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94 Cards in this Set
- Front
- Back
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which molecule measures plasma volume
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radiolabeled albumin
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which molecule measures ECF volume
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inulin
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which 2 molecules can be used to estimate GFR
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inulin (is freely filtered, not reabsorbed or secreted), creatinine clearance also estimates it (small amount is secreted so slightly overestimates it)
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Clearence equation
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CL=V*U/P
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which molecule estimates RPF, equation for RBF
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PAH clearence (is both filtered and secreted), RBF=RPF/(1-Hct)
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changes in RPF and GFR when you constrict AA
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decr RPF, decr GFP
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changes in RPF and GFR when you constric EA
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decr RBF, incr GFR
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changes in RPF and GFR when you dilate AA
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incr RBF, incr GFR
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changes in RPF and GFR when you dilate EA
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incr RBF, decr GFR
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how to calculate free water clearence
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ability to dilute urine; C(H20) = V - C(osm); C(osm) - U(osm)V/P(osm); with ADH C(H2O)<0 (retention of free water); without ADH C(H2O)>0 (excretion of free water)
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filtered load
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FL = GFR X [plasma]
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excretion rate
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ER = V x [urine]
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Reabsorption rate
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RR = filtered load (GFR x [plasma]) - excretion rate (V x [urine])
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secretion rate
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excretion rate (V x [urine]) - filtered load (GFR x [plasma])
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effects of ANP
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secreted in response to incr BP, causes incr in GFR and incr Na filtration WITHOUT a compensitory incr in Na+ reabsorbtion in the distal nephron
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diarrhea causes which type of metabolic disturbance
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normal anion gap metabolic acidosis
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which metabolic disturbance causes tingling and why
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respiratory alkylosis; you have less H+ ions to bind to protein, so more Ca++ binds instead, this lowers free Ca++ and causes tingling
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most common cause of adult nephrotic syndrome
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membranous GN (diffuse), caused by drugs (NSAIDs, captopril), infections (HBV,syph) and SLE
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most common glomerular dz in HIV patients (and IV drug users)
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focal (some glomeruli) segmental (part of glom affected) glomerulosclerosis
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what can be associated with Wilms tumor (3)
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aniridia (iris hypoplasia), GU malformation, mental-motor retardation (WAGR)
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where is EPO made
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in the endothelial cells of the peritubular CAPs
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what arteries supply the bladder
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vesciular branches of internal iliacs
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podocytes
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make the BM/visceral layer in Bowman's capsule
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course of the ureters
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pass under the uterine artery and under the vas deferens (water under the bridge)
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what % of total body weight is water, what % of that is ECF/ICF, what % of that is plama vs. interstitial
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60% of weight is water, of that 1/3 is ECF and 2/3 is ICFl of the ECF, 1/4 is plasma and 3/4 is interstitial
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implication if CL of a substance is either higher or lower than GFR
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if CL<GFR then there is reabsorption; if CL>GFR then secretion; if = then neither
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what makes the glomerular BM negatively charged
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heparin sulfate
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filtration fraction
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fraction of RBF that is actually filtered; FF=GFR/RBF
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threshold for glucose reabsorption
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at 200 you see glucosuria, at 350 its saturated
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tubuloglomerular feedback
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incr renal artery pressure causes incr delivery of fluid to the macula densa, causes constriction of nearby AA and causes incr resistence to maintain normal RBF
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where in the nephron does PTH act
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in the PT it inhibits Na/phosphate cotransport to cause P excretion, also stimulates 1a-hydroxylase; in the distal convoluted tubule it incr Ca/Na exchange (pump on the basal side)
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AT II effect on nephron
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stimulates Na/H exchange in the PT, incr Na and H2O reabsorption (can lead to contraction alkylosis)
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which sections of the nephron have low/no H20 permeability (diluting segments)
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thick ascending loop, early distal convoluted tubule
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which ADH receptors are resonsible for incr H20 perm in the collecting ducts
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V2
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intercalated cell of collecting tubules
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has H+/K+ exchanger on luminal
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AT II's effect on HR
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affects baroreceptor function, limits reflex bradycardia that would usually accompany its pressor effects
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JG and MD cells
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JG: modified SM cells in AA, secrete renin in response to decr RBF, decr Na delivery to DT and incr symp tone; MD: part of distal convoluted tubule, Na sensor
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what causes vasodilation of AA
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PG's, secreted by endothial cells of the AA
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Na and K levels in DKA patient
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low Na and high K+
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effect of salicylates on arterial pH
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initial resp alk due to stimulation of resp center, then it interferes with TCA and cuases met acidosis; eventually may die of hypo-K+ and dehydration
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causes of incr anion gap met acidosis
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methanol, uremia, DKA, paraldehyde, Iron, INH, lactic acidosis, ethylene glycol, salicylates
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type I renal tubular acidosis
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defect in H/K ATPase in collecting tubules leads to an ability to secrete H+, can lead to hypokalemia
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type II renal tubular acidosis
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defect in PT HCO3- reabsorption, can lead to hypokalemia
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type IV renal tubular acidosis
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hypoaldo leads to hyperkalemia leads to inhibition of ammonium excretion in PT, causes a decr in urine pH due to decr buffering capacity
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granular muddy brown casts
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ATN
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nephritic syndrome presentation (6)
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inflammatory process; causes hematuria, RBC casts, azotemia, oliguria, HTN, proteinuria <3.5
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nephrotic syndrome presentation (4)
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due to loss of - charge on BM; massive proteinuria, hyperlipidemia, edema, ascites
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acute poststrep glomerulonephritis
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type III HS, nerphritic, follows skin or pharyngeal strep infection, typically presents with peripheral and periorbital edema; glomeruli are hypercellular, lumpy bumpy; subepithelial immune complexes (granular)
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crescentic GN
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Goodpastures, Wegner's, presents as nephritic
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diffuse proliferative GN
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nephritic, subendothelial IC's, incr # cells, "wire looping", most common cause of death in SLE
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Berger's
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IgA nephrophathy, presents as nephritic or nephrotic, commonly follows URI, IC's in the mesangium, episodic bouts of hematuria
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Alport's syndrome
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mutation in type IV collagen, can cause nephritic syndrome; also associated with nerve disorders, ocular disorders and deafness
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membranous GN (diffuse membranous)
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most common cause of adult nephrotic, caused by drugs (NSAIDs, captopril), infections (HBV, syph), SLE; diffuse CAP and BM thickening, subepithelial deposits
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minimal change
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presents in kids as nephrotic syndrome; foot process efacement on EM, often postinfectious
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focal segmental GS
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segmental sclerosis and hyalinosis, most commonly in HIV pts, nephrotic syndrome
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membranoproliferative GN
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nephrotic, sometimes associated with HBV, subendothelial deposits, tram track due to GBM splitting
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composition of Ca kideny stones
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Ca oxalate or Ca phosphate or both
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kidney stone that is radiolucent (won't show up on x-ray)
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uric acid; urine must be acidic for these to form
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syndrome and gene deletion associated with renal cell CA
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von Hippel-Lindau, gene deletion on chromosome 3
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paraneoplastic syndromes associated with renal cell CA
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ectopic EPO, ACTH, PTHrp, prolactin
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painless hematuria
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suggestive of bladder CA
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exposures associated with transitional cell CA (4)
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phenacetin, smoking, analine dyes, cyclophosphamide
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drug induced interstitial nephritis (include presentation)
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acute interstitial renal inflammation; presents with fever, rash, oliguria, eosinophilia, hematuria; occurs 2 weeks after admin of drugs (penicillin derivitives like methicillin, NSAIDs, diuretics); combo of type I and type IV HS
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ischemic ATN
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often due to hypovolemia; causes damage to endothelial cells which acts to vasoconstrict AA and decr GFR,; also causes damage to tubular cells which can detach and obstruct the lumen causing oliguria; BM damaged;
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nephrotoxic ATN (including most common cause)
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aminoglycosides most common cause, primarily damages PT cells, BM intact
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drugs most commonly causing hematuria
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anticoags
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renal handling of BUN and creatinine
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BUN is reabsorbed, creatinine is not
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prerenal azotemia
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most often due to hypovolemia, also NSAIDs and ACE-I; decr RBF causes decr GFR, urea (along with Na and H2O) is retained in the kidney, so the BUN/creatinine ratio incrs as the body attempts to conserve water
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urine osmolality, urine Na, FeNa, serum BUN/Cr levels for prerenal ARF
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UO: high, UNa: low, FeNa: low, serum BUN/Cr >20
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urine osmolality, urine Na, FeNa, serum BUN/Cr levels for renal ARF
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UO: <350, UNa: >20, FeNa: >2%, serum BUN/Cr <15
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urine osmolality, urine Na, FeNa, serum BUN/Cr levels for postrenal ARF
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UO: <350, UNa: >40, FeNa: >4%, serum BUN/Cr >15
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associated problems in ADPKD
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berry aneurysms, mitral valve prolapse, HTN (cysts impair glomeruli perfusion, cause incr in renin secretion)
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where are simple cysts of the kidney found
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only in the cortex
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Na disturbances
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low: disorientation, stupor, coma; high: irritability, delerium, N/V
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K disturbances
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low: U waves (small hump on EKG after T-wave), flattened T waves, arrhythmias; high: peaked T-waves, wide QRS, arrhythmias
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medullary cystic dz
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medullary cysts, US shows small kidney, poor prognosis
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medullary sponge dz
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collecting duct cysts, good prognosis, may have stones, UTIs, hematura
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where in the nephron is urine most hypertonic if ADH is absent or present
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absent: most hypertonic at the bottom of the descening limb of henle, b/c it passes through the medulla which is hypertonic and it is permeable to H2O, water flows out, making urine hypertonic, if no ADH, then no water is reabsorbed in the collecting tubules; if ADH is present, water is reabsorbed in the collecting tubules and this the end of the CT is the most hypertonic area
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important pumps in PT (3)
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Na/glucose cotransporter (also responsible for AA, PO4), Na/H pump, Cl/base transporter (secretion of ammonium to act as a buffer)
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important pump in TALH
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Na/K/2Cl, also Mg/Ca paracellular transport
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important pump of distal convoluted tubule
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Na/Cl cotransport
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effect of acidosis/alkylosis on K+ secretion
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acidosis leads to decr K+ secretion, alkylosis leads to incr K+ secretion
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presentation of ethylene glycol poisoning
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sudden onset back pain, hematuria, oliguria; incr anion gap metabolic acidosis, Ca-oxaloacete kideney stones
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causes of metabolic alkylosis (4)
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diuretic use (contraction alkalosis), vomiting (losing acid from stomach), antacid use, hyperaldo (incr H+ excretion, incr HCO3 reabsorption)
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nephritic dzs (5)
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acute post-strep GN, rapidly progressing (cresentic) GN, diffuse proliferative GN, Berger's, Alport's
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nephrotic dzs (6)
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membranous GN, minimal change, amyloidosis, DM glomerulonephropathy, focal segmental GS, membranoproliferative GN
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Diabetic nephropathy
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NEG of GBM causes incr permeability, thickening; NEG of effecrent arterioles (hyalinized) leads to incr GFR and mesangial damage
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renal cell CA
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often invades the IVC and renal vein, incr incidence with smoking and obesity, polygonal clear cells which contain glycogen and lipid, gross: hemorrhage and necrosis
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Wilms tumor
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presents with huge, grey, necrotic palpable flank mass, contains embryonic glomerular structures plus a stomal component which can contain SM, often makes renin and can cause HTN and hematuria
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renal papillary necrosis (4)
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DM, acute pyelonephritis, chronic phenacetin use (ex: acetaminophen, esp if used with asprin), sickle cell anemia
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renal failure diet
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decr protein, ecr PO4, incr carbs, moderate fat, minimal H2O and Na
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Mg++ disturbances
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low: neuromusclular irratibility, arrythmias; high: delerium, decr DTRs
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HUS
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E. Coli, microangiopathic hemolytic anemia related to vascular intimal hyperplasia, fibrinoid necorisis and thickened BM
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bladder CA
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usually arises from the transitional epithelium, tumor penetration through the mucosa is invasive CA, often papillary
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