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Flashcards

Renal 1

Sterling Schwartz STEP test prep COMP Inglês 42 flashcards

Flashcards do conjunto (42)

  1. 1What substance's clearance is affected by desmopressin administration?H2O and Urea. The permeability is increased allowing more to be reabsorbed. This creates for more concentrated urine.
  2. 2What gene is commonly deleted in Renal cell Carcinoma?VHL on Chr. 3. This is common in both familial and sporadic forms of RCC.
  3. 3Anti GBM diseaseNephritic syndrome. Liner deposition of IgG and C3 on BM. CRESCENTS form (rapidly progressive glomerulonephritis)
  4. 4When are ACEI/ARB contraindicated?Renal artery stenosis. This is because Angiotensin II vasoconstricts the efferent arterioles. Without this action GFR falls and it is already decreased in renal artery stenosis.
  5. 5What disease presents with absent alpha galactosidase A? What are the findings and complications?Fabry Disease. XR. There is an increase in globotriaosylceramide. Pnts may have meuropathic pain, Hypohidrosis, telangiectasias, CV disease, and Cerebrovascular disease. RENAL FAILURE can also result due build up of GB3. PNTS have proteinuria. Pain is brought on by exercise/stress.
  6. 6SirolimusBlocks IL 2 signal transduction, by binding FKBP which inhibits mTOR. Used in immunosuppression.
  7. 7Clear Cell CarcinomaRound/polygonal cells w/ clear cytoplasm. most common form RCC. the clear cytoplasm is due to glycogen and lipids.
  8. 8Tumor lysis SyndromeOccurs when cells w/ increased turnover are rx w/ chemotherapy. This causes a build up of Uric acid that precipitates at low pHs such as those found in the distal tubule and collecting ducts.
  9. 9Creatinine Secretion and GFRNon linear relationship. At steady state Creatinine synth=secretion. Relatively small decreases in GFR result in large increases in serum creatinine. Increased GFR causes creatinine decrease.
  10. 10PAHParaaminohippuric acid. Freely Filtered and secreted by cells of the proximal tubule. The filtering process is not saturable but in secretion the carrier proteins can be saturated.
  11. 11Idiopathic Membranous nephropathyAssoc w/ circulating IgG ab to Phospholipase A2 receptor.
  12. 12Presentation of RCCUsually clear cells, Sx develop late in course as Hematuria flank pain, palpable abd. mass, fever, malaise, anorexia, and weight loss. paraneoplastic syndromes can happen (polycythemia and erythrocytosis). Metastisis to the lungs most common, followed by bone, LN, Adernals, and liver
  13. 13Fetal hydronephrosisUsually transient. most common cause is kinking at the uteropelvic junction.
  14. 14Risk factors for NephrolithiasisHypercalciuria, Hyperoxalauria (Crohn disease), Hypocitraturia (Distal tubule acidosis), hyperuricemia.
    Low fluid, low Ca, high Na/Oxalate/protein/Fructose
  15. 15What is the best early indication of Diabetic Nephropathy?Elevated urine Albumin
  16. 16Hyperacute RejectionPreformed antibodies against graft. Acts in min-hrs w/ mottling. cyanosis, fibrinoid necrosis and thrombotic occlusion of capillaries.
  17. 17Action of aldosteroneIncreases Na/K-ATPase pump and apical Na channels. Promotes K and H section in the collecting duct. This is inhibited by K sparring diuretics.
  18. 18SE of ACE inhibitorsCough, Hyperkalemia, and decreased GFR (increased creatinine)
  19. 19Findings and Signs of EmbolismAcute kidney injury (oliguria, azotemia), Blue toes, livedo reticularis (purple lace like discoloration). On microscopy there are cholesterol clefts (dissolved cholesterol, forms needle like clefts) in the arteries.
  20. 20Eosinophil FunctionParasite defense: stimulated by IL-5, eosinophils response to IgG/E covered Parasites, binding the Ig causes eosinophil degranulation and release of basic protein and ROS. AB DEP MECH.
    Type I hypersensitivity: Synthesize PG, LKT, and cytokines seen in late phase hypersensitivity and Chronic allergy.
  21. 21Stress incontinenceLeakage w/ coughing, lifting, sneezing. Caused by decreased Urethral spinster tone, or urethral hypermobility.
  22. 22Type II hypersensitivity reactionIgG and IgM, and COMPLEMENT ACTIVATION, NK cell, neutrophils, and Macrophages. occurs in Autoimmune hemolytic anemia, good pasture syndrome and hemolytic transfusion reactions.
  23. 23What structure does the ureter pass over within the pelvis?Internal illiac arteries. lies behind uterine artery lower down.
  24. 24What diseases present w/eosinophilic hyaline material w/in intimate and media of small arteries and arterioles?HTN and Diabetes
  25. 25Filtration Fraction from Hematocrit, Flow rate, filtration fraction, and GFR.FF=GFR/RPF
    RPF=RBF*(1-HCT)
  26. 26What is important to obtain in work up for metabolic acidosis?Urine Chloride and volume status. The most common causes of metabolic alkalosis are vomiting.nasogastric suctioning (loss of Cl and H ions), Thiazides/loop diuretics (Blocks Na and Cl reabsorption, thus Cl wasting), Mineralocorticoid excess (Cl, H, and K wasting there is increase Na reabsorption and Relative HCO3 increase).
  27. 27IgA nephropathyDeposition if IgA complexes. Mesangial hypercellularity on light microscopy. OnIF there is IgA in Mesangium Starts 5-7 days post URI and returns every few months or w/ URI.
  28. 28PTH related proteinIncreased in Squamous cell/Renal/Bladder/Breast/Ovarian Tumors. iIt acts as a PTH mimic resulting in hypercalcemia.
  29. 29Grapefruit juice.Inhibits P450 enzymes in the Liver and the GI tract. This causes a rise in drugs like Cyclosporin which are degraded by P450 in both GI and Liver.
  30. 30How is Bradykinin affected by ACE?ACE decreases bradykinin. This is important because the increase in bradykinin during ACE inhibitor rx can result in angioedema from bradykinin vasodilatory effects.
  31. 31ChlorthalidoneA thiazide diuretic.
  32. 32Electrolyte disturbances of Thiazide diureticsLoss of K and H. This can result in hypokalemia (muscle cramps/weakness), and metabolic alkalosis.
  33. 33What part of the Nephron unit is impermeable to H2OThin/Thick ascending loop of henle and the early distal tubule (late DT is affected by ADH).
  34. 34In terms of Renin, Ang I, Ang II, ADO, and Bradykinin what effect do Beta blockers have on the RAS system?Beta blockers inhibit Juxtaglomerular cells from producing renin thus decreasing Ang I/II and ADO. Because ACE is not affected Bradykinin is affected.
  35. 35Rx for prevention of Ca stonesThiazide Diuretics. They increase Ca reabsorption by inhibiting Na/Cl cotransport. Also by causing hypovolemia Thiazides increase Na and H20 reabsorption by which Ca reabsorption also increase.
  36. 36NSAID kidney injuryAssoc w/ chronic use. Concentration of NSAIDs leads to Chronic interstitial nephritis (interstitial infiltrate w/fibrosis, tubular atrophy, papillary necrosis, and scarring). Because NSAIDs inhibit prostaglandin synthesis vasoconstriction can occur and cause ischemic papillary necrosis.
  37. 37Oxalate CrystalsAppear in the Proximal tubule after Ethylene glycol poisoning.
  38. 38Sx of Ethylene Glycol PoisoningAcute renal failure (oliguria, anorexia, flank pain), 24-72 hrs after ingestion. High anion gap metabolic acidosis may be present.
  39. 39Renal Metabolism of what amino acid is important for Acid excretion?Glutamine. Metabolized into Glutamate then into alphketoglutarate then into Glucose. In the first two steps NH3 is released This accepts an H ion in the tubular lumen. In this way excess ammonium production is seen in Chronic acidosis.
  40. 40RBF from Urine flow, PAH clearance, and hematocritRBF=PAH clearance/(1-HCT)
    PAH CL=(urine PAH*UFR)/Plasma PAH
  41. 41From which cells does RCC originate.Epithelium of the proximal renal tubules
  42. 42Thrmobocytopenic thrombotic pupura-Hemolytic Uremic syndrome (TTP-HUS)fever, neuro symptoms, renal failure, anemia, and thrombocytopenia. PLT activation, microvascular thrombosis, Microangiopathic hemolytic anemia w/schistocytes. PT/PTT are NORMAL

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COMP STEP test prep FlashCards sobre Renal 1, criado por Sterling Schwartz em 04-08-2017.
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