|light amyloid chain (seen in which type of amyloidosis: systemic or local?)
|heavy amyloid chain deposition in which type of amyloidosis (systemic or local)? ||localized ie heart amyloidosis, kidney|
|hib vaccine mixed with what toxoid component,
what is its formal name,
and why is this done? ||diptheria toxiod or tetanus toxoid -> T cell stimulation -> further b cell stimulation by T cells -> Class switching from IgM to IgG -> much better immunity.
protein is PRP polyribiose ribitol phosphate
|HIb vaccine schedule? ||2, 4, 6, 15 months
|kawasaki disease is associated with which cardiac complication ||myocardial infarction, and coronary artery aneurysm |
|pulmonary hypertension seen most commonly in which autoimmune disease? ||Scleroderma|
|which systemic vasculitis causes hepatic necrosis ||PAN (also viral hepatitis)|
|MHC 1 consists of ? ||B2 Microglobulin and HEAVY chain only -
heavy chain is highly polymorphic|
|MHC 2 consists of ? ||alpha and beta polypeptides|
|Argatroban use, montior with, MOA? ||use:anticoagulant, use in thrombosis in pts with Heparin Induced Thrombocytopenia, and percutaneous coronary intervention.
MOA : direct thrombin inhibitor.
DOES NOT REQUIRE ANTITHROMBIN III, therefore used in patients already on heparin. |
|most common cause of thrombocytopenia in hospitalized patients is? ||heparin (mostly with unfractioned heparin ,vs low molecular weight heparin>)
|how to treat thrombosis in Heparin Induced Thrombocytopenia patients? ||argatroban (direct thrombin active site inhibitor), lepirudin , hirudin, bivaliruden|
|all normal females are mosaic at x chromosome : T or F - What is the Mechanism and the microscopic result ||True - all females with 46 xx - one x is deactivated by LYONIZATION - randomly -
makes all normal females MOSAIC.
Mechanism is formation of heterochromatin (low transcriptional activity) and BARR BODY is result. |
|euchromatin formed by ?
Heterochromatin formed by ? (MOA) ||Euchromatin is HISTONE ACETYLATION -> high transcriptional activity
Heterochromatin - condensed via methylation - > CYTOSINE -> MethylCYTOSINE.
|standard rx for CHF and one extra drug which improves overal survivability - what is the mechanism of this - (low or high dose required) ||Standard rx = Ace Inhibitor, Diuretic (not spiro) and Digoxin.
extra drug is spiro /epleronone -> blocks ALD - (aldosterone increases cardiac remodeling -> fibrosis) |
|process and intracellular locations of insulin production ||starts in beta pancreatic cell -
proinsulin forms -> RER - > packaged and sent to GOGI apparatus
here, convertase cleaves it into
1)insulin 2)C-peptide 3) 2 pairs of BASIC amino acids.
C pep+insulin packed secretory granules- >equimolar release |
|common presentations of neurofibromatosis type 1 , genetic defect and chromosome,
tumor, and origin ||vonrecklinghausen disease - NF1 , ch 17
cafe au lait spots, rubbery tumors -> neurofibromas -> tumor of schwann cells -> neuroectoderm. buttonholing |
|Ectoderm develops into? ||skin, appendages, nasal, oral epithelium, anal to dentate line, lens and cornea|
|Neuroectoderm gives rise to? ||all neurons, neurohypophysis, retina, pineal gland, pregant autonomic fibers, astrocytes, ependymal cells, choroid plexus.|
|mesoderm - dived into? gives rise to? ||3 sections - para-axial, intermediate, lateral
leads to muscles bones blood genitals, dermis and most organs - not liver, pancreas, lungs, outpouching of gut, or thyroid (base of tongue)|
|endoderm - ||thyroid (base of tongue), epithelial lining of GIT, lung, urethra, ear.
also LIVER, PANCREAS, LUNG becuase these are all outpouching of privitive gut tube|
|Notocord- ||regreses but leaves vestigal structure nucleus pulposus (vertebrae form form paraaxia mesoderm)|
|organophosphorous poisoning - symptoms and MOA ||MOA - anticholinestrase at both N and M rec.
symptoms are : DUMBELS
d-diarrhea&diaphroesis, U-urination, M-miosis (pupillary sphincter), B-bronchospasam and + secretions, E - emesis, L - lacrimation and S - salivation|
|type 1, alpha error ||reject null when null is really true
ie - seeing a difference when no differece is there - convicting an innocent man of being guilty. alpha is the probability of this happening. depends on p=0.05 ~ 5% chance that you will get thiserror type 1 = b/(b+d)|
|type 2, beta ||fail to reject null but null was truly false.
ie seeing NO effect, but there was one. declaring a guilty man innocent.
beta is the probability - set at 0.2 there 80% chance of rejecting null when null is truly false. |
|how is trypsinogen activated? where? what ezyme? ||trypsinogen from pancreas -> trypsin by
duodenal epithelial cells - enteropeptidase.
trypsin -> breaks down protein to dipeptide and AA's. activates other proteases ie carboxypeptidase, elastase, and chymotrypsin.|
|what enzyme allows usage of glycerol in liver? ||glycerol kinase - TG is broken down into Glycerol and Fatty Acid
FA -> beta oxid or ketogenesis, Glycerol -> GLYCEROL KINASE (liver only) to glycerol3p->Dhap->glycolysis/neogenesis.
TG stored in adipose-mtblz to FFA+glycerol by hormone sensitive lipase|
|hepatic angiosarcoma -
true origin cells? ||polyvinyl chloride (plastic), thorotrast (radioisotope), arsenic (pesticide)
express CD 31 AKA PECAM 1 (seen on vascular endothelial cells for WBC migration - thus true origin is vascular endothelial cells|
|injury to axillary nerve caused by what injury and what symptoms ? ||anterior dislocation on shoulder -> paralysis of deltoid and teres minor and sensory loss to upper lateral arm.|
|violent stretch between head and shoulder causes? symptoms? ||upper trunk -> erb duchenne palsy -> adducted, pronated extended elbow.|
|mastectomy or any axillary surgery - damaged nerve? symptoms? ||long thoracic nerve -> serratus anterior paralysis -> winging scapula and inability to abduct arm beyond 90 degrees.|
|hepatic angiosarcoma -
true origin cells? ||polyvinyl chloride (plastic), thorotrast (radioisotope), arsenic (pesticide)
express CD 31 AKA PECAM 1 (seen on vascular endothelial cells for WBC migration - thus true origin is vascular endothelial cells|
|injury to axillary nerve caused by what injury and what symptoms ? ||anterior dislocation on shoulder -> paralysis of deltoid and teres minor and sensory loss to upper lateral arm.|
|violent stretch between head and shoulder causes? symptoms? ||upper trunk -> erb duchenne palsy -> adducted, pronated extended elbow.|
|mastectomy or any axillary surgery - damaged nerve? symptoms? ||long thoracic nerve -> serratus anterior paralysis -> winging scapula and inability to abduct arm beyond 90 degrees.|
|defective CFTR transmembrane protein gating of Cystic Fibrosis? ||ATP-gated! pumps cl- out of epithelial cells against  gradient using ATP - drawing water and Na along with it - hydrating and promoting secretion (airways, gut, pancreas)
|why high chlordie in sweat of Cystic Fibrosis patients? ||in eccrine sweat glands, sweat starts as isotonic to plasma but in transportation, salt is removed by CFTR but the defect prevents this thus high sweat chloride - good screening test |
|antibiotics causing hearing and vestibular function loss ||aminoglycosides and vancomycin
rarely also cause neuromuscilar blockade (aminoglycosides)|
|hepatic function monitoring required with whhich anti TB drugs ||iNH, rifampin, pyrazinamide|
|complete blood count monitoring with which antibiotics? ||chloramphenicol, dapsone, TMPSMX
|most renal toxic AB's? ||AM-B and aminoglycosides -> ATN|
|optic neuritis, scotoma, colorblindness, decrease visual acuity caused by which AB? ||ethambutol|
|forcarnet - details about it - activation?
administration. ||pyrophosphate analog, no activation required .
inhibits DNA pol in HERPES and RTase in HIV. IV admin, rx advanced Advanced sids w/ acyclovir resistant herpes and gancyclovir resistnt CMV|
|Acyclovir MOA ||nucleoside analog.activated intracellularly to MONOPHOSPHATE by viral THYMIDINE KINASE, convert monophosphate THEN is converted to TRIphosphate by CELLULAR KINASE - which is active - inhibits herpesvirus DNA polymerase mediated replication .|
|Lamivudine ||cytosine analog -NRTI - must phosphorylate by cellular kinase. inhibits HIV rev transcription through viral DNA CHAIN TERMINATION.|
|Saquinavir ||no intracelluar activation required- is a PROTEASE INHIBITOR binds catalytic site of HIV ASPARTIC PROTEASE - prevents cleavage of polyprotein precursors necessary for generation of functional viral proteins. |
|Gancyclovir ||guianine nucleoside analog - structurally simiar to acyclovir. requires conversion to monophosphate - has GREATER ACTIVITY THAN ACYCLOVIR VS CMV Dna Polymerase.|
|Amantadine - ||antiviral agent - no activation - bind and INHIBITS M2 ion channel protein of Influenza A, blocking viral UNCOATING after host cell endocytosis. |
|oseltamivir ||no activation required, sialic acid analogue - inhibits influenza A and B (vs amantadine ONLY A)|
|platelets release what factors to cause proliferation of atherosclerotic plaques ||PDGF, TGF-b, SMC.
these stimulate smooth muscle cell migration from media into intima as well as SMC proliferation. |
|beta lactamase producing bacteria list
how to make penicillins work against these? ||S.aureus, H.influenza, bacteroides, gram - bactera.
rx with sulbactam, tazobactam, clavulinic acid. |
|CEA -> ?
AFP -> ?
CA-125 -> ||AFP - liver DZ, cirrhosis, yolk sac tumor
CA-125 - not effective screener - ovarian ca, endometrial, lung, breast, pancreas ca - benign also ie endometriosis , PID, cirrhosis.
Acid Phosphatase - prostate esp osteoclastic bone activity.
CEA - ca colon|
|alzheimers MRI what is atrophied ON MRI || hippocampal atrophy is first to be seen and better seen on MRI - later its generalized cortical atrophy|
|Idiopathic Membranous Nephropathy - common in what group, exactly pathophysiology ||elderly - find serum AB's vs PLA2R phospholipase A2 Receptor IgG4 -> immune complex deposition. PLA2R mostly found in GLOMERULAR Podocytes - is the major antigen in IDIOPATHIC memb glom neph. |
|Mixed cryoglobulinemia ? assx what disease, what Ig? , what thickens? ||HEP C - IgM deposition in GLOMERULUS -> BM thickens + cellular proliferation. |
|Mesothelioma vs adenoca lung ||Hemorragic pleural effusion, nodular or smooth pleural thickening on xray - lung parenchyma intact - EM gold standard - tumor cells with numberous long slender microvilli with abundant TONOFILAMENTS (vs adenoca has short, plump microvilli)|
|ALL - T all vs B all - presentation and immunohistochemical staining difference? ||IHC - both Tdt - B ALL - 10, 19, 20
T-all 2, 3, 4, 5, 7, 8
T all presents as mediastianl mass -> esophageal compression and dyphagia, stridor, dyspnea. - more RESP symptoms. |
|some viruses are polycistronic - entire mrna transcript gets translated and then the proteins are cleaved by proteases to make functional proteins. which viruses have this type of replication? name a virus like this ||single stranded, positive sense, linear
non-segmented RNA virus, SS+ - these have genome that is independently infective if transferred into a host cell and that functions as its own mRNA.
ECHOVIRUS has a SS+ RNA genome so exhibits this characteristic.|
|pleura innervation , pain felt where? ||pleura = visceral (lung) and parietal (other)
visceral-pain felt by phrenic, but referred to c3-c5 area, on neck and shoulder. (diaphramatic, mediastinal and visceral pleura)
parietal pleura -> somatic sensory nerves- capable of sharp localized pain. |
|99mmTc pertechnetate scan detecs? ||gastric mucosa - thus Meckel's Diverticulum.
(right lower abdominal area)|
|Meckels Diverticulum - failure to obliterate what?
presentation? ||omphalomesenteric duct.
Lower GIT Bleeding in young patient due to acid secretion by ectopic gastric mucosa in diverticulum. -> Melena, and right lower quadrant pain. looks like appendicitis. red currant jelly stool.|
|failure of veneral and dorsal pancreatic buds to FUSE leads to? ||pancreas divisum (asymptomatic, incidental finding)|
|Hindgut is part of primitive gut, gives rise to distal 1/3 transverse colon, descending colon, rectum and upper part of anal canal.
failure of proper descent leads to ?
Descends along what artery? ||anal agenesis or imperforate anus
DESCENDS along Inferior Mesenteric Artery|
|abnormal midgut ROTATION AROUND ________ artery, leads to ___________?
pathophys? ||superior mesenteric artery -
intestinal MALROTATION -
fixed fibrous adhesive bands -> intestinal obstruction. |
|Dihydrotestosterone comes from what precursor and what enzyme and results in development of what in male embryo, and adult ||testosterone -> 5 alpha hydroxylase -> DHT
P P S - penis prostate scrotum.
facial hair, baldness, muscle mass, libido.
|2 types of 5 alpha reductase.
type 1 in postpubescent SKIN
type 2 in GENITALS
deficiency of type 2 -> diminished conversion of testosteroneto DHT in tissues . if male fetus has this defect, internal genitalia normal development under testosterone but? ||external does not develop due to low DHT -> pseudohermaphrodism. genitalia at birth is either small penis + hypospadias, or female type. may be raised as female until puberty then masculinization and testis descent occurs. |
|Pancoast tumors cause which syndromes ||Horner Syndrome, SVC syndrome, Arm weakness,
arm paresthesia, and haorsness - due to invasion of paravertebral sympathetic chain.
|Meissners plexus , layer of GIT and other name ||Meissners Submucosa|
|Auerbach plexus ||muscular layer , myentric plexus. |
|Corticosteroid rx can increase which cell type and why? ||neutrophils increase due to demargination (release of all neutrophils which were attached to vessel walls)
Note - lymphocytes are decreased t>b, within minutes by redistributing them into spleen, bone marry and lymph nodes.|
|what is + trendelenberg test and why does it happen - muscles and nerves involved? ||when patient walks away from examiner, hip dips to the opposite side - ie pt stands on right leg, hip sinks to left side. due to paralysis of gluteus medius and minimus - supplied by superior gluteal nerve|
|obturator nerve injury causes? ||weak thigh adduction and medial thigh sensory loss|
|sciatic nerve innervates which muscle group -- except ? ||innervates all hamstrings except SHORT HEAD of biceps femoris.|
|thiazide diuretics cauase what HYPER problems and what HYPO problems ||HYPER - hyperuricemia, calcemia, glycemia, lipidemia (INCREASE CHOLESTEROL and LDL - BAD IN HYPERTENSIVES because trying to lower cardiac risk)
HYPO problems:hypokalemia, hypotension-reduce BP via blood volume and decrease vascular resistance.hyponatremi|
|drugs causing DISULFIRAM like rxn ||disulfiram, metronidazole, cephalosporins,chloramphenicol, ritonavir, sulfonylureas (chlorpropamide etc)|
|neurtal protesases (elastase) come from what cells in lung.
how is their activity counterbalanced?
what diseases result from overactivity/under balace? ||neutrophils (azurophil/primary granules) and alveolar macrophages/
alpha 1 antitrypsin in SERUM
centriacinar and panacinar emphysema.|
|lung transplant patient comes with pneumonia - what virus is implicated commonly and what does the histo look like ||CMV - enveloped double stranded, DNA Virus
-intranuclear and cytoplasmic inclusion bodies.
|bilateral acoustic neuromas are associated with what disease - chromosomes? ||Neurofibromatosis type 2 - autosomal dominant, NF2 gene on ch 22.|
|Strep Pyogenes - classification and major virulence factor? ||Group A, Beta hemolytic - B-BrAs -
bacitracin- group B resistant (S.agalactiae)
group A sensitive (s.pyogenes.)
M-protein is important virulence factor.
it is antiphagocytic, anticomplement, cytotoxic to neutrophils AND mediates bacterial attachment|
|Streptolysin O - oxygen labile, extracelular protein from S.pyogenes - what does it do? ||lyses RBC (b-hemolytic) and PMN's
is the antigen responsble for AB's - ASO.
Does NOT convey phagocytosis resitance.
|DNase - enzyme in Streptococcus - what does it do> ||depolymerizes viscous DNA in Pus and disintegrates PMN's allowing the bactera to move freely in dissue.
|Streptokinase is an extracellular enzyme - catalyzes what? why? ||plasminogen ---> Plasmin -> fibrin digestion facilitating spread of streptococci in infected tissue - used as a thrombolytic.
|Aspirin binds what enzymes?
WHich enzyme is always present in cells, and which is inducible?
when is it inducible?
what is the molecular of weight of the inducible enzyme -
contrast with INFLIXIMAB ||COX 1 & COX 2 - Cox 1 is always expressed but 2 is undetected except in inflammation. COX 2 is INDUCIBLE - blocked by NSAIDS - molecular wt is 72kD.
Infliximab also binds to an inflammatory protein but COX 2 is an ENZYME but TNF is a PROTEIN.|
|Infliximab targets what?,
used for what dieases? ||TNF alpha
crohns, Rheumatoid arthritis
toxicity is REACTIVATION OF LATENT TB|
|Trastuzumab herceptin ||monoclonal AB vs HER2 (erb-b2) kills breast cancer cells which overexpress her2 - use in metastatic breast cancer.
|Imatinib (gleevec) ||vs philadelphia chromosome brc abl tyrosine kiase inhibitor
use in CML, GI stromal tumors.
|Rituximab: ||monoclonal ABs vs CD20 found in b cell neoplams - use in NHL, Rheumatoid arthritis w/ Methotrexate.|
|omalizumab used in which patients ||severe asthma with high IgE, or triggered by special allergic trigger -
is AB vs IgE - useful in patients resistnat to steroids or trying to get off steroid.|
|penicillins inhibit which enzyme.
what does this enzyme do?
structural analog of ? ||transpeptidase enzyme - catalyzes final crosslink step in peptidoglycan cell wall formation - joining of the amino acid in 3rd pos of peptidoglycan to terminal d ala-d ala , penicillins are structural analogs of D-ala-D-ala. inhibits cell wall synth.|
|most important test to work up cushings syndrome? ||dexamethasone suppression test.
normal: suppress ACTH+cortisol
if ACTH high, and cortisol is <50% suppressed -> Pituitary adenoma.
if ACTH high but no suppression of cortisol, ->ectopic ACTH
low baseline ACTH and no suppression -> primary adrenal tum|
|ACTH stimulation test is used in? ||adrenocortical deficiency. |
|antiepileptic drugs using NA channels ||phenytoin, carbamezapine, valproic acid.|
side effects ||calcium T type channels blocked.
EFGH + stevens johnson
Ethosuximide Fatigue GI upset Headache |
|phenytoin side effects ||nystagmus, diplopia, ataxia, sedation, gingival hyperplasia, hirsuitism, megaloblastic anemia, fetal Hydantoin syndrome, SLE like syndrome, inducer of P450|
|carbamezapine side effects ||dipolpia, ataxia, blood dyscrasia,s - agranulocytosis, aplaistic anemia, liver toxicity, teratogenic, induce p450, siadh, SJS aka exfoliative dermatitis|
|Valproic acid side effects - ||GI disress, hepatotoxic *measure LFT*
NEURAL TUBE DEFECTS SPINA BIFIDA|
|dexrazoxane? ||iron chelating agent prevents anthracycline induced doxorubicin cardiotoxicity.|
|amifostine? ||cytoprotective free radical scavenger agent used to decrease cuymuative nephrotoxicity associated with platinum contaiing alkylating chemotherapeutics|
|mesna used to block hemorragic cystis caused by what? ||cyclophosphamide or ifosfamide - blocks toxicity to uroepithelial cells caused by ACREOLIN which is the metabolic product formed in KIDNEY |
|how does TNF a, catecholamines, glucocorticoids and glucagon and high free fatty acids induce insulin resistance? ||activation of SERINE KINASES - this leads to phosphorylation of Insulin Receptor Serine 1 IRS1 serine residues. this inhibits IRS1 tyrosine phosphorylation by insulin (of beta subunits). phospohorylation of THREONINE resides do the same.|
|Serine and Threonine Residue phosphorylation by SERINE kinases leads to what?? ||INSULIN RESISTANCE - tNFa, catecholamines, glucocorticoids, glucagon, high FFA.|
|Pagets disease of bone - what is the progress of disease ||first - osteoCLAST breakdown bone. then osteoblasts regenerate it.
net result is increased bone resorption and formation of abnormal bone. new collagen deposits haphazardly(not linear) -> mosaic pattern w/ cement lines represent previous areas of reabx.|
treatment? ||90% metabolized in liver by sulfatin and flucuronide conjugation, 10% by p450 enzymes ->NAPQI which is toxic and dangerous. at low doses, NAPQI is metabolzed by hepatic glutathione . if toxicity, then glutathione exhausted -> centrilobular necrosis.|
|rx acetaminophen poisoning. ||N acetyl Cysteine which is a sulfylhydryl donor, glutathione substitute in liver. enhances non toxic sulfation elimination of acetaminophen. |
|vagal stimulation on lungs causes what ?
what receptors mediate this?
where are the receptors located in the histology
how does this affect work of breathing? ||bronchial smooth muscle contraction,
and increase mucus secretion
mediated by m3 receptors
this overall INCREASES WORK OF BREATHING|
|difference between wallerian degeneration and axonal reaction? timeframes? ||wallerian degen is in SEVERED part of axon distal to injury - swelling, irregularity, destruction by schwann cells and macrophages. de3generatoin of PROXYMAL segment occurs to node of ranvier.|
|what happens to proxymal axonal part of severed axon injury? ||axonal reaction 0 cellular edema in cell body, swoled , round, nucleus displaces to periphery of cell and dispersion of NISSIL substance - with fine , granular changes -> central chromatolysis. 1 day -12 days after injury.|
|degenerative disesae of neurons characterized by what on histology/ ||reactive glial changes - neuronal loss is selective - affects well definded neuronal groups - alz, picks, huntingtons etc|
|which cardiac drugs slow AV conduction> ||digoxin, CCHB's B-blockers |
|hyper parathyroid bone changes? ||subperiosteal thinning on medial side of 2 and 3 phalanxes of hand and salt and pepper appearance of the skull. appendicular skeleton is mostly involved (pectoral, pelvic and limbs)|
|hyperparathyroid presentation? ||bone loss, renal stones, gastrointestinal
GIT ulcers and psychiatric disorders.
85% parathyroid ademona 15% hyperplasia|
|vitamin D deficiency bone changes? ||unmineralized osteoid with widened osteoid seams. low bone mineral density, high fracture risk|
|trabecular thinning with fewer interconnections is characteristic of? ||osteoporosis
total bone mass is decreased and normal bone architecture is disrupted.|
|mosaic pattern of lamellar bone with irregular sections of lamellar bone with cement lines (representing previous resorption) ? ||Pagets DZ bone|
|Osteopetrosis histological bone changes? ||marble bone disease - decreased osteoclastic bone resorption - persistence of primary unmineralized spongiosa in medullary canals . in NORMAL people, the bone marrow replaces spongiosa. |
|metalloproteinases are enzymes secreted from macrophages - what are they notorious for ? ||remodeling the fibrous cap of atherosclerotic plaques, making MI more likely.|
|embolus in which artery produces hemorragic infarct in lungs and which produce wedge shaped infarcts? ||wedge shaped - peripheral branches of pulmonary artery.
other infarcts cause hemorrhagic infarcts because of dual blood supply from pulmonary and bronchial arteries.
|brown gallbladder pigment stones caused by? ||infections of biliary tract|
|black gallbladder stones caused by? ||intravscular hemolysis|
|cysteine stones develop dude to? ||autosomal recessive transmembrane cystine transport in intestine and kidney/.|
|uric acid stones ||psoriasis, leukemia.|
|gallbladder hypomotility leads to ? ||biliary sludge - contains cholesterol monohydrate crystals, calcium bilirubinate, mucus .
pregnancy, rapid wt loss, long use of TPN or OCTREOTIDE and high spinal cord injuries. |
|paramesonephric ducts (mullerian ducts) become? inhibited by?
stage of development? ||beome uterine tubes, uterus, cervix and upper vagina.
inhibited in males by Mullerian Inhibiting Factor MIF from SERTOLI CELLS
DUCTAL stage develop under ESTROGEN from mother|
|Wolffian Ducts - Mesonephric Ducts ||become epididymis , ductus deferns, seiminal vesicles.|
|GENITAL STAGE -
genital tubercle - ?
urogenital folds - ?
Genital Swellings - ?
Urogenital Sinus - ? ||Genital Tubercle -> glans penis, clitoris
Urogenital folds -? venteral aspect penis, labia minora
Genital Swellings - scrotum and labia majora.
Urogenital Sinus -> bladder, urethra, prostate, bulbourethral glands , or lower vagina and bartholin glands.|
|3 stages of genital development in embryo? ||GONADAL STAGE, DUCTAL STAGE, GENITAL STAGE|
|primary biliary cirrhosis has what immunological markers? ||Anti Mitochondrial AB(vs pyruvate dehydrogenase complex E2),ANA=prognostic anti-actin Ab,and Anti-centromere antibody (prognostic for portal HTN)Interlobar bile duct dmg+intra epithelial wbc+periductal granuloma w/ epitheloid cells
|rx primary biliary cirrhosis ||use GGT test
check gluten sensitivity (differentiate pagets dz)
rx ursodeoxycholic acid + cholestyramine, vit ADEK and Calcium.|
|Primary sclerosing cholangitis ||image ducts w/ MRCP - beading of intra+extrahepatic bile ducts. P ANCA+ assx 80% churg strauss, ulcerative colotis, HLA dr3, HLA B8|
|alkaline phosphatase also comes from (other than osteoclastic bone activity) > ||bile duct cells -> obstructive jaundice high ALP|
|Budd Chiari Syndrome - occlusion of IVC or hepatic veins with centrilobular congestion and necrosis(acetaminophen tox) leading to congestive liver disease -> hepatomegaly, ascites, abd pain, liver failure. varicies, abd and back veins, ABSENT JVD ||cuased by the following conditions - hypercoagulability (polycythemia, OCP, pregnancy) Hepatocellular carcinoma.|
|differentiate budd chiari vs rt heart failure - ||HIGH JVD in RT HEART|
|alcoholic hepatitis - liver finidngs? ||hepatitis - swollen necrotic hepatocytes with neutrophilic infiltration . Mallory odies (intracytoplasmic eosinophilic inclusions) AST>ALT ration >1.5|
|alcoholic cirrhosis irreversible micronodular, shrunken, hobnail, sclerosis around CENTRAL VEIN = ZONE III, liver failure, portal HTN, hepatocellular CA |
|methacholine ||muscarinc cholinergic agonist |
|scopolamine is ||antagonist of muscarinic cholinergic receptrs used for motion sickness|
|phenoxybenzamine is a non selective ? ||alpha adrenergic antagonist used in rx pheochromocytoma. |
|isoproterenol is ||nonspecific beta adrenergic agonist - alpha = beta ? CHECK
used in asthmatics - bronchodilator|
|ipratopium bromide ||like scopolamine - antagonist of muscarinic cholinergic receptors.|
|all betablockers and drugs that decrease av conduction in heart increase WHAT INTERVAL ||PR interval ONLY|
|type 3 hypersensitivity rxn example SERUM SICKNESS caused by what common antibiotic? serum findings? ||Trimethoprim/sulfonamides. - fever, skin rash, itching, arthralgia, glom-neph, lymphadenopathy - 5-10 days pst exposure.
immune complex deposits -> compliment activation -> HYPOCOMPLEMNTEMiA low serum c3|
|Sulfonamides cause what kinds of hypersensitivity rxns/ ||type 3 - serum sickness 5-10 days after
type 2 - thrombocytopenia|
|transcription factors and DNA enhancers bind to what to increase TRANSCRIPTION - how many bases upstream? to the 5' or 3' end?
what enzyme binds this area?
Pro or Eukaryote? ||Promotor regions - two of importance in EUKARYOTES - CAAT box 60-80 bases upstream (5') and TATA Box 25 bases upstream. enzyme is RNA POLYMERASE 2|
|rubella caused by what virus? what lymphnodes are classically involved ||TOGAVIRUS - german measles - rubella -
post auricular and occipital nodes|
|rubeola caused by what virus? ||paramyxovirus|
|appetite suppressants like fenfluramine, dexfenfluramine and phentermine used for 3 months or more cause what? ||secondary pulmonary hypertension -> dyspnea weakness, dizziness, syncope) -- eventually becomes cor pulmonale so RV hypertrophy.|
|causes of bilateral upper lobe pulmonary fibrosis ||coal worker, silicosis, tuberculosis, histoplasmosis, sarcoidosis, allergic bronchopulmonary aspergillosis, ankylosing spondylitis.|
|tzanck smeark ||herpes mostly HSV 2
|side effects of SSRI's like sertaline.
contrast with side effect of TCA's (imipramine, doxepin, amitriptyline, clomipramine. ||SSRI - sexual dysfunction most common
TCA - urinary retention (anticholinergic effect, worse in BPH) arrhythmia rare but feared -quinidine like, prolnged QRS and QT
seizures, orthostatic hypotension a1 antagonism, sedation (histamine block)|
|most common cause of aseptic viral meningitis? ||enterovirus - coxsackie, echo, polio.
polio can cause LMN and meningitis.|
|sexually transmitted viruses -> meningitis ||HIV HSV1 2 EBV CMV|
|resp secretion viruses -> meningitis? ||varicella, mumps, adenovirus.|
|Arboviruses - insect bites -> meningitis
examples? ||togavirus (east, west and venezuelan equine encephalitis), flaviviridae (st lous encephalitis)
bunyaviridae (california encephalitis)|
|lactase deficient patients have what findings ? ||increased stood osmotic gap, increased breath hydrogen content, decreased stool pH.|
|Stool osmotic gap - number? constituents? diseases? ||maximum is 290 mOsm/kg (same as blood) normally its much lower closer to 50.
constituents are mostly Sodium and Potassium. if electrolytes are the main component, ~50mOsm. if poorly absorbed substances, then osmotic gap goes up ~100mOSM ie Lactose intol.|
|lactose intolerance test- describe. ||50g lactose w/ blood level measured at 0 60 120 min. if blood glucose increase <20 mg/dl and there are symptoms (bloating, flatulence diarrhea etc) then the dx is confirmed.
|d xylose test? what it is and why ||d-xylose is a monosaccharide. its abx does not require pancreatic enzymes - not affected by pancreatic insufficiency or pancreatectomy. orad admin fixed dose used to differentiate MALABSORPTION Gi vs pancreat. |
|Apocrine sweat glands ||apocrine (dermis and subcutaneous fat of breast areolae, axillae, genitals) membrane bound sweat vesicles into hair follices (not directly to skin surface. adrenergic fibers of SYMP system - not functional until puberty. smell comes from bacterial action.|
|Holocrine glands ? ||associated with sebaceous glands. holocrine secretion entails discharge of entire secretory CELLS that undergo breakdown to release secretory product. |
|eccrine / Merocrine glands ||skin of most of the body not lips, glans penis etc. secrete watery na cl solution directly to skin surface. |
|paracrine sweat glandsq ||similar to endocrine glands by secretions reach target cells by DIFFUSION through EXTRACELLULAR SPACE|
|how does heptatitis B virus increase chance of hepatocellular carcinoma? ||2 mechanisms. 1 - incorporation of HBV DNA into host genome causes chronic liver cell injury and regenerative hyperplasia increasing mutational probablity. second, HBV codes for HBx protein activated MULTIPLE GROWTH PROMOTING GENES and p53 inactivation.|
|urticaria - 2 types what are they, MOA ||1 antigen induced>IgE>mast cell
2 NO IgE - direct mast cell stim by opiates, antibiotics, radiographic contrast media. BOTH cause microvasculature hyperpermeability , resolve hours, days weeks. may coalesce>annular, linear, acriform.|
|HISTOLOGY of urticaria ||mild superficial infiltrate composed of mononuclear cells and some EOSINOPHILS around dermal VENULES. Superficially - COLLAGEN BUNDLES PARTED by dermal edema and lymphatic channels dilate with TRANSUDATE. No epidermal changes. |
|acanthosis ? ||increased thickness in stratum SPINOSUM (prickle cell layer) between granular cell layer and basal layer. Psoriasis - acanthosis.|
|spongiosis ||INTERcelluar epidermal edema histo:increase width of space between cells. assx spongiotic dermatitis which includes eczema.|
|acantholysis ||loss of cohesion between keratinocytes of epidermis or adnexal structures. assx spongiotic dermatitis, incl eczema.
|dyskeratosis ||abnomal premature keratinization of keratinocytes . dyskeratotic cells are EOSINIPHILIC and have small basophilic nuclear remnant. dyskeratosis found in Squamous Cell Ca. |
|which colon cancer type involves PROTO Oncoges, ANTI oncogenes, and DNA Mismatch repair genes?
how many of these dna mismatch repair genes exist. names?> ||SPORADIC COLON CA=PROTO/ANTI oncogenes APC, k-ras, p53 DCC.Polyp type. LEFT SIDE, older than 50
HNPCC involves DNA mismatch repair genes MLH1 MSH2 MSH6 PMS2. NO POLYPS, RIGHT SIDE, younger than 50|
|lynch 1 ||family predisposition to COLON ADENOCARCINOMA|
|lynch 2 ||predisposition to colon cancer with similar features to lunch 1, AND extraintestinal cancers, endometrial, ovarian, stomach, pancreas, urothelial.|
|APC gene is responsible for intercellular ATTACHMENT. mutation leads to formation of? ||polyps from norml mucosa. APC mutation detected in most sporadic colon cancers and all familial .|
|Polymyalgia Rheumatica is associated with what disease in more than 50% cases
neck torso shoulder pelvic girdle pain and morning stiffness, with fever fatigue and weight loss ||temporal arteririts / GCA|
|protein C - ||vitamin K dpenedent factor , syth in liver, anticoagulant degrading factor Va and VIIIa|
|Factor XII hageman - synth in liver, activated by? triggers? ||endothelial injury. triggers intrinsic pathway|
|Urokinase is thrombolytic for MI and PE, MOA? ||plasminogen to plasmin, which degrades fibrinogen to fibrin and FDP.|
|to decrease GFR by 50 %, what % of renal glomeruli need to be involved? ||75%
septic emboli from endocardial vegetations CANNOT DO THIS MUCH DAMAGE, more likely to be IMMUNE COMPLEX disease|
|nonpolar hydrophobic AA's? ||valine alanine isoleucine, methionine, phenylalanine|
|where are nonpolar hydrophobic AA's like alanine, valine isoleucine , methionine, phenylalanine located and for what? ||interiorly on globular proteins where they are shielded from direct contact with water. classic plasma membrane spanning proteins are executors for glycoprotein hormones TSH.LH.FSH-gProt-coupled memb bound recptrs|
|why is Creatine Kinase elevated in hypothyroidism/ ||muscle biopsy in hypothyroid shows - pale fibers with decreased striation and deposition of mucinous material. atrophy of type 2 fibers .
|other causes of elevated CPK are Statins, autoimmune polymiositis dermatomyositis, muscular dystrophy like duchenne |
|hypertrophic cardiomyopathy - genetics? genes involved? how many cases are genetic? defect? ||nearly ALL cases due to Auto DOM mutations
in CARDIAC SARCOMERE PROTEIN. MOST COMM IS BETA-MYOSIN HEAVY CHAIN.
single point MISSENSE mutation in beta myosin heavy chain MHC (50%), Myosin binding protein C (25%) or Tropomyosin (5%) |
|Dilated cardiomyopathy - how many cases are genetic? mutation? ||1/3 cases are genetic, AUTO DOM, cardiac myocyte CYTOSKELETAL PROTEINS DYSTROPHIN
recall dystrophin mutation also seen in duchenne and becker muscular dystrophy.|
|what % of erythroid precursors are destroyed in b12 / folic acid deficiency? is the bone marrow hyper or hypo cellular?
can neuropathy of b12 occur in absence of anemia? - which senses / tracts go first.
MCV >? , other causes of MCV ? ||hypercellular marrow, 90% erythroid precursors are destroyed before release. MCV >80 usually around 100. >110 is highly indicative of b12/folate def. other causes: liver dz hypothyroid, alcoholism. >6 lobes neutrophil. degen post and lateral column|
|mannitol - what kind of diuretic? where does it act in kidney? common s/e? serious s/e? use? ||osmotic diuresis - used to decrease ICT
act in PROX TUBULE AND LOOP OF HENLE. s/e volume deprletion and hypernatremia
pulm edema, and RISE IN PLASMA VOLUME -> triggers viscious cycle>release of K and h20 release from celle>rise>hypoNA met acid, hypoK.|
|bumetanide is a loop diuretic - inhibits nak2cl in asc loh. blocks na cl transport so increases their secretion.
|osteoclasts come from what cell lineage?
how are they stimulated and controled?
relationship b/w osteoblasts and clasts ||clasts are from monocyte phagocytic cells. they are controlled by MCSF and RANK L which come from osteoblasts. interaction b/w rankL and clasts is inhibited by BLAST secreted osteoprotegrin OPG. bone turnover + if rankL + and OPG -.|
|Arsenic Poisoning - MOA? Rx? ||blocks Sulfhyldryl groups on multiple enzymes -> cellular metabolism shut down -> GIT symptoms + garlic breath. USE DIMERCAPROL or penicillamine (also for mercury, copper, gold) displases arsenic form SH groups.
|ulcerative colotis ||rectum always involved, imflammation is limited to mucosa and submucosa only, mucosal damage is continuous. complications megacolon -> perforation. high risk of adenoca colon.|
|crohns disease ||noncaseating granuloma, perianal fistulae, transmural inflammation|
|most common CNS metastasis comes from? ||lung , breast and melanoma|
|melanocytes are what embryological cell lineage? ||neural crest cells. -
|melanomas metastasize commonly to ? ||brain, GIT, bone, liver and lungs.|
|surface ectoderm - ||epidermis, appendages, mammary glands (modified sweat glands), lens , adenohypophysis.|
|irregularly irregular tachyarrhyphmia in conscious patient? ||atrial fibrillation - most common chronic arrhythmia. ABSENT P WAVES, irregularly spaced ventricular contractions=(variable R R interval)|
|QT interval ventricular depolarizaiton and repolarization . QT prolonged in ||ventricular tachycardia aka torsades de pointes - heart rate is usually regular.|
|high QRS voltags in precordial leads ||ventricular htphy - usually from untreated hypertension. does not usually cause irregular rhythm|
|QRS prolonged interval - ||ventricular dyssynchrony or slowed intraventricular impulse conduction. BBB - regular HR. |
|b6 cofactor in ||transamination and decarboxylation of aminoacids for gluconeogenesis and other processes.|
|b1 thiamine cofactor for ||transketolase, alphaketoglutarate dehydrogenase and pyruvate dehydrogenase|
|b2 Riboflavin ||dehydrogenases using FMN and FAD|
|b3 ||dehydrogenases using NAD and NADP
|biotin ||carboxylases - 4 of them.
pyrivate carboxylasse, acetyl coa carboxylase, propionyl coa carboxylase and 3 methylcrotonyl coa carboxylase.|
|blood transfusion - relatinship with calcium and potassium? ||whole blood is mixed with citrate anticoagulant before storage. this CHELATES serum CALCIUM > HYPOCALCEMIA (normal 8-10) -> PARESTHESIA, tingling toes and fingers.
stored blood cells lose intracelular K -> hyperkalemia |
|HIV1 protease inhibitors resembles cushings syndrome |
|cave exploration, mississippi and ohio? ||hisOHIOplasMISSISSIPPI CAVEuslatum
lives in macrophages, RESEMBLES RESPONSE TO TB
|6th position, beta globin gene , GA -> Valined ||sickle cell trait|
|delta 508 deletion in CF what is deleted? ||phenylalanine|
|peroxisomes - where in cell? what enzymes? where are they most abundant? function? ||cytoplasmic - oxidative enzymes Catalase, D-amino acid oxidase oric acid oxidase.
ubiquitious in eukaryotes, most in Liver and kidney where detox happens. in liver, also break down fatty acids.|
|etoposide and podophyllin - MOA, Use? ||topoisomerase 2 causes chromosome breaks and then reseals them to relieve + super coiling.
these drugs block that : etoposide testicular and small cell ca lung. podophyllin for genital warts |
|5FU and 5Deoxyuridine block thymidylate synthase ||methotrexate blocks dihydrofolate reductse|
|irinotecan, topotecan inhibit topoisomerase 1, induces single strand breaks to relieve negative supercoiling. ||vinca alkaloids like vincristine and vinblastine build TUBULIN monomers, disrupting microtuble necessary for separating chromosome strands during mitosis. |
|Taxanes like paclitaxel cause microtubular dysfunction like vinca alkaloids |
|renal PLASMA flow = renal art pressure - renal vein pressure / renal vascular resistance OR? ||RBF=PAH clearance=urinePAHxurine flow/plasmaPAH
|rheumatoid arthritis, cardiac involvement? ||Fibrinous pericarditis|
|tertiary syphilis cardiac involvement ||aortitis, aortic aneurysm, aurtoic regurg.
rare mitral valve lesions.|
|glucagonoma presentation? ||rare pancreatic tumor with necrolytic migratory erythema, elevated erythematous rash in groin, hyperglycemia, stomatitis, cheilosis,, abdominal pain. measure serum glucagon.|
|somatostatin inibits what? presentation? ||abdominal pain, gall stones, constipation and steatorrhea due inhib of insulin, glucagon, gastrin, cholecystokinin, and secretin and inhibit directly GIT motility. |
|which toxins are superantigens? ||enterotoxins, exfoliative toxins, and TSST, cross link MHC 2 to TCR -> huge recruitment of T cells and macrophages -> release of IL2 and TNF -> Toxic shock syndrome.|
|trochlear nerve palsy causes ? ||vertical diplopia like walking down stairs, reading or looking toward nose. |
|auer rods are deformed azurophilic granules found in cytoplasm of myeloblasts staning positively for myeloperoxidase. abundant in AML M3 ||stain with MYELOPERXOIDASE|
|hairy cell leukemia stains + for what? ||TRAP tartarate resistant acid phosphatase. neoplasts b lymphocytes are precursors and are cd20+ - splenomegaly, fatigue, pancytopenia. |
|normal aging of heart? ||deposition of lipofuscin, shrinking left ventricle and sigmoid shaped septum - bulges into left ventricular outflow tract!|
|light microscope finding in GBS, presentation? ||segmental demyelination and endoneural inflammatory infiltrate. ascending weakness, loss of DTR's even bells palsy and resp paralysis.|
|werdnig hoffman syndrome pathophys? ||anterior horn cell dmage, LMN - flaccid weakness, areflexia, atrophy and fasciculation - floppy child syndrome.|
|Thiamine deficiency demyelination ||unlike GBS, no PERINEURLA INFLAMMATION IS SEEN.
pain and parestheisa, weakness, afrelexia, and distal lower limb weakness is seen.|
|duchenne muscular dystrophy - inheritance, type of mutation? ||frameshift mutation, x linked|
|spherocytosis incareas risk of what kind of gall stones?
what virus precipitates aplastic crisis ||parvovirus b19
|Lithium toxicity presentation?
how it is handled in the kidney?
what drugs for what conditions increae the reabx of lithium -> toxicity? ||presents as tremors, twitching, agitation, ataxia and delerium.
handled by kidnye like SODIUM - in PT >60% reabx. dehydration, CHF, volume depletion - body increases NA reabx, and LI too -> tox.
ACE INHIB, NSAID, THIAZIDE DIURETICS (not loop) |
|1st line RX for isolated systolic HTN - in regular pt and in diabetic pt? ||normal: thiazide diuretic or dihydropyridine CCB
diabetic - ACE inhibitor or ARB
|acid fast uses what dye and what decolorizer? ||carbolfuschin and alcohol
stains for MYCOLIC acid.|
|SLE assiciated with what part of T lymphocyte mutation?
what function of CTL's is lost with this mutation? ||FAS mutation -> failure of CLONAL DELETION of autoreactive TL's|
|primidone is an antiepileptic drug metabolized to what? ||metabolized into phenobarbital and phenylethylmalonamide PEMA, which are also anticonvulsants.
|h influenza - 2 types . capsulated and non-capsulated.
type B has was unique feature?
do non capsulated strains cause disease?
what disease do they cause? ||type B has RIBOSE instead of hexose.
its pathogenic because capsule protects vs phagocytosis.|
|hyaluronidase is used by which bacteria? ||staph, strep group A, and clostridium difficle|
|adenovirus is common in people living in close quarters - pharyngoconjunctival fever - pharyngitis, cough, nasal congestion, conjunctivitis and lymph nodes ||calcivirus = norwalk virus - Gastroenteritis
paramyxovirus = parainfluenza (croup),RSV (bronchiolitis in infants), measles and mumps
parvovirus = b19 aplastic crisis in sickle cell anemia, spherocytosis and fifths disease, hydrops fetaliss
|arenavirus = lymphocytic choriomeningitis virus (LCV) febrile aseptic meningoencephalitis or influenzalike illness from HAMSTERS AND MICE ||poxviruses = smallpox, vaccinia, cowpox, monkeypox and molluscum contagiousm.|
|base excision repair - types of DNA damage that is corrected by this ||defect in single bases - spontaneous, chemical (depurination), thymine dimer formation UV rays - breaks in DNA chain/oxidative dmg (ionizing radiation), cross links, intercalation, alkylation - chemical/drugs. |
|base excision repair -order of enzymes ||glycosylase - removes BASE
endonuclease - removes SUGAR-PHOSPHATE
LYase assists in this (endonuclease ->5', lyase 3')
DNA polymerase -replaces missing nucleotide, ligase reconnects strands
glycosylase-endonuclease-lyase-dna polymerase - ligase.|
|ACE inhib's do what to renal filtration fraction? who is this dangerous is? what is the lab test that reflects this/ ||creatinine rises transiently.
filtration fraction is decreases due to decrease efferent constriction because of angiotensin 2, dangerous in renal artery stenosis - in whom blood flow is low , the effernt constriction is maintaining GFR -> renal failure.|
|most common thyroid cancers? ||1) papillary thyroid cancer
2) follicular thyroid cancer
both arise from follicle epithelium.|
|papillary thyroid cancer histology ||most common thyroid cancer. FNAC ->thyroidectomy. branching papillae with bibrovascular stalk lined by single or multiple layers of cuboidal epithelium, GROUND GLASS NUCLEI, psammoma bodies. good prognosis.INTRANUCLEAR GROOVING. also a tall cell variant|
|follicular thyroid cancer - hiso? ||2nd MCC. well differentiated, simulating normal thyroid, or less well differentiated with sheets of follicular cells or large cells with eosinophilic cytoplasm HURTHLE CELLS. different from PTC:ground glass nuclei and pasmmoma body.|
|anaplastic thyroid carcinoma ||aggresive poor prog. 2 yr mortality 100%, invades locally and mets. large pleomorphic cells, large multinucleated osteoclast like cells, and small cells mixed in with spindle cells. no psamm, or ground glass nuclei.|
|medullary thyroid cancer ||from parafollicular C cells, 20% familial MEN 2a 2b, bilateral, preceded by c cell hyperplasia. uniform polygonal or spindle shaped cells CALCITONIN STAIN + extracellular amyloid deposits from calcitonin are present - CONGO RED STAIN.|
|follicular adeonma ||benign thyroid tumors difficult to differentiate from follicular thyroid cancer. look for ABSENT CAPSULAR and VASCULAR INVASION.|
|hashimotothyroiditis ||MONONUCLEAR infiltrate Lymphocytes+plasma cells, GERMINAL CENTERS. METAPLASIA of thyroid follicluar epithelium -> large oxyphilic cells with granular cytoplasms = hurthle cells (follicluar thyroid ca also) anti TPO ab's|
|hurthle cells seen in ? ||large oxyphilic cells eosinophilic cytoplasm)
hashimoto thyroiditis (metaplastic change)
medullary carcinoma thyroid.|
|riedels thyroiditis ||extensive fibrosis extending into surrounding structures. hard fixed gland simulates malignancy. anti antithyroid peroxidase maybe + (autoimmunity possible)|
|antithyroid peroxidase + ||hashimoto and ridel|
|de quervain thyroiditis ||mixed cellular infiltration with occasional multinuclear giant cell aka granulomatous thyroiditis. maybe virally triggered -> thyrotoxicosis, painful tender gland - then hypothyroid, finally euthyroid.|
|thyroid follicular cells arise from? ||outpouching of pharyngeal epithelium. they then migrate to lower neck and fise with parafollicular C cells from 4th pharyngeal pouch and form the thyroid. follicular cell cancers are Papillary and Follicular.|
|capillary endothelial cells arise from?
Von Hippel Lindau disease?
||primitive endothelium. VHL - capillary rich hemangioblastomas. VHL gene regulates transcription of Hypoxia inhibitive factor 1 HIF1 (++VEGF and erythropoetin) ->mutation = hemangioma.|
|EF2 is necessary for what exactly process? ||translation : ef2 is necessary for tRNA to insert NEW amino acid into growing protein chain .|
|clostridium perfringens releases what special toxin causing cell destruction? ||cytolytic toxin aka alpha toxin or phospholipase C -> degrades cell membrane phospholipids and destroying the cell.|
|what is ebsteins anomaly?
what drug causes it? ||Atrialization of right ventricle aka apical displacement of tricuspid valve
Lithium causes it - rx manic / bipolar.|
|valproic acid is used as? (2 specific differnt functions) ||anticonvulsant AND mood stabilizer - use in epileptics with bipolor / depression
also in absence(2nd after ethosuximide), myoclonic(DOC), GTC. as mood stabilizer:prevents mania in rapid cycling bipolar disorder(<4 episodes/yr), and mania.|
|sertraline is SSIR used in what disorders/ ||depression, OCD, panic.|
|S.aureus is the usual cause of of soft tissue infections. which drug is empirically used to rx this ||NAFCILLIN - used for folliculitis, abscesses.
treats S. aureus (usually produces b-lactamase)
nafcillin is not effective vs MRSA|
|lung abscesses in alcoholic pts is usually treated with ||clindamycin|
|causes of AVASCULAR NECROSIS OF FEMORAL HEAD ||4 causes:
Sickle cell DZ -embolic
SLE - vessel wall vasculitis
Steroid Therapy - unknown
Alcoholism - unknown
no swelling or erythema - MRI most sensitive.|
|micicarmine stain for what fungus? ||cryptococcus neoformans|
|nonseptate hyphae that branch at wide angles are from what fungi? ||Micor and Rhizopus.|
|Candida albicans forms germ tubes (sprouts of true hyphae from yeast cells) in incubated in 37 deg C for 3 hours. this differentiates C. Albicans from what other fungi? ||other candidal fungi.|
|Spherules (round with endosores) found in coccidioides immitus causing what disease? ||lung disease - meningitis is not common.|
|Sporangium is a structure that contains spores - present in MOLD fungi. |
|does cryptococcus have mold, yest or dimorphic ||yeast ONLY NOT DIMORPHIC|
|protamine sulfate used for? ||counteract OD heparin
protamine sulfate comes form salmon sperm!|
|VItamin K reveresed OD ||WARFARIN|
|Aminocaproic acid (comes form lysine)and tranexamic acid inhibit what? used in OD of what drugs? ||streptokinase. inhibit plasminogen activation|
|Shigella is NON motile vs salmonella is motile.
Shigella is non lactose fermenting and produces ACID instead of GAS like Ecoli.
Shigella does not produce H2S compared to salmonella which does.
||Salmonella mechanism is Mucosal invasion.
via M cells in peyers patches . after entering M cells, shigella lyses into containment vacuole and enter CYTOSOL. causes APOPTOSIS and spread into adjacent cells w/ ACTIN POLYMERIZATION|
|shigella releases shiga toxin ->inhibits protein synthesis. is AB toxin 1A binds 5Bs. A inactivtes 60s rib -> no prot synth, cell death. toxin is less important than mucosal invasion. non toxigenic strains cause disease also. ||Prolferation in lymph nodes is not characteristic of shigella - but is seen in yersinia enterocolitica and salmonella typhi.
yersinia enterocolitica causes lymph node infection - inflamed mesernteric nodes - pseudoappendicitis.|
|pseudoappendicitis is caused by? ||enlarged lymphnodes in yersinia enterocolotica.|
|distended macrophages in intestnal lamina propria seen in what disease ||Whipple Disease|
|collections of neutrophils in crypt lumina in intestine seen in ? ||ulcerative colotis.|
| intestinal inflammation with scatered non-caseating granulomas ||crohns disease|
|massive infiltration of intestinal lamina propria with atypical lymphocytes seen in? ||GIT LYMPHOMAS.|
|lactose deficiency patients have what mucosal changes? || none|
|bullous pemphigoid - disease of elderly - ABs vs ?
||Hemidesmosomes - AB's attack these along dermal epidermal junction at basement membrane - compliment fixation -> tissue injury. SUBEPIDERMAL NONACANTHOLYTIC blister appers w/ edema and perivasc lymphocytic infiltrate. vacuolations in basal layer >blister.|
|young woman with skni rash, arthralgia, and POSITIVE VDRL TEST ||SLE - antiphospholipid AB's make VDRL +, reactive vs cardiolipin.
APLA -venous thrombosis, arterial thrombosis, miscarriage. Lupin anticoaglant 10-30% SLE pts. MISCARRIAGE bc inhib tPA activity necessary for trophoblastic invasion of uterus.|
|trophoblastic invasion of uterus , blocked by antiphospholipid antibodies of SLE, physiologically requires what substance? ||tPA|
|transmural infarct has what ECG finding ||ST elevation.|
|rupture of ventricle post MI happens after how long/ ||4-5 dyas , range 1-10 days. at this time coagulative necrosis, neutrophil infiltration and enzymatic lysis of connective tissue has weakened the infarcted myocardium. |
|if ventricle wall ruptures, how does patient die? what will ECG show? || profound hypotension due to cardiac tamponade.
ECG shows electrical activity but body is pulseless -> hypotension, shock, death.|
|gram + actinomycete T.Whipelli involves small intestine, joints and CNS. what are the histo findings? ||Mucosa of Small intenstive with ENLARGED FOAMY MACROPHAGES packed with 1) Rod shaped bacilli 2) diastase resistant, PAS + granules. |
|relative risk is in COHORT studies.
what is the equivalent in CASE CONTROL studies?> ||Exposure odds ratio|
|blastomycosis dermatitidis is dimorphic fungus causing pulmonary infection in what immune status host? ||immunoCOMPETENT.|
|bastomycosis is seen in what area? what other fungi is seen in this area? ||OHIo/Mississippi valley, great lakes
also see histohioplasmississippi
cauess asymptomatic or flylike illness with cough and sputum, hemoptysis and pleuritic chest pain. maybe chronic. granuloma +++|
|transverse cervical ligament is also known as cardinal ligament -extends from where to where? ||cervix and lateral fornix of vagina to lateral pelvic wall. |
|transverse cervical ligament aka cardinal ligament contains what artery and should be ligated during what procedure.? ||UTERINE artery - ligate in radical hysterectomy/|
|nerves and vessels to OVARY are delivered through what ligament. when shoudl this ligmanent be ligated? ||suspensory ligament of ovary. shoudl be ligated in any surgery involving ovary.|
|broad ligament of uterus is formed by mesovarium which covers the ovaries. |
|ovarian arteries are branch of? ||abdomainal aorta bilaterally. left ovarian VEIN drains into left renal vein, right directly into IVC. parasymp innervation of ovary - VAGAL.
|common complication of ovarian surgery causing bleeding? ||accidental ligation of ureter instead of suspensory ligament.|
|etanercept (enbrel) is an anti TNF a drug used in rheumatoid arthritis esp in those who have failed with methotrexate. what screen needs to be done before using this drug? ||it causes immunosuppression therefore PPD test for latent TB must be done. cannot use in any patient with infection. |
|make sure to do what test when using Methotrexate and Leflunomide? ||Liver Function tests.|
|acellular pertussis vaccine contains what immunogenic material? ||purified components of B pert and detoxified pert toxin. toxoid|
|hep b vaccine contains? ||purified inactivated hbsag particles from YEAST through recombinant DNA tech|
|varicella vaccine contains? ||line attenuated varicella virions|
|bcg vaccine contains ||live attenuated strain of m.bovis.|
|salk (sulks cause it sucks) = IPV ||dead inactive killed virus|
|sabin - OPV - ||live attenuated virus|
|wiskott aldrich syndrome presentation :
mutation? ||eczema, infection, thrombocytopenia(petichae, hematemesis, epistaxis.
X chrom mutuation (males only)
B and T disorder - esp pyogenic inf(failed humoral vs polysaccharide capse n.men, h.inf, s.pneum.) opportunistic.p.jirovec.esp after maternal igg iga @6|
|rx wiskott aldrich syndrome ||hla matched bone marrow trx.|
|tzanck smear uses what stain? what tissues are tested with this smear? what viruses does it identify? ||Herpes Simplex or VZV virus.
uses Wright Giemsa Stain.
Scrapings from oral ulcer base.|
|herpetic gingivostomatitis is the most common manifestation of PRIMARY HSV1 infection - at what age is this commong? ||1-3 years, fever, vesicoulcerative lesions in oral membranes and localized lymphadenopathy.|
|secondary reactivation of hsv1, 2, vsv, cmv like orolabial herpes. ||confined to one side, 1/10 involvement of initial infection
|hsv 1 remains latent where
CMV? ||hsv in trigeminal ganglia
vzv in dorsal root ganglia
cmv many tissues. - interstitial pneymonitis, retinitis, hepatitis, colitis and generalized disease|
|patient with anaphylaxis - what can be used as marker alternative to histamine? ||tryptase - comes from mast cells only
therefore is a good serum marker for mast cell activation
|primary cns lymphomas esp those in immunosuppressed are associated with EBV, what are common markers found on these cells? ||CD 20, CD 79A
may present with mental status change, seizures, progressive focal neurologic deficit. high grade anaplasia, poor response to chemo.|
|von hippel lindau syndrome presentation? genetic inforamation? ||autosomal DOM. VHL gene, chromosome 3p DELETION.
presentation cerebellar hemangioblastoma, clear cell RCC, pheochromocytoma.
rcc in 40% pts. strong assx 3p . rcc only assx with this deletion.|
|rb oncogene is located on ch 13. mutations lead to? ||retinoblastoma and osteosarcoma|
|NF 1 is on ch 17 mutations causes ||vonrecklinghausens diseae|
|WT1 anti-oncogene ch 11, assx? ||wilms tumor.|
|BRCA 1 - ||breast and ovarian ca|
|when to use colchicine?q ||in gout pts with contraindications to NSAIDS like
renal faiure, peptic ulcer dz |
|drugs highly CLEARED by liver (bile feces) (not 'metabolized or biotransformed' by liver)
have what characteristics/ ||high lipophilicity!
high volume of distribution. these same drugs tent to be poorly cleared by kidney as they can cross tubular cell membranes after filtration and enter tissues again. high lipid soluble allows drug to enter hepatocytes - excreted.|
|low volume of distribution drugs are confined to bloodstream and do not diffuse readily through hepatocytes into bile. low Vd is highly plasma prot bound and hydrophilic, excreted unchanged in urine. |
|what are epitheloid cells? ||activated macrophages/|
|what is the essential cofactor for hepatic microsomal carboxylase that converts glutamyl residues into gamma carboxyglutamates.
required for functioning of factors vii, ix, x - allows for calcium binding sites that interact with phospholipid surface -> ||Vitamin K -
calcium binding sites interact with PL surface to produce THROMBIN.|
|enoxaparin is a low molecular wt heparin MOA? ||potentiates antithrombin 3 therefore mostly inhibiting factor xa which prevents prothrombin -> thrombin.|
|enoxaparin is a low molecular wt heparin MOA? ||potentiates antithrombin 3 therefore mostly inhibiting factor xa which prevents prothrombin -> thrombin.|
|tissue plasminogen activator tPA converts plasminogen to plasmin, breaking down fibrin, -> thrombolysis. CLOT SPECIFIC thrombolysis ||plasminogen is bound by thrombolytic agents streptokinase urokinase and tPA, these agents assist in cleavage to plasminogen to plasmin |
|prothrombin factor II is vit K dependent. along with 7 9 10 - all of these are therefore depleted by? ||warfarin.|
|prothrombin factor II is vit K dependent. along with 7 9 10 - all of these are therefore depleted by? ||warfarin.|
|methotrexate enters cells and gets polyglutamated, which keeps it in the cell along with ? ||dihydrofolate reductate. thus these 2 are increased in cell in MTX use.|
|methotrexate enters cells and gets polyglutamated, which keeps it in the cell along with ? ||dihydrofolate reductate. thus these 2 are increased in cell in MTX use.|
|presentation of mutiple myeloma ||easy fatigue (anemia)
bone pain (back and ribs, due osteoCLAST activating factor from myeloma cells -> bone lysis)
|what causes renal failure in multiple myeloma ||multifactoria : hypercalcemia, hyperuricemia, kidney infiltration by myeloma cells, AL amyloidosis , infections.
|what is classic myeloma kidney aka myeloma cast nephropathy ||due to excess excretion of
FREE LIGHT CHAINS - bence jones protein (light chains) filtered in glom, then reabx into tubules. when exceeds reabx capacity, then appear in urine. precipitate with TAMM HORSFALL protein ->eosinophilic casts NOT EOSINOPHILS|
|what do bence jones light chain do in tubular epithelium and tubules? ||obstruction and compression -> renal failure.
B J Prot is directly toxic to tubular epithelium causing atrophy - > see large glassy eosinophilic casts|
|ischemic tubular necrosis presents how? ||muddy brown granular and epithelial cell casts along free tubular epithelia cells.|
|acute pyelonephritis would present with ? ||pyuria, WBC casts|
|hypersensitivity interstitial nephritis manifests as? ||sterile pyuria and history of some drug . peripheral eosinophilia and eosinophiluria is non specific but suggests hypersensitivity interstitial nephritis.|
|NSAID causes what kind of nephritis? ||papillary necrosis and chronic interstitial nephritis.|
|aminoglycosides renal damage? ||accumulates in CORTEX, acute tubular necrosis.|
|chronic lead exposure , what effect on kidney? ||chronic tubulointerstitial nephritis -> renal failure.|
|failed fusion results in ? ||endocardial cushoin defect - ostium PRIMUM ASD|
|failed proliferation -> ||unilateral aplasia of fibula|
|apoptosis failure in embryo? ||autoimmune DZ and persistecnce of autoreactive T/B immune cells.|
|obilteration ||branchial cleft cyst|
|migration ||hirschprung dz - neural crest cells|
|fusion ||hypospadias (failed urethral FOLDS)|
|TGA failure? ||septation (spiralling) of aorticopulmonary septum|
|if you see GOBLET cells in esophageal epithelium is this normal?
if not, what does it represent. ||it is not normal, it represents adenocarcinoma / barrets esophagus |
|most common eshophageal benign tumor ||leiyomyoma|
|ronchi and wheezing in a neonate / child indicates closing airways - either asthma or bronchiolitis. most common cause of bronchiolitis is RSV - what is the management of rSv ||supportive - if very severe, then add aerosolized ribavirin|
|MOA of ribavirin and viruses it works on ||RSV and hepatitis C
is a nucleoSide analog, inhibits guanine nucletides|
|ganciclovir is anti herpes virus guanine nucleoside analog (other guanine nucleoside analog is ribavirin) .. ganciclovir is different from acyclovir how> ||ganciclovir is more active vs CMV Dna|
|Oseltamivir is a sialic acid analogue inhibits what parts of influenza virus? ||neuraminidases of both type A and B influenza.
this can cause bronchiolitis in children but RSV is more commo|
|amantadine impairs what part of influenza infectivity> ||uncoating of influenza A ONLY - this uncoating happens after endocytosis|
|what is the most importnat part of abscess formation on a biochemical immunology level? ||spilling of lysosomal enzymes from macrophages and neutrophils. this creates further chemotaxis and damages surrounding lung tissue making abscess possible.|
|interferon gamma - what is its function> ||phagolysosome formation, inducible nitric oxide synthase release and development of granulomas and caseous necrosis. |
|interleukin 12 does ||stimulates NK cells to destroy target, is responsible for T helper cell seretion of IFN gamma. |
|selegiline is an inhibitor of MAO B. pretreatment with this prevents what/ ||progression of parkinsons.|
|dopamine is a d2 agonist, stimulates central d2 receptors - only helps early parkinsons but may delay introduction of ldopa by years |
|use of carbidopa (blocks peripheral conversion of l-dopa to dopamine) ||l dopa is abx in small intestine by large NEUTRAL amino acid transporter system then converted to dopamine by enzyme dopa decarboxylase. the peripheral conversion causees all the side effects (GI effects) carbidopa does not cross BBB so prevents it.|
|picornaviruses/ ||echo, rhino, hepatitis a, enterovirus, polio|
|which picornaviridae are
acid labile ||labile - rhinovirus - no GI disease
stable - enterovirus (all are but notably entero)
|fetal defects and their mechanism? ||malformation, deformation, disruption, sequence, agenesis.|
|malformation defects/ ||primary defect in cells,
holoprosensephaly(5th wk, trisomy 13, 18)
anencephaly, congenital heart disease, poly/syndactyly|
|deformation - ||fetal anomales due to extrinsic mechanical forces ie uterine constraint -> hip dislocation/breech presentation. (not potters synd which is a SEQUENCE)|
|disruption / amniotic band syndrome ||secondary breakdown of previously normal tissue / structure - rupture of amnion during development leads to band formation which compresses or amputates limbs.|
|sequence occurs when a number of abnormalities results from single primary defect ie? ||oligohydramnios -> potters syndrome|
|how do cancer cells become resistant to chemotherapy drugs/ ||multidrug resistance genes ie MDR1|
|describe MDR 1 gene ||transmembrane protein P-glycoprotein which is ATP DEPENDENT EFFLUX pump. p-gly. is normally on intestinal and renal tubular epithelial cells and eliminates foreign compounds.also in capilly endothelium of BBB. prevents penetraion. removes drugs if mutated|
|function of p glycoprotein (as seen on MDR1 gene giving resistance to turmor cells from drugs) ||found on intestinal and renal tubular epithelial cells - eliminates toxins
found on capillary endo in BBB - prevents penetration of toxins into brain
found on tumor cells , eliminates drugs from cancer cells as toxins - gives resistance.
|process of apoptosis is separated into what 2 phases ||initiation and execution - initiation brings protein hydrolyzing caspases . execution ; the caspases bring about cell death by cleaving cellular proteins and activating DNAses|
|initiation phase of apoptosis ||signals from 2 pathways -mitochochondrial or death receptor (extrinsic). mito becomes permeable to pro-apoptotics,
antiapoptotic bcl2 bclx finish and bax bim cause release of cytochrome C|
|proapoptotic factors bax bim
anti-apoptotic, bcl2 bclx
once anti finish, then pro cause mito permiability and release of cytochrome c -> apoptosis |
|extrinsic pathway : ||death receptor engaged on cell surface (tumor necrosis factor receptor family) TNFr1 and FAS cd95 - multiple bound fas receptors come together and make a binding site for death domain containing adapter FADD>binds caspase and activates it. |
|mechanism of opioid tolerance ||involves phosphorylation of opioid receptors by protein kinase.
chronic tolerance may involve increased adenylyl cyclase or NO levels.|
|morphine tolerance shows what Neurotransmitter to interact with opioid pathway ? ||glutamate (normally excitatory) binds NMDA receptors -> phopshorylates NMDA receptors (activate)
DEXTROMETHORPHAN reverses opioid tolerance through nmda antagonist properties. glutamate plays a role in morphine tolerance|
|what neurotransmitter specifically plays a role in morphine tolerance ||NMDA receptors and glutamate action.|
|glycine is a co - binder for glutamate. what do the 2 do in the cns? ||allow for activation of nmda receptors. it does not play a role in morphine tolerance however.|
|vasovagal syncope from ear canal is still mediated by ||vagus x |
|posterior part of external auditory canal is innervated by small auricular branch of vagus nerve. remainder is supplied by ||mandibular trigemianl through auriculotemporal.. |
|inner surface of tympanic memb supplied by what nerve ||ix glossopharyngeal. via typanic branch.|
|what is the most common arrhythmia in myocardial ischemia as in heart attack? therefore most common cause of sudden cardiac death ||ventricular fibrillation|
|most lethal arrhythmias in acute MI patients are? ||vent fibrillation or vent tachycardia.|
|most common cause of MI death after actute prehospital phase (which was vent fib, or vent tach) ||ventricular failure |
|wall rupture or ventricular septal rupture occurs how long after MI/ ||3-7 days |
|adenosine and acetylcholine act on what part of the cardiac myosite depolarization? ||phase 4 which is the slow upward automaticity part before 0 spike then 3 repolarization .
phase 4 mechnaism - slow na+ leak + closing of k+ channels. then at -50, T-type ca channels open and speeds up depol to -40 after which depolarization happens|
|adenosine mechanism of acting on phase 4 of cardiac depolariation ? ||activates K+ channels - preveents depolarization.
also inhibits L type calcium chanels - which are active in phase 0, prolongs time to threshold.|
|mechanism of acetyl choline on cardiac myosite - ||opens specific k_ channels and increase k conductance and at the same time, slows inward Ca influx. - slows the heart. |
|norepinephrine effect on cardiac myocites/ ||acts in L type ca channels and na channels in phase 4. - increase ca and na influx, rapid depolarization incrased heart rate.|
|which drugs are anti TNF a action -(synovitis, joint erosion, rheumatoid arthritis, slow disease progression) ||etanercept, adalimumab, infliximab.
increase infection risk, esp TB - do PPD skin test First.|
|purine pyrimidine agents - are tey used in rheumatoid arthritis? ||yes - methotrexate is 1st line agent.|
|what immune complex vasculitis assx igA, c3, presenting with leukocytoclastic angiitis in SMALL vessels of dermis and GIT - abdominal pain, purpuric rash, polyarthralgia and complicated by glomerulonephritis , in males mosly 3-11 yrs ||HSP|
|GCA and takayasu do not have iga or c3.
may present with weakened pulses in extremities .
TAO is not assx iga or c3 either. |
|hypersensitivity myocarditis presentation and cause? ||due to a new drug with cross reacting atopic response - periVASCULAR infiltrate with abundant eosinophls |
|s100 protein is a protein seen in ||melanoma, schwannoma, inflammation, clear cell sarcomas,
has antimicrobial activity.|
|reed sternberg cells seen in what disease ||hodgkins lymphoma|
|follicular lymphoma sows what kinds of cells? what age group? ||2 important cells - centrocytes (small cleaved cells) , centroblasts, large, non cleaved cells.
|burkitt lymphoma presentation? ||high grade lymphoma - mass in abdomen pelvis or jaw, starry sky apparance due to monotonous population of medium sized lymphocytes with a few tingible macrophages. |
|b12 neuropathy = ||dorsal columns (position and vibration, gait abnormal, sensory ataxia)
lateral corticospinal tract - UMN sign - spastic, hyper refflexia, babinski sign
axonal degen, can cause numbness or paresthesia|
|syringomyelia - cyst within spinal cord destroys central portion of spinal cord - ||lateral spinothalamic tracks are affected, bilateral loss of pain and temp - involvement of motor neurons of AHC' >flaccid paralysis and atrophy of intrinsic muscles of hand. |
|damage to dorsal column and dorsal roots are? ||tabes dorsalis - unlike combined degen of b12, later tract is not involved.|
|ALS - upper and lower motor neuron lesion |
|anterior spinal artery syndrome - result of compression / occlusion of artery in front of spinal cord. compression from bone fragments or disc herniation - ||complete loss of strength below level of injury and loss of pain and temp sens but PRESERVED VIBRATION.|
|thiazolidinediones TZD - like pioglitazone, rosaglitazone act how? ||stimulate NUCLEAR RECEPTOR PPAR gamma which is transcriptional regulator of genes involved in glucose and lipid metabolism. -> TRANSACTIVATION|
|most important gene regulated by PPAR gama (stimulated by TZD"s like pioglitazone) ||Adiponectin (its levels are LOW in dm 2) rx wx TZD's increases adiponectin to N levelx.|
|sulfonylureas bind to what? ||Katp channels on beta cells |
|insulin acts by? ||binding cell surface receptors . receptor is tetrameric with 2a and 2b subunits - a is extracellular and is binding site. b is intracellular w/ tyrosine kinase domains.|
|enzyme inactivation is an important mechanism for action of metformin and alpha glucosidase inhibitors . metformin decreases enzyme activity responsible for gluconeogenesis in hepatic microsomes . alpha glucosidase inhibitors decrease enzyme activity of? ||membrane bound disaccharidases on intestinal brush border. |
|2 classes of dopamine agonists: ||ergot compounds - bromocriptine and pergolide
NOn ergot compounds - pramipexole and ropinerole|
|bromocriptine is ergot dopaminergic - used to treat parkinsons or hyperprolactinemia. |
|role of amantadine in parkinsons ||indirect and direct dopaminergic , alleviates motor symptoms. enhances endogenous dopamine.has some anticholinergic so reduces tremors.|
|decreased central dopamine degradation by what drug ||selegiline MAO B inhibitor prevents degradation of dopamine in brain|
|COMT and dopadecarboxylase inhibitors decrease breakdown of ||levodopa in peripheral tissues, increasing the amount available to briain.|
|most common urea cycle defect? ||ornithine transcarbamoylase deficiency - increase ammonium and carbamoyl phosphate -> neurological damage.
major cases present in children, minor may present in adults.|
|propylthiouracil vs methimazole ||PTU - safe in Pregnancy and decreases Peripheral conversion
|antithyroid drug pneumonics
propylthiouracil, methimazole, thiocyanate, perchlorate ||THIroid peroxidase inhibitors I- -> I2 block
Na->I PUMP Blockers - thiocyaNAte and perchlorate.|
|patient on antithyroid drug - agranulocytosis is complication - presentation and appropriate test? ||WBC count with differential is the right test,
presents with fever and sore through
0.5% ppl have this side effect, usually in early rx, but may be at any time. |
|why not use aspirin or ibuprofen for thyroid patients with fever and sore throat? ||first suspect agranulocytosis - so symptomatic management is not enough.
also thes drugs displace thyroid hormones from binding sites - worsening thyrotoxic state ,
|pulm HTN definition ||>25 mmhg|
|causes of Pulm Artery Htn? ||Major: sporadic or idiopathic - MCC
left heart failure
chronic hypoxia - COPD, sleep apnea,
chronic thromboembolism, HIV|
|genetics of PAH? ||auto DOM with variable penetrance. abnormal BMPR2 bone morphogenetic protein receptor type 2. this predisposes to pulm vasc disease., then, infections drugs, ion channel defects>DZ begins-++ endothelin (vasoconstr), inhib NO, PGi2|
|pathophysiology of pulm artery htn ||vasoconstriction, vasc smooth muscle proliferation , fibrosis, thrombosis of pulm art/ateriole, endothelial cell growth, elevated pulm pressure. -> right vent hypertrophy, failure, dyspnea, pain, distended neck veins. increases p2 and holosystolic tricusp|
|murmur of pulmonary art hypertension ||accentuated p2 at left sternal border. holosystolic tricuspid insufficiency accentuated with inspiration,
|rx pulmonary artery hypertension ||epoprostenol|
|pantothenic acid b5 becomes CoA. where is Coenzyme A required ||many reactions but importantly TCA CYCLE
where it binds oxaloacetate + coA -> citrate -> succinyl coA.
also imp in vit A, D, cholesterol, steroid, heme, fatty acid, Amino Acid, and protein synth.
|how does pantothenic acid become coA ||actively transported into cells, ATP dependent phosphorylation -> coA.|
|symptoms of b5 pantothenic acid deficiency ||burning feed, numbness, paresthesia/dysestheisas. |
|rx neisseria meningitis? ||ceftriaxone for minimum 2 weeks.|
|FF = gfr / rpf
normal FF = 20%
filtered load = GFR x plasma concentration
rpf best estimate with PAH
gfr estimate with creatinine
||why use renal PLASMA flow instead of renal BLOOD flow for filtration equations?
|mycobacterium avium intracellularae - infects immunosuppressed and competent hosts. more comming in hiV with CD4 counts BELOW 50 - diagnose with blood culture of AFB - prevention and treatment? ||weekly azithromycin prevents
treat with clarithromycin/azithromycin + rifabutin/ethambutol - must use combo and use HIV rx to bring counts above 200|
|isoniazid used prophylactically in HIV pts exposed to M. TB with POSITIVE PPD
what is cosidered + PPD in HIV pts? ||induration of 5mm or more.|
|rifampin is used in those exposed to? ||N.meningitidis, and H.influenzae.
not useful against mycobacterium avium intracellularae.|
|penicillin rx classically in waht dz ||treponemal, neisseria, and gram+
|TMPSMX used in HIV for prevention of what diseases? when do those disesases become especially likely? ||cd4 count 200 -Pneumocystin jiroveci
cd4 100 - toxoplasma gondi|
|maternal insulin does not cross placenta but sugar does so fetal hyperglyemia results in diabetic mothers causing hyperinsulinemia (transient) but also excess calorie storage as fat. fetus has hypoglycemia for how long? ||1 week or so.|
|treatment of toxoplasmosis ||pyremethimine and sulfadiazine|
|if you see EBV on spinal tap of hiv patient with cns manifestions , think of> ||b cell lymphoma|
|mycoplams requires what nutrient to grow on media ||cholesterol|
|narrow zone of b hemolysis on sheep blood agar (resembles b hemolytic strep) and has tumbling motility at 22 deg c, and cultured at low temps even 4 deg c ||listria monocytogenes
eliminiated by cell mediated immunity (intracellular)|
|bupropion causes agitation insomnia and seizures
acts on NE but not SE, ach, or histamine.
bupripion used for ||depression assx psychomotor retardation (because it is stimulatory)
also treats nicotine dependency, used in depression where ssris cause sexual dysfunction
|crohns dz predisposes to gall stones by what mechanism ||increased bile acid wasting,
not because of increased delivery to liver|
|screen all newborns for? ||hypothyroid, phenylketonuria and galactosemia|
|frontal lobe syndrome (possible due to injury) ||3 categories
disinhibited, disorganized, apathetic -
all 3 characteristics are present but one will dominate.|
|arb's block AT 1 receptors and therefore what what effects/. ||increased renin, increased AT1 increased AT 2
DECREASED ALDOSTERONE (due to vasc smooth muscle relaxation) and NO CHANGE in bradykinin levels.|
|some drugs that can be used in early rheumatoid arthritis
usual management of it is methotrexate, add leflunomide and TNF a inhibitors if needed. ||sulfasalazine, hydroxychloroquine, minocycline|
|side effects of minocycline ||photosensitivity and autoimmune hepatitis.|
|naproxen is an NSAID works by blocking PG synth
side effecs. ||gi bleed, fluid retention, hypertension becomes WORSE, elevation of liver enzymes.|
|side effects of methotrexate ||stomatitis(oral ulcers), hepatotoxic - hepatitis, fibrosis and cirrhosis.
myelosuppression -> infection. b cell lymphoma, pulmonary fibrosis.
folinic acid reduces stomatitis.|
|patients with CHF - what drug can reduce all cause mortality and slowing progress of heart failure? ||BETA BLOCKERS, especially CARVEDILOL
which blocks a1 b1 b2
also remember SPIRO does similar by preventing cardiac remodeling though blocking aldosterone actions. |
|positive osmotic fragility test is seen in ||spherocytosis, not sickle cell anemia
|formation of pigment gallstones in hemolytic anemia? ||increased bilirubin from rbc precipitates as calcium bilirubinate forming pigmented stones.
mature pigmented stones combine calcium bilirubinate, bilirubin polymers and calcium salts.|
|copper management? wilsons disease affects what ||wilsons AutoRec-copper liver brain eye. 60% ingested copper (.6-3mg/day) abx stomach duod, bound albumin->liver>binds a2globulin = ceruloplasmin->secreted to plasma=95%circulating copper) normal body copper 50-150mg. extra secreted bile>stool, 10% renal.|
|septic arthritis usually due to ? ||gonococcus. use ceftriaxone empirically to cover this in any inflamed monoarthrotis while waiting for confirmation. - complications of waiting -0 joint destruction, osteomyelitis, sepsis|
|first step in screening for malabsorption is stool test with which stain? ||sudan III - testing for quantitative fat analysis. >7gm/day fot excreted is malabx|
|what can be diagnosed by duodenal aspiration or jejunal biopsy - ||too invasive to use early in a workup but help to establish diagnosis of crohns, whipple, celiac sprue and others|
|panacinar emphysema ||a1 antitrypsin deficiency - is a form of copd, affects LOWER LOBES (vs centriacinar - smoking - afects upper lobes) caused by neutrophil elastase in alveoli, lower lobes worse because greater perfusion |
|centriacinar emphysema || upper lobes, assx smoking, destructive proteases from macrophages and neutrophils cause acinar wall destruction. reflects lower perfusion in upper lobes, and low presnece of a1 antitrypsin in serum|
|diastolic pressures >120 cuase hyperplastic arteriosclerosis ||onion like concentric thickening of walls of arterioles of laminated SMC's and reduplicated basement membranes - malignant nephrosclerosis - retinal hge, exudate, pappiledema = malignant hypertension.|
|homogenous deposition of hyaline materia in intima and media of small arteries and arterioles characterizes ||hyaline arteriosclerosis - assx LOWER levels of hypertension |
|pyruvate to lactate uses NADH and turns it back into NAD, which is used by? ||glyceraldehyde 3p -> 1,3 BPG turns NAD+ into NADH|
|3 types of colonic adenomatous polyps ||tubular , villous, tubulovillous|
|tubuar - d ||dysplastic colonic mucosal cells with tubular shaped glands - smaller, pedunculated|
|villous ||dysplastic epithelial cells form villi like projections extending from polyp surface down to stroma . look like cauliflower, lower gi bleeding - guaiac+, anemia, intestinal obstr, mucus secretion, secretory diarrhea, high risk of adenocarcinoma.|
|what hco3 level is normal and what is 'compensated' renally? ||25 is normal, 30+ is compensated renally
recall too many H+ = acidosis , we try to excrete the excess h+ which causes retention of hco3|
|contraction alkalosis - ||overuse of diuretics cause volume loss, causes increased aldosterone - causes na h20 retention and loss k and h+ renally. loss of h+ produces met alk, aka contraction alk . lab: high ph, high hco3 and high pco2|
|diabetic ketoacidosis ||low ph, low hc03 and low pco2 (due resp kussmaul)|
|SaO2 less than what is required to cause hypoxic secondary polycythemia (increased rbc mass) ||less than 92%
a pao2 of 70mmhg corresponds to sao2 of 94%|
|erythrocytosis is defined as?
what do you need to look at to determine if it is relative or absolute erythrocytosis ||>52% male >48% female hematocrit
Look for RBC MASS - if normal, then RELATIVE erytyrocytisis|
|gout occurs in patients with ACTIVATING MUTATIONS in PRPP synthetase - due to? ||increase purine production -> hyper uricemia|
|small 5mm cavities in basal vang, post limb int capsule, pons, cerebellum are lacunar infarts.
what are the primary causes of lacunar infarcts/ ||lipohyalinosis and microatheromas|
|lipohyalinosis ||destructive vessel lesion w/ loss of normal architecture, muram foam cells and fibrinoid necrosis.|
|microatheromas ||accumulation of lipid laden macrophages in intimal layer of vessel. - they occur near the branch off from feeding artery|
|mitral valve disease and carotid atherosclerosis can cause cerebran infarction secondary to embolism - also release microemboli but are not as common as the main 2, which aree? ||lipohyalinosis and microatheroma|
|oligodendrocyte apoptosis occurs in multiple sclerosis |
|cystic fibrosis patients with mild cftr mutations may have normal sweat chloride test
in them what other test can you do> ||nasal transpeithelial potential difference -(between surface of resp epithelia and interstitial fluid). CF pts have more NEGATIVE baseline nasal potential than normal due to increase luminal sodium resorption. see pic. this abx in all gland but sweat no.|
|s4 gallop is presystolic sound, before s1. left sided s4 hear best at apex with pt in left lateral decubitus.
rt sided s4 heart along lower left sternal border (tricuspid area) ||s4 hear when sudden rise in end diastolic ventricular pressure caused by atrial contraction against ventricle that is maximally full. s4 in any condition causing stiff ventricle ie LVH|
|5 year old, bounding pulse , thrill on upper left sternal border, continuous machinery murmur =?
what aortic arch? ||patent ductus arteriosus - embryonically allows fetal blood from pulm into systemic circuluation , bypassing lungs. closes at birth w/ pgE2 and O2. after closing = ligamentum arteriosum. 6th aortic arch!!!!|
|PDA comes from what aortic arch ||6th arotic arch|
|sinus venosus ||embryologic structure in heart gets blood from vena cavae - in adult, becomes smooth portion of FA canned sinus venarum|
|bulbus cordis ||beginning of ventricular outflow tract in embryo - is the smooth part of left and right ventricle |
|primitive atrium gets blood from sinus venosus , transmits to ventricle - becomes the rough part of RA and LA. |
|VCN thayer martin for neisseria (esp colistin does this) nystatin for fungi, vancomycin for gm + - what type of medium ||selective medium|
|enrichment media have sepcial factors ||XV factors for haemophilus or anaerobic conditions for clostridia|
|differential media for ||differentiating based on metabolic properties like Macconkey and EMB agar
|reducing media ||culture organisms that reduce iron or sulfur|
|PSVT rx - valsalva increases refractory period in AV node prevents reentrant circut - due to increased vagal tone . if this failed then what rx? ||adenosine|
|hyper IgM is inability of b cells to class switch - due to? ||HEAVY CHAIN CONSTANT REGION that wont change, deficeint CD40 Ligand - recurrent sinopulmonary infection (differentiate CF)
see lymphiod hyperplasia due to too much IgM. rx IvIg|
|pulmonary finding in CHF (ie post MI) ||decreased lung compliance due to pulm edema -> TRANSUDATE in interstitium. |
|drug of choice in gonoccal urethritis ||ceftriaxone|
|failed rx with ceftriaxone for urethritis = ||NGU, commonly c.trachomatic or ureaplasma urealyticum, also mycoplasma or trichomonas. azithromycin is rx.
|chlamidya trachomatis is intracelular has cell wall but NO :PEPTIDOGLYCAN . considered gram - , difficult to stain. has PBP's!!? this is called chlamidyal anomaly ||what is chlamidyal anomaly - chlamidya has penicillin binding protins but no peptidoglycan |
|ureaplasma urealyticum lacks cell wall, does not stain and is not susceptible to ceftriaxone, so rx with? ||macrolides or tetracyclines|
|how to treat chlamidya or ureaplasma? ||antiribosomal antibiotics macrolides or tetracyclines|
|chlamidya requires what from its host cell that it cannot produce on its own, but ureaplasma cAN produce ||ATP - is required for growth and replication|
|how does tetanus vaccine protect from tetanus ||does NOT prevent bacterial growth rather gives immunity to bacterial product through cirulating antibodies|
|pro-carcinogens are metabolized by cytochrome p450 monooxygenase, prensent in ? ||hepatic microsomes and endoplasmic reticulum of other tissues.|
|cytochrome p450 monooxygenase metabolizes steroids, alcohol, toxins and other substances by rendering them soluble and easier to excrete. this process can cause what HARMFUL effect ||turning procarcinogens into carcinogens and causing mutations > cancer|
|chemicals can induce cancer, most of these chemicals start in harmless PRO-carcinogenic state and must be made into active carcinogens. what system in the body does this? ||cytochrome p450 monooxygenase, from hepatic microsomes and
endoplasmic reticulum of other tissues.|
|glutathione s transferase is involved in? ||DETOX, inactivates carcinogens.|
|mitochondrial cytochrome oxidase cytochrome a+a3 is part of ETC, reacts with what to produce what? ||reacts with oxygen to produce water -|
|difference between mitochondrian cytochrome oxidase cytochrome a+a3 vs microsomal monooxygenase cytochrome p450 ||cytochrome a+a3 mitochondrial cytochrome oxidase is part of ETC - turns o2 into water
cytochrome p450 microsomal monooxygenase turns procarcinogens into carcinogens. (hepatic microsomes and endoplasmic reticulum)|
|superoxide dismutase converts what into what ||superoxide into oxygen and hydrogen peroxide during phagocytosis|
|space constant is? ||measure of how far along an axon , an electrical impulse will travel.
|what is space constant used for ||reflects increased charge dissipation if decreased - results in impaired stimulus transmission along axon.|
|what is purpose of myelin ||to increase space constant therefore increase the distance traveled by impluse down axon|
|demyelination has what effect on space constant - ||decrease and therefore decreased signal transduction.|
|temporal summation vs spatial summation ||temporal refers to sequential impulses frm same neuron over time
spatial summation refers to impulses from several different neurons |
|neisseria gonorrhea - infection does not provide lasting immunity becuse? ||1 high antigenic variation - and immunity only against single epitope
2 poor antibody response to gonococcus (IgG, IgM) and very low titre is released. |
|resistance of n.gonorrheae to what antibiotics? ||mostly penicillin,
still sensitive to 3rd gen cephalosporins.
|gonorrhea is frequently co infected with what infection?
therfore rx shoudl include what drugs/ ||chlamydia trachomatis - include 3rd gen cephalosporin ceftriaxone and azithromycin/doxycycline|
|repeated neisseria infectino can be caused by what deficiency of the complement system? ||terminal complement deficiency ->inability to form MAC|
|best place to harvest gret saphenous vein for CVS procedures? ie bypass surgery in atherosclerosis ||just below pubic tubercle
|if left anterior descending artery alone is occluded by atherosclerotic plaque, what is the best replacement vessel for bypass grafting? ||left internal mammary artery aka left internal throacic artery - why? becuase superior short and long term patency rate compared to saphenous vein graft. |
|if multiple coronary artery grafts are required, where to harvest the vessels from> ||great saphenous vein - longest in body, superficially located.|
|course of great saphenous vein. ||medial malleolus, medial leg, thigh, drains into femoral vein at femoral triangle. graft here, below pubic tubercle - sartorius muscle laterally, adductor longus medially. |
|short/small saphenous vein course? ||lateral aspect of foot, goes posteriorly drains into popliteal fossa.|
|parvovirus b19, erythrovirus aka fifth disease (is the 5th on the list of childhood viral exanthems) replicates WHERE int he body and why there?
how is it transmitted? ||transmission is respiratory droplets AND blood bourne infection.
replicates in BONE MARROW
why? becuase blood group P antigen = globoside is a b19 virus receptor expressed on RBC, rbc precursors, megakaryocytes, endothelial cells, placenta, and fetus |
|parvovirus b19 causes ||arthritis in adults,
fifth disease in children
aplastic crisis (no new rbc production and this is dangerous in those with existing hemolysis ie spherocytosis or sickel cell)
complication in HIV
hydrops fetalis in first trimester|
|treatment for hodgkins lymphoma - ||vinca alkaloids, vincristine most likely|
|how do vinca alkaloids work ||inhibit microtubule formation - bind b tubulin prevent polymerization of microtubule proteins. inhibition of microtubule causes cell cycle specific cytotox in M PHASE . |
|what is the toxicity to arresting in M phase of cell cycle. ||inhibition of microtubules as in vinca alkaloids causes replicated chromosomes to be unable to align and then separate into daughter cells. |
|vincristine assx ||neurotoxicity, peripheral neuropathy. - disruption of microtubule formation - transports cellular products from neuron body down axon|
|why does microtubule inhibiton cause neuropathy, what drug is characteristic of this ||vinca alkaloids - vincristine - microtubules transport cellular nutrients from neuronal body down axon. vincristine disrupts neuronal microtubuls.|
|patients with COPD, asthma , what beta blockers to give? ||selective beta blocker is required - metoprolol, atenolol, acebutolol, esmolol|
|why not to give propranolol in copd / asthma ||nonselective beta blockers cause bronchoconstriction and peripheral vasospasm and predispose diabetics to hypoglycemia by blunting hypoglycemic symptoms|
|nitrates are vasodilators and decrease BP, how can this paradoxically increase myocardial o2 demand and how can this be prevented ||vaso dilation, decrease BP - body sympathetic system kicks in >catecholamines > beta 1 stimulation, REFLEX TACHYCARDIA - prevent by blocking beta 1 = metorprlol, esmolol, atenolol|
|n-acetyl cysteine is medication used in? ||acetaminophen tylenol od
also renal protective prior to administration of iv iodine contrast for radiological studies.|
|hydralazine causes arteriolar dilation ->what is the negative effect of this? how do we overcome this ||reflex tachycardia - overcome with coadmistration beta blockers.|
|nifedipine is a peripherally acting CCB - causing reflex tachycardia due to arteriolar effect. how to overcome? ||use cardioselective CCB's like diltiazem or verapamil - slow av nodal conduction but beta blockers blunt tachycardia if required.`|
|drugs causing reflex tachycardia
||nitrates, hydralazine, non cardioselective CCB's like nifedipine|
|ischemic colitis due to systemic hypotension happens where first and presents how?
why? ||splenic flexure and sigmoid colon are watershed areas between sources of perfusion. splenic flex is between SMA and IMA. presents with pain and bloody diarrhea|
|what drugs act on PPAR ? what do they do? ||ppar gamma is glitazones for diabeties , increases sensitivty to insulin - hepato and cardio toxic
PPAR Alpha - FIBRATES used to decrease TG's, upregulate LPL causing increased TG clearance.never give with statins (more muscle liver tox)
|most common Congenital adrenal hyperplasia cause ||21 alpha hydroxylase deficiency - decrease cortisol, aldosterone, increases sex hormones, salt wasting and hypOtension.
a NON SALT DEPLETING FORM ALSO EXISTS|
|what is the genetic inheritance of 21 alpha hydroxylase deficiency ||chromose 6, autosomal recessive|
|treatment of CAH? ||deficiency enzymes cause failed ACTH regulation so ACTH goes way up, Rx is administer minimum effective dose of cortisol to keep acth suppressed.|
|omphalomesenteric duct connects midgut lumen with yolk sac cavity. it obliterates at 7th week. if it is abnormal, what defects can result? ||persistent duct aka vitteline fistula is complete failure to close>intestine to umb>meconium leak - diverticulum mcc, partial closure patent part on ileum, fibrous band to umb.
sinus=partial close, patent part at umb.
duct cust (enterocyst) |
|what is enterocyst ||umbilical and ileal part of omphalomesentric duct obliterate as normal by central patent part remains.|
|Li Fraumeni is autosomal dominant mutation in 1 allele of p53 gene predisposing to cancers at young age after second allele mutates. p53 produces p53 protein arresting cell in g1/s until dna damage is repaired, or else inducing apoptosis. what cancers? ||breast, brain, adrenal cortex, sarcoma, leukemia - all before age 45|
|Rb gene regulats g1 S check point w/ rb protein tumor suppressor. what cancers if mutated? ||retinoblastoma and osteosarcoma|
|brca 1 tumor suppressor gene what cancers ||breast and ovary|
|NF2, tumor suppressor gene - ||bilateral acoustic neuroma (schwann cells) in cerebello pontine angle - hearing loss vertigo tinnitus|
|APC gene - familial polyposis syndrome, sporadic colon cancer, and melanoma. what does the gene do? ||maintains low levesl of b catenin (which is oncogenic) and for intracelllar adhesion. |
|how to explain neurological and rash findings that are associated with fat embolus? ||fat globules escape lungs through precapillay av sungs that open due to increased pulm art pressure>fat to CNS, confusion etc. thrombocytopenia and petechiae are b/c platelet adherence and coating of fat microglobules|
|focal necrosis of alveolar wlls with intralaveolar hemorrage seen in/ ||goodpasture, vasculitis ass hge, pulmonary hemosiderosis - basically pulm hemorrhage syndromes|
|red thrombus vs fat embolus? ||red thrombus in pulm artery is DVT or deep veinous source. - no rash or CNS involvement in |
|mechanism of alcohol withdrawal ||ethanol binds inhibitory gabaA and potentiates effects of GABA>sedation .long use>downregulation of gaba recepotrs.also block NMDA(excitatory), so upregulates
also increased synth excitatory mediators ie NE,5ht, dopamine>TOLERANCE and withdrawl|
|alcohol w/d happens 10 hrs after last drink, maximum intensity in 3 days, subsides 5 days presentation/ ||shakes, tremor, autonomic dysfunction - tachycardia, high resp, temp, nausea vomiting, insomnia, agitation, anxiety. seizures at 48 hours (GTC)|
|delrium tremens begins 2-3 days after drink, possibly fatal, sympathetic hyperactivity, high bp, temp, perspiration, hallucinations, confusion , formication=bugs under skin |
|ischemic infarcts of brain look cystic!, coaused by atherosclerosis commonly - necrosis takes place - neurons become red then die - macrophages clean up, stay there for months, lastly what cell comes and walls off the cavity/ ||astrocytes in proces called gliosis|
|wht are the 3 distributions of pneumonia ||patch, involving a number of lobules = broncho/lobular
inflam infiltrate confined to alveolar walls - interstitial
entire lobe = lobar|
|4 stages of lobar pneumonia ||congestion 24 hours
red hepatization 2-3 days
gray hepatization 4-6 days
|congestion 24 hrs ||lobe is red, heavy and boggy
vascular dilation, alveolar exudate his mostly bacteria|
|red hepatization 2-3 days ||red, firm, liver like!hepatization. exudate contains neutrophils and rbs and fibrin|
|gray hepatization, 4-6 days ||gray brown firm lobe, rbc disentigrated, edudate contains neutrophils and fibrin -
note RBC Disintegrated|
|difference between red and gray hepatization ||time frame red, then gray - rbcs are broken down in gray - therfore gray, not red |
|resolution ||restoration of normal - enzymatic digestion of exudate|
|porcelain gallbladder ||seen on x ray, bluish, brittle, calcium laden GB on outline. ca deposits intramurally due to irritation or natural progression , may be asymptomatic - assx callbladder carcinoma 30%! cholecystectomy recomended|
|findings in gallbladder with fluke infection is? ||NOT porcelain GB, find brown pigment stones|
|most common benign lung tumor , finding? ||hamartoma. peripherally located - appear as COIN LESION 50-60 yrs pts. consisnt of disorganized cartilage , fibrous and adipose tissue
disorganized cartilage! fibrous and adipose tissue.|
|neuroendocrine markers are seen in what lung tumor ||small cell ca and carcinoid tumors|
|celecoxib is a sulfa drug, inhibits reversibly cox 2, but spares cox 1. why is this useful ||cox 2 blocks inflammation , cox 1 spared leaves gi mucosa intact , use in patients who need NSAIDs but have GIT problems
toxicity thrombosis, sulfa allergy.|
|rituximab is monoclonal AB vs what? used for what? ||rx lymphomas , vs cd20|
|ADH acts where? ||PRINCIPAL cells (think adh=vasopressin=principal) in medullary collecting duct. v1 + > vasoconstriction and increased protaglandin release. v2+>antidiuretic response|
|sunscreen contains what active ingredient?
active against what wavelengths? what time of UV? ||PABA paraaminobenzoic acid esters - used vs UVB 290-320 nm, do not absorb UVA (320-400)
uvb causes sunburn, immunosuppression, photo aging, and carcinogenesis. UVA is not as harmful but compounds are added ie avobenzone for uva1 uva2
zinc oxide vs all|
|probenecid decreasees renal clearance of penicillins by? ||inhibiting tubular organic acid secretion system. prolongs action of penicillin.|
|clavulinic acid, sulbactam and tazobactam all inhibit ||BETA LACTAMASES|
|non-dihydropyridine CCBs (verapamil and dildiazem)
+ beta blockers cause what bad effect ||significant sinus bradycardia, even sinus arrest and severe hypotension
|why do fibrates predispose to gallstones? ||suppression of cholesterol 7alpha hydroxylase, reduces conversion of cholesterol into bile acids -> more cholesterol in bile - precipitates, gallstones. |
|drugs predisposing to cholesterol stones AND any other factors? ||fibrates (7a hydroxylase), octreotide, ceftriaxone|
|what antibiotic causes increased risk of gallstones (cholesterol) ||ceftriaxone|
|SAH>rupture berry aneurysm or AV malformation - what causes morbidity a week after. prevent? ||vasospasm due to impaired brain autoregulation - rx NIMODIPINE selective CCB|
|anti Ro SSA and LA SSB seen in sjogren syndrome increaed risk of what cancer/ ||non hodgkin lymphoma|
|when to suspect legionella> ||pneumonia and diarrhea|
|how to test for legionella ||sputum is UNRELIABLE use
uRINE ANTIGEN test|
|another bacteria like legionella that inhabits water systems - ||mycobacterium kansasii|
|ace inhibitor allergy reaction is characterized by what ||tongue, eyelid, face lips swelling, due to BRADYKININ, not anaphylaxis|
|what is non immune mediated mast cell degranulation - what causes it? ||non IgE stimuli ie drugs, chemicals heat etc. = pseudoallergic reaction - similar to hypersinsitivity but no ige involvement. - VANCOMYCIN|
|why do fungi mucor absidia mostly rhizopus have affinity for DKA patients? ||presence of KETONE REDUCTASE ENZYME gives affinity for ketones and high sugar. proliferate in blood vessel walls, cause necrosis downstream. - spreads to CNS, death.
|microscope findings in mucormycosis ||broad nonseptate hyphae with RIGHT ANGLE BRANCHING , tissue invasion of Blood vessels , thrombosis and tissue necrosis.
|what to differentiate mucormycosis from? ||aspergillus - also affects sinuses in immunocompromised and has similar sx, seen with v shaped 45 degree branching hyphae|
|diagnosis of bronchopulmonary allergic aspergillosis vs paranasal aspergillus - ABPA - high IgE and antibodies to aspergillus fumigatus. skin hypersensitivty is also + |
|carbon tetrachloride causes what kind of hepatic injury? ||free radical injury - CCL4 is oxidised by p450 oxidase -> CCL3 freeradical forms -> lipid degredation and h202 = lipid peroxidation. hepatocyte necrosis ensues|
|place an IVC filter in patients contraindicated for anticoagulation ||prevents DVT reaching lungs or other parts of body|
|adrena gland tumor, yellowish most commonly is aldosterone secreting = conn syndrme. presentation? ||hyperaldosterone = na retention, k secretion = hypertensionand hypokalemia, also metabolic alkalosis. hypokalemia causes muscle weakness (hypokalemic paresis) and alkalosis causes paresthesias|
|age related macular denge leading caues of blindness in usa - degen of central retina, dry: subretinal drusen or pigment change.
wet: neovasc + hge/gray mebm
rx? ||dry: vitamins and zinc
wet: vgef inhib + laser phototherapy.
RX ranibizumab and pegaptanib|
|anti epidermal growth factor receptors used in non small cell lung ca ||erlontinib, getitinib|
|anti-interleukin 2 is for immunosuppression in gvhd or transplant pts |
|why use methadone in heroin addiction rx ||potent, long acting opiate with good oral availability - key is it has a very long half life so it suppresses withdrawal long as to break addiction.|
|how does head and neck of femur get blood supply?
what vessel is most likely injured in femoral neck fracture ||trochanteric anastomosis = medial and lateral femoral circumflex arteries.
medial circumflex femoral makes the largest contribution and is most likely to be injured|
|HAART has what effect on the HIV virus ||resistance via POL mutations (reverse transcriptase)|
|what kind of genome on hiv virus ||diploid genome 2 molecules of RNA|
|p24 is? ||capsid protein, GAG|
|gp41 is for ||fusion and entry = envelope protein|
|gp120 is for ||attachment to t cells = envelope protein|
|env gene is for ? ||gp 120, and gp41|
|reverse transcriptase synthesizes dsDNA from rna. the ds dna then integrates into host genome ||RECOMBINATION is posisble due to 2 same RNA strands present|
|hiv binds to? ||cxcr4 cd4 on t cells
ccr5 and cd4 on macrophages
homoczygouls ccr5 mutation gives immunity, heterozygous ccr5 gives delayed infection time|
|how do get immunity to HIV? ||homozygous ccr5|
|presumptive diagnosis of hiv with eliza - highly sensitive good for seeing positives, so rule out , then what test to confim ||western blot - specific, high fasle negative rate- use to rule IN
|what is use of hiv pcr/viral load in hiv? ||monitoring drug therapy with viral load.|
|aids diagnosis <200cd4, normal 500-1500.
or cd4/cd8 ration less than 1:1.5 ||
|babies are false positive HIV due to what?
maternal IgG vs gp120 |
|hiv infections at cell count #'s
400-candida, tenia, shingles, TB, bacterial
200 - HSV, cryptosporidiosis, isospora, coccidiodiomycosis, pneumocystis j. ||100 candida esophagitis, toxoplasmosis, histoplasmosis
50 CMV retinitis, esophagitis, MAC, cryptococcal meningoencephalitis.|
|hiv assx neoplasms - kaposi sarcoma, hhv 8, cervical ca hpv, cns lymphoma b cell, NHL |
|eggshell calcification seen in ||hydatid cyst|
|empty can test with sensitivity in shoulder or weakness is specific for what ? ||supraspinatus tendon injury|
|why is supraspinatus most commonly injured? ||friction on acromion, most superior position|
|muscles of rotator cuff ||anterior - subscapularis
posterior infraspinatus, teres minor|
|what collagen related process is responsible for aging and wrinking skin ||collagen fibril production decreases
NOT proline hydroxylation or collagen corss linking or fibrillin synth or collagenase.
only decreased collagen production.|
|how does 2 3 BPG bind to HB? ||pocket formed my 2 BETA chains (only HBA not HBF) the pocket has +charge AA's binding to negative phosphates in 23 dPg. it does not bind oxyHB, only deoxy.|
|why can fetal hb not bind to 2.3 bpg and therefore has higher affinity for o2? ||becuase hbf has 2 gamma chains instead beta chains and the beta chains form a pocket for 23BPG and also HISTIDINE is very important.
|what happens if the histidine on beta chain of HB mutates ||cannot bind to 23BPG then and increaes affinity for o2|
|can 2,3bpg bind all kinds of HB? || no only DE OXY HbA
|sexually active adult with polyarthralgia , swollen, and aspirate w/ neutrophils and intracellular organisms ||neisseria gonorrheae.|
|potassium iodide blocks thyroid uptake of radioactive iodine how? ||competitive inhibition|
|first dose hypotension is an adverse effect when starting ace inhibitors. what drugs coadministered make this phenomenon more likely? ||diuretics causing hypovolemia or hyponatremia etc|
|phenoxybenzamine has what unique characteristics ||irreverisble and a1 and a2|
|why is inhibin low in undescended testes ||becuase inhibin comes from semineferous tubules which involute in undescended testes. - atrophic and hyalinized. FSH is elevated due to loss negative inhibition by inhibin.|
|leydig cells are not sensitive to temperature therefore what will be the finding in undescended testes ||normal testosterone, sexual dvelopment but undescended testes, low sperm and inhibin and high FSH|
|why do reticulocycets appear blue compared to RBC. what stains bring this about and what component are staining blue.
why is this especially noticable after iron therapy. ||anemic gets iron therapy ++erythropoiesis , high reticulocytes also. stain with WRIGHT GIEMSA, see bluish RETICULAR MESH LIKE NETWORK OF RESIDUAL RIBOSOMAL RNA.
after 24 hours in blood stream they mature.|
|non bacterial thrombotic endocarditis is not caused by bacteria or calcium! it is caused by HYPERCOAGULABLE STATE. if NBTE is caused by hypercoagulability is is caused marantic or marasmic endocarditis. what other syndrome is this similar pathology to? ||Trousseau's syndrome - migratory thrombophlebitis also caused by malignancy and hypercoagulability pancreas and lung|
|which cancers are NBTE and trousseaus syndrome closely associated with ||mucinous adenocarcinoma pancreas
|HIV what are NEf and Tat? ||Tat - viral replication
Nef - decreases expression of MHC class 1 on infected cells.|
|precocious puberty definition and causes/ ||males <9 females <7
CAH, ovarian and adrenal tumors
if neurologic abnormalities ie gaze problem(parinaud) then brain tumor|
|parinaud syndrome aka ||dorsal midbrain syndrome - paralysis of upward gaze. MCC Germinoma of pineal gland|
|germinoma originate from what cell line ||embryonic germ cells - |
|symptoms of pineal germinoma ||precocous puberty due -b-hcg production
aqueductal compression ->obstr hydrocephalus
parinaud syndrome - paralysis of upward and convergence - due to compression of tectal midbrain|
|heme oxygenase plays what role in bruises ||heme -> biliverdin (green bruise)|
|axillary lymph node dissectin is a risk for chronic lymphedema of the arm. what cancer does this predispose to?> ||multiple violaceous nodules on the arm - angiosarcoma.|
|LM of shingles shows? ||intranuclear inclusion in keratinocytes and multinucleated giant cells (tzanck smear). skin biopsy shows - acantholysis (loss of intracellular connections) and keratinocytes and intraepidermal vesicles. dermal inflam, and wbc vasculits.|
|what is extrahepatic biliary atresia ||congential obstr of extrahepatic bile ducts. - total obstr by 3rd wk of like - obstr jaundice picture, enlarged liver.
high direct bili, ask phos, ggt.|
|liver biopsy findings in biliary atresia? ||diagnostic :
1 marked intrahepatic bile ductule proliferation
2 portal tract edema, and fibrosis
3 parenchymal cholestasis
rx? surgical release or else biliary cirrhosis by 6 month|
|non-caseating granuloms in ||sarcoidosis and chrons|
|sarcoidosis has elevated ACE levels. |
|sarcoidosis GRAIN? ||gammaglobulinemia, rheumatoid arthritis, ace incre3ase, interstitial fibrosis, noncaseating granuloma|
|epithelial granulomas of sarcoidosis contain ||schaumann and steroid bodies|
|elevated vit d of sarcoidosis is due to increase ||1 alpha hydroxylase activity|
|injury to fibular neck injures what nerve - what loss is seen ||common peroneal nerve also called common fibular nerve
foot drop, and sensory loss on dorsum of foot and lateral aspect of knee|
|common causes of metabolic alkalosis are ||loss of hydrogen from body ie vomiting , stomach suction. this causes decreased cl- (less than 10 meq/l) this is saline responsive
2 thiazide diuretic use increase loss of na cl and reabx hco3-> ++aldosterone >save na but still lose cl - contraction alk|
|third common cause of metabolic alk continued from previous slide ||conn syndrome -hyper aldosterone secretion - save na, save hco3, lose h but lose cl and k. urinary cl is elevated (20=meq/l) this is saline resistant metabolic alkalosis.|
|treatment of the common causes of met alk ||1 stomach / hydrogen loss type - saline rx
2 diuretic thiazide esp - rx saline
3 aldosterone type - saline resistant |
|what test is very important when suggestiv of met alk - always check URINE CL
findings ||vomiting / hcl loss - serum cl low, urine cl low
thiazide dirutetic, urine cl high serum cl low
aldosterone type, urinary cl high (20+)
|met alk is characterized by what findings on lab ||high ph, high hco3 high pco2
|bleeding time and and PTT elevation suggests ||vWD - because platelets are inhiited and factor viii also.
differ from hemophilia - only viii involved so ptt elevated but not BT|
|factor xiii def causes what findings ||it is a transglutaminase that corss links fibrin polymers and stabilizes clots - xiii def causes delayed bleeding but not PT PTT oR BT|
|mitral stenosis has opening snap due to ||abrupt halting of motion of stenotic mitral valve leaf during mitral valve opening . most commonly due to prior rheumatic carditis|
|xeroderma pigmentosum deficient enzyme is ||UV specific ENDONUCLEASE
not 3'5' exonuclease
|what disease is associated with dna exonuclease 3' 5' proofreading failure - ||defective repair of mismatched bases = hnpcc|
|in alzheimers disease , where does amylod deposit and what is it derrived from. what is its specific name ||deposition in parenchyma and blood vessels of the brain of (congo red +) amyloid = A beta amyloid comes from cleavage of APP amylod precursor protein. - 2 places senile plaques (core is a beta) and amyloid angiopathy-media and BM of cerebral vessels |
|where can krukenberg tumors originate ||stomach, breast, pancreas and gallbladder|
|what do ovarian tumor cells look like in krukenberg tumor ||signet ring cells mucin producing in ovarian stroma|
|stomach is most common source of krukenerg tumor - breast in 5-20% - how does seeding occur> ||peritoneal seeding |
|what characteristic nodes are enlarged in GIT malignancy ||sister mary joseph nodule (paraaortic ) and virchows node|
|aortic regurg causes widened pulse pressure and therfore head bobbing. |
|lacunar infarcts are ISCHEMIC infarts and thus do not show up immediately on CT but show up weeks later as LAKE LIKE - why do they happen> ||Hypertension -> hyaline arteriosclerosis _> narrowing of lume -> occlusion|
|where do lacunar infarcts occur and what do they cause there ||pure motor hemi - post limb int cap
pure sensory VPL VPM thalamus
ataxia hemiplegia syndrome - base of pons
dysarthria clumsy hand synd-base of pons or genu of int cap|
|charcot buchard aneurysms are microaneurysms less than 1 mm (vs 15 mm of lacunar) - small penetrating arterioles of basal gang, pons, subcortifcl white matter ||due to hypertension also but not causing hyaline arteriosclerosis
these are hemorrhagic strokes and will be evident on CT
|COAL amino acids cystine ornithine lysie and arginine are dibasic amino acids that share a comon transport mechanism in kidney and intestinal lumen. in GIT, these AA's are reabx w. high affinity transporter on JEJUNAL cells. in kidney? ||substances are filtered at glomerulus and reabx by similar transmemb channel on PROX TUB - the defect causes failure of this so there is excessive excretion of COAL AA's into urine (failure to reabx)|
|the pka of coal aa's is ? 8.3 but urine is acidic so they precipitate - esp CYSTEINE -> cysteine stones ||lifelong urolithiasis and cystinuria |
|cystinuria is inborn error of transporter of COAL aa's . AUTO RECESSIVE, only clinical problem is ||recurrent nephrolithiasis , how to diagnose?
hexagonal cystine crystals. (rhomboid calcium, needule urate) |
|mycolic acid is in cell wall of mycobacterium , makes it acid fast - can be treated with what analog of vit b6 ||inh - is similar to b6 - causes what side effects - neuropathy hepatoxicity 450 inhibit|
|in cerebral hypoperfusion like shock or decreased co, what parts of the brain are injured first ||pyramidal cells of hippocampus = sommers sector
purkinje cells of cerebellum.
if continued ischemia, then watershed zones - border between ant and mid cerebral arteries - wedge shaped areas of necrosis over cerebral convexitie, laterla to fissure.|
|cyclosporine and tacrolimus act on calcineurin - what is it? ||in normal t cells, it is a protein phosphatase activated by + of receptor. once activated, it dephosphorylates NFAT, allowing it to enter nucleus , binds IL2promotor -> IL2|
|Neurofibromin is a tumor suppressor protein on NF1 gene ch 17 - protects vs cancer becuase it suppresses? ||RAS gene - which activates cell growth and proliferation |
|BCL2 (bcell leukemia / lymphoma 2) is an apoptosis inhibitor. if overexpressed, cell death delayed- follicular cell lymphoma (t 14:18, q32;q21 ) ||p53 is a tumor suppressor causing cell cycle arrest and apoptosis. ineffective in most cancers and li fraumeni syndrome|
|choriocarcinoma and moles are associated with what kind of cyst ||theca leutin cysts (bilateral and multiple)|
|yolk sac tumors have 50% what bodies? ||schiler duval bodies - resemble glomeruli|
|grnulosa cell tumor has call exner bodies ||hcg secreting tumors are dysgerminoma and horiocarcinoma|
|granulosa theca cell tumors secrete estrogen and have call exner bodies - present? ||fenizing - precocious puberty but more commonly seen in post menopausal women causing endometrial hyperplasia - small gland like structures with acidophilic material is call exner body - is immature follice |
|using hands to raise from squat or from chair (proxymal muscle weakness) is called> ||gowers sign - |
|why is distal muscle hypertrophy seen in those with proxymal muscle weakness ||to compensate for proxymal muscle weakness. |
|gower sign and calf enlargement in child 3-6 = duchenne - deletion of gene coding for dystrophin - located on x chromosome , also recessive ||only males are affected but females are carriers. - dystrophin is a structural compoent of skeletal muscle fibers , links cytoskeleton actin to transmembrane proteins alpha and beta dystrophiglycans - loos results in myonecrosis. |
|histology of duchennes ||widespread muscle necrosis , on LM, variation of muscle fiber size and angulated fibers seen . some fibers have centrally located internalized nuclei|
|charcot marie tooth disease is caused by mutation of genes responsible for ||synthesis of myelin - abnormal myelin is made , decreased nerve conduction velocity - presents as weakness of dorsiflexion due to common peroneal nerve involvement |
|endomysial inflammation is seen in polymyositis ||perifascicular inflammation is seen in dermatomyositis.
both cause prox musc weak but no distal hypertrophy|
|endoneural inflammatory infiltrate seen in ||GBS|
|tuberous sclerosis ||Skin - sebaceous adenoma, seizure, shagreen patch
4 tubes- CVS rhabdomyoma, Renal tube angiomyolipoma, CSF ependymoma(astrocytoma), skin tube - sebaceous adenoma, shagreen, ash leaf|
|achalasia failure of what plexus ||myentric / auerbach think
achalasiauerbach , and cardia (muscle) so myentric) |
|metronidazole uses? get gap on the metro ||gardenrella, entameba, trichomonas
giardia anaerobes pylori|
|dresseler syndrome ||weeks after MI - fibrinous pericarditis , autoimmune|
|wagr complex ||wilms tumor - renal , mcc in early childhood 2-4 yrs
|km= ||km=[s] @1/2 Vmax
is a substrate concentration allowing the enzyme to do its thing.
if you need less substrate then it means the enzyme has high affinity , if you have to have lots of substrate, then it means the enzyme has a low affinity. |
|lineweaver burke plot what is eq for slope? ||km/Vmax|
|verapamil or quinidine toxic effect with digoxin why/
digoxin and and furosemide >? ||they displace it from its plasma protien causing digoxin toxicity
furosemide causes hypokalemia - causes digitalis tox.|
|what drugs make lithium toxicity more likely?
what is the teratogenic effect of lithium? ||Li behaves like sodium. it crosses BBB freely.
anything causing increased sodium retention , also acts on Li ie ace inhibitors, thiazides, NSAIDS!
|what is ebstein anomaly associted with li? ||ventriculization of right atrium and atrialization of right ventricle - ie displacement of tricuspid valve to apex.|
|low therapeutic index drugs ||phenobarbital, digoxin, warfarin, heparin, lithium|
|3 kinds of antagonism ||pharmalogical, chemical, physiological.|
|physostigmine fixes ||atropine poisoning , crosses BBB, use in glaucoma too|
|why is dopamine beta hydroxylase used in stains? what does it do? ||catalyzes dopamine to NE in the brain.
it is unique to NE containing areas of the brain therefore it can be stained for to find NE containing areas.|
|differnt shocks with appropriate treatment ||anaphylactic shock - epinephrine
septic shock - nor epinephrine (only alpha action but less heart action)
septic shock aslo use dopamine for d1 effect on renal perfiusion
cardiogenic shock - want heart only so b1 - dobutamine
|why is dobutamine used in cardiac stress testing ||specific to beta1 - increased action so increased o2 demand |
|b2 receptors in uterus prevent contraction ||ritodrine and terbutaline |
|which two beta blockers reduce mortality after MI? ||metoprolol and carvedilol |
|thyroid storm ||propranolo|
|non selective beta blockers ; how to remember which ones ||letters p-z except labetalol (has Alol, means it also blocks Alpha - is a nonselective a and b.)
|labetalol and carvedilol ||Alol and I lol -> have alpha activity also|
|alll beta blockers a-m are ? ||b1 selective|
|propranolol use ||migraine prophylaxis (also lithium, and one more - refer to flash cards??), phobia, anxiety, danger with alcohol
use in essential tremor and thyroid storm and prevents t4-t3 conversion|
|how do beta blockers decrease renin secretion - ||beta receptor blockade on renal JGA cels|
|antihypertensive effects of beta blcokers ||decrease heart beta 1 stim, decrease TPR and blod volume due to JGA blockade and decrease aldosterone|
|which beta blockers are goodin patients with pulmonary disease ||A BEAM - acebutolol, betaxolol, esmolol, atenolol ,metoprolol
these are selective beta 1, do not affect b2 - no broncho constr
|which beta blockers have ISA intrinsic sympathetic activity , mimicing NE ie is a partial agonist, (also do not increase blood lipids) ||acebutolol and pindolol. |
|what is beta blocker of choice in portal HTN patients with esophageal variceal bleeding>> ||NADOLOL|
| never give a beta blocker to patient on beta blocker
why? ||cocaine raises BP due to a1 but is a b2 action is slightly there - si moderately high BP.
if added beta blocker, then no b2 effect so only a1 -> massive increase in BP|
| beta blockers are drug of choice in pateints with aortic dissection || they not only decrease the bp but decrease the SLOPE OF THE RISE OF THE BP , and high slope rise of BP increases the tearing of aortic dissection|
| review interactions on page 247 ||review beta blcokers 242 and graphs on 241 and earlier. |
|admin of analgesics like morphine (less so meperidine have what pain causing effect in upper GIT ||spasm of sphincter of oddi -> biliary colic|
|hypokalemia findings on ECG (as caused by amphotericin B) ||T wave FLAT
U wave PROMINENT
premature atrial and ventricular contraction.
ventricular tachycardia or fibrillatoin .|
|oseltamivir is a neuraminidase inhibitor used in inf A B. neuraminidase is required for release of virus from infected cells and spread w/in resp tract. neuraminidase inhibitora cause newly synth virions to adhere to cell surface>aggregate, no spread. ||muyst be taken w/in 48 hrs, slows viral penetration of mucous secretions protecting resp epithelium, preventing infection. |
|amantidine operates how? ||impairs uncoating or disassembly of virus (inf A only) after endocytosis.|
|ototoxic diuretics? ||furosemide (oh dang)
|NITRATE DRUGS causes muscle relaxation how?
simulate nitric oxide (EDRF) ||NO->guanylate cyclase which turns GTP-->cGMP
this incases the cGMP in cell, causing DECREASED CALCIUM, decreasing activity of MLCK, and then dephosphorylation, then smooth muscle relaxation. |
|glanzmann thrombasthenia and the drug which mimics it ||glanzmann is congenital def of GP2b3a receptor.
ABCIXIMAB is AB vs GP2b3a|
|anastrozole is an aromatase inhibitor that blocks estrogen production. where does most estrogen come from ? ||androstendione from adrenal, to estrone in liver/muscle/fat
used in post menopausal women with breast ancer|
|CMV rx in AIDS? ||ganciclovir, foscarnet, cidofovir.
|foscarnet is a pyrophospahate analog, and chelates calcium and wasting of MAGNESIUM . so Low MG and Ca cause? ||PTH -> even more low ca -> SEIZURES.|
|in morphine addicted patients, what drug will precipiate withdrawal ? ||pentazocine - is a mu agonist but only partial agonist. is an analgesic with low abuse potential|
|what is the drug of choice for listeria - ||ampicilin - ceftriaxone does NOT cover it|
|risperidone is good rx for schizophrenia but caues what side effect in women/ ||hyperprolactinemia, causing amoenorrhea
prl is inhibited by dopamine.
dopamine acts on D2 lactotrophs - resperidone is anti dopamine, loss of feedback inhib,more prl>hypogonadism due inhibis gnrh|
|verapamil CCB + beta blocker || very low BP, rate and heart block|
|1 non depolarizing neuromuscular blocker
2 depolarizing N M blocker ||1 vecuronium
2 ONLY ONE is succinyl choline|
|3 c's of measles ||cough coryza conjunctivitis|
|pregnancy bHCG + when? ||fertilization ->implantation 6 days
Blood serum hcg 6-8 days after implantation
urine 14 days after|
|conjugation ||sex pilus, f plasmid
e coli first, most bacteria are capable|
|transduction (recall transversion is substitution of purine for pyrimidine) ||movement of DNA material from one species to another through bacteriophage. -
AB resitance, and virulence factors|
|transformation ||non pathogenic straings can take up DNA from other lysed bacteria around, express their virulence factors and become pathogenic.
S.pneumoniae, H.influenzae, N. Meningitidis. (all encapsulated)
is the example of 2 non pathogenic strains mixed>lethal|
|what gram+ bacteria secrets ENDO toxin ||Listeria |
|ecoli - toxigenic ETEC - has cholera like toxin - ST and LT segments what does LT do and why is ST not inactivated by heat?
LT ++ what receptor ?
St ++ what receptor? ||LT ++ Gs-adenylyl cyclase
ST is not inactivated beacuse it is very small!
ST++ cGMP through guanylyl cyclase on apical membranes of gut mucosal cells.
pili are responsible for adhesion to GIT mucosa, kidney/bladder. K capsule for meningitis.|
|Stacked Brick Intestinal Adhesion is? ||EAEC - enteraggregative e.coli. adhere to jejenum and ileum in aggregative stacked brick pattern but do NOT invade->persistent diarrhea in 3rd world|
|Shiga like toxin from? ||EHEC inactiavtes 60S|
|Fick's principle (fuck principle) = ||CO = Rate of O2 Consumption / (art o2 content - venous o2 content)|
|local defense vs candida what cells?>
systemic defense vs candida is by? ||Local - T CELLS
HIV -> Local candida
Neutropenic ->systemic candida|
|renal cell carcinoma originates from what cells? ||proxymal tubule renal EPITHELIAL CELLS|
|hypertrophic cardiomyopathy, which valve is pressing against the hypertrophic septum? ||MITRAL VALVE NOT AORTIC|
|eukaryotic gene transcription - RNA pol 2 uses DNA to crease mrna
associated with ENHANCERS AND PROMOTERS ||1) Promotors are bindings sites for transcription factors and RNA pol 2 - TWO TYPES OF PROMOTORS TATA/hogness box 25 bases upstream and CAAT box 80 bases upstream.
|ENHANCERS increase rate of transcription initiation through protein binding and interaction with trasncription factors bound to promotor sequences. ||enhancers are located upstream OR DOWNSTREAM OR IN THE GENE ITSELF - ie vARIABLE LOCATIONS.
|Repressor elements ||similar to enhancers , but DECREASE instead of increase transcription rates.|
|resistance in SERIES ||just add them all up|
|resistance in PARALELL ||1/total = 1/r1+1/r2+1/r3 etc
add the FRACTIONS and then INVERT THE ANSWER
remember 1/2+1/2+1/2+1/2 = 4/2 (denominator stays same)|
|goodpasture syndrome is caused by antiGBM vs? ||alpha 3 chain of collagen type 4
attacks lungs and kidneys, glomnephritis+pulm hge - CRESENT FORMATION w/ fibrin. - LINEAR IgG and C3 , rbc casts and mild proteinuria , hypertension.|
|Wegeners - involves upper and lower resp tract, and kidneys RPGN - granulomatosis and polyangiitis, C-Anca+ (anti NEURTOPHIL CYTOPLASMIC antibody. ||RPGN of wegeners is Pauci Immune - no anti GBM antibodies or immune complex deposition (compare to goodpasture syndrome. |
|cardiac cell cytoskeletal protein or mitochondrial enzymes defect leads to what condition ||Dilated Cardiomyopathy|
|mutation in Cardiac Cell sarcomere proteins (beta-myosin heavy chain) underlie hypertrophic cardiomyopathy ||syncope of HCM is onset with exertion, no ECG abnormalities.|
|unprovoked syncope with congenital prolonged QT interval is defect in Potassium channels - what 2 syndromes? ||Romano Ward, Jarvell Lange Neilsen syndrome|
|dexrazoxane is what? ||iron chelating agent prevents anthracycline induced (doxorubicin) cardiotoxicity|
|cisplatin (platinum) based chemotherapy causes nephrotoxicity - how to prevent this/ ||aggressive Nacl hydration (drug remains inactive in high cl solution) and drug AMIFOSTINE thiol based cytoprotective free radical scavenging agent used to decrease cumulative nephrotox of platinum agents.|
|follicular lymphoma is most indolent NONHODGKINS lymphoma in adults, origin, defect etc?
Waxing and Waning lymphadenopathy ||t14;18, characteristic and results in overexpression of bcl2|
|hairy cell leukemia presents with splenomegaly and pancytopenia in older men LN's are not enlarged , leukemic cells have hair like cytoplasmic projections , + for TRAP tartarate resistant acid phosphatase ||Mycosis Fungoides: cutaenous T cell lymphoma - proliferating cd4+ infiltrate skin->pautrier microabscesses - plaques like eczema/psoriasis.erythroderma|
|ALL - MCC in children - lymph nodes, liver spleen enlarged, fever, bleeding, bone pain. neoplastic cells are pre b or pre t
||burkitt assx ebv , aggressive very susceptible to chemo|
|what tissues cannot use ketones and why/ ||any tissue w/o mitochondria - RBC's
and liver cannot becuase it lacks Succinyl Coa Acetoacetate Coa transferase (thiophorase)|
| SHiN ? ||
strep pneumo, HiB, N.Meningitis - IgA Protease +
|spore forming bacteria ||bacilus (cereus, anthracis)
Clostridium (perfringens, botulinum, tetani)
Coxiella Brunetti |
|clostridium perfringens toxin ||alpha toxin is Lecithinase - acts as phospholipase , destroys cell membranes
test with NAGLER REACTION in egg yolk
gets DOUBLE ZONE HEMOSYSIS on BLOOD agar|
| dangerous infections in neonates? ||Groub B strep (Agalactiae) (beta hemolytic)
|diptheria toxin is coded by what> ? what medium?
what is volutin? ||beta prophage, loeffler coagulated serum medium
volutin are metachromatic ble and red granules .
RECALL ELEK TEST distinguishes diptheria from other diptherioids|
|mechanisms of AB resitance ||vancomycin chnage in peptidoglycan later penicilin binding protein d-ala d-ala to d-ala d-lac, PBP2, protein 2a replaces transpeptidase
sulfonamides decrease affinity of enzyme mutations and active transport of AB out of cell
|mechanism of tetracycline and gram - bacterial resistance> ||tetracycline - active export out of cell
gram - bacteria , conjugation plasmids give AB resistance - especially VRE enterococcus , gamma hemolysis) - get resistance very quickly and pass on plasmid.|
|tetanus toxin blocks gaba and glycine release causing spastic paralysis from what cells, and where ||renshaw cells in spinal cord
remember toxin is transported INTRAAXONALLY and binds GANGLIOSIDE RECEPTORS|
| recall vancomycin is normally given IV becuase of very poor oral abx - when can you give oral vancomycin> ||c diff colotis|
|c diff and c botulinum both have double zone hemolysis ||c diff has stormy fermentation of milk media .|
|listeria and d diff polymerize actin filaments - actin rockets |
|only bacteria to have poly peptide capsule with d glutamate is ||anthrax|
|vaginal transmission during birth ||strep agalactiae (swap , if + at 36 rx penicillin and ampicillin)
|listeria has what kind of motility and what other special movement trait ||actin rockets (like c diff) and tumbling motility
can cause amnionitis , septicemia, abortion and granulomatosis infantiseptica rx ampicillin gentamycin - has listeriolysin o|
|nocardia vs actinomyces abscess in brain/ ||actinomyces 1 single brain abscess
nocardia, multiple abscesses|
|TNF alpha blockers ||all are antibodies - adalimumab, etanercept, infliximab - all used for same purpose -
INFLIXIMAB PREDISPOSES TO TB REACTIVATION
etanercept is a TNF DECOY RECEPTOR|
|type 1 diabetes is what kind of hypersensitivty rxn> ||type FOUR not type two|
|pallegra is 3d's caused by what ||niacin deficiency , OR b6 deficiency
recall tryptophan --> niacin THROUGH b6
isoniazid also blocks this|
|when calculating incidence, dont forget what important point/ ||those currently with or those previously + for it are NOT CONSIDERED AT RISK|
|what diseases is ESR important in? ||polymyalgia rheumatica
OSTEOMYELITIS!! high esr should raise clinical suspicion
|fluoroquinolones work on what enzymes? what 2 steps does it block?
what genes code for these enzymes?
what genes mutate to give resistance to FQ's? ||topoisomerase 2 and 4 - come from genes PARC and PARE
4-separation of daughter dna chromosome before cell division (recall semiconservative replication)
resist by mutation in gyrA gyrB genes , altered affinity of binding.|
|DsDNA antibody is specific to RENAL involvement in SLE |
|what disease are + ANA (antinuclear antibody) ||lupus, sjogrens, scleroderma, polymyositis , dermatomyosits rheumatoid arthritis |
|what type f hypersensitivity reaction is Polyarteritis Nodosa ,
what type is eczema ||PAN - III
Eczema type I
|anti microsomal antibody ||SLE sjogren, rheumatoid arthritis, hashimoto, others|
|ANA is progrnostic in what diseae ||primary biliary cirrhosis|
|anticentromere antibody is prognostic for what - ||portal hypertension |
|histo finding in primary biliary cirrhosis - periductal granulomas, intra epithelial lymphocytes,, epitheloid cells ||associated with gluten sensitivty , rx ursodeoxycholic acid and cholestyramine and vitamin adek|
|primary sclerosing cholangitis - assx churg strauss p anca +, 80% assx ulcerative colitis - ||image ducts with MRCP see BEADING of intra and extra hepatic bile ducts. |
|what is ANCA ||igG vs cytoplasmic antigens in neutrophil granulocytes, measured with elisa and immunflouresence. pANCA is perinuclear staining - c ANCA is cytoplasmic staining|
|c anca is cytoplasmic staining ||p anca is perinuclear staining. |
|coefficient of determination? ||r2 , r is pearsons coefficient |
|is chlamidya reportable? ||no - but gonorrhea, syphilis and hiv are|
| what is the basic ADDICTION pathway in the brain ||DOPAMINERGIC - ++->positive reinforcement, medial forebrain bundle, -> nucleus accumbens -> venteral tegmental area
inverse relationship - dopamine is like gas pedal serotonin in forebrain is like brakes. |
|cravings come from ||insular cortex through its projections to thalamus and amygdala (emotional anticipation and conditioned response) |
|when in apgar given? whats the best score ||given at 1 min and 5 min - thus given twice total
best score is 10
apgar - appearance pulse grimace activity respiration
| treatment for restless leg syndrome ||dopaminergic agents - like roperinole and premipaxole , levo carbi dopa
avoid caffeine, clonazepam gabapentin or opiods in extreme
|what is secreted from suprachiasmatic nucleus ||NorEpinephrine - controls ACTH prolactin, melatonin and nocturnal NE. |
|what is the pathway of circadian rhythm ||Retina _> suprachiasmatic nucleus,- NE release , Pineal gland , melatonin. |
|what drugs can reduce risk of hiv transmission from mother to child ||azathiaprine reduces breast milk risk by half. (risk was 50% with breast feeding)
Nevirapine - given around labor , reduces risk of delivery trasnmission by half also
high compliance required for AZT rx|
|what are the risks associated with transmission of HIV ||uncircumcised at higher risk, risk of sex with low risk male is 1/5 million, high risk make i 1/20-1/2. needle stick injury 1/250 , blood transfusion 2/3
vertical - 20% with no intervention - recall all infants test + due maternal AB:S. after 1 year, 20|
|what is fanconi syndrime ||proxymal tubular defect of resorption - leads to polyuria, acidosis, electrolyte imbalance, and growth failure|
|von hippel lindau syndrome - chromosome, type of transmission and associated malignancies ||chromosome 3, autosomal dominant and 4 cacners
IS A TUMOR SUPPRESSOR GENE MUTATION
3 systemsn - BLOOD VESSELS - hemangioblastoma and angiomatosis
RENAL RCC , ADRENAL - pheochromoctoma. |
| fanconi anemia ||genetic dz , short stature, high incidence of tumors, leukemia, aplastic anemia - p53 mutation - AML COMMON |
|Wilsons disease - autosomal RECESSIVE, mutation of
ATP7B on chromosome 13.
||reduced formation and secretion of CERULOPLASMIN and hinders copper metabolism reducing formation and decreasing copper secretion into biliary system. -copper free radical damage to liver, then blood, gets to basal gang and cornea.|
|liver involvement in wilsons disease ||asymptomatic liver function tests
fulminant hepatitis, protal hypertesniion
|neurological sequela of wilsons disease ||parkinsonian like tremor (resting and pill rolling) common due to both in basal ganglia
rigidity, catatonia, ataxia, slurring speech, personality changes, depression or paranoia. |
|how to diagnose wilsons disease - liver biopsy showing quantitative hepatic copper level higher than 250 mcg/gram dry wt. - or, low serum ceruloplasmin (<20 mg/dl)+keyserflecher rings ||CT of head can show the degenerative changes but not specific to wilsons disease and not part of diagnosis |
|lymph node malignancy is MONOCLONAL as assessed by GENE REARRANGEMENT ON T CELL RECEPTOR GENES. ||see single allele for V REGION of TCR.
similar is true in B cells = clonal rearrangement of HEAVY CHAINS is b lymphoma|
|viral infections associated with intracytoplasmic inclusion ||herpes virus and measles (differentiate with koplik spots of measles)|
|rx ADHD ||methylphenidate ritalin
atomoxitine, nonstimulant SNRI = dexedrine
|rett disorder is x linked dominant !
only seen in females because males die in utero ||seen in girls - apparently normal for 6 months.years then loss of development, retardation, loss of communication, ataxia and stereotyped handwriting. - midline hang wringing
deceleration of head growth! |
| why does purging, vomiting cause hypokalemic, hypochloremic alkalosis? ||loss of H+ and Cl- in vomiting = hypochloremic alkalosis -
low K because - body tries to compensate by dumping H+ from cells into serum in EXCHANGE for k + leading to low K in serum
|how do anorexics and starvation patients get LANUGO> ||low fat -> low fat based hormones ie GnRh - > low sex hormones -> lanugo, amenorrhea - same mechanism|
| neurotransmitters in psychiatric disease: ||
|anxiety : ||+NE
- GABA (rx benzo)
- 5HT (ssris , flluvoxamine also in OCD)|
|depression ||- NE
|alzheimers ||- ACH|
|Huntingtons ||- ACH
- GABA therefore never give anticholinergics in alzheimers and huntingtons patients|
|schizophrenia ||+ dopamine |
|parkinsons ||- dopaine
recall benztropine - muscinic atagonist is used|
|differentiate dementia vs pseudodementia ||dementia , patients may not be aware of memory loss -
pseudodementia - usually depression in elderly - and they are away are irritated by their dementia|
|mini mental status exam used for what ||dementia diagnosis|
|genetics associted with alzheimers disease ||presinilin 1, 2 on chromosomes 1, 14.
APP gene (amyloid precursor protein) on chromome 21 seen in DOWN SYNDROME
apolipoprotein E gene on ch 19|
|lewy bodies are seen in > ||lewy body dementia ( parkinsonism with visual halucinations and repeated falls)
, parkinsons disease and lewy body type alzheimers|
|hirano bodies seen in? ||intracellular aggregate of ACTIN , rod shaped cryatals, eosinophilic.
|oligclonal band of igG seen in CSF in what diseasee? gamma portion of electrophoresis ||MS (igG vs oligodendrocytes)
syphilis, SLE, sarcoidosis|
|high potency neruoleptics ||haloperidol, flufenazine |
|medium potency neuroleptis ||trifluperazine, molindone|
|low potency ||thioridizine, chlorpromazine|
|what is dantrolene used for ||malignant hyperthermia (caused by inhalational agents and succinyl choline) in people with RYR1 gene mutation.
Neuroleptic malignant syndrome (antipsychotics)(dopaminergic)
mechanism - prevents release of calcium from sarcoplasmic ret. in SKEL MUSCLES|
|C C T T
thioridizine causes? ||corneal deposits for cpz
reTinal deposits for Thioridizine (also retrograde ejaculation)|
|EPS high in high potency antipsychotics
||anticholinergic SE's high in low potency antipsychotics|
|if rx of schizophrenia makes the symptoms worse? ||organic brain lesion in dominant temportal hemisphere
|antipshychotic use presents with what dental complication ||cavities because it produces metalic tase in mouth and patients eat candy
|Tardive dyskinesia vs cerebelar disease ||cerebellar disease - tremor present always , TD tremor REDUCES while reaching for an object)
|RYR1 gene mutation is for what? ||fever and hyperthermia when use of succinylcholene and antipsychotics -, neuroleptic malignant syndrome and malignant hyperthermia are very similar
RYR1 gene codes for ryanodine receptors of skeletal muscles. |
|typical antipsychotics vs atypical = ||typical block d2
atypical block d2 and 5ht - prevents a lot of side effects becuase 5ht is also blocked.
h2 and alpha is blocked in both causing hypotension, and weight gain from h2|
|olanzapine ||OCD, depression, anxiety, mania , bipolar, tourettes
also use other atypical antipsychotics
|olanzapine and quietapine cause major gain of ||weight -> diabetes|
|respiridone how does it cause amenorrhea ||through increasing prolactin
also causes agranulocytosis like clozapine |
|diphenhydramine and antihistamines worsen what? espeially in what dangerous age group? ||extrapyrimidal side effects in elderly like delerium. use bezos instead.or TRAZODONE|
|trazodone is used in rx depression or insomnia in demented patients ||less potency, and anticholinergic side effects than TCA's
itself is a serotonin modulator.|
|patient with dementia needs help sleeping or to reduce agitation , what antipsychotic to use/ ||use HIGH potency becuase has less anticholinergic side effects (worsen delerium)
do not use low potency because it has high anticholinergic side effects|
|manic episode lasts how long
signs? ||1 week DIG FAST
distractable, irresponsible (hedonistic), grandiosity, flight of ideas
|one manic episode =? ||bipolar 1|
|one hypomanic episode ||bipolar 2|
| rx bipolar ||lithium valproic acid carbamezapine|
|lithium used for what
acts through phosphoinositol pathway -> IP3 ||bipolar, aggression, cluster headaches, causes NEphrogenic Diabetes insipidius so used in rx siadh. |
|side effects of lithium LMNOP ||lithium, movement (tremors)(replaces sodium -> tremors )
hypOthyroid, pregnancy problems ie fetal cardiac defect EBSTEIN ANOMALY|
|uses of streptomycin and mechanism of action ||tuberculosis (blocks 30s ribosome, halts protein synth)
plague yersinia pestis
tularemia - francisella tularensis|
|What anti TB drug causes it to lose acid fastness ||the stain is taken up by mycolic acid int he cell wall of TB
INH acts by inhibiton of mycloic acid synth - thus is specific to mycobacteria.
recall INH is toxic to Neurons and Hepatocytes|
|parkinsons patient therapy is losing effectiveness, why? ||multivitamin with b6 - increases peripheral metabolism of levodopa decreasing its effectiveness.
|cimetidine causees gynecomastia and inhibits cytochrome p450 causing increase in what drugs ||warfarin, phenytoin, propranolol metoprolol quinidine and theophylline|
|retrolental fibroplasmia is mediated through what growth factor ||vgef stimulated by high concentration o2|
|phylloquinone is plan baesd vitamin k ||menoquinone is flora based vit k|
|breast milk has all vitamins except ||vit d and k|
|increased diagnostic accuracy (lead time bias)
increases what ||incidence AND prevlaence
contrast with improving survival of patients which only increases prevalence|
|which genes are on apical ecdodermal ridge (ectodermal thickening at the end of the developing limb) ||wnt 7 and fgf.|
|what does sonic hedgehog gene do ||at base of limbs in zone of polarizing activity ZPA, involved in patterning , along Ant Post axis -- determines correct location of limbs. is ECTODERMAL - deficiency causes holoprsencephaly|
|wnt 7 - at apical ecodermal ridge ||necessary for proper organization along dorsal ventral axis|
|FGF gene ||achondroplasia - also on apical ectodermal ridge - stimulated mitosis of mesoderm causing limb lengthening|
|homeobox gene - skelegtal organization in cranio caudal direction - codes for transcirption regulators, |
|hox d13 ||synpolydactylyl between 3-4th digit
retinoic acid mutates it.|
|smudge cells seen in ||b - cll|
alpha granules ||dense bodies - ADP, Ca(vit K),
alpha granules - vWF and fibrinogen and PF 4 - TXa2 is not preformed - rather synthesized |
|affinity is binding strength
IgG ||avidity - mullti point binding
|cisapride is a promotility agent that was removed from market for causing arrhythmias - which? ||Torsades De Pointes|
|foregut from where to where,
what artery supplies ||pharynx to duodenum
|midgut ? ||duodenum to splenic flexure
|hindgut ||splenic flexure to rectum
|developmental anomalies of ROSTRAL FOLD ||Sternal defects|
|failure of Lateral fold ||omphalocele and gastroschiesis|
|Caudal fold ||bladder extrophy|
|what is the covering in omphalocele ||amnion on peritoneum
other anomalies are associated 50%|
|gastroschiesis is extruding viscera NOT covered by sac. ||other anomalies not common,
liver is never found protruding|
|how do we activate the dehydrogenase complex ||exercise higher NAD/NADH ration
high ADP and high calcium|
|arsenic blocks lipoic acid |
|3 different dehydrogenase complexq ||akG
branched amino acid dehydrogenase |
|branches of internal pudedal artery ||I love going places in my very own underwear
I L G P I M V O U
iliolumbar, lateral sacral, gluteal (sup inf), pudendal (int), inf vesical, middle rectal, vaginal, obdurator, umbilical |
|causes of mitral valve prolapse
||MVP may occur with greater frequency in individuals with Ehlers-Danlos Syndrome, Marfan syndrome  or polycystic kidney disease. Other risk factors include Graves' disease. and chest wall deformities such as Pectus Excavatum |
|what is the result of untreated congenital hip dislocation ||EROSIVE arthropathy |
|primordial germ cell migration from yolk sac failure results in ||extragonadal germ cell tumor = teratoma.|
|achondroplasoia (autosomal dominant)
FGFr3 - membranous ossification is NORMAL so normal head. vs endochondral ossification ||defect is constituitive ACTIVATION of FGFR3, causing causing INACTIVATION of chondrocytes|
|duodenal atresia - failure to recanalize
assx trisomy 21 ||apple peel atresia is jejunal, ileal, or colonic atresia is due to VASCULAR ACCIDENT|
|Tracheo esophageal fistula is a MESODERMAL problem ||foregut midgut hindgut all endoderm
developmental defects of ant abdominal wall ECTODERMAL|
|midgut development is herniation at 6 weeks
reenters abdominal cavit at 10 weeks, rotates around SMA - volvulus ||summary - malrotation of midgut causes = omphalocele, intestinal atresia or stenosus, voluvlus. |
|coelom is the embryonic cavity in mesoderm (middle layer) gives rise to? ||pleura, pericardium and peritoneum|
|most common location of obstruction in fetus causing hydronephrosis is uretropelvic junction - why? ||by 10 weeks, before metanephros ->kidney starts making urine, the uterters are fully canalized. failure at uretropelvic junction is most common abnormality|
|amniocentesis showing acetylcholinestrace is indicative of wht defect ||failure of FUSION - NTDs |
|NTDs happen at whta time frame, and where ||4th week failure of fusion of anterior or posterior neuropores.
anterior is encephalocele or anencephaly
posterior is more common, spina bifida, menengocele or meningomyelocele|
|mesonephric ducts - what do they do in both genders ||in males, they become epidydamus, ductus deferns, seminal vesicles and ejaculatory ducts,
in females they become gartners ducts
they never fuse.|
|paramesonephric ducts in males? ||vestigial testicular appendix|
|fusion of urethral folds forms urethra in both males and females ||failure of fusion of urethral folds = hypospadias|
|Pagets disease of bone is osteoCLASTIC
these osteoclasts are multinucleated 100+ (normal is 2-5) what is this stimulated by? ||++ by osteoblasts
RANK L and M-csf
macrophage colony stumlating factor
receptor for activated nuclear factor kappa - beta ligant |
|alkaline phosphatase increased in all osteoCLAST diseases ||stress fractures,
|gastric bypas surgery complication ||dumping syndrome - (stomach food storage function is lost) - accelerated dumping -> sugary food especially - anxiety /bloating, diarrhea, "butterflies" |
|DLco is diffusion limited carbon monoxide (rate of diffusion) what does this measure? ||surface area and thickness of membrane
- reason is because is ALways is diffusion, we can therefore predict the rate of diffusion.
emphysmea and fibrosis DECREASE
|resolved ARDS usually becomes? ||interstitial fibrosis - look for decreased DLCO|
|what does the cresent consisit of in RPGN ||plasma proteins c3, fibrin, parietal cells, monocytes, macrophages|
|metastatic prostate cancer to bone looks like?> ||pleomorphic cells arranged into duct like structures (remember its ADENOcarcinoma)|
|somites are what cell lineage? ||mesoderm - somites are masses of mesoderm give rise to muscles.|
|basophils are never present in cancer cells |
|if children dont talk by 18 months, then check?
or just general crying and babbling ||hearing.|
|findings in DIC
(common cause retained fetus) ||prolnged PT PTT
elevtaed FBP's fibrin split producsts aka d dimerslow factor v and viii levels.|
|which clotting factors are low in DIC ||V VIII|
|site of attachment of renal stones in kidney is ||renal papilla which is junction b/w pyramids (cortex) and the minor calyx ->major calyx -> renal pelvis -> ureter|
|all renal stones (calcium, oxalate, phosphate and uric acid PRECIPITATE in ACIDIC ph.
Ca can precipitate in Neurtal Ph
ONLY ONE KIND OF STONE PRECIPITATES IN ALKALI? ||STRUVITE|
|urease positive bugs are
PARTICULAR KINDS HAVE UREASE ||P K H U
proteus, Klebsiella, h pylori, ureaplasma|
| bacterial toxins that inhibit protein synthesis ||EHEC vero/shiga toxin, shigella toxin - both act through inhibition of 60s ribosome unit
diptheria and pseudomonas toxins work though EF2 mechanism|
|lysine instead of glutamic acid at 6th postio on beta globin gene causes ||HBC - this lysine is BASIC so on electrophoresis HbC travels SLOWEST
recall valine for glutamic acid is the sickle cell mutation|
|sickle cell train Valine for glutamic acid at 6 causes what kind of interaction, making it so dangerous of a disease ||hydrophobic interaction - recall valine is NON polar but glutamic ACID is POLAR so LOSS OF CHARGE/polarity |
|normal folding of the globin chains - alpha? beta? secondary ? tertiary? ||8 alpha helical stretches is secondary folding
8 beta bends is tertiary structure -
sickle cell or hbc does not cause major change in the structure. however PROLINE substitution would do this|
|HbM disease is formation of methemoglobin - prevents formation of ferrous iron - remains in ferric form - ||this is due to HISTIDE -> TYROSINE in heme binding pocket of alpha or beta chain|
|rapid induction of anaesthesia , or truth serum is done with sodium thiopental - ultra short acting barbiturate - acts on gaba and increases inhibition. - why is it ultra short acting> ||very quickly redistributes into skel muscle and fat tissues|
|best rx in MI arrhythmias , why? ||lidocaine and amiodarone - specific to depolarized and depolarizing rapidly cells - which describes MI - so these drugs are specific to infarcted types of tissue , treatment of choixe|
|verapamil is used to treat atrial tachyarrhythmia - why is it important to not give in ventricular tachyarrhythmia ||because it cauess vent fibrillation and death|
|digoxin is used as an antriarrhythmic, why? ||slows AV nodal conduction -> use in atria tachyarrhythmias|
|atypical phenylketonuria causes what symptoms and what is the deficiency ||tetrahydrobiopterin reductase , requred for phenylalanine>tyrosine and tyrosine>dopa - , also required for Nitric oxide and serotonin - symptoms are then high prolactin because no dopamine so no inhibition of prolactin. also neurological abnormalities|
|reed sternberg cells ||hodgkins lymphoma|
|differential for heart valve thickening with vegetations ||SLE - libman sacchs-most common, involves coronaries also
|dermatomyositis - autoimmune so perivascular ischemic necrosis,
associated with? ||myocarditis, interstitial lung disease , vasculitis|
|churg strauss - necrotizing vasculitis commonly seen in ATOPIC patients ||coronary artery necrotizing vasculitis is seen but NOT cardiac valve defects
- assx asthma, eosinophilia.
p24 and p 7 - what gene
gp41 gp120 -?
replication regulation? ||p7 p21 - GAG
gp41 gp120 - ENV
enzymes - Pol
regulation of replication TAT and REV|
see lipid laden macrophages
and OLIGODENDROCYTE depletion - loss of white matter
oligoclonal bands of IgG ||also see oligodendrocyte depletion in progressive multifocal leukoencephalopathy|
|chloramphenicol inhibits ? ||50s subunit and peptidyl transferase so inhibits protein synth|
|homeobox genes code for? ||DNA TRANSCIPTIONAL FACTORS which regulate expression of genes and location of organts and tissues called morphogenesis|
|reserpine is a cheap antihypertensie used globally causing what symptoms? ||blocks packaging of NE, dopamine and serotonin, at the stage of packaging into vesicles. they are not vesicated, therefore get broken down by MAO. this causes depression! and suicidal ideation,
also nasal congestion and hypersecretion of gastric acid|
|granulomatous vasculitis of MEDIA, arterial only ||takayasu - mostly aortic arch but also temporal - women less than 40
temporal arterititis , mostly temporal , greater than age 50|
|luekocytoclastic vasculitis, hypersensitivity vasculitis, microscopic vasculitis ||preesnt in small arterie with FIBRINOID necrosis ,
arterioles, capillaries, veinules. similar to PAN, igA|
|PAN - immune complex vasculitis causing what kind of necrosis?
affects medium and small arteries ||FIBRINOID necrosis - immune complex goes into vessel wall, brings complement and plasma proteins making an eosinophilic fibrinoid smudge |
|rheumatoid arthritiis vasculitis ||similar to PAN - fibrinoid type, causing infarcts of organs in long time rheumatic arthritis patients|
|orthostatic hyptension ||phenelzine (mao inhibitor) and TCAs|
|drugs causing seizure ||imipenem !!
isoniazid IF GIVEN WITHOUT PYRAZINAMIDE|
|skin brusises ||petichae less than 5 mm
purpura 5mm - 1cm
ecchumosis 1cm +
do NOT blanche - unlike telangiectasias|
|apc gene -> adenomatous polyps are premalignant. ||adenoma to carcinoma sequence involves kras p53 and DCC gene|
|what enzyme increased causes increase chance of colon cancer ||COX - therefore cox2 inhibitors are shown to DECREASE colon cancer.|
|cardiac tamponade can occur in relation to viral illness how? ||viral pericardidtis -> serous fluid accumulation , tamponade.
jugular distension, pulsus paradoxus and low blood pressure are seen.
recall constrictive pericarditis is a chronic process|
|becks triad of cardiac tamponade is? ||1) distended jugular
2) distant muffled heart sounds
|myocardial infarction can cause signs similar to becks triad however it would also present with PULMONARY EDEMA - ||remember you must HEAR SINGS oF edema - dyspnea and fatigue will be signs in both so cannot be assumed to be caused by pulm edema|
|HSP is a IgA mediated LEUKOCYTOCLASTIC vasculitis affecting young boys after infection || the IgA is vs the infecting organism and then deposit in small vessels causing JOINT PAIN, PALPABLE PURPURA and ABDOMINAL PAIN
can be hematuria and tarry black stool|
|joint pain in HSP is in what joints why? ||knees and ankles, because of dependent location - > more immune complex deposition|
|pinealoma is not originating from pineal gland, rather just in the area of the pineal gland. tey are most commonly what ? ||germinomas - cause perinaud syndrome, obstructive hydrocephalus and precocious puberty|
|size of adenomatous polyps increases risk of malignancy ||less than 1 cm - 0%
more than 4cm - 50%
|which gene converts normal mucosa to polyp - is APC ||which gene makes the cells proliferate in existing poyps so they become larger and more likely malignany - K RAS
|final malignant transformation of a large polyp into cancer cells requires
DCC and p53 ||K ras is a proto-oncogene , after mutation is becomes an oncogene.
normally it codes for a protein that regulates cell cycle. after mutation , loss of function makes it oncogenic.|
|enfurvitide is an HIV fusion inhibitor MOA? ||binds gp41 prevents entry into genome of uninfected CD4+ T cells|
|ritonavir is a protease inhibitor prevents maturation and assembly of virions makes them uninfective ||zidovudine is an NRTI - requires activation by thymidine kinase before it can be in its functional triphosphate form|
|nevirapine, efavirenz and delaviridine are NNRTI's , prevent RNA -> Dna, no activation required. ||most dangerous s/e is life threatening hepatic failure with encephalopathy - preceeded by flu like symptoms with abdominal pain, jaundice - this happens within 6 wekks.
stevens johnsons within 18 wks|
|erythema nodosum ||most common in strep pyogenes pharyngitis,
also s aureus, sarcoidosis, fungal infections, chlamidya|
|anterior uveitis causes ||herpes, syphilis, lyme disease and hla b7 assx reactive arthritis|
|bilateral absence of vas deferens seen in ||cystic fibrosis|
|lipofuschin is due to ||lipid peroxidation and free radical damage seen in heart and liver of aged or malnourised, diseased patients.|
|transciption, regulation and degradation of mRNA in cytoplasm is mediated by what ||cytoplasmic P bodies|
|what are the post transcriptional modifications done to mrna to turn it form hnRNA into mRNA ||poly A tail, cap on 5' end, intron splicing|
|hepatic adenomas are seen in young women especially after using OCP's ||epigastric or RUQ pain, asymptomatic or incidentally discovered.
may rupture and cause life threatening bleeding.|
|granulomas in lung, other than TB ||fungi, berrylium, foreign body, sarcoidosis, histiocytosis wegeners|
|fanconi syndrome of kidney is due to chronic NSAID - chronic interstitial nephritis ||loss of k, p, amino acids and glucose|
|pathophys of chronic nsaid interstitial nephritis ||medullary concentration+vasa recta ischemia due to inhib PG's+cellular damage due to mitochondria oxidative decoupling -> reversible interstitial inflammation, calyceal architecture distruction, tubular atrophy.|
|duodenum breaks down lipids, jejenum absorbs it. ||this remains true in cholecystectomy patients|
|valine leucine threonine methionine cholesterol and odd chain fatty acids catabolized to propionyl coa through what enzyme ||branched chain alpha keto acid dehydrogenase|
|porpionyl coa > methylmalonyl coa through biotin dependent carboxylation > succinyl coa through ISOMERIZATION and b12 ||defeciencty of methylmalonyl coa isomerase causes increased methyl malonyl coa in serum and urine|
|PRIMIDONE is metabolized to? ||phenobarbital -
patient with overdose symptoms who is epileptic but shows high blood levels of phenobarbital - it was primidone overdose , metabolized into this.
used in rx seizures and epilepsy but avoided for lethargy |
|what type of cell predominates in sarcoidosis patients bronchoalveolar washings ||cd4+t cells
look for high cd4 : cd8 ratio in bronchioalveolar lavage
5:1 - 20:1
this ratio is DECREASED in hiv, hypersensitivty pneumonitis|
|foscarnet is a pyrophosphate analog that does not require activation
it inhibits directly dna polymerase in herpes and reverse transcriptase in HIV ||used in HIV patients with herpes virus not responding to acyclovir and CMV not responding to gancyclovir|
|drugs that are metabolized and excreted by liver tend to be highly lipophilic and have a HIGH VOLUME OF DISTRIBUTION ||highly lipophilic drugs with high VD are poorly renally excreted becuuse they pass lipid membranes easily and are reabsorbed by kidney|
|histo of pilocytic astrocytoma - most common cerebellar tumor in children, can also arise in brainstem, hypothalamus, or optic pathway ||cystic, micro-cysts, well differentiated spindle cells with hairy proceses.
eosinophilic granular bodies and rosenthal fibers present|
subcortical white matter, butterfly ||has ASTROCYTES (keep straight with pilocytic astrocytoma which has WELL DIFFerentiated SPINDLE CELLS) this tumor has POORLY DIFFERENTIATED cells pleomorphic marked nuclear atypia and brisk mitotic activity NECROSIS, VACULARITY|
|medulloblastoma - second most common posterior fossa tumor of children ||small poorly differntiated cells with high mitotic activity SCANT CYTOPLASM, LITTLE STROMA AND HOMER WRIGHT ROSETTES|
|ependymoma ||pseudorosettes, gfap +
roof of 4th vent in children
spinal in adults|
|neuroblastoma is most common extracranial tumor in children. renal medulla ||small round blue cell tumors, neuritic process called NUEROPIL is pathognomonic.
NSE,chromogranin,s100,synaptophysin all +. GFAP NEGATIVE
HVA VMA high and CH 2, N-MYC gene (transcription factor)|
|splenic findings in sickle cell ||children - sequesteration which is congestion and hypovolemia where all RBC clumps get stuck in spleed.
repeated sequesteration / congestion leads to atrophy and fibrosis in years so adults do not present with sequesteration, they present with fibrosis|
|muromonab is ? ||vs cd3 - use in kidney transplant having rejection|
|rituximab ||vs cd 20 use in b cell lymphoma or severe rheumatoid arthritis|
|omalizumab ||anti IgE used in refractory asthma|
|anti epidermal growth factor is? ||CETuximab vs cancers like pancreating, NON SMALL CELL lung|
|bevacizumab is vs ||VEGF used in colon cancer and GIT cancers|
|leukemoid reaction vs CML ||both have myelocytes, metamyelocytes, promyelocytes and band cells
differentiate with ALKALINE PHOSPHATASE
LOW IN CML , (philadelphia BCR ABL 9:22)
HIGH IN Leukemoid reaction|
|cml - blasts must be less than 10 % |
|rank L high osteoprotegrin (decoy receptor) Low -> bone resprotion by osteoclasts ||rank l and m csf come from osteobasts . PTH works through this mechanism - BLASTS ++ rank L/mcsf > ++ rankL : osteoprotegrin ratio >resorption|
|Rifampin ||inhibits DNA dependent RNA synth causing so preventing transcription therefore no mrna so no protein
resistance is through modification of rifampin binding site on dna dependent rna polymerase|
|INH needs to be activated by enzyme Catalase Peroxidase !!! then it inhibits mycolic acid synthesis ||alteration of this catalase peroxidase enzyme is resistance mechanism vs INH|
|30 s subunit ||aminoglycosides (gentamycin, streptomycin)
|50 s subunit ||chloramphenicol, clindamycin, linezolid, macrolides (azythromycin erythromycin clarithromycin)|
|alkaline phosphatase reflects osteoBLASTS
comes also from placenta, liver, intestines ||tartarate resistant ACID phosphatase, urinary hydroxproline and urinary deoxypyridinoline are for osteoCLASTS - urine deoxypyridinoline is most sensitive|
|differentiate between alkaline phosphatase elevated due to intestine or liver? ||bone = boil
bone specific ALP is easily denatured by heat
also can use electrophoresis or monoclonal ABs|
|calcitonin marker in ||medullary carcinoma thyroid from parafollicular c cells|
|post auricular lymph nodes german measles rash face to trunk ||togavirus|
|aorta riding anterior and to the right of pulm art is ?
TGV ||failure of Septum to SPIRAL NORMALLY during SEPTATION|
|embryological failure: |
|fusion ||failureof urethral folds to FUSE is HYPOspadias|
|aptosis ||autoimmune diseses due to failure of slection process|
|obliteration ||branchial cleft cyst - lateral! 3rd
differentiate from thyroglossal (endodermal) base of tongue, central, moves with swallowing, surgically remove the track|
|migration ||neural crest -> hirschprung|
|proliferation ||unilateral aplasia of fibula|
|pda machinery murmur, bounding pulse, thrill at left upper sternal border ||6th aortic arch derivative |
|triple test done 16-18 wks tests for ||afp, hcg and estrIOL if high, then do ultrasound.
if dates are correct and ultrasound abnormal, do amniocentesis|
|afp from fetal liver, git and yolk sac ||if high, wrong dates!!!, NTD, abdominal wall defects (gastroscheisis or omphalocele) multiple gestation
LOW IN DOWNS|
|decreased estriol means placental insufficiency |
|herieditary hemorrhagic telangiectasia on skin and mucosa , present with melena and epistaxis is ||osler weber rendu|
|leptomenengial angioma + facial port wine stain ||sturge weber |
|retinal hemorrhage , bilateral renal cell carcinoma liver cyst and hemangioblastomas on cerebelum ||von hippel lindau|
|aneuploidy is ||chromosomal nondysjunction during meiosis or mitosis|
|meiotic nondysjunction is a type of ||aneuploidy|
|pleitropy is one gene that affects many outcomes |
|definitive dx of downs ||first triple test (confirm dates) see low AFP , then do amniocentesis and karyotype for final diagnosis|
|polyploidy ||2 or more complete chromosomes in 1 cell ie partial mole|
|law of separation - mendels first law ||parent chromosomes split so child gets half from each parent|
|downs patients are at increased risk of what cancer ||ALL AML|
|chromosomal instability syndrime ||are NOT fragile x syndrme -
consisint of xeroderma, bloom sydrome, ataxia telangiectasia , fanconi anemia|
|fragile x syndrom ||hypermethylation of FMR 1 gene on long arm chromosome x results in profound mental retardation due to CGG trinucleotide repeats.
remember hypermethylation of cytosine , deactivating the gene is the mechanism|
|mantle cell lymphoma - b cell 11:14 results in? ||ACTIVATION OF CYCLIN D GENE|
|15:17 ||apml M3 (recall 8:21 is m2) - many auer rods, peroxidase + -> DIC|
|8:14 ||burkitts lymphoma - c-myc , next to immunoglobulin heavy chain gene, gets heavy expressed , so increased prodction of ONCOGENE|
|9:22 bcr abl has what ckind of activity ||tyrosine kinase|
|retinoblastoma RB gene - requires 2 hits to become malignant ||is a tumor suppressor gene on ch 13|
|clara cells are nonciliated and in terminal resp epithelium ||secrete clara cell secretory protein CCSP, which does 2 things - 1) surfactant 2) contains p450 enzymes, helps metabolize |
|myoclonus obsoclonus (is paraneoplastic) is uncoordinated random eye movements seen in children associated with? ||neuroblastoma - N myc gene
also see orbital metastasis (proptosis, diplopia)
brain mets - EPIDURAL SPACE = dumbell tumor - compresses spinal tissue|
|low c1 estrase is Hereditary Angioedema (auto dom) ||do not give captopril |
|enveloped viruses are destroyed by ether and other organic solvents. these have a lipid bilayer coming from host cell nuclear or plasma memb
||non-enveloped viruses are resistant to ether |
|proteus mirabilis has what kind of flagella ||peritrichous flagella|
|serpiginous chains with caput medusae appearance on LM is what bacteria ||anthrax|
|listeria the only gram + bacteria with endotoxin |
|vitamin e def leads to ||oxidative stress of all lipid bilayers , especially RBC and neurons - long neurons and axons becuase they have more surface areas>more oxidative damage.
loss of vibraration and proprioception seen
ie cystic fibrosis, abetalipoproteinemia|
|cholecystitis - x ray is not helpful becuase most stones dont have enough calcium to be opaque , ultrasound finds stones in most asymptmatic individuals ||diagnosis with HIDA SCAN - give radio dye, watch for liver filling, then direct excretion into duodenum and bypass of gallbladder is diagnostic|
|bcl -2, 14 translocates to 18 near IgG heavy chain gene - overexpression - excessive protein is synthesized from bcl 2 causing? ||inhibition of apoptosis - follicular lymphoma
find cd 19, 20, 21, 79a in B cells|
|subdural hge ||between dura and arachnoid -due to tearing of bridging cortical veins|
|Subarachnoid hge between arachnoid and pia ||due to rupture berry aneurysm, ant communicating, post communicating and middle CEREBRAL artery (not middle MENINGIAL)|
|ischemic tubular necrosis presents with ||oliguria and muddy brown casts NOT SEEN IN SICKLE CELL DZ, OR NSAIDS, OR DIABETES OR ANYTHING ISCHEMIA --- RECALL ISCHEMIC KIDNEY DISEASE LEDS TO PAPILLARY NEcROSIS|
|Papillary necrosis caused by? ||Sickle cell, diabetes (not enzymatic glycosylation->vasc wall compromise>ischemia), acute pyelonephritis and urinary obstruction
|the true ischemia diseases or kidney cause? ||PAPILLARY NECROSIS, NOT ischemic tubular necrosis|
|papillary necrosis ||see yellow tips of renal pyramids distal 2/3
sloughing papillae, COAGULATIVE INFARCT, with tubular outlines preserserved. pain, hematuria and passage of clumps |
|cd 40 is on B cell binds with Cd 40LIGNAD on activated T cells.
CD? ||cd 154 is cd 40 L|
|ethosuximide works on t type calcium channels ||especially in thalamic neurons
use in absence seizures |
|benzo barbiturates and alcohol act on GABA A ||it is a ligand gated CL channel . these POTENTIATE gaba and INCRESE CHLORODIE CURRENT
|valproate acts on ||NMDA, POTASSIUM and SODIUM AND GABA|
|gallbladder fluke infection leads to what kind of stone ||brown pigment stones|
|homocystineuria develops because of cystatione synthase deficiency - conversion of homocysteiine into cystathione and cystine requires b6. if the enzyme is deficiency ,then b6 offers relief by converting some homocysteine to cysteine ||PRESENTS LIKE MARFANS SYNDROME !! arachnodactyly , scoliosis, elongated limbs and ectopia lentis|
|homocystinuria presents like marfans syndrome ||rx b6|
|ALS is umn and LMn degen - thinning of anterior horn cells and loss of corticothalmaic tract - see SPASTICITY along with LMN . see loss of cranial nerve nuclei and precentral gyrus atrophy . ||find mutations of SOD 1 gene -for copper zinc superoxide dismutase
rx with RILUZOLE which decreases gaba release|
|reason for decreased chest expansion in hla b27 ank spond? ||costochondral enthesitis|
|group a strep (pyogenes) causes rheumatic FEVER , see? ||myocarditis with granulomas are aschoff bodies - contain mostly binuclear cells
also find caterpillar cells aka anitsckow cells=plump macrophages with slender bodies inside - these are chromatin Ribbons . overtime these become aschoff giant cells.fibroti|
|in diptheria toxin myocarditis, find ? ||no granulomas (ARF)
see MACROPHAGES and PLEOMORPHIC BODIES|
|aortic stenosis is assx atrial fibrillation.
cardiac output is already low, if at fibb starts, it goes even lower due to loss of 'atrial kick' (ejection from atria) what symptoms are seem ||profound hypotension|
|how do COMT inhibitors entacapone and tolcapone work? ||inhibit BREAKDOWN OF LEVODOPA SO MORE CAN CROSS BLOOD BRAIN BARRIER
entacapone prevents PERIPHERAL METHYLATION
TOLCAPONE PREVENTS BOTH PERIPHERAL AND CENTRAL.|
|amantadine acts how on dopamine? ||increases synth, release and reuptake|
|which drugs CENTRALLY prevent BREAKDOWN OF LEVODOPA ||selegeline (through MAO B)
Tolcapone through COMT|
|anterior cerebral arteries suppy medial side of hemispheres - damage here causes ||contralateral loss of sensation, and motor deficits of legs, genitals and personality changes|
|von willerbands disease causes ||poor platelet aggregation (gp1b IX) and shorter life of VIII (antihemophelic factor) (halflife w/ vwf 12 hr, w/o 2 hr)
so see both clotting abx and PTT abx.
platelet bleeding is mucocutaneous, and menorrhagia
post surgical/dental is VIII def|
|hegeman factor XIII causes PTT deficiency but is usually asymptomatic and discovered accidnetally |
|riboflavin deficiency -> less FMN/FAD - TCa cycle inhibited at succinate dehydrogenase -RECALL DEHYDROGENASE COMPLEX
b1-TPP, b2-FMN b3_NAD b5/6? and lipoic acid ||also affects electron reception in ETC -
metabolic changes to b2 are made in heart, liver and kidney|
|classic galactosemia is most common - def of? ||galactose 1 p uridyl transferase
causes lethargy, failure to thrive, hyprchloremic metabloic ACIDOSIS
amino aciduria - rx no lactose (galactose and glucose)- galactitol through galactitol reductase -> liver and lens damage|
|galactokinase is less severe, less common - most common effect is ||cataract|
|diptheria becomes dangerous when it aquires TOX gene - how does it get this ||lysogeny - from coryneyphage beta|
|what is the role of 16s subunit of 30 s in ribsosomes ||16s contins 'complementary base pairs to mrna" to the shine dalgaro sequence which is 10 bases upstream from AUG. this 16s is the first ribosome to bind and initiated protein translation|
|which ribosome created peptide bonds between the amino acids? ||23s of the 50 s |
|translocation is movement of ribsosome complex along mrna strand - how is this powered ||elongation factor G, powered by GTP|
|verapamil is a non dihydropyridine CCB, selective for heart and used in atrial fibrillatin angina and hypertension ||causes constipation, has negative inotropic effect do not give in CHF
causes AV block - this is the MOA but also causes most side effects
GINGIVAL HYPERPLASIA AND BRADYCARDIA|
|amilodipine is selective on vasc smooth muscle. ||cause reflex tachycardia - increases myocardial workload , do not use in heart failure, or coronary syndromes|
|lidocaine is used in ventricular arrhythmias especially after MI ||digoxin also slows AV nodal conduction like verapamil , both are rx for atrial tachycardia|
|CCB'S !! 1 2 3 ||VERAPAMIL IS MOST CARDIOSELECTIVE
NEFIDIPINE/AMILODIPINE MOST ON VASC SMOOTH MUSCLE
DILTIAZEM - BOTH|
|raloxefene is a SERM , blocks estrogen in breast and uterus but SIMULATeS estrogen in bone and blood ||decreases breast cancer risk but also increses bone mineral density preventing osteoporosis|
|cancer cells can :
1) detach from existing area due to loss of E Cadherins
2) bind to new basement membranes and invade due to laminin and fibronectin
||3) destroy and invade healthy tissue with metalloproteinaes - using zinc to melt tissues|
|dubin johnson is "defect in excretion of bilirubin glucuronides across canalicular membrane" - so dubie isnt letting out smoke ||liver becomes black.see pigment granules composed of 'epinephrine metabolite polymers' (making the liver black) on electron spin resonance. see NORMAL liver function + conjugated jaundice (>50% vs unconj or else N liver. URINE COPROPORPHYRIN 1!|
|reason for increased lipid profile in nephrotic syndrome ||find increased synth of lipoporteinsto compensate decrease COP (cholesterol, TH, VLDL, LDL, Lipoprotein a, apolipoprotein, apoprotein), LOW Lipoprotein lipse so no destruction, and abnormal carrier proteins carrying lipids.
|Muscular atrophy can be caused by corticosteroids - what other drug can have a similar presentation ||chloroquine |
|PAN typically spares pulmonary circulation and very rarely involves bronchial circulation. commonly involves? ||all organs especially heart kidney liver and mesenteric vessels - creates BEAD LIKE aneurysms on mesenteric vessels
PAN is segmental, transmural and necrotizing - can rupture leading to hemorrhage |
|defective growth hormone receptor -> LARON dwarfism
||serum high growth hormone with low igf1 (liver)|
|growth hormone works through JAK STAT (janus kinase and stat 5) |
|igf 1 comes from 2 places - ||central (hypothalamus ) causes BRAIN growth, does not affect body growth
liver - affects body growth|
|crohns renal stones? ||calcium oxalate-ileum doesnt absorbe bile acids - so cholesterol is free to bind calcium - soap - this is unabsorbable - calcium oxalate stones form|
|rheumatic heart disease and mitral valve prolapse (more common) are most common predisposers to ||bacterial native valve endocarditis -> give emboli causing strokes|
|sphrocytes seen in ||spherocytosis, hemolytic anemia, old blood samples and BURNS|
|global cerebral ischemia -> ||hypocammpus .pyramidal cells.
cerebellum .purkinje cells.]|
|transmural arterial inflammation with FIBRINOID NECROSIS - PAN |
|large amounts of fat and lysosomal enzymes cause LIQUIFACTIVE NECROSIS ||seen in brain and fat |
|most common type of necrosis in other organs other than fatty organs is ||coagulative necrosis|
|PAS+ granules on liver biopsy ||look for pulmonary signs - panacinar emphysema -
this is alpha 1 anti trypsin granules |
|N-acetyl cysteine in CF patient ||breaks down disulfide bridges - releasing mucous|
|SPINOCEREBELLAR AND DORSAL COLUMN INVOLVED IN ||freidrich ataxia OR VITAMIN E DEF -(LBW babies, fat malabx, abetalipoproteinemia|
|tnf alpha causes what paraneoplastic syndrome ||cachexia -
is released by tumor cells and macrophages
therefore tnf a is aka cachetin
increases insulin resistance, decreases appetite and action of lipoprotein lipase|
|abciximab - vs 2b3a , causes significant neutropenia in 24 hours ||used in stent placenent and acute coronary sydromes|
|ticlopidine is alternative to clipidogrel and aspirin - blocks ADP preventing 2b3a . ||rarely used if others can be used due to serious side effects - NEUTROPENIA AND MOUTH ULCERS IN 1%- MONITOR BLOOD COUNT / 2 WKS |
|cavernous hemangioma is most common benign tumor of liver - spontaneous regress, or surgical removal. usually less than 5 cm, no immediate risk but do bleed after biopsy and not diagnostically helpful - do not biopsy .
these GROW BY ECTASIA NOT HPL/HPTHY ||not related to OCP (that is hepatic ADENOMA)|
|mycoplasma pneumoniae causes hemolysis how ||cold agglutinins produced as defensive ABs produce hemolysis. when immune rxn goes down as infection is cleared, then hemolysis stops.
also see STEVENS JOHNSONS SYNDROME|
|opening snap - S2 time difference is best guage of severity of mitral STENOSIS AKA a2 os interval ||less time is more severe
more time is less severe|
|EBV binds on CD21 |
|cd 21 present on b cells espeically in nasopharyngeal epithelium ||EBV binds to cd 21 via its GP350. it binds on the C3D portion.
|vitmain c - > scurvy - deficiency takes place in ||RER|
|cholestasis causes elevated ||alkaline phosphatase - ie
primary biliary cirrhosis|