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108 Cards in this Set

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