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Step 1 12.12.12

Renal II

QuestionAnswer
When is atrial naturetic peptide secreted? What does it do and what is the net effecT? secreted when atrial P is high. incr GFR, and Na+ filtration = Na+ and volume loss
When is renin secreted? in low blood volume
When is Parathyroid hormone (PTH) secreted? when plasma Ca++ is low, or plasma PO4--- is high or vit D is low
What does PTH cause? incr Ca++ reabsrobtion in DCt, decr PO4--- reabsorbtion in PCT, incr vit D production. also incr Ca++ and PO4 absorbtion from the gut
When is angiotensin II shynthesized? in response to decr BP
What does Angiotensin II do? What is the net effect? incr GFR but with compensatory Na+ reabsorbtion in PT, DCT. net effrect: preserves renal function in low volume state and reabsorbs Na+ to decr fluid loss
When is aldosterone secreted? secreted in response to decr BV (AT II) and incr plasma K+
What is the effect of aldosterone? incr Na+ reabsorbtion, incr K+ secretion, incr h+
When is ADH secreted? secreted in response to incr plasma osmolarity and decr blood volume
What is the action of ADH (vasopressin)? binds to receptors on principal c ells causing incr water channels and incr H20 reabsorbtioon
What are 6 causes of hyperkalemia by a shift of K+ from the ICF to the ECF? 1insulin deficiency 2. Beta adrenergic antagonists 3. acidosis, exercise 4. hyper osmolarity 5. digitalis 6. cell lysis
How is hyperkalemia caused by insulin deficiency? decr the Na+/K+ ATPase
How is hyperkalemia caused by beta adrenergic antagonists? decr Na+/K+ ATPase
How is hyperkalemia caused by acidosis or severe exercise? incr K+/H+ exchanger
How does digitalis cause hyperkalemia? blocks Na/K+ ATPAse
What are 4 things that cause a hypokalemia by shifting K+ into the ICF? 1. insulin 2. Beta adrenergic agonists 3. alkalosis 4. hypo osmolarity
How does inuslin, beta adrenergic agonists cause hypokalemia? activate the Na+/K+ ATPase
How does alkalosis cause hypokalemia? incr K+/H+ exchanger
What are the sx of hyponatremia? disorientation ,stupor, coma
What are the sx of hypernatremia? neurologic:irritability, delirium, coma
What causes hypochloridemia? secondary to met alk., hypokalemia, hypovolumeia, incr aldosterone
What causes hyperchloridemia? secondary to non-anion gap acidosis
What are the ECG sx of hypokalemia? U waves on ECG, flattened T waves, arythmia, paralysis
What are the ECG sx of hyperkalemia? peaked T waves, wide QRS, arrythmia
What are the sx of hypocalcemia? tetany, NMJ irritability
What are the sx of hypercalcemia? delerium, renal stones, abdominal pain, not necc. calciuria
What are the sx of hypomagnesia? NMJ irritability, arrythmias
What are the sx of hypermagnesia? delerium, decr DTRs, cardiopulmonary arrest
What are the sx of hypophosphatemia? low mineral ion product causes bone loss, osteomalacia
What are the sx of hyperphosphatemia? high mineral ion product causes renal stones, metastatic calcification
What happens to the pH, PCO2, and [HCO3-) in a metabolic acidosis? decr pH, decr pCO2, decr HCO3-
What happens to the pH, PCO2, and [HCO3-) in a metabolic alkalosis? incr pH, incr pCO2, incr HCO3-
What happens to the pH, PCO2, and [HCO3-) in a respiratory acidosis? decr pH, incr pCO2, incr [HCO3-]
What happens to the pH, PCO2, and [HCO3-) in a respiratory alkalosis? incr pH, decr PCO2, decr HCO3-
What is the compensatory response in a metabolic acidosis? immediate hyperventialation
What is the compensatory response in a metabolic alkalosis? immediate hypoventialtion
What is the compensatory response in a respiratory acidosis? incr Renal HCO3- reabsorbtion (delayed)
What is the compensatory response in a respiratory alkalosis? decr renal HCO3 reabsorbtion (delayed)
What is the henderson hasselbach equation for blood pH? pH= pKa+ log [HCO3-]/0.03 PCO2
What is Winter's formula for compensation in a metabolic acidosis? PCO2 incr 0.7 for ever 1 HCO3-
What are some major causes of respiratory acidosis? Hypoventialation: airway obstruction, acute lung disease, chronic lung disease, opioids, weakening of resp muscles
How do you calculate the anion gap? Na+-(HcO3- + Cl-) normal is 8-12
What is a mnemonic for the major causes of anion gap metabolic acidosis? MUDPILES: Methanol (formic acid), uremia, DKA, paraldehyde or Phenoformin, Iron tablets, lactic acidosis, EtGly, Salicylates
What are the major causes of a normal anion gap metabolic acidosis? diarrhea, glue sniffing, enal tubular acidosis, hyperchloremia
what is normal HCO3 and CO2 on ABG? CO2=40, HCO3= 24
What are some major causes of respiratory alkalosis? hyperventialation: high altitude, aspirin injestion (early)
What are some major causes of metabolic alkalosis? hypoventialtion with comp: diuretics, vomiting, anatacid use, hyperaldosteronism
What is Type 1 Renal tubular acidosis? What is it associated with? defect in collecting tubules ability to excrete H+. assoc: hypokalemia and risk for calcium kidney stones
What is Type 2 renal tubular acidosis? What is it associated with? defect in proximal tubule HCO3 reabsorbtion. associated wiht hypokalemia, and hypophosphatemic rickets
What is Type 4 renal tubular acidosis? What is it associated with? hypoaldosteronism or lack of collecting tubule response to aldosterone. assoc: hyperkalemia, inhibitoon of ammonium excretion in PT. leads to decr urine pH due to decr buffering capacity
What 3 conditions are RBC casts seen? glomerular nephritis, ischemia, malignant HTN
What 3 con ditions are WBC casts seen in the urine? tubulointerstitial inflammation, acute pyelonephritis, transplant rejection
When are muddy brown granular casts seen in the urine? acute tubular necrosis
When are waxy casts seen in the urine? advanced renal disease/CRF
What do casts in general indicated? that the hematuria or the pyuria is of renal origin
What will bladder cancer or kidney stones produce in the urine? blood, no casts
What will acute cystitis produce in the urine? pyuria, not casts
What does focal glomerular disease mean? few glomeruli invovled as in FSGS
What does diffuse glomerular disease mean? all glomeruli invovled as in diffuse proliferative GN
What does proliferative glomerular disease mean? hypercellular glomeruli as in mesangial hypercellularity
What is a membranous glomerular injury? thicking of GBM, as in membranous GN
What is a primary glomerular disease? only the glomeruli are invovled as in minimal change disease
What is a seconday glomerular disease? invovles glomeruli and other organs as in SLE, and nephropathy
What are 4 major GNs which produce nephritic syndrome? 1. acute post strep GN 2. rapidly progressive GN 3. Berger's IgA glomerulopathy 4. Alport syndrome
What are 5 major GN producing nephrotic syndrome? 1. focal segmental GN 2. membranous GN 3. minimal change disease 4. amyloidosis 5. diabetic glomerulopathy
What are 2 major GN which can cause both nephrotic and mephritic syndromes? 1. diffuse proliferative GN 2. membranoproliferative GN
Is Nephritic or nephrotic syndrome inflammatory? nephritic
What are some sx associated with nephritic syndrome ? hematuria, RBC casts, azotemia, oliguria, HTN, proteinuria
What is the clinical picture and outcome of acute post streptococcal glomerulonephritis? most frequently seen in children. peripheral and periorbital edema and dark urine. resolves spontaneously
What is seen on LM in acute post streptococcal glomerulonephritis? glomeruli enlarged and hypercellular, neutrophils. lumpy bumpy appearance
What is seen on EM in acute post streptococcal glomerulonephritis? subepithelial immune complex humps
What is seen on IF in acute post streptococcal glomerulonephritis? granular appearance due to IgG, IgM, and C3 on GBM and mesangium
What are 3 major diseases that can lead to rapidly progressive ( crescentic) glomerularnephritis? 1. Goodpasture's (type II hyper sens), Ab to GBM and alveolar BM 2. Wegener's granulomatosis 3. microscopic polyangitis
What is seen on IF and what are the common sx of Goodpasture's syndrome? linear IF on GBM, see hematuria coupled with hemoptysis
What Ab is seen in microscopic polyangitis vs. Wegener's granulomatosis? MP:pANCA WG: cANCA
What is seen on LM anf IF in rapidly progressive ( crescentic) glomerularnephritis? crescent moon shaped consisting of fibrin and plasma proteins (C3b) with glomerular parietal cells, monocytes, macrophabges
What is the prognosis in rapidly progressive ( crescentic) glomerularnephritis? poor. rapidly deteriorating renal function
What are 2 processes causing diffuse proliferative glomerular nephritis? SLE or MPGN
What is seen on LM in diffuse proliferative glomerular nephritis? wire looping of capillaries
what is seen on EM in diffuse proliferative glomerular nephritis? subendothelial and sometimes intramembranous IgG ICs often with C3
What is seen on IF in diffuse proliferative glomerular nephritis?? granular
How do SLE and MPGN present? can present as nephrotic and nephritic together. diffuse proliferative glomerular nephritis is the most common cause of death in SLE
Henloch Schonlein purpura is related to what GN? Berger's disease (IgA nephropathy)
How does Berger's disease (IgA nephropathy)present? flares of URI and acute gastroenteritis. intermittent hematuria
What is seen on LM in Berger's disease (IgA nephropathy)? mesangial proliferation
qWhat is seen on EM in Berger's disease (IgA nephropathy)? mesangial IC depositis
What is seen on IF in Berger's disease (IgA nephropathy)? IgA ICs in mesangium
What is the pathophysiology of Alport Syndrome? mutation in type IV collagen-->split basement membrane
What sx is Alport syndrome associated with? nerve disroders, orcular defects, deafness, X-linked
How does nephrotic syndrome present? What is it associated with? massive proteinuria (>3.5 g/day), hyperlipidemia, fatty casts, edema. Associated wiht thromboembolism (hypercoagulable state due to ATIII loss in urine) and incr infection
What is seen on LM in focal segmental glomerularnephritis? Who is most likely to get? most common GN in HIV pt. see segmental sclerosis and hyalinosis
What causes membranous glomerularnephritis (diffuse mebranous glomerulopathy)? When is it most commonly seen? caused by drugs, infection, SLE, solid tumors. most common cause of adutls with nephrotic syndrome
What is seen on LM in membranous glomerularnephritis (diffuse mebranous glomerulopathy)? diffuse capillary and GBM thickening
What is seen on EM in membranous glomerularnephritis (diffuse mebranous glomerulopathy)? spike and dome with subepithelial deposits
What is seen on IF in membranous glomerularnephritis (diffuse mebranous glomerulopathy)? granular. SLE's nephrotic presentation
What causes minimal change disease? who gets it? How is it tx? can be triggered by infection or immune stimulus. most common in children. responds to corticosteroids
What is seen on LM in minimal change disease? normal
What is seen on EM in minimal change disease? foot process effacement. slective loss of albumin due to GBM polyanion loss
What is amyloidosis associated with in the kidney? chronic conditions like multiple myeloma, Tb, RA
What is seen on LM in amyloidosis? congo red stain, apple green birefringence
what is seen generally in membranoproliferative glomerular nephritis? subendothelial ICs with granular IF
What is seen in type I membranoproliferative glomerular nephritis LM? tram track appearance due to GBM splitting caused by mesangial in growth
What is seen on EM in type II membranoproliferative glomerular nephritis? dense deposits
How can membranoproliferative glomerular nephritis present? either as nephrtic or nephrotic
What is Type I MPGN associated with? HBV, HBC
What is Type II MPGN associated with? C3 nephritic factor
What is the pathophysiology of diabetic glomerulo-nephropathy? nonenzymatic glycosylation of GBM--> incr permeability, thickening
What is seen on LM of diabetic glomerulo-nephropathy? mesangial expansion, GBM thickening, eosinophilic nodular glomerularsclerosis (Kkimmelstiel-Wilson lesion)
What are the severe complications of kidney stones? Hoe to you tx and prevent? can lead to severe complications like hydropnephrosis and pyelonephritis. tx and prevent by encouraging fluid intake
What is the x ray and what pH precipitates calcium kidney stones? What are the 2 types? acidic or neutral pH. radiopaque on XR. either Ca oxalate or Ca phosphate
What conditions can lead to calcium kidney stone? hypercalcemia conditions like cancer, PTH.
What conditions could lead to a Calcium oxalate stone? ethylene glycol or vitamin C abuse
What is the x ray and what pH precipitates ammonium magnesium phosphate (struvite) stones? alkaline pH, radiopaque
What causes ammonium magnesium phosphate (struvite) stones? what can they lead to? infection with urease positive magnesium and radiolucent buds like Proteus, Staphylococcus, Klebsiella. can form stagcorn stones which predispose to UTI
What conditions can worsen ammonium magnesium phosphate crystals? alkaluria
What is the x ray and what pH precipitates of uric acid stones? acidic pH, radiolucent
What conditions can predispose to uric acid stones? gout, leukemia
What is the x ray and what pH precipitates cysteine stones? acidic pH, radiopaque
What do cysteine stones look like? how do you treat them? hexagonal. tx with alkalinization of urine
What is hydronephrosis? What does it cause? results from urinary tract obstruction. causes dilation up to obstruction and parenchymal thickening chronically
What is the origin or renal cell carcinoma? What does it look like on histology? originates from renal tubular cells. see polygonal clear cells filled with lipids and carbohydrates
Who gets renal cell carcinoma? What are the major RF? most commonly in men 50-70 y/o. incidence incr with smoking and obesity
How does renal cell carcinoma present clinically? hematuria, palpable mass, secondary polycythemia, flank pain, fever, weight loss.
What does a renal cell carcinoma invade and where does it spread? invades IVC and spreads hematogenously to lung and bone
What is a key genetic association of renal cell carcinoma? von-Hippel Lindau syndrome and gene deletion at 3p
What paraneoplatic syndromes is renal cell carcinoma associated with? ectopic EPI, ACTH, PTHrP, prolactin
Who gets Wilm's tumor? What will it contain? most common renal malignancy in age 2-4. contains embryonic glomerular structures
How does Wilm's tumor present? huge, palpable flank mass and or hematuria
What is the genetic component of Wilm's tumor, What syndrome can it be a part of? deletion of WT1 tumor surpressor on Chr 11. can be part of WAGR complex: Wilm's tumor, aniridia, genitourinary malformation, mental motor Retardation
Where can transitional cell carcinoma occur? What is a key finding on urinalysis? can occur in renal calyces, pelvis, ureters, bladder. painless hematuria with no casts suggests bladder cancer
What are the major RF for transitional cell carcinoma? Mnemonic? problems in the Pee SAC: phenacetin, smokings, aniline dyes, cyclophosphamide
How does acute pyelonephritis present? What does it affect? fever, CVA tnederness, n/v. affects cortex with sparing of glomeruli
What is seen on histology in chronic pyelonephritis? coarse, assymetric corticomedullary scarring. tubuloes can contain eosinophilic casts (thyroidization of kidney)
What is a classic urinalysis findings for chronic pyelonephritis? What is required for the development? white cell casts are classic. need vesicouteral reflux to develop chronic pyelopnephritis
What causes drug induced interstitial nephritis? What is seen? diruetics, NSAIDs, penicillin derivatives, sulfonamides, rifampin causing pyuria and azotemia. acute interstitial inflammationm
How does induced interstital nephritis present? fever, rash, hematuria, CVA tenderness. azotemia 1-2 weeks after drug admistration
What is diffuse cortical necrosis? acute generalized cortical infarction of both kidneys. like due to vasospasm and DIC
What is diffuse cortical necrosis associated with? obstetric catastrophes and septic shock
What are the 3 stages of acute tubular necrosis? 1. inciting event, 2. maintenance phase : oliguric lasts 1-3 weeks with risk of hyperkalemia 3. recovery:= polyuric, BUN and SeCr fall, risk of hypokalemia
What are some key assocations of acute tubular necrosis? renal iscehmia, crush injury, toxin
Muddy brown granular casts are a key finding in? acute tubular necrosis
What is the pathophysiology and etiology of renal papillary necrosis? sloughing of renal papillae-->gross hematuria, proteinuria. may be triggered by recent infection or immune stimulus.
What are 4 key associated conditions with renal papillary necrosis? 1. DM 2. acute pyelonephritis 3. chronic phenacetin use 4. SCA and trait
How do you define acute renal failure? abrupt decline in renal fx with incr Creatinine and incr BUN over several days
What causes prerenal azotemia? What is seen? What happens to BUN/Cr? due to decr renal blood flow. see decr GFR, Na+ and H2O retained by kidney and an attempt to conserve volume so BUN/Cr ration incr
What causes intrinsic renal failure? What is seen? What happens to BUN/Cr? ATN or ischemia or toxins or rarely RPGN. patchy necrosis leading to debris blocking the kidney and fluid backflow. see decr GFR, epithelial/granular casts, decr BUN/Cr ration due to decr BUN reabsorbtion
What causes postrenal failure? What is seen? What happens to BUN/Cr? sue to outflow obstruction like stones, BPH, neoplasia. only develops if obstruction is bilateral
What urine osm is seen in prerenal vs. renal vs postrenal failure? Pre: >500. Renal: <350 Post: less than 350
What urine Na+ is seen in prerenal vs. renal vs postrenal failure? Pre: <10 Renal: >20. Post: >40
What FeNa is seen in prerenal vs. renal vs postrenal failure? Pre: <1% Renal: >2% Post: >4%
What Serum BUN/Cr is seen in prerenal vs. renal vs postrenal failure? PRe:>20. Renal: <15. Post: >15
What are the consequences of Na/H2O retention in renal failure? CHf, pulmonary edema, HTN
What are the major consequences of renal failure? 1. Na/H2oO retetnion 2. hyperkalemia 3. Metabolic acidosis 4. uremia 5. anemia, 6. renal osteodystrophy 7. dyslipidemia (esp TGs) 8. growth reatrdation and developmental delay
What marks the clinical syndrome of uremia? incr BUn , Cr, nausea and annorexia, pericarditis, asterixis, encephalopathy, platelet dysfx
What is renal osteodystrophy? failure to hydroxylate vit D-->Ca++ wasting and Po4 retention-->secondary hyperPTH. decr intestinal absrobtion along wiht decr Ca++ due to hyper PO4. causes subperiosteal thinning of bones
What is seen grossly in ADPKD? multiple, large, bilateral cysts that destroy the kidney parenchyma
How does ADPKD present? flank pain, hematuria, HTN, urinary infection, progressive renal failure
What is the genetic issue in ADPKD? What are some key associated problems of ADPKD? auto D mutation in PKD1 or PKD2. death from CKD or HTN due to incr renin. Associated wiht: polycystic liver, berry aneurysm, mitral valve prolapse
What are some key associated conditions with ADPKD? congenital hepatic fibrosis. Potters, after neonatal period: HTN, portal HTN renal insufficency
What are dialysis cysts? cortical and medullary cysts resulting from long term dialysis
What are simple cysts? beingn, commion, incidental finding. non enhancing and cortical and fluid filled
What is medullay cystic disease? medullary cysts can sometimes lead to fibrosis and progressive insufficiency. ultrasound shows small kidney. 70% develop kidney stones. poo prognosis
What diuretic acts primarily at the PCT? acetazolamide
What diuretic acts primarily at the proximal striaght tubule? mannitol
Where do loop diuretics primarily work? thick ascending limb
Where do thizaide diuretics primarily work? DCT
Where do K+ sparing diuretics primarily work? collecting tubule
Where doe ADH antagonists primairly work? collecting duct
What is the mech of mannitol? osmotic diuretic, incr tubular fluid osm, incr urine flow
What is the use of mannitol? shock, drug OD, incr intracranial and intraocular P
What are the major Se of mannitol? pulmonery edema, dehydration,. CONTRAI in anuria, CHF
What is the mech of acetazolamide? carbonic anhydrase inhibitor. causes self limited NaHCO3 diuresis and reduction of body stores of HCO3
What is the clinical use of acetazolamide? glaucoma, urinary alkalinization, metabolic alkalinosis, altitude sickness
What are the major SE of acetazolamide? hyperchloremic metabolic acidosis, neuropathy, NH3 toxicity, sulfa allergy
What is the mech of furosemide? sulfonamide loop diuretic. inhibits the Na/K/Cl cotransporter of thick ascending limb of loop of henle. abolishes the hypertonicity of the medulla preventing concentration. incr Ca++ excretion
What is the effect of furosemide on PGE? What can inhibit it? stimulates PGE release (vasodilates afferent arteriole), inhibited by NSAIDs
What is the clinical use of loop diuretics? edematous states (CHF, cirrosis, nephrotic syndrome, pulm. edema), HTN, hypercalcemia
What are the major SE of furosemide? Mnemonic? OH DANG! Ototoxicity, hypokalemia, dehydration, allergy (sulfa), Nephritis (interstitial), Gout
What is the mech of ethacrynic acid? phenoxyacetic acid derivative which inhibits Na/K/CL in thick ascending limb of LoH.
What is the clinical use of ethacrynic acid? diuresis in pt with allergies to sulfa drugs
What are the major SE of ethacrynic acid? similar to furosemide (OH DANG), can be use in hyperuricemia and acute gout
What is the mech of hydrochlorothiazide? thiazide diuretic. inhibits NaCl reabsorbtion in early distal tubule. reducing diluting ability of nephron, decr Ca++ excretion
What is the clinical use of hydrochlorothiazide? HTN, CHF, idiopathic hypercalciuria, nephrogenic DI
What is are the major SE of hydrochlorothiazide? hypokalemic metabolic alkalosis, hyponatermia, hyper glycemia, hyperlipidemia, hyperuricemia, hypercalcemia. sulfa allergy. hyperGLUC
What is the class of Spironolactone, triameterne, amiloride? K+ sparing diuretics
What is the mech of spironolactone? competitive aldosterone receptor antagonist in cortical collecting tubule
What is the mech of amiloride and triamterene? act at cortical collecting tubule by ccblocking Na+ channels
What is the clinical use of spironolactone, triameterene, amiloride? hyperaldosteronism, K+ depletion, CHF
What are the major SE of spironlactone? hyperkalemia, gynecomastia
What are the SE of amiloride and triamterine? hyperkalemia
What happens to urine Na and serum Na+ in diuretic use? urine incr, serum decr
What happens to urine K+ in diuretic use? incr in all except K+ sparing diuretics
What diuretics could cause an acidemia? Carbonic anhydrase inhibitors ( decr HCO3 reabs), K+ sparing (aldosterone blockade prevents H+ secretion), hyperkalmeia causes K+ to enter cells in exchange for H+
How can loop and thiazide diuretics cause an alkalemia? 1. volume contraction-->incr AT II--> incr Na/H exchange in PT= incr HCO3 2. K+ loss leads to K+ exiting cells for H+ entering cells 3. in low K+, H rather than K is exchanged for Na+ in CCT leading to alkalosis and paradoxical aciduria
How does urine Ca+ vary with loop vs thiazide diuretics? incr in loop diuretics, dec in thiazides. thiazides incr reabsorbtion in PT and LoH
What is the mech of lisinopril, enalapril, captopril? inhibit ACE, reducing levels of Ang II and preventing bradykinin inactivation. renin release is incr due to loss of feedback inhbitiosn
what is the mech of the -sartans? What is a key diff between them and the prils? angiotensin II receptor blockers. do NOT incr kallikrein= NO cough
What is the clinical use of the -prils? HTN, CHF, diabetic renal disease. prevent heart remodeling in chronic HTN
What are the major SE of the prils? Mnemonic? CAPTOPRIL: Cough, angioedema, proteinuria, tasts changes, hypOtension, Pregnancy damage, Rash, incr renin, Lower angII. also hyperkalemia
What condtion besides pregnancy should -prils be avoided? bilateral renal artery stenosis b/c ACeI decr GFR causing incr in SeCr
Created by: tjs2123