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Pathophysiology
UWORLD + FA pathophysiology review
| Question | Answer |
|---|---|
| What kind of acid-base imbalance is seen with Emphysema? | Respiratory acidosis with compensatory metabolic alkalosis. |
| PaO2 < 75 mmHg on room air | Hypoxemia |
| What is the normal pH range? | 7.35 - 7.45 |
| Normal PaCO2 range? | 35 - 45 |
| What is the HCO3- normal range? | 22-26 |
| What is the normal range for PO2? | 65-105 |
| If the pH and PaCO2 are going in opposite direction? | Respiratory imbalance |
| If pH and PaCO2 are moving in same direction? | Metabolic disorder |
| Left-sided Heart failure: | cause Secondary Pulmonary HTN via left-sided diastolic filling pressure transmitting backwards to the pulmonary veins |
| What is the end result of Secondary Pulmonary Hypertension? | Pulmonary venous congestion |
| What is the MCC of secondary Pulmonary HTN? | Left-sided heart failure |
| Hypoxia-induced vasoconstriction? | underlie pulmonary HTN that occurs secondary to chronic obstructive pulmonary disease |
| Primary Biliary cholangitis? | Chronic autoimmune liver disease characterized by lymphocytic infiltrates and destruction of the small and mid-sized intrahepatic bile ducts. |
| What disease or condition demonstrates similar hepatic findings as in PBC? | Graft vs Host Disease |
| Acetaminophen overdose is characterized by: | damage to the CENTRILOBULAR arase causing necrosis |
| Alcoholic hepatitis is characterized by: | Hepatocellular swelling and necrosis, Mallory bodies, neutrophils infiltration, and fibrosis |
| What is a common complication of long-standing Rheumatoid Arthritis? | Vertebral malalignment (subluxation) |
| What medical emergency procedure may damage the vertebral of RA patients? | Intubation for mechanical breathing |
| What is the clinical presentation of Cervical subluxation? | Neck pain, stiffness, and neurologic findings (sensory loss, muscle weakness) |
| Compression of the Spinal cord causes: | Flaccid paralysis, with decreased or absent reflexes below the compression |
| What is a common cause of Compression of the Spinal cord? | Cervical subluxation in RA patients. |
| What cells are involved in Pheochromocytoma? | Neuroendocrine cells in the Adrenal Medulla |
| What gene mutations are associated with Pheochromocytoma? | VHL, RET and NF-1 genes |
| Pheochromocytoma symptoms are due to: | Increased Catecholamine secretion |
| What are the featured symptoms of Pheochromocytoma? | EPISODIC headache, tachycardia/palpitations, sweating and hypertension |
| Neuroendocrine cells stain positive for: | Synaptophysin, Chromogranin, and Neuron-specific enolase |
| Neuron-specific enolase is a marker for __________________ derived cells. | Neuroendocrine |
| Acne associated bacteria: | Propionibacterium |
| Propionibacterium is associated with: | Anaerobic bacteria responsible for the development of acne. |
| UV exposure causes: | Pyridine dimers formation |
| What kind of expuresu is needed for formation of Pyridine dimers in DNA? | UV light exposure |
| How are Pyridine dimers involved in DNA repair? | Specific endonuclease complex is recognized and initiates the process of repair by nicked the damaged strand on both sides of the Pyridine primer. |
| UV damaged DNA repair process: | 1. UV exposures creates THYMINE dimers 2. Endonuclease complex recognized the deformed helix 3. single stranded cleavage on both sides of segment 4. Damage DNA is discarded 5. DNA polymerase synthesis of replacement segment 6. DNA ligase helps the remaining gap sealed |
| What are Cholesteatomas? | collections of SQUAMOUS CELL DEBRIS that form a mass behind the tympanic membrane. |
| Pearly mass behind the tympanic membrane? | Cholesteatomas |
| Where is the location of Cholesteatomas? | Behind the tympanic membrane |
| Cholesteatomas may cause hearing loss due to: | Erosion into the Auditory ossicles |
| Cholesteatomas cause: | 1. MCC of painless otorrhea 2. Conductive hearing loss 3. If large enough may compress the Vestibular apparatus and facial nerve causes of vertigo or Facial palsy |
| What kind of hearing loss is seen with Cholesteatomas? | Conductive hearing loss |
| Range of time seen in Rupture of the Left ventricular free wall? | 5-14 days after the MI |
| What is the consequence or result of Left Ventricular Free wall rupture? | Rupture lead to Hemopericardium and cardiac tamponade, causing profound hypotension and shock with rapid progression to pulseless electrical activity and death |
| Right ventricular failure: | Acute; Seen with Hypotension , clear lungs and Kussmaul sign |
| Papillary Muscle rupture is seen how long after MI? | Acute or 3-5 days |
| What are the clinical features of Papillary muscle rupture? | 1. Severe MR with flail leaflet 2. New holosystolic murmur 3. Severe Pulmonary edema |
| Interventricular Septal Rupture occurs either acutely or after ________________ since MI. It is associated with: | 3-5 days; Chest pain, New Holosystolic murmur, biventricular failure, shock, and step up in O2 level from RA to RV. |
| What are the accompanying symptoms of Ventricular Free Wall rupture? | Chest pain, Cardiac tamponade, shock Ditant heart sounds |
| Left ventricular Aneurysm: | Seen after weeks or months from MI. Characterized by Subacute heart failure and Stable angina. |
| What is the neurotoxin released by C. tetani? | Tetanospasmin |
| Tetanospasmin: | Blocks the release of GLYCINE and GABA fro the spinal inhibitory neurons that regulate the lower motor neurons |
| Inhibition of LMNs in Tetanus is seen with: | Activation of muscles leading to spasms and hyperreflexia |
| What are the main characteristics seen in Tetanus? | - Difficulty opening the Jaw (Trismus) - Fixed sardonic smile (Risus sardonicus) - Contracting back muscles resulting in backward arching (Opisthotonus) |
| C. botulinum toxin? | Inhibits the release of ACh, leading to flaccid paralysis |
| Flaccid paralysis due to toxin | Botulism |
| V. cholerae: | Serotonin release form enterochromaffin cells in the GI tract |
| The increased secretion of Serotonin in V. cholerae infection accounts for: | Extreme secretion of fluid in cholera. |
| Fibromyalgia symptoms are: | 1. Widespread musculoskeletal pain 2. Fatigue 3. Impaired attention ad concentration 4. Psychiatric disturbance (depression and anxiety) 5. Symptoms lasting more than 3 months |
| Multiple tender joints + Absence of joint or muscle inflammation. Suspected Dx? | Fibromyalgia |
| Polymyalgia rheumatica | Inflammatory disease that affect patient >50 yo; subacute pain and stiffness in the shoulder and hips, weight loss, fever and malaise. |
| UMN signs include: | Abnormal plantar flexion (Babinski sign), Spastic paralysis, increased muscle tone, Clasp-knife rigidity, hyperreflexia, pronator drift, and Pyramidal weakness |
| What is Pyramidal weakness? | Weakness more pronounced in the lower extremity flexors and upper extremity extensors. |
| What are the LMN signs? | 1. Flaccid paralysis 2. Weakness with hypotonia and muscle atrophy 3. Fasciculations 4. Suppred or absent reflexes |
| Abscess formation | largely driven by NEUTROPHIL RECRUITMENT and activation leading to the release of cytotoxic granules that kill bacteria but can liquefying necrosis of surrounding tissue. |
| What is the common CXR description of an lung abscess? | "cavitation with air-fluid level" |
| Dendritic cells and APCs: | release IL-2, which stimulates the differentiation of Th1 helper cells and production of INF-gamma by T-cells |
| Left ventricular afterload is determined by: | 1. Balance of resistance between forward flow (aortic pressure) and 2. Regurgitant flow (left atrial pressure) |
| Imbalances in the forces responsible for Left ventricular afterload, lead to the development of ___________________________. | Mitral regurgitation |
| What is the result of a reduction in systemic vascular resistance in regards to MR? | Increases the ratio or forward regurgitant flow and improves cardiac output. |
| What is the clinical characteristics of Primary (Psychogenic) Polydipsia? | Excessive intake of free water leading to Hyponatremia and production large volumes of dilute urine |
| What it the treatment for Psychogenic polydipsia? | Water restriction |
| Primary polydipsia presents with ___________ sodium, ______________ urine osmolarity after water deprivation test, and _____________ with the addition of vasopressin. | Low sodium; Increased water osmolarity after water deprivation test; No change with Vasopressin injection |
| How is the Serum Na (sodium) levels in Nephro and Central DI? | Both have high serum Na+ levels. |
| If the patient presents with polydipsia, polyuria, hypernatremia and large increase change in urine osmolarity with Vasopressin. Dx? | Central DI |
| What are the 3 main effects of ACE inhibitors? | 1. Systemic Vasoconstriction 2. Preference contricito of Glomerular EFFERENT arteriole 3. Enhancement of Adrenal Aldosterone secretion |
| What value is used to distinguish between metabolic and respiratory alkalosis? | pCO2 levels |
| Increased pH + pCO2 less than 40 mmHg --> Dx? | Respiratory alkalosis |
| Low pCO2 in the setting of increased pH means | Respiratory alkalosis |
| Metabolic alkalosis is characterized by: | - pH > 7.45 - high pCO2 (>40 mmHg) -accumulation of HCO3- due to hypoventilation (compensation) |
| What is measured further in metabolic alkalosis in order to investigate the further the pathogenesis? | Urine Chloride levels |
| Urine Chloride levels are measured in _____________________. | Metabolic alkalosis |
| Metabolic alkalosis + Low Urine Cl- levels are due to: | - Vomiting, Nasogastric aspiration - Prior diuretic use |
| Metabolic alkalosis + High Urine Cl levels is caused by: | In case of: - Hypovolemia ---- Current diuretic use - Euvolemia ---- Bartter and Gitelman syndrome - Hypervolemia ---- leads to excess mineralocorticoid activity, presented with: Primary Hyperaldosteronism Cushing Disease Ectopic ACTH production |
| What is a Keloid? | Excessive collagen formation during the remodeling phase of wound healing |
| What is the clinical presentation of an Keloid? | Raised, painful, and pruritic nodules that grow beyond the wound borders. |
| Gallstones are most likely composed of ___________________. | Cholesterol |
| What substances aid in the prevention of gallstone formation? | Bile acids and Phosphatidylcholine, both help to dissolve cholesterol and prevent gallstone formation. |
| What are Target cells? | Erythrocytes that have reduced cell volume or excessive membrane. |
| Target cells with reduced cell volume are associated with: | Thalassemia or Iron deficiency |
| Target cells with excessive membrane are associated with: | Obstructive liver disease, and Postsplenectomy |
| What is the main organ responsible to "prune" RBCs? | Spleen |
| Structural mutation to Hb are seen in __________________ which presents ___________________. | Sickle cell ; Target cells. |
| What is "splenic conditioning"? | Process in which spleen macrophages "prune" out ecemembres membrane form RBC. |
| Spherocytes: | have low area-to-surface ratio and are susceptible to osmotic stress; |
| Spherocytes are seen in: | Hemolytic anemia and Spherocytosis |
| What type of RBC cells are at increased risk of Osmotic stress? | Spherocytes |
| Pappenheimer bodies: | aggregated iron deposits in RBCs |
| In what conditions are pappenheimer bodies seen? | Sideroblastic anemia |
| Howell-Jolly bodies are: | clusters of DNA remnants |
| Why are Howell-Jolly bodies produced? | Found in RBCs due to hypersplenism or asplenism |
| DNA remnants in RBC; Peripheral round, dark purple, blue or red inclusions. Describe? | Howell-Jolly bodies |
| What are Heinz bodies? | Denatured Hb seeing in RBC in patients with G6PD deficiency or thalassemia. |
| In what disease we can see Heinz bodies? | G6PD deficiency and Thalassemia |
| What is Basophilic stippling? | blue granules dispersed within the cytosol of RBC due to precipitated ribosomes. |
| Precipitated ribosomes in cytoplasm? | Basophilic stipplings |
| What conditions are associated to Basophilic stippling? | Thalasemia, EtOH abuse, and lead/heavy metal poisoning. |
| Centiacinal emphysema: | associated with chronic, heavy smoking, which involves the release of proteases, especially ELASTASE, from infiltrating neutrophils and alveolar macrophages. |
| What is the main protease released by Neutrophils in Centriacinar emphysema? | Elastase |
| Chronic, heavy smoking is associated with _________________ emphysema. | Centriacinar |
| Common description of CXR emphysema | Dilated air spaces |
| The secretion of Elastase produces: | Creation on new O2 free radicals, which impair the function of Protease inhibitors, such as AAT-1, leading to: - Acinal wall destruction - Irreversible airspace dilation distal to terminal bronchioles |
| Renal artery stenosis: | Causes significant renal HYPOPERFUSION which results in decreased GFR and activation of RAAS |
| What are the Juxtaglomerular cells? | Modified smooth muscle cells with Renin-containing zymogen granules. |
| What is the effect of RAS in the Afferent glomerular arteriole? | The modified smooth muscle (JG) cells in the wasl of the AFFERENT glomerular arterioles increase the release of renin. |
| What is PCP? | atypical fungal infection seen mainly in those with impaired cell -mediated immunity (AIDS) |
| What is the clinical and CXR presentation of PCP? | Pulmonary symptoms, hypoxia and BIlateral interstitial infiltrates on CXR. |
| What is commonly seen in patients with PCP? | Oropharyngeal candidiasis |
| White plaques on oral mucosa on an immunocompromised patient. Dx? | Oropharyngeal candidiasis |
| What is the clinical presentation of an patient with an Lung abscess? | Pulmonary infection , presenting with several days of fever, cough productive of Copious sputum (foul smelling) |
| What are the 2 MCC of lung abscess? | 1. Anaerobic bacteria form the oropharynx 2. Untreated pneumonia |
| Squamous cell neoplasm of the ear? | MC malignant ear canal tumor |
| What is the distinctive symptoms of squamous cell neoplasm of the ear? | Local or regional pain with an ulcerated plaque or nodule |
| What are the two main compensatory mechanisms for Hypovolemia? | 1. Activation of RAAS 2. Increased ADH release |
| What is the result of RAAS activation and increased ADH release? | Increase renal Na+, Cl-, water and UREA reabsorption with increased K+ excretion. |
| What area is most commonly affected in Crohn's Disease? | Terminal ileum |
| What kind of gallstones are seen in Crohn's Disease? | Cholesterol |
| The decrease reabsorption of Bile acids in Crohn's disease lead? | The development of cholesterol gallstones. |
| What is the function of Bile acids? | Emulsify fat droplets to form water-soluble micelles, which can be ten used to hydrolyze TGs into fatty acids and monoglycerides. |
| Gallbladder hypomobility | contribute to cholesterol gallstone formation in those with spinal cord injury or those patients receiving total parenteral nutrition |
| Pigment stones | Seen with patients chronic hemolytic anemias; due to increased secretion of bilirubin into bile |
| What is at risk of developing in case of too much bilibin been deposited into bile? | Pigment stones |
| Calcium oxalate stones are associated to: | Kidney stones developed in Crohn's disease. |
| What is pathogenesis of Lactose intolerance? | Due to acquired conditions that injure the Brush border of the Small intestine where lactase is expressed. |
| Labs seen in Lactose intolerance? | 1. Increased Breath Hydrogen content 2. Reduced stool pH 3. Elevated stool osmolarity |
| Patient diarrhea als an elevated stool osmolarity, reduced stool pH, and increased breath hydrogen content. | Lactose intolerance |
| Spherocytosis is seen with: | Increased MCHC (mean corpuscular Hb concentration) due to dehydration of teh RBC |
| What are the markers for Hemolysis? | Elevated lactate dehydrogenase, reticulocytosis, and decreased haptoglobin |
| Spherocytosis has a ____________________ MCV. | normal |
| Hypovolemia may be due to | excessive diuresis, can cause acute kidney injury due to reduced renal blood flow (prerenal azotemia) |
| Prerenal azotemia has: | Low Urine Na+ and FeNa and the BUN:Cr ratio is increased. |
| Intrinsic Renal injury is seen with what conditions? | ATN and Interstitial nephritis |
| Muddy brown casts | ATN |
| Interstitial Nephritis | UA usually presers with pyuria, WBC casts, and eosinophils |
| Epoposterol: | Synthetic prostacyclin; used in the treatment of pulmonary HTN, peripheral vascular disease, and Raynaud phenomenon. |
| Prostacyclin is made from _______________________ by _____________ in vascular endothelial cells. | Prostaglandin H2; Prostacyclin synthase |
| The actions of PGI2 oppose those of: | Thromboxane A2 |
| PGI-2 actions: | 1. Inhibits platelet aggregation 2. Causes vasodilation |
| Tumor arising from chromaffin cells of the adrenal medulla, characterized by excess production of catecholamines. | Pheochromocytoma |
| What is the cause of Hepatic Encephalopathy? | Increased level of ammonia and other neurotoxins i the circulation that lead to increased inhibitory NT and empired eceitaroy N release. |
| What is the treatment options for Hepatic Encephalopathy? | Lactulose and Rifaximin |
| What is the mode of action of Lactulose? | Acidification of colonic contents, which then converts absorbable ammonia into non-absorbable ammonium ions, trapping in the stool and thereby increase fecal nitrogen excretion ----> decreased ammonia concentration. |
| Ventricular Free-wall rupture is seen with: | Chest pain, tamponade, shock, and distant heart sounds |
| What is the pathogenesis ventricular free wall rupture? | The rupture lead to hemopericardium and cardiac tamponade, causing profound hypotension and shock with rapid progression to pulseless electrical activity and death. |
| Septic shock may be precipitated by _______________ or ____________. | Hyperthermia or Hypothermia |
| What are the changes in forces in Septic Shock? | Decrease in systemic vascular pressure, central venous pressure, and PCWP, and an increase in Cardiac Output. |
| Hypovolemic Shock: | All related forces are decreased except for , SVR (afterload) which increased. |
| What are the associated antibodies in Polymyositis and Dermatomyositis? | Antinuclear (ANA) and anti-tRNA synthetase (anti-Jo-1) |
| Anti-Jo-1 represents | anti-tRNA synthetase antibody involved in Polymyositis |
| Bx of Polymyositis: | Patchy endomysial inflammatory infiltrate |
| Bx of Dermatomyositis? | Perivascular inflammation (localized around blood vessels and septa between muscle fibers). |
| What are the complications of Polymyositis? | - Interstitial Lung Disease - Myocarditis |
| Pathologic features of Polymyositis? | 1. Elevated muscle enzymes (CK and aldolase) 2. Autoantibodies (ANA, anti-Jo-1) 3. Bx ---> Endomysial mononuclear infiltrate, Patchy necrosis. |
| How does GLUCAGON increases serum glucose? | 1. Increasing Hepatic Glycogenolysis 2. Increasing Gluconeogenesis |
| What is the relation between glucagon and insulin> | Glucagon stimulates insulin release from the pancreas. |
| Glucagon has little or no effect on? | Skeletal muscle, adipose tissue, and renal cortex. |
| Epinephrine and Glucagon both increase glucose by: | Increase In hepatic glycogenolysis and gluconeogenesis |
| Epinephrine: | 1. Decrease glucose uptake by skeletal muscle 2. Increased release of Alanine form Skeletal muscle, which serves as source of gluconeogenesis in the liver. 3. In adipose tissue, increase the breakdown of TGs, thereby increasing circulating free fatty acids and glycerol that can be tutilized as a gluconeogenic substrate. |
| Silicosis pathogenesis: | Inhaled particles lead to IMPAIRED MACROPHAGE FUNCTION by disrupting phagocytosis and promoting apoptosis. |
| Which lobes are most affected by Silicosis? | Upper lobes |
| Silicosis often increases the risk of infection by? | Mycobacterium tuberculosis |
| Cystic fibrosis: | seen with impaired mucociliary clearance, which result in recurrent pulmonary infections due to impaired pathogen clearance. |
| What are three main values seen in Pulmonary Functions tests? | FEV1, FVC, and FEV1/FVC ratio |
| What is the normal value for FVC and FEV1? | >80% |
| What is the normal value of FEV1:FVC? | >70% |
| FVC, FEV1 & FEV1/FVC are all _______________ in COPD. | decreased |
| How is the value of FEV1 : FVC altered in restrictive lung disease? | Normal to increased |
| FEV1 and FVC are ______________ in restrictive lung pattern. | Decreased |
| What is DLCO? | Diffusing capacity of Carbon monoxide |
| What does DLCO measure? | The amount of oxygen that travel from the lung alveoli to the bloodstream. |
| What conditions tend to reduce DLCO? | - Fibrosis and alveolitis - Restrictive lung disease - COPD (emphysema) |
| What conditions can be associated with an increased DLCO? | Polycythemia, and Asthma most commonly. |
| What is Mastocytosis? | abnormal proliferation of Mast cell sand increase histamine release. |
| What are the effects of increased histamine in mastocytosis? | Causes hypersecretion of Gastric acid by the Parietal in the stomach as well as a variety of other symptoms such as hypotension, flushing and pruritus |
| KIT is associated with: | Mastocytosis |
| What is KIT? | receptor tyrosine kinase involved in Mast cell proliferation. |
| Atrophic gastritis presents with: | Nausea, indigestion and epigastric discomfort |
| WHat are the MC causes of gastritis? | 1. Colonization on H. pylori 2. Autoimmune gastritis by Pernicious anemia |
| Gastrinoma: | - Secretes gastrin - associated with Zollinger- Ellison Syndrome |
| Somatostatinoma: | Secretes somatostatin; causes diarrhea, cholestasis, and hyperglycemia. |
| VIPoma: | Pancreatic tumor that secretes VIP, thus causing watery diarrhea, achlorhydria, and hypokalemia. |
| What is Tumor Lysis syndrome? | The breakdown of cellular content during chemotherapy of a rapid turnover cancer, such as lymphoma or leukemia |
| What are the most common serum abnormalities seen with Tumor Lysis syndrome? | Potassium, phosphorus, and uric acid |
| Where and why in the nephron is there uric acid precipitation? | Uric acid is soluble at normal pH, but can preti in acidic environments, in the distal tubules an collecting ducts. |
| Where does calculi of uric acid may be found in the nephron? | In the DCT and Collecting ducts |
| How is uric acid precipitation prevented? | Alkalinization of urine and proper hydration. |
| Does a high or low blood flow favors the precipitation of stones in the nephron? | Low or slow blood flow |
| What is the MCC of liver hydatid cysts? | Echinococcus granulosus infection |
| Accidental spill of hydatid cysts in the liver may cause: | Anaphylactic shock and death |
| What people in the U.S.A are more susceptible to E. granulosus infection? | Those living the Southwestern region and have constant contact with sheep an dogs. |
| Gene mutation to trypsin | Common cause of Hereditary pancreatitis, as it leaves trypsin unable to inactiva. |
| Where Are the Direct tissue effects of Growth hormone? | 1. Increase insulin resistance 2. Increase fat utilization 3. Increase protein synthesis |
| The increment of IGF-1 production in the liver produces: | Growth and development of bone, cartilage, and soft tissue. |
| What hypothalamic hormone stimulates the release of GH from the anterior pituitary? | GnRH |
| Dermatomyositis: | Proximal muscle weakness resembling polymyositis, with additional inflammatory features involve the SKIN |
| What are the cutaneous features distinctive of Dermatomyositis? | 1. Heliotrope rash 2. Gottron Papules |
| What are the common paraneoplastic syndromes associated with the development of Dermatomyositis and/or Polymyositis? | P Neoplasms of the Ovary, or Lung, or Pancreas. |
| Hepatitis C infection: | associated with Porphyria cutanea tarda (PCT), which presents with skin , fragility, and a blistering -rash in sued exposed areas, and mixed cryoglobulinemic vasculitis, which presents as non-blanching palpable purpura. |
| What is dystrophic calcification? | occurs in damaged or necrotic tissue in the seetin o normal calcium levels |
| When do you see Metastatic calcification? | In normal tissue but with hypercalcemia |
| What is the difference between Dystrophic vs Metastatic calcification? | Dystrophic occurs in necrotic or damage tissue but normal serum calcium, while, Metastasis occurs in normal tissue in the setting of Hypercalcemia. |
| Calcification in necrotic tissue and normal blood calcium? | Dystrophic calcification |
| Calcification in normal tissue in the setting of hypercalcemia? | Metastatic calcification |
| A common manifestation of Dystrophic calcification is: | Psammoma bodies |
| Autoimmune reaction following an untreated group A streptococcal pharyngitis? | Acute Rheumatic Fever |
| What is the pathogenesis of Rheumatic fever? | Anti-group A Strep antibodies (anti-M protein, anti-N-acetyl-B-D-glucosamine) CROSS REACT and attack cardiac and CNS antigens. |
| What is the common presentation of RF? | Arthritis, Mitral regurgitation (III/IV holosystolic murmur), sydenham chorea, erythema marginatum, and Subcutaneous nodules. |
| What criteria is seen in RF? | JONES criteria |
| What is Sydenham Chorea? | Non-rhythmic movements of hands, feet and face, which may involve voice pitch and volume. |
| Erythema ___________________ is associated with acute RF. | Marginatum |
| The malabsorption seen in Celiac disease leads to the poor absorption of _____________________. | Lipid soluble Vitamins A, D, E, K |
| Vitamin D deficiency presents with: | 1. Decreased serum Phosphorus 2. Increased serum PTH (secondary Hyper PTH) 3. Low serum Calcium |
| What marks the high bone turnover in Celiac disease> | Elevated level of Alkaline phosphatase |
| What is the antibody of Celiac Disease? | anti- tissue transglutaminase antibody |
| Positive for tissue-transglutaminase antibody. Dx? | Celiac disease |
| What are the MCC of Thyrotoxicosis? | 1. Endogenous hyper-TH or, 2. Over-replacement of TH in hypothyroid patients. |
| Agranulocytosis is a side effect of which drugs? | PTU and methimazole |
| PTU adverse effects include: | Agranulocytosis and Hepatotoxicity |
| Goiter in hypothyroid patients: | due to chronic stimulation of the thyroid by TSH |
| Thyroid cancer is: | Potential long-term complication of Radioiodine therapy for hyperthyroidism. |
| Multiple Myeloma is associated with: | Increased bone resorption due to the production of Tumor-related cytokines |
| What are the labs seen in Multiple Myeloma? | INCREASED: serum Calcium and Urine Calcium DECREASED; PTH and 1,25-(OH)2 Vitamin D |
| What is the cause of development for Gout? | Deposition of monosodium urate crustal in joints and soft tissues. |
| Gout synovial fluid analysis: | Needle-shaped negatively birefringent sodium crystals |
| What two main categories are the causatives for Gout? | 1. Increase Urate production 2. Decrease Urate clearance |
| What condition are associated with increased urate production? | Primary gout Myeloproliferative/ Lymphoproliferative disorders (PCT) Tumor Lysis syndrome HGPT deficiency |
| What are the two condition associated with decreased urate clearance and subsequent development of gout? | 1. Chronic Kidney disease 2. Thiazide/Loop diuretics |
| What joints are most affected in Gout? | Knee, 1st MTP, and ankle. |
| Pseudogout: | Not associated with Myeloproliferative disorders. Rhomboid shaped calcium crystals Positive birefringence |
| Severe Tricuspid Regurgitation (TR) may lead to: | Right heart failure, evidenced by JVD, hepatomegaly and lower extremity edema, and no evidence of Pulmonary edema. |
| Why is the placement of a permanent pacemaker (implantable) may produce Tricuspid Regurgitation? | The end of the probe will go through the Tricuspid valve orifice, producing a possible gap during its closure, leading to backflow,and development of regurgitation |
| Where is TR best heard? | Left-lower sternal border (LLSB); increase intensity with inspiration and leg raise. |
| REM sleep is characterized by: | Dreaming and voluntary muscle paralysis, and occurs towards the final third of the night. |
| Nightmares occur during: | REM sleep |
| Night terrors: | a NON-REM parasomnia shared by incomplete arousal and lack of recall of dream content |
| NON-REM SLEEP is dived into 3 stages: | Stage -1; Theta waves Stage 2: (ligight, stable sleep) - Theta waves - Sleep spindles and K-complexes Stage 3: - Slow - wave speed or deep sleep - NON-REM arousal (Night terrors) |
| Pathologic atrophy: | it can be caused by decreased physical workload, loss of innervation, decreased blood supply, inadequate nutrition, absent endocrine stimulation, or mechanical pressure. |
| Chronic smoking: | Causes metaplasia (not atrophy) of lungs columnar epithelium |
| Long-term use of Glucocorticoids: | Leads to suppression of H-P-A axis, which in turn lead to bilateral adrenocortical atrophy of Z. Fasciculata and Reticularis. |
| What can cause an adrenal crisis? | sudden cessation of corticosteroids |
| Patients with excess ACTH | Adrenal gland cortical hyperplasia and hypertrophy |
| How long after initiation of ischemia do cardiomyocytes start presenting effects? | 60 seconds |
| After how much time, without reversal and treatment, is ischemic damage IRREVERSIBLE in cardiac tissue? | After 30 minutes |
| Light-chain cast nephropathy is associated or related to: | Multiple Myeloma |
| What are some clinical manifestations of Multiple Myeloma? | Osteolytic lesions, hypercalcemia, anemia, aor acute kidney injury. |
| Polymyositis: | Causes symmetrical proximal muscle weakness. |
| Polymyositis is seen with: | Overexpression of MHC I proteins in sacomema which leads to inflammation of CD8+ T lymphocytes and myocyte damage. |
Created by:
rakomi
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