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108 Cards in this Set
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three parts of embryologic dev of urinary system
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1) pronephros -- primitive, completely regresss; 2) mesonephros: regresses except for some gonadal tissues (wolffian ducts in males --> ductus, epidydymis); 3) metanpehros: origin of the "true kidney"; develops caudally from tissues of ureteric bud --> collecting system of kindey, and metanephric mesoderm: glomerulus, bownmans space, tubules;
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what variables affect dialysis:
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proportional: pressure gradient, surface area, solubility of substance; inverse: membrane thickenss, molecular weight of molecule
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upper gi bleed in an alcoholic
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probably Mallory-Weiss tea: result of forceful retching agiainst tight LES --> high intragastric pressures
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pH changes with repetitive vomiting
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metabolic alkalosis (loss of acidic gastric secretions); remember, when you throw UP, pH goes UP, when you have diarrhea (down), pH goes DOWN (loss of HC03
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how is urea processed in the glomerulus?
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filtered at glomerulus, passively reabsorbed in proximal tubule and inner medullary collecting ducts, net 10-70% urea excreted
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aldo effects
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NA/K-ATPase activation --> absorbs Na, secretes K= (and H+)
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treatment for acute cerebral edema
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mannitol (osmotic diuretic)
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size of albumin vs IgG
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IgG is more bulky
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mechansim of albuminuria in MCD
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albumin is small enough to squeeze through pores in GBM, but charge barrier prvetns this; in MCD, loss of charge selectivity (negatively charged molecules) allows albumin loss
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when can low molecular weight proteins (Ig light chains, amino acids, etc.) be seen in urine?
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normally reabsorbed in PT --> appear when PT damaged (eg tubulointerstitial nephritis); also can happen if overload proteinuria (eg multiple myeloma)
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where does ADH act?
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medullary segment of collecting duct
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pH effects on uric acid stones
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soluble at physiologic pH, can precipitate in acidic environments of distal tubules / collecting ducts; --> alkalinize urine to prevent uric acid stones in tumor lysis syndrome
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from what cells do renal cell carcinomas originiate:
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epithelium of PROXIMAL RENAL TUBULES
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where can a horseshoe kidney get stuck?
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under IMA during its ascent;
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morphology of post strep glomerulonephritis
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granular IgG, IgM and C3 deposits along BM and in mesangium of glomeruli ("lumpy bumpy" appearance); subepithelial humps of ICs on EM
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effects of vasopressin
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increase in water and urea permeability at luminal membrane of inner medullary collecting duct --> increased water and urea reabsorption
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causes of membranous glomerulonpehritis
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85% idiopathic; rest are: systemic dz (DM, tumors, SLE), drugs (gold, penicillamine, NSAIDs), infections (HBV, HCV, malaria, syphilis)
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histo of membranoproliferative glomerulonephritis vs membranous glomerulopathy
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MPGN: large hypercellular glomeruli (hence "proliferative); MGN: diffuse thickening of capillary wall WITHOUT increas in celluarlity
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most common cause of nephrotic syndrome in adult pts in US
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FSGS (previously MGN)
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None
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wegener's granulomatosis vs goodpasture syndrome
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wegener's involve URT (sinusitis, nasal ulceration) in addition to GP-like hemoptysis and RPN; also, Wegener's is a/w c-ANCA and considered "pauci-immune" b/c there are no anti-GBM antibodies or immune complex deposition
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liver changes in nephrotic syndrome
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decreasd plasma albumin conc --? liver ups synth of all proteins (incl lipproteins --> inc chol, TG, VLDL, LDL, etc.)
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course of the ureters
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"water under the bridge:" ureters lie behind (retroperitoneal) to uterine artery and ductus deferens
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fraction of Total body weight that is water, intracellular, and extracellular
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60% water (40% intracell, 20% extracell)
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how to measure extracellular volume
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inulin
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how to measure plasma volume
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albumin
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how to measure total body water?
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D2O (heavy water)
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what is responsible for charge barrier of glomerulus
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heparan sulfate (negatively charged)
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estimated renal plasma flow (ERPF) vs renal plasma flow (RPF)
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ERPF approximated using PAH (filtered + secreted), tends to underestimate true RPF by ~10% (not ALL PAH is secreted…)
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renal plasma flow (RPF) vs renal blood flow (RBF)
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RPF is SMALLER (RPF is RBF minus the blood component); RPF = RBF (1 - HCT)
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effect of prostaglandins / NSAIDs on kidney
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prostaglandins DILATE AFFERENT aretriole --> inc RBF, inc GFR, FF remains constant; NSAIDs inhibit prostaglandin synthesis ==> dec GFR, potential renal failure
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calculation of free water
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Cl_h20 + Cl_osm = V_urine; Cl_osm = U_osm * V / P_osm
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at what plasma glucose level does glucosuria begin? What's this called?
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200 mg/dL = Threshold
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at what level of plasma glucose does the transport mechanism become saturated?
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350 mg/dL
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mechanism of AA reabsorption
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2' active transport in proximal tubules (w/ Na+)
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henderson-hasselbach eqn
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pH = pKa + log ( [HCO3-] / (0.03*PCO2) )
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role of early proximal tubule
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"workhorse of kidney:" REABSORBS almost all GLUCOSE and AA, along with MOST of the SODIUM, BICARB, BUN (rest w/ ADH) and WATER; also SECRETES AMMONIA to buffer secreted H+
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where does PTH act in kidney
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acts on Distal Convoluted Tubule (DCT) to increase Calcium reabsorption
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by what other name is the DCT known?
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"cortical diluting segment" -- actively reabosrbs Na/Cl while water absorption is blocked (membrane impermeable to H2O)
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where and how is Mg++ reabsorbed? What else is reabsorbed this way?
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thick ascending loop of henle: NaKCl2 transporter bring in even charge, but K+ leaks back out to lumen ==> net positive charge in lumen; electrical gradient drives Ca++ and Mg++ to be reabsorbed paracellularly
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where and how is Ca++ reabsorbed? What regulates it?
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Ca++ reabsorbed in TAL by same mech as Mg++ (electrical gradient); also reabsorbed in DCT via basolateral Ca/Na antiporter under PTH control
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what are the two types of cells in the collecting tubules and what are their roles?
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1) INTERCALATED cells: secrete H+ via apical H+ATPase under Aldo control; 2) PRINCIPAL cells: reabsorb Na (aldo), urea (ADH), and H2O (ADH), secrete K+
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what are the two hormones that act on the convoluted tubles, what are their receptors, and what are their functions?
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1) ALDO: intracell receptor; increased Na reabsorption in principal cells (stims Na and K channels apically as well as NaK ATPase basolaterally); also increases H+ secretion by intercalated cells; 2) ADH: acts on membrane V2 receptor to increase aquaporin (H2O) channels on apical membrane --> increased water reabsorption; also increases urea reabsorption
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what causes increased distal potassium excretion? (5)
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1) inc diet; 2) inc aldo; 3) inc pH (save H+ in exchange for K+); 4) diuretics (non k-sparing); 5) inc anions in lumen
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what changes serum potassium levels?
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insulin, beta-agonists, and alkalosis all PUSH K+ INTO cells; exercise, cell-lysis, increased Posm (K+ escapes with H2O) and acidosis all increase EXTRACELLular K+
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stimuli for JG release of renin (3)
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1) dec renal blood pressure; 2) dec Na+ delivery to distal tubule; 3) inc sympathetic tone
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mech of NSAID nephrotox
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inhibit renal production of prostaglandins which keep afferrent arterioles vasodilated ==> dec GFR --> acute renal failure
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stimuli for aldosterone secretion
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1) dec blood volume --> ATII; 2) inc k+
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stimuli for and effects of ANP (atrial natriuretic peptide/factor)
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secreted in response to increased atrial pressure; causes dec Ra, inc Re, and inhibits renin ==> inc GFR, inc Na/H2O excretion; (effectively a "check" on the RAA system that protects overloaded heart)
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anion gap eqn
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AG = Na - (Cl + HCO3); should be 8-12
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causes of anion gap metabolic acidosis
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MUDPILES (Methanol, Uremia, DKA, Paraldehyde/Phenformin, Iron supplements/INH, Lactic acidosis, Ethylene glycol, Salycilates
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causes of non-anion gap metabolic acidosis
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diarrhea, glue sniffing, hyperchloremia, renal tubular acidosis (types I, II, and IV)
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causes of respiratory acidosis
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retention of CO2 b/c of hypoventilation: COPD, acute pulm infection, obstruction, medullary depression (opiods, narcotics), respiratory muscle weakness (guillain-barre, MS, ALS, Polio)
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causes of respiratory alkalosis
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hyperventilation, aspirin ingestion (early), psychogenic
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aspirin effects on body pH
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early respiratory alkalosis (direct stim of medullary receptors --> hyperventilation); followed by anion-gap metabolic acidosis (salicylate tox); tx with alkalinzation of urine, eg acetazolamide
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causes of metabolic alkalosis
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vomiting, diuretic use, hyperaldosteronism, antacid use
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contraction alkalosis
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fluid loss --> inc aldo --> inc HCO3- reabsorption (inc H+ secretion); tx with saline and supplemental K+
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vomiting effects on body pH
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1) loss of HCl --> non-anion gap metabolic alkalosis; 2) fluid loss --> dec renal perfusion pressure --> inc aldo --> inc HCO3 reabsorption (inc H+ secretion) ==> MORE metabolic alkalosis
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acid-base compensation for metabolic acidosis
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Winter's formula: PCO2 = 1.5 * HCO3 + 8 +/- 2
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acid-base compensation for metabolic alkalosis
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for every +1 HCO3 --> +0.7 PCO2
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acid-base compensation for respiratory acidosis, acute and chronic
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a: +10 PCO2 --> +1 HCO3; c: +10 PCO2 --> +3.5 HCO3
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acid-base compensation for respiratory alkalosis, acute and chronic
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a: -10 PCO2 --> -2 HCO3; c: -10 PCO2 --> -5 HCO3
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what do RBC casts in urine suggest? (3)
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glomerular inflammation (NEPHRITIC SYNDROMES), ischemia, or malignant HTN
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what do WBC casts in urine suggest? (3)
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tubulointerstitial disease, acute PYELONEPHRITIS, glomerular disorders
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what do granular casts in urine suggest?
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acute tubular necrosis (breakdown of necrotic cells); can also see epithelial cell casts in ATN (if not broken down into granular casts)
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what do waxy casts in urine suggest?
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advanced renal disease / CRF (end product of cast evolution --> must be from low urine flow / stasis); also tend to be larger (b/c of stasis --> dilated ducts)
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what do WBCs in urine without casts suggest?
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cystitis (bladder infection)
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what do RBCs in urine without casts suggest?
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bladder cancer
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what do hyaline casts in urine suggest?
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nonspecific
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glomerulopathy with spike and dome appearance
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membranous glomerulonephritis
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glomerulopathy with "lumpy bumpy" appearance on LM
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post-strep glomerulonephritis
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glomerulopathy with linear pattern on IF
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goodpasture's
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subtypes of RPGN
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TYPE I (IC): PSGN, SLE, IgA; TYPE 2 (Ab): Goodpasture; Type 3 (pauci-immune, ANCA+): Wegener's
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crescentic glomerulonephropathy
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RPGN
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glomerulopathy with "tram track" appearance on EM
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membranoproliferative glomerulonephritis
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alport's syndrome
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split BM (collagen IV mutation) --> nephritic syndrome, nerve deafness, and ocular disorders (cataracts + lens dislocation)
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nephritic syndrome with peripheral and periorbital edema
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acute post-strep glomerulonephritis
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glomerulopathy with granular pattern on IF
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anything with IC deposition (MGN, PSGN, SLE IV?)
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subENDO vs subEPI humps
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subENDO: MPGN; subEPI: MGN, PSGN
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lipid nephrosis
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minimal change disease
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glomerulopathy with criss-cross fibrillary pattern on EM
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amyloidosis
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glomerulopathy with slowly progressing renal disease
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MGN, MPGN
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SLE glomerulonephropathy type V
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MGN
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glomerulopathy with segmental sclerosis
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FSGS
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glomerulopathy that responds well to steroids
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minimal change disease
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name 4 kinds of kidney stones
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CALCIUM (most common), STRUVITE (aka ammonium magnesium phosphate, 2nd most common), URIC ACID, CYSTINE
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what is the shape of calcium stones?
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"envelope"
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what is the shape of struvite stones
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"coffin" (predisposed by urease-pos bacteria in kidney -- PUNCH to the kidneys and you're dead)
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staghorn calculi
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formed in struvite stones, can be a nidus for UTI
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what is the shape of uric acid stones
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rhomboid plates / rosettes
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form of cystine stones
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hexagonal, yellow-brown
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spread of RCC
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invades RCC --> hematogenous spread, poor survival (like liver?)
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paraneoplastic syndromes a/w RCC
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EPO, ACTH, PTHrP, prolactin
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WAGR complex
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Wilms Tumor, Aniridia, GU malformations, Retardation (mental-motor)
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causes of transitional cell carcinoma
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PeeSAC (Phenacetin, Smoking, Aniline dyes, Cyclophosphamide)
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thyroidizaton of kidney
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CHRONIC PYELONEPHRITIS: renal tubules with eosinophilic casts (looks like thyroid)
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causes of diffuse bilateral renal cortical necrosis
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generalized infarction, usu due to vasospasm + DIC
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fanconi syndrome
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impaired prox tubular reabsoprtion --> glucosuria, Aauria, inc urinary phosphate, acidosis
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crush injury
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traumatic rhabdomyolysis: crushing injury to muscle --> rhabdomyolysis --> shock, ARF/ATN
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cause of intrinsic renal failure
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ATN --> epithelial/granular casts, obstruct tubule --> dec GFR
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renal failure's effects on K
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HYPERkalemia --> cardiac arrythmias
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leaf-shaped patches of skin lacking pigment
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tuberous sclerosis
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tumors a/w tuberous sclerosis
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cortical tubers, subependymal hamartomas in brain (--> seizures, MR), cardiac rhabdomyomas, facial angiofibromas, ash-leavf patchess
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prognostic factor in PSGN
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age (kids more likely to recover completetly)
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morphology of RPGN
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crescent-shaped on light microscopy; crescents consist of parietal cells, monocytes, macrophages, and fibrin --> sclerosis --> disrupted glomerular function
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IgA nephropathy vs PSGN
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both occur post-infection (URI / skin); IgA develops a few days afer, PSGN takes a few weeks; also, IgA has normal complement levels, PSGN has low C3 levels; finally, mesangial IgA deposits are not seen with PSGN
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tx for calcium stones
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thiazides (increase clacium reabsorption)
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what parts of nephron are most suceptible to hypoxia?
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proximal tubules and TAL (located in outer medulla -- lower blood supply); also, both are involved in ATP-consuming xport --> more O2 dependent
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muddy brown casts
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pathognomonic for acute tubular necrosis
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