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59 Cards in this Set
- Front
- Back
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Blood flow through kidney from renal a to v?
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Renal a, interlobar a, interlobular a, afferent arteriole, efferent arteriole, peritubular caps, vasa recta....
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How do you measure plasma vol, extracell vol, TBW?
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Plasma - radiolabeled albumin, Evans blue
Extracel - inulin, mannitol, sulfate TBW - tritiated H20, D20, antipyrene |
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What is the glomerular filtration barrier composed of?
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Size and charge!
Fenestrated endothelial cells Fused BM - heparan sulfate (neg) Podocyte epithelial cells |
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How do you calc clearance?
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Vol of plasma cleared of substance per unit time.
C=UV/P |
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How can you measure GFR? Which is more accurate?
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Clearance of inulin (freely filtered, not reabsorbed/secreted)
Clearance of Cr (slightly secreted so overestimated GFR a bit) |
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How can you measure effective renal plasma flow? (ERPF)
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Clearance of PAH - freely filtered and completed secreted by prox tubule. All PAH entering kidney is excreted. PAH con is lowest in Bowman's capsule, then secreted in PCT, and con can increase if more water is reab later along nephron.
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How can you measure renal blood flow? How does this differ from ERPF?
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RBF=ERPF/(1-Hct)
ERPF underestimates RBF by less than 10%. |
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What is the filtration fraction? Filtered load?
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FF=GFR/RPF=20%
Filtered load = GFR x P |
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How do NSAID's and ACEI each affect GFR?
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NSAID - decrease PG, decrease dilation of afferent arteriole, decrease GFR.
ACEI - decrease constriction of efferent arteriole, decrease GFR because hydrostatic P lowered, can't push as much across GBM. |
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How does filtration fraction change with PG and angiotensin II?
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PG - dilate afferent, increase RPF and GFR so FF constant
AII - constrict efferent, decrease RPF, increase GFR so FF increases. |
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How does constriction of the ureter affect RPF, GFR, and FF?
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RPF unchanged
GFR decreased (pressure - think Starling forces) FF decreased |
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How is glucose normally handled by kidney? 160-200? 350?
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Normal range: glc completely reabsorbed in PCT by Na-glc cotransport.
160-200: glycosuria begins >350: transporter fully saturated (Tm) |
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How are AA's handled by kidney? Do they competitively inhibit each other?
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Reabsorbed by Na-dependent transporters in PCT, 3 diff one, competitively inhibit each other.
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What 3 actions does PTH have in the nephron?
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PCT - activates 1alpha-hydroxylase to increase conversion to active Vit D
PCT - inhibits Na/P cotransport to increase P excretion. DCT - stim Ca/Na exchanger to increase Ca reabsorption. |
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Where does AII work in the nephron?
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PCT - stim Na/H exchange during volume depletion, allowing for contraction alkalosis.
Efferent arteriole - constricts to maintain FF in times of low renal blood flow. |
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Where do aldosterone and ADH work in the nephron?
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CT - Aldo binds aldo receptor and stim reab of Na with loss of K and H.
ADH binds V2 and inserts aquaporins in luminal side to increase water reab. |
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Where is ammonia buffer generated and secreted in nephron?
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PCT - buffers secreted H
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What happens in the tDLH? How?What is it impermeable to? What is its nickname?
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Passive reabsorption of water ONLY due to medullary hypertonicity - "concentrating seg" makes urine hypertonic. Impermeable to solutes.
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What happens in the TALH? What is it impermeable to?
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Na/K/2Cl cotransport, indirect paracellular reab of Mg, Ca. Impermeable to water.
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What happens in the DCT? What is its nickname?
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Na/Cl cotransport, Na/Ca channel exchanger (PTH stimulated). "Diluting seg" because actie reab of NaCl.
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What happens in the principal cells of CT? Intercalated cell?
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Principal - aldo activated eNaC, secretion of K for charge balance, ADH activated aquaporins.
Intercalated - H/K exchanger secretes H for charge balance |
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What happens to concentration of Cr and inulin along length of PCT? Why?
What happens to Cl as it goes along the PCT? |
Concentration (but not amnt) increases due to reabsorption of water. NOT due to secretion/reab of either solute.
**Note - Cr is slightly secreted, making it overestimate GFR. Cl is initially reab at a slower rate than Na, but then catches up to the rate of Na reab more distally. |
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How does AII affect baroreceptor fxn? Na reabsorption?
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Limits reflex bradycardia, which would normally be caused by its pressor effects. Increases Na reab by constricting efferent arteriole to increase GFR and FF....WITH compensatory reab of Na in distal nephron. Also stim Na/H exchanger in PCT, allowing for contraction alk.
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How does ANP act as a check on RAAS?
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ANP released from atria in vol overload states. Dilates smc of afferent arteriole via cGMP to increase GFR and decrease renin. Net loss of Na and water with NO compensatory Na reab in distal nephron!
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What stimulates secretion of renin? From which cells?
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Low BP detection by JG cells of afferent arteriole
Low Na delivery to macula densa in DCT Increased sym tone via beta1 receptors Renin secreted by JG cells (modified smc) of afferent arteriole. |
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What composes the juxtaglomerular apparatus?
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JG cells - modified smc of afferent arteriole, secrete renin
Macula dense - Na sensor in DCT |
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Which cells secrete the following?
EPO 1,25-OH2 Vit D Renin PG's |
EPO - endothelial cells of peritubular caps
Vit D - conversion in PCT Renin - JG cells (modified smc) of afferent arteriole PGs - paracrine secretion |
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How does ANP differ from AII in regards to Na reab?
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Both increase GFR and filtration rate of Na. BUT....ANP has no compensatory reab in distal nephron (net loss Na), and AII does (net gain Na).
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How do insulin def and BB cause hyperK?
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Decreased activity of Na/K ATPase.
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What kind of acid-base disturbance do iron tablets and INH cause?
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Metabolic acidosis
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Type 1 RTA
Type 2 RTA Type 4 RTA |
Type 1 - DCT can't secrete acid, kidney stones.
Type 2 - PCT loses bicarb, no stones, hypophosphatemic rickets Type 4 - hypoaldo/no response to aldo. Inability to excrete ammonium in PCT. HyperK, low urine pH due to decreased buffering capacity. |
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Post-strep GN - LM, EM, IF
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LM - lumpy bumpy, PMN
EM - subepithelial humps IF - granular |
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Membranoproliferative GN - LM, EM, IF.
Type I, Type II are assoc with what? |
Nephrotic or nephritic syndrome
LM - wire looping caps, tram-track splitting of BM by mesangial ingrowth in Type 1 EM - subendothelial deposits, dense deposits in Type 2 IF - granular Type I - hepB/C Type II - C3 nephritic factor |
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IgA Nephropathy (Berger's) - LM, IF
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LM - IgA deposits in mesangium
IF - IgA immune complexes in mesangium *often seen after acute URI or gastroenteritis |
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Membranous GN - LM, EM, IF
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LM - diffuse cap and BM thickening
EM - subepithelial spike and dome IF - granular |
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GN associations?
Membranous Membranoprolif FSGS |
Membranous - solid tumors
Membranoprolif - HBV, HCV (cryoglobulinemia) FSGS - HIV, heroin abuse |
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In terms of glomerular disease, what do the following mean?
Focal Diffuse Proliferative Membranous |
Focal - only a few glomeruli
Diffuse - all glomeruli Prolif - hypercelluar, blue dots Membranous - membrane, pink |
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What is the defect in minimal change disease? Causes?
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Cytokines destroy neg charge barrier (heparan sulfate) of GBM, making podocytes fuse. This happens in ALL nephrotic syndromes!
Children HL |
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What causes glom injury in nephritic vs nephrotic?
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Nephritic - PMN
Nephrotic - cytokines damaging neg charge barrier, fusion of podocytes |
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What happens in DM glomerulonephropathy?
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Non-enzymatic glycosylation (NEG) of GBM - increase perm, thickening.
NEG of efferent arteriole - increase GFR, mesangial expansion. |
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RCC - histo, gross, paraneo syndromes?
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Renal tubular cells become polygonal clear cells.
Gross - yellow, necrotic/hem mass. Ectopic paraneo syndromes! EPO, ACTH, PTHrp, prolactin |
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Wilm's Tumor (nephroblastoma) - gene, Chr?
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Deletion of WT1 tumor sup gene on Chr 11.
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What is WAGR Syndrome?
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Wilm's tumor
Aniridia GU malformatoin Retardation |
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Transitional Cell Carcinoma - assoc causes?
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phenacetin
smoking aniline dyes cyclophosphamide |
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Acute pyelo - histo
Chronic pyelo - histo |
Acute - Cortical PMN infiltrate only.
Chronic - Corticomedullary lymph infiltration and scarring, blunted calyx, tubules with eosinophilic casts |
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What is diffuse cortical necrosis? Causes?
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Acute cortical infarct of BOTH kidneys, due to vasospasm and DIC. (Septic shock, obstetric comps)
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What is renal papillary necrosis? Causes?
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Sloughing of renal papillae causing hematuria, proteinuria.
DM Sickle cell Analgesic nephropathy (phenacetin) Acute pyelo |
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2 causes of death in ADPKD?
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CKD - cysts destroy kidney parenchyma
HTN - increase renin release |
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What is ARPKD assoc with?
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Congenital hepatic fibrosis
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Mannitol - tox, contraindications?
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Pulm edema, dehydration.
CI in CHF and anuria. |
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Acetazolamide - MOA, use, tox?
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CA inhibitor causes bicarb diuresis, reduction in total body bicarb.
Use - resp/met alk, urinary alkalinazation (cystinuria), glaucoma, altitude sickness Tox - hyperCl met acidosis, neuropathy, sulfa allergy, NH3 toxicity. |
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Furosemide - MOA, tox?
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Inhibits Na/K/2Cl in TALH, washing out hypertonic medulla, prevent con of urine.
Tox - ototoxicity, nephrotox, sulfa allergy, hypoK, dehydration, Ca loss, gout. |
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Ethacrynic acid - MOA, use, tox?
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Same as furosemide but NOT a sulfa drug and does NOT cause hyperuricemia. Use in pt allergic to sulfa, gout.
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HCTZ - tox?
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Hyperlipidemia
Hyperglycemia HyperCa Hyperuricemia Sulfa allergy HypoK, met alk, dehydration |
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K sparing diuretics - names, MOA?
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Spirinolactone, eplerenone - Aldo receptor blockers.
Amiloride, triamterene - eNaC blockers |
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When are ACEI contraindicated?
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Bilat renal artery stenosis, angioedema, cough.
Prevent constriction of efferent arteriole and signif decrease GFR. |
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Which diuretics cause acidemia, how?
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CA inhibitors - lose bicarb.
Aldo inhibitors - no lose H, and no lose K, rel hyperK shifts H out of cells. |
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Which diuretics causes alkalemia, how? (3 ways)
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HCTZ, furosemide.
-Vol contraction, AII, stim Na/H receptor in PCT to reab Na and lose H. -HypoK shifts H into cells. -HypoK causes you to lose H instead of K in PCT, causing paradoxical aciduria. |
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How do thiazides cause hyperCa? (2 ways)
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-Vol depletion, upreg Na absorption in PCT and TALH, increase paracellular Ca in TALH.
-Block Na/Cl cotransport, Na gradient, increase Na/Ca exchanger. |
