Help
Options
Didn't know it?
click below
click below
Knew it?
click below
click below
Don't Know
Remaining cards (0)
Know
retry
shuffle
restart
0:00
Embed Code - If you would like this activity on your web page, copy the script below and paste it into your web page.
Normal Size Small Size show me how
Normal Size Small Size show me how
UWORLD
QUESTIONS
| Question | Answer |
|---|---|
| Ureters important landmarks | OVER: Common/External Iliac vessels UNDER: Gonadal Vessels (injury during ligation of Ovarian Vessels) LATERAL: Internal Iliac MEDIAL: Gonadal Vessel as they enter true pelvis |
| Structure injured during ligation of uterine vessels in Histerectomy | Ureter |
| Chi-Square | Association of 2 CATEGORICAL variables |
| t-Test | Means of 2 GROUPS |
| ANOVA (ANALYSIS OF VARIANCE) | Means of 3 or more GROUPS |
| Meta-analysis | Pools data and integrates results from several similar studies to reach an overall conclusion (LIMITED BY: quality of individual studies or bias in study selection) |
| ANTERIOR Drawer sign | ACL (anterior cruciate ligament) injury |
| POSTERIOR Drawer sing | PCL (posterior cruciate ligament) injury |
| Common injury in contact sports due to lateral force applied to a planted leg. | Damage to ACL, MCL and lateral meniscus |
| Determines the dose rate required to maintain a steady state plasma concentration (Css) | Clearance= Vd x Ke= rate elimination/plasma drug concentration |
| Maintenance Dose | Cp x CL/F |
| Most important steps for prevention of central venous catheter infections | *Proper hand washing * Full barrier precautions durin insertion of a central line *Chlorhexidine for skin disinfection *Avoidance of the femoral insertion site *Removal of catheter(s) when no longer needed |
| Gram (+) infects prosthetic devices and intravenous catheters | Staphylococcus epidermidis (Novobiocin sensitive; Biofilms) |
| Patient with ATYPICAL depression who has a hypertensive crisis after a wine and chefs party! | MAO inhibitor-tyramine crisis (especially Phenelzine) |
| MAO inhibitors MOA | Nonselective Monoamine Oxidase Inhibitors, increase level of amine neurotransmitters (NE, 5-HT, Dopa) |
| Most common cardiovascular syndrome associated with SLE | Pericarditis |
| Same sex twins | Dichorionic/diamniotic (2 oocytes, 2 sperm, 2 amnios, 2 chorions) |
| Acute onset neurologic abnormalities + Hypoxemia + Petechial Rash | Fat Emboli (patient with severe long bone fracture and/or pelvic fracture) |
| Types of PE | FAT BAT (Fat, Air, Thrombus, Bacteria, Amniotic fluid, Tumor) |
| Test of choice for a PE | CT Pulmonary Angiography |
| Necrotizing Fasciitis | 1) Streptococcus Pyogenes (Group A strep) 2) Staphylococcus aureus 3) Clostridium Perfringens |
| Pyrrolidonyl Arylamidase (PYR) positive | Streptococcus Pyogenes (Group A strep)--> Gram (+), catalase (-), beta hemolytic, bacitracin sensitive, forms chains |
| Posterior Fossa malformations | Arnold Chiari Dandy- Walker |
| Symmetric muscle weakness, endomysial inflammation with CD8+ Tcells, MHC I | Polyomyositis (LAB: increased CK, (+) ANA, (+)anti-Jo-1, (+)anti-SRP) |
| Low EF, poor contractility, often 2º to Ischemic Heart disease or DCM | Systolic Dysfunction |
| Isolated RHF | Cor Pulmonale |
| Most common cardiomyopathy (90% cases) | Dilated Cardiomyopathy (S3, Echo->dilated heart, CRX->balloon appearance of heart) |
| Eccentric hypertrophy of heart (sarcomeres added in series) | DCM |
| Yeast and pseudohyphae (dimorphic), Positive Germ tube test at 37ºC | Candida albicans |
| Four primary features of Neuroleptic Malignant Syndrome | 1. Hyperthermia 2. Extreme generalized rigidity 3. Autonomic Instability 4. Altered mental status Treatment: Dantrolene (D2 agonist) |
| MOA of Typical Antipsychotics (Haloperidol + ¨-azines¨) | Block dopamine D2 receptors, increasing cAMP |
| 2 most common causes of 1º eugonadotropic amenorrhea | 1. Imperforate hymen 2. Mullerian Duct abnormalities |
| 1º amenorrhea in a female with fully developed 2º sex characteristics and normal levels of estrogens, gonadotropins | Mullerian duct abnormality |
| Triad of abnormalities in ECG of Wolf Parkinson White | 1. Delta wave at the start of QRS complex 2. Shortened PR interval 3. Widened QRS |
| Most common type of Ventricular Pre-excitation Syndrome | Wolf Parkinson White (abnormal fast accessory conduction pathway from atria to ventricle; bundle of Kent, bypasses AV node) |
| BH4 is used as a cofactor for the synthesis of | 1. Tyrosine 2. Dopamine 3. Serotonin 4. Nitric Oxide |
| Mononucleosis Monospot (-) | CMV |
| (+) Monospot-heterophile antibodies detected by sheep agglutination RBCs | EBV |
| Confirm Menopause | INCREASED FSH (loss of negative feedback on FSH due to low estrogen) |
| Menopause before age 40 | premature ovarian failure |
| Hormonal changes in Menopause | Increased: FSH, LH, GnRH Decreased: Estrogen |
| Should be removed from a patients diet suffering from Aldose B deficiency (Fructose Intolerance) | decreased intake BOTH: fructose+sucrose |
| Phosphodiesterase Inhibitors (Cilostazol,Dipyridamole) cause | Increase cAMP= VASODILATION |
| Oxaloacetate forms aspartate while reacting with glutamate, whats the essential cofactor for this reaction | Pyridoxine (vit B6) |
| ALL current cases | Prevalence |
| New cases | Incidence |
| Incidence rate | # NEW cases specified time period/Population at risk during SAME time period |
| Prevalence | Prevalence= Incidence x Time |
| Prevalence > Incidence | Chronic diseases |
| Fever, urticaria, arthralgias, proteinuria, lymphadenopathy, decreased serum C3 levels following drug use | Serum sickness (Immune complex disease, type III Hypersensitivy) |
| Most serum sickness is now caused by drugs (not serum) acting as | Haptens |
| NORMAL urinary excretion in Pancreatic insufficiency, DECREASED with Intestinal mucosa defects or bacterial overgrowth | D-xylose absorption test |
| DIAGNOSE Pancreatic Insufficiency | 1. Normal D-xylose absorption test 2. Increased neutral fat in stool |
| MOST gastric ulcers occur in? | Lesser Curvature (Transitional zone) |
| Enzyme activated responsible for pathogenesis of Acute Pancreatitis | Trypsinogen (converted to trypsin by enterokinase enteropeptidase, a brush border enzyme on the duodenal and jejunal mucosa) |
| Pupillary light reflex | Illumination on 1 eye= bilateral pupillary constriction |
| Decreased bilateral pupillary constriction when light is shone in AFFECTED eye relative to UNAFFECTED eye | Marcus Gunn Pupil (Afferent pupillary defect- due to optic nerve damage or severe retinal injury) |
| Degranulation of MAST CELLS | IgE-Fc receptor aggregation on the cell surface |
| Digoxin (Cardiac Glycoside); MOA | Direct inhibition of Na+/K+ ATPase leads to indirect inhibition of Na+/Ca2+ exchanger/antiport. INCREASING [Ca2+]i---> positive inotropy. Stimulates vagus nerve---> decreasing HR. |
| Digoxin (Cardiac Glycoside); CLINICAL USE | 1. CHF (increases contractility) 2.Atrial fibrillation (decreases conduction at AV node and depression of SA node) |
| 1º line treatment for Atrial Fibrillation with Rapid Ventricular Response | 1. Ca2+ channel blockers (class IV, Antiarrhythmics): Diltiazem 2. Cardioselective beta blocker |
| 2º line treatment for Atrial Fibrillation with Rapid Ventricular Response | Digoxin |
| Treatment for Rheumatoid Arthritis | TNF-alpha inhibitors |
| lnfliximab, Adalimumab (TNF-alpha inhibitor) | 1. Crohn's disease 2. Rheumatoid arthritis 3. Psoriatic arthritis, 4. Ankylosing spondylitis 5. Inflammatory bowel disease (IBD) |
| All TNF-alpha inhibitors predispose to | INFECTION including reactivation of latent TB. TNF blockade prevents activation of macrophages and destruction of phagocytosed microbes. |
| What test should be performed before starting treatment with a TNF-alpha inhibitor | PPD skin test |
| TNF-alpha inhibitors | 1. Etarnecept 2. Infliximab, adalimumab |
| Anti-TNF-alpha monoclonal antibody | Infliximab, adalimumab |
| Hypertension, hypokalemia, metabolic alkalosis and LOW plasma renin | Conn Syndrome (1º Hyperaldosteronism) |
| Conn Syndrome (1º Hyperaldosteronism) is caused by | 1. Adrenal hyperplasia 2. Aldosterone-secreting adrenal adenoma |
| Treatment for Conn Syndrome (1º Hyperaldosteronism) | 1. Surgery 2. Spironolactone (K+ sparing diretic, aldosterone antagonist) |
| Single MOST important risk factor associated with Aortic Disecction | Hypertension |
| CT shows intraluminal tear forming a ¨flap¨ separating true and false lumen | Aortic Disecction |
| Aortic Disecction associated with | 1. Hypertension 2. Bicuspid aortic valve 3. Connective tissue disorders (Marfan syndrome) |
| Clinical LAB features of Legionella pneumophila | -High fever (>39ºC) -Headache and confusion -Watery diarrhea -Hyponatremia -Sputum gram stain showing many neutrophils, but few or NO organisms -CXR: unilobar infiltrate that progresses to consolidation |
| Sputum gram stain showing many neutrophils, but few or NO organisms | Legionella pneumophila (gram-negative, facultative intracellular) |
| stain used for Legionella pneumophila | Silver stain |
| Legionella pneumophila grows on | Charcoal yeast extract culture with iron and cysteine |
| Legionella pneumophila detected clinically by | Antigen in urine. |
| Associate Legionella pneumophila | Smokers and patients with Chronic Lung disease. Aerosol transmission from environmental water source (air conditioning systems, hot water tanks,etc) |
| X-linked defect affecting the methylation and expression of the FMRI gene. | Fragile X; Trinucleotide repeat disorder (CGG) |
| 2nd most common cause of genetic mental retardation (after Down syndrome) | Fragile X |
| Macroorchidism, long face with a large jaw, large everted ears, autism, mitral valve prolapse. | Fragile X (X-linked; FMRI gene;Trinucleotide repeat disorder (CGG)) |
| Trinucleotide repeat disorder (CGG) | Fragile X (X-linked defect affecting the methylation and expression of the FMRI gene) |
| ACE inhibitors | INCREASE: renin, AT I, bradykinin DECREASE: AT II, aldosterone |
| Acute hemolytic cystitis (dysuria+hematuria) in children | Adenovirus (naked, dsDNA, linear) |
| Thrombocytopenic purpura, recurrent Infections, Eczema | Wiskott-Aldrich syndrome |
| Wiskott-Aldrich syndrome treatment | HLA-matched bone marrow transplantation |
| mutation in WAS gene (X-linked recessive); T cells unable to reorganize actin cytoskeleton. | Wiskott-Aldrich syndrome |
| Findings in Wiskott-Aldrich syndrome | 1. Decreased to normal: IgG, IgM 2. Increased: IgE, IgA 3. FEWER and SMALLER PLATELETS |
| Aminoacids with 3 titratable protons | Histidine Arginine Lysine Aspartic acid Glutamic acid Cysteine Tyrosine |
| Can be injured during axillary node dissection after mastectomy | Long thoracic nerve (C5-C7) |
| Inability to anchor scapula to thoracic cage--> cannot abduct arm above horizontal position | Mucle deficit: Serratus anterior Injury: Long thoracic nerve (C5-C7) |
| ¨winged scapula¨ | Long thoracic nerve (C5-C7) injury |
| Wide pulse pressure, bounding pulses and head bobbing | Aortic regurgitation |
| Female>65yoa with unilateral headache, jaw claudication, pelvic girdle pain and morning stiffness | Temporal (giant cell) arteritis |
| Temporal (giant cell) arteritis is associated with | Polymyalgia rheumatica. |
| Lab finding in Temporal (giant cell) arteritis | INCREASED ESR. LM: granulomas in the media of the arteries, consisting of mononuclear infiltrates and multinucleate giant cells |
| Temporal (giant cell) arteritis should be treated with high-close corticosteroids prior to biopsy to PREVENT | Vision Loss |
| Temporal (giant cell) arteritis most commonly affects | Branches of Carotid Artery |
| Most common cause of Acute Gastroenteritis in children and adults in INDUSTRIALIZED COUNTRIES | Campylobacter (Comma or S-shaped, oxidase positive, grows at 42°C) |
| Campylobacter transmission | Fecal-oral through foods such as poultry, meat, unpasteurized milk. |
| Major cause of bloody diarrhea, especially in children. | Campylobacter (Comma or S-shaped, oxidase positive, grows at 42°C) |
| Common antecedent to Guillain-Barre syndrome and reactive arthritis. | Campylobacter (Comma or S-shaped, oxidase positive, grows at 42°C) |
| Histone that ties nucleosome beads together in a string. | H1 Histone |
| ONLY histone that is NOT in the nucleosome core | H1 Histone |
| Single amino acid replacement in beta globin chain; substitution of Glutamic acid for Valine at position 6 | Missense mutation; Sickle Cell anemia |
| Metalloproteinases | secreted by inflammatory macrophages in the intima and may reduce plaque stability by degrading collagen |
| Bilateral metastases to ovaries. Abundant mucus, signet ring cells. | Krukenberg's tumor (Stomach Cancer) |
| Vaccine contains type B capsular polysaccharide (polyribosylribitol phosphate) conjugated to diphtheria toxoid | H. influenzae Hib conjugated vaccine: increased IMMUNOGENICITY |
| Death from cardiac cause within 1 hour of onset of symptoms | Sudden Death |
| sudden cardiac death most commonly due to | lethal arrhythmia (e.g., ventricular fibrillation) |
| Lippid-lowerin agent that can EXACERBATE Gout | Niacin (Vitamin B3) |
| Niacin (Vitamin B3) side effects | 1. Red, flushed face 2. Hyperglycemia (acanthosis nigricans) 3. Hyperuricemia (exacerbates gout) |
| Contralateral hemianopia with macular sparing | PCA |
| Post-traumatic stress disorder | Disturbance lasts > I month, with onset of symptoms beginning anytime after event |
| Persistent reexperiencing previous traumatic event. Nightmares, flashbacks, intense fear, helplessness, or horror. Leads to avoidance of stimuli associated with the trauma and persistent arousal. | Post-traumatic stress disorder |
| Post-traumatic stress disorder, Treatment | psychotherapy, SSRis. |
| Acute stress disorder | 3 days- 1 month |
| Most common childhood systemic vasculitis. Often follows URI | Henoch-Schonlein purpura |
| Henoch-Schonlein purpura, Classic triad: | Classic triad: • Skin: palpable purpura on buttocks/legs • Arthralgia • GI : abdominal pain, melena, multiple lesions of same age |
| Henoch-Schonlein purpura associated with | IgA nephropathy |
| Vasculitis 2º to IgA + C3 complex deposition | Henoch-Schonlein purpura |
| Virchow's triad | • Stasis • Hypercoagulability (e.g., defect in coagulation cascade proteins, most commonly factor V Leiden) • Endothelial damage (exposed collagen triggers clotting cascade) |
| Gestational Diabetes | •Increased INSULIN-->Islet cell hyperplasia= HYPOglycemia in neonate |
| The pancreas is derived from | Duodenal portion of the Foregut |
| GI embriology | Foregut-pharynx to duodenum. Midgut-duodenum to proximal 2/3 transverse colon. Hindgut-distal 1/3 transverse colon to anal canal above pectinate line |
| The ventral pancreatic bud becomes | 1. Uncinate process 2. Pancreatic head 3. Main pancreatic duct |
| The dorsal pancreatic bud becomes | Everything else! 1.Tail 2.Body 3.Isthmus 4. Accessory pancreatic duct |
| Airway an GI infections, Autoimmune disease, Atopy, Anaphylaxis to IgA containing products | Selective IgA deficiency (Most common 1º immunodeficiency) |
| Most common 1º immunodeficiency | Selective IgA deficiency |
| The consistency and reproducibility of a test (reliability). Absence of random variation. | Precision |
| Reduces precision in a test. | Random error |
| Increases precision in a test. | Decrease in standard deviation. |
| Deficiency of surfactant | Patchy alveolar atelectasis (collapse) |
| Causes hepatocellular cytoplasm to take finely granular, eosinophilic appearance ¨ground glass¨-like | HBV |
| Infection with N. gonorrhea does NOT result in lasting immunity due to | Its ability to modify its outer membrane protein, ANTIGENIC VARIATION |
| 1º cause of urinary tract obstruction in elderly male patient | BPH (Benign Prostatic Hyperplasia) |
| Distension/dilation of renal pelvis and calyces | Hydronephrosis |
| Most common site of obstruction (hydronephrosis) in fetus. | Ureteropelvic junction |
| Causes of Hydronephrosis | -Urinary tract obstruction (e.g, renal stones, BPH, cervical cancer, injury to ureter) -Retroperitoneal fibrosis -Vesicoureteral reflux |
| Systolic heart sounds | 1. Aortic/Pulmonic stenosis 2. Mitral/Tricuspid regurgitation 3. Ventricular septal defect |
| Diastolic heart sounds | 1. Aortic/Pulmonic regurgitation 2. Mitral/Tricuspid stenosis |
| Most common congenital cardiac defect | VSD (L-to-R shunt) |
| L-to-R shunts; frequency | VSD>ASD>PDA |
| L-to-R shunts; LATE cyanosis ¨blue KIDS¨ | 1.VSD 2.ASD 3.PDA 4.Eisenmenger syndrome |
| Holosystolic, harsh-sounding murmur. Loudest at tricuspid area, accentuated with hand grip maneuver due to increased afterload. | Ventricular septal defect |
| R-to-L shunts; EARLY cyanosis ¨blue BABIES¨; 5 T´s | 1) Truncus arteriosus (1 vessel) 2) Transposition of great vessels (2 switched vessels) 3) Tricuspid atresia (3=tri) 4) Tetralogy of Fallot (4=tetra) 5) TAPVR (5 letters in the name); Total anomalous pulmonary venous return |
| Follows opening snap. Delayed rumbling late diastolic murmur. Enhanced by maneuvers that increase LA return (e.g., expiration). | Mitral Stenosis |
| Opening snap | Mitral Stenosis |
| Chronic Mitral Stenosis results in | LA dilation |
| 3 points of insertion of Sternocleidomastoid Muscle | 1. ¨Sterno¨: manubrium of Sternum 2. ¨Cleido¨: medial part of Clavicle 3. ¨Mastoid¨: Mastoid process of the skull |
| Sternocleidomastoid Muscle function and innervation | -CN XI -Function: turn head in the opposite direction |
| Loss of high-frequency hearing 1st; sudden extremely loud noises can produce hearing loss due to tympanic membrane rupture. | Damage to stereocilliated cells in organ of Corti |
| Damage to stereocilliated cells in organ of Corti | Noise-induced hearing loss |
| Beta1-selective antagonists (Beta1 > Beta2) | 1. Acebutolol (partial agonist), 2. Betaxolol, 3. Esmolol (short acting), 4. Atenolol, 5. Metoprolol |
| Beta 1 receptors are found in | -Cardiac tissue -JGA cells |
| Law of Laplace | Collapsing pressure (P)= 2 (surface tension)/radius |
| 2º Hyperaldosteronism | -Renal artery stenosis, -Chronic renal failure, -CHF, -Cirrhosis, -Nephrotic syndrome -Malignant HTN -REnin-secreting tumor (reninoma) |
| Renal perception of low intravascular volume results in an overactive renin-angiotensin system. Associated with HIGH plasma RENIN. | 2º Hyperaldosteronism |
| Hypertension, HIGH= plasma RENIN, HIGH= plasma ALDOSTERONE | 2º Hyperaldosteronism |
| Treatment of 2º Hyperaldosteronism | Spironolactone |
| Acute salicylate toxicity | Respiratory alkalosis |
| Chronic salicylate toxicity | Metabolic acidosis with compensation (hyperventilation), Increased anion gap |
| NADPH is required for | -Reductive reactions, e.g., glutathione reduction inside RBCs, Fatty acid and Cholesterol biosynthesis. -Ribose for nucleotide synthesis and glycolytic intermediates. |
| 2 distinct phases of HMP shunt (oxidative and nonoxidative), occur in | CYTOPLASM |
| HMP shunt sites | Sites: lactating mammary glands, liver, adrenal cortex (sites of fatty acid or steroid synthesis), RBCs. |
| Interferes with Gamma-carboxylation of glutamic acid residues | Warfarin |
| Vitamin K deficiency | Decreased synthesis of factors II, VII, IX, X, protein C, protein S. vWF carries/protects VIII. |
| Warfarin inhibits | Epoxide reductase |
| Warfarin; CLINICAL USE | Chronic anticoagulation (after STEMI, venous thromboembolism prophylaxis, and prevention of stroke in atrial fibrillation). |
| Follow Warfarin administration with | PT/ INR values |
| Thyroid hormones alter gene transcription by binding to receptor situated inside | NUCLEUS |
| Diagnosis of Strongyloides stercoralis | Rhabtidiform (non-infectious form) in stool |
| Route of transmission; Strongyloides stercoralis | Filariform larvae (infectious form) in soil penetrates the skin |
| UMN lesion signs | 1. Hyperreflexia 2. Hypertonia 3. Babinski (+) 4. Spastic paralysis 5. Clasp knife spasticity |
| LMN lesion signs | 1. Weakness 2. Atrophy 3. Fasciculations 4. Hypotonia 5. Hyporeflexic 6. Flaccid paralysis |
| Major virulence factor of S. pyogenes (Group A streptococci) | M protein |
| deficiency causes Cheilosis, Angular Stomatitis, Corneal vascularization. | Riboflavin (Vitamin B2) |
| Component of flavins FAD and FMN, used as cofactors in redox reactions,e.g, the succinate dehydrogenase reaction in the TCA cycle | Riboflavin (Vitamin B2) |
| Screen pregnant women at 35-37 weeks. Patients with positive culture receive intrapartum penicillin prophylaxis. | Streptococcus agalactiae (group B streptococci) |
| Intrapartum penicillin prophylaxis. | Streptococcus agalactiae (group B streptococci) |
| Streptococcus agalactiae (group B streptococci) | -Bacitracin resistant, -Beta-hemolytic, -Produces CAMP factor, -Hippurate test positive. Colonizes vagina; causes pneumonia, meningitis, and sepsis, mainly in babies. |
| 1º line treatment for Essential Tremor | Propranolol (non-specific beta-adrenergic antagonist) |
| Action tremor; exacerbated by holding posture/limb position | Essential Tremor |
| Autosomal dominant. Patients often self-medicated with EtOH, which decreases tremor amplitude. | Essential Tremor |
Created by:
heidy39
Popular USMLE sets