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135 Cards in this Set
- Front
- Back
JG cells located where, action
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afferent arteriole, if sense decrease in BP secrete renin
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Macula densa cells located where, senses what, 2 actions
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on DCT on top of glomerulus
if sense decrease in NaCl, it causes dilation of afferent arterioles to increase GFR back to normal and causes renin secretion |
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Ureter passage relative to uterine artery and ductus deferens
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"water passes under the bridge"- ureter passes under uterine artery and ductus deferens
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60-40-20 rule of body weight
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60% of body weight water
40% is intracellular, 20% extracellular |
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extracellular body fluid is intersitial compartment?
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3/4 (only 1/4 is plasma volume)
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Glomerular filtration barrier:
what composes size barrier? what is responsible for electric barrier? what layer are podocyte foot proccesses? |
fenestrated endothelium is size barrier
heparan sulfate bound to BM provides negative charge podocytes compose epithelial layer |
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what happens if negative charge on glomerular BM lost?
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nephrotic syndrome
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Clearance equation and units
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C = (urinary conc. * urinary volume)/ plasma concentration
ml/min |
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what is starling equation for GFR
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C = Kf (Pressure glomerular capillary - bowmans space) - (oncotic pressure glomerular capillary - oncotic pressure bowmans space)
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what substance best to determine GFR? what is calculation? what is normal GFR?
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GFRinulin = C*V/P
(just clearance of inulin) normal is about 100 ml/min |
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does creatinine over or underestimate GFR?
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overestimates because moderate secreted into tubule
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what is effective renal plasma flow and what substance is used to estimate it?
is it the same as renal perfusion rate? |
flow of blood through the renal arteriole
Cpah= U*V/P PAH because all PAH is excreted renal perfusion rate is about 10% higher |
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Filtration fraction equation?
use what to estimate it? normal value? |
filtration fraction = GFR/RPF
GFR = clearance of inulin or creatinine RPF = clearance of SAH normal = 20% |
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Filtered load equation
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GFR * plasma concentration
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change in GFR, RPF, FF if dilate afferent arteriole?
1 substance that dilates? 1 substance that constricts? |
GFR increases
RPF increases FF stays the same prostaglandins dilate afferent arteriole NSAIDs constrict afferent arteriole |
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what is pathway of blood from efferent arteriole to renal vein?
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efferent arteriole, vasa recta, interlobular vein, interlobar vein, renal vein
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Constriction of efferent arteriole changes:
GFR RPF FF 1 substance that preferentially constricts efferent arteriole |
GFR increases
RPF decreases FF increase Angiotensin II (so ACE inhibitor causes efferent dilation) |
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if decrease plasma protein concentraion, what changes:
GFR RPF FF |
GFR increases (less oncotic pressure in glomerular capillary)
RPF doesn't change FF increases |
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if ureter constricts, what changes:
GFR RPF FF |
GFR decreases
RPF doesn't change FF decreases |
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how do you calculate resorption and secretion rates
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secretion = excretion - filtration
reabsorption = filtration- excretion filtered load = GFR*Plasma conc. excretion rate = U*V |
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glucose reabsorbed where by what
at what level does glucosuria start? at what point is transporter saturated? |
in PCT by Na/glucose cotransporter
160-200 mg/dL 350 mg/dL saturated |
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where are AAs reabsorbed in kidney, by what type of transporter
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PCT by Na+ cotransporter (at least 3 distinct carrier systems)
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what deficiency of kidney tubule reabsorption can cause pellagra (dermatitis, dementia, diarrhea)?
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Hartnup disease - deficiency of neutral amino acid transport (including tryptophan, which is needed to make niacin)
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PCT absorbs all what (2)?
absorbs most of what (5) what type of absorption (isotonic/hypertonic/hypotonic)? actively secreted what? |
absorbs all glucose and AAs
Na, HC03, Cl-, H20, K+ isotonic actively secrete NH3 |
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PTH inhibits what to increase phosphate excretion?
what to stimulate Ca reabsorption? |
inhibits phosphate/ reabsorption in PCT
stimulates Ca++ reabsorption in DCT |
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Angiotensin II stimulates what transporter in PCT?
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Na/H+ antiporter so Na and H20 reabsorption increase (but can cause contraction alkalosis)
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Thick ascending loop:
directly reabsorbs? indirectly reabsorbs (2) |
directly reabsorbs Na, K, 2 Cl
indirectly absorbs Mg and Ca concentrates urine as it ascends |
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thin ascendig loop absorbs what, how
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passively reabsorbs water by medullary hypertonicity (concentrates urine)
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DCT makes urine more dilute or hypertonic?
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more dilute by absorbing more NaCl (inhibited by thiazide diuretics)
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2 actions of principal cell, location
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in Collecting duct
1. stimulated by aldosterone to insert Na+ channels on luminal side and reabsorb Na+ while excreting H+ and K+ 2. stimulated by ADH (via V2 receptor) to insert aquaporin channel on luminal surface |
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Intercalated cell, secretes what, reabsorbs what, located where
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in collecting duct
secretes H+, reabsorbs HC03 |
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3 stimulators of renin secretion, what cells secrete it?
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decreased BP sensed by juxtaglomerular cells
decreased Na delivery to DCT sensed by macula densa cells--> stimulat JG cells increased sympathetic tone |
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ATII effects on:
hypothalamus pituitary adrenals kidney glomerulus vasculature |
hypothalamus- stimulates thirst
Pituitary - stimulates ADH secretion Adrenals - stimulates aldosterone release Kidney - stimulates Na+ reabsorption in PCT glomerulus - stimulates efferent arteriole contraction vasculature - stimulates vascular smooth muscle contraction |
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ADH respond to osmolarity or BP?
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both, primarily osmolarity but can be overriden by low BP
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ANP
messenger system? effect on GFR? renin? |
cGMP (increases, vasodilates smooth muscle)
increase GFR, decrease renin acts to inhibit RAAS system |
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Is there reflex bradycardia when angiotensin II causes peripheral vasoconstriction?
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No, because ang II prevents reflex bradycardia by affecting barorecptor function
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PTH stimulates what enzyme in kidney
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1 alpha-hydroxylase (converts 25OH vitamin D to 1,25-OH vitamin D)
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how can NSIADs cause acute renal failure
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inhibit prostaglandins which dilate afferent arteriole, so GFR decreases
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Net effect of Atrial Naturetic Peptide? secreted from where
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secreted from atria in response to increased blood volume
dilates vascular smooth muscle (inc. cGMP), inc. GFR, increase Na+ filtration, DOES NOT REABSORB Na+ so more Na and H20 excreted |
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2 stimulatory conditions for aldosterone secretion
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decrease blood volume, increased [K+]
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6 situations K+ shifted out of cell (hyperkalemia) and 2 transporters involved
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Acidosis (inc. K/H+ exchanger)
Beta adrenergic antagonists (dec. Na/K ATPase) Digoxin (dec. Na/K ATPase) Hypoinsulinemia (dec. Na/K ATPase) cell lysis hyperosmolarity |
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what is presentation in low Na serum osmolality
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disorientation, stupor, coma
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presentation for Na high Na serum osmolality
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agitation, delirium, coma
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Cl- high in what states:
metabolic state kalemia volemia aldosterone level |
Cl- high in
metabolic alkalosis hypokalemia hypovolemia increased aldosterone (think of overactive loop diuretics) |
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when is Cl- low?
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2ndary metabolic acidosis
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U waves in ECG indicate
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hypokalemia
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wide QRS indicates what lab abnormality
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hyperkalemia
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Peaked T waves indicate what lab abnormality
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hyperkalemia
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arrhythmias in hypokalemia or hyperkalemia
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both
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neuromuscular irritability and tetany seen in what lab abnormality
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hypocalcemia
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delirium, kidney stones, abdominal pain seen in what lab abnormality
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hypercalcemia
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neuromuscular irritability and arrhythmias seen in what lab abnormality
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low Mg2+
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decreased tendon reflexes, pulmonary edema, can become cardiovaascular collapse (eletcrolyte imbalance)
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high Mg2+
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renal stones and metastatic calcifications seen in what lab abnormality
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high P04
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In metabolic and respiratory disorders, does compensation increase in same direction or opposite direction as primary change?
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same direction (HCO3 increase.decrease in respiratory abnormalities slow so may initially not be same direction
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for every -1 HCO3 change, change in pC02?
for every +1 HC03 change, change in pC02? |
-1 HCO3 = -1.2 pCO2
+1 HCO3 = + 0.7 pCO2 |
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Anion Gap Acidosis causes (and anion gap equation)
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AG (9-12 normal) = Na - (HCO3 + Cl)
MUDPILES Methanol Uremia DKA Phenformin, paraldehyde INH, Iron, Ibuprofen Lactic Acid Ethylene Glycol Salicylates |
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2 causes of respiratory alkalosis
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hyperventilation (early high altitude exposure)
early aspirin overdose |
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4 causes of metabolic alkalosis
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vomiting
diuretic use antacid use hyperaldosteronism |
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4 causes non-ionic gap metabolic acidosis
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diarrhea
glue sniffing renal tubular acidosis hyperchloremia |
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Renal Tubular Acidosis Type 1
cause? affects where? 2 complications? |
decreased H+ excretion in CCT
hypokalemia calcium kidney stones |
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Renal Tubular Acidosis Type 2
cause? affects where? 2 complications? |
decreased reabsorption of HC03 in PCT
hypokalemia hypophosphatemic rickets |
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Renal Tubular Acidosis Type 4
cause? affects where? 2 complications |
due to hypoaldosteronism or lack of nephron response (in principal cell of CCT)
HYPERkalemia (with decreased urine pH) decreased NH4+ excretion in PCT |
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5 types of renal casts
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RBCs
WBCs Granular hyaline waxy |
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2 causes of RBC casts
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glomerulonephritis
ischemia malignant HTN |
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3 causes of WBC casts
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tubulointersitial nephritis
pyelonephritis transplant rejection |
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cause of granular cast
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renal tubular necrosis
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waxy casts indicate
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chronic renal failure
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what presents with pyruia but no casts
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acute cystitis
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what presents with hematuria but no casts (2)
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bladder cancer, kidney stone
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5 characteristics of nephritic syndrome
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azotemia
rbcs/casts in urine proteinuria (>3.5 g/day) HTN oliguria |
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2 nephritic syndromes with granular appearance on immunoflorescence
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poststreptococcal glomerulonephritis, diffuse proliferative glomerulonephritis (SLE or MPGN caused)
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nephritis with peripheral and periorbital edema
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Acute post-streptococcal glomerulonephritis
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what changes occur in poststreptococcal glomerulonephritis
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immune complexes deposit subepithelially, PMNs infiltrate to clear, causes a
"lumpy-bumpy" appearance on light microscope |
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List 2 disease classes that present with rapidly progressive (crescentic) glomerulonephritis
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Anti-GBM diseases
ANCA diseases |
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Anti-GBM diseases
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have linear immunoflurescent stain
Anti-GBM crescentic glomerulonephritis Goodpasture's disease (lung hemorrhage) |
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ANCA diseases (4)
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all have non-linear immunoflurescence
1. pauci-immune glomerulonephritis 2. microscopic polyangiitis (p-ANCA) 3. Wegner's Granulomatosis (granulomatous lung involvement) 4. Churg-Strauss (granulomas plus eosinophilia) |
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p-ANCA association
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microscopic polyangiitis
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c-ANCA association
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Wegner's granulomatosis
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crescent shapes in glomeruli indicate what class of nephritis and are composed of what
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rapidly progressive (crescentic) glomerulonephrits
fibrin, C3b, plasma proteins poor prognosis (renal failure in days-weeks) |
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2 causes of diffuse proliferative glomerulonephritis
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SLE and MPGN
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kindey disease with "wire-looping" capillaries granular immunofluorescent staining?
what is causing problem? |
Diffuse Proliferative Glomerulonephritis
DNA-antiDNA immune complexes (type III hypersenstivity) cause subendothelial deposits SLE and MPGN are causes |
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nephritis after URI or gastroenteritis?
what is being deposited, where, to cause damage? |
IgA nephropathy (Berger's Disease)
IgA complexes deposit in mesangium |
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nephritis and deafness?
inheritance? |
Alport's syndrome
can also present with ocular and nerve disorders problem with type 4 collagen, will split basement membrane X-LINKED DOMINANT inheritance |
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Nephrotic syndrome:
4 characteristics 2 associated complications |
characteristics: dyslipidemia, proteinuria (>3.5g/day), edema, fatty casts
associations - increased risk of thromboembolism, infection (decreased immunoglobulins) |
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most common adult nephrotic syndrome is what and looks like what
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Membranous glomerolnephropathy,
thickening of BM and capillary "spike and dome" appearance of subepithelial deposits |
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neprhotic syndrome with subepithelial deposits, 4 causes
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membranous glomerulnephropathy
most common adult nephropathy "spike and dome" deposits SLE (nephrotic presentation), drugs, tumors, infections |
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Most common nephropathy in kids
can be triggered by what selective loss of what (not foot processes, though this too) treatment? |
Minimal change disease
can be triggered by recent infection selective loss of albumin because of loss of heparan sulfate maintaining anionic BM charge. no loss of Ig tx- corticosteroids |
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Diabetic Glomerulonephropathy:
change in GFR? what part of glomeruli changes what is damage pattern |
nonenzymatic glcosylation of BM causes expansion of mesangium
more leaky, GFR increases nodular glomerulosclerosis (with Kimmelsteil-Wilson lesions) |
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nephropathy with segmental sclerosis and hyalinosis?
most common nephropathy in what patient population? |
Focal segmental glomerulosclerosis
HIV patients |
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nephropathy: subendothelial IC deposits and granular immunofluorescence? Association with types?
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Membranoproliferative Glomerulonephropathy
Type 1- with "tram-track" lines - associated with HBV, HCV type 2- with "dense deposits" - associated with C3 nephritic factor |
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which type of membranoproliferative glomerulonephropathy/nephritis has "dense deposits?" association?
"tram lines?" association? |
type 1 - tram lines (split BM from mesangial expansion), associated with HBV and HCV
type 2 - dense deposits, associated with C3 nephritic factor (will have very low serum C3 levels) |
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4 types of kidney stones
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-calcium (most common)
-ammonium magnesium phosphate -uric acid (radioluscent) -cystine |
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hexagonal, radiopaque kidney stone is? tx?
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Cysteine (usually associated with cysteinuria)
tx- alkalinization of urine |
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what is radioluscent kidney stone made of?
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uric acid (gout, leukemia and other high cell turnover states)
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2 causes of calcium oxalate kidney stones
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ethylene glycol poisoning, vitamin C abuse
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what are calcium kidney stone components
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either calcium phosphate or calcium oxalate
seen in PTH, cancer |
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Staghorn canaliculi seen with what type of stone?
complication of staghorn canaliculi? |
ammonium magnesium phosphate crystals
can be nidus for UTI |
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3 causes of Ammonium magnesium phosphate crystals?
worsened by what condition |
bacteria = staph, klebsiella, proteus
alkaline urine |
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cancer composed of polygonal clear cells arising from renal tubular cells
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Renal Cell Carcinoma
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2 risk factors for RCC
2 places it likes to spread (and likes to spread through what) |
smoking, obesity
likes bone and lung, spreads through IVC |
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4 paraneoplastic substances produced by RCC
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Prolactin
Epo ACTH PTHrp |
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huge palpable flank mass with hematuria in kid 2-4 is?
association? |
Nephroblastoma (Wilm's tumor)
WAGR complex (Wt1 gene, chromsome 11) Wilm's tumor aniridia genitourinary abnormalities retardation |
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painless hematuria suggests?
3 causes |
transitional cell bladder cancer (occurs anywhere from renal calyces to bladder)
associated with problems in your Pee SAC pheniacetin Aniline dyes cyclophosphamide |
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Acute pyelonephritis usually affects what, spares what, has what in urine
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affects cortex
spares glomeruli white casts in urine |
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eosinophilic casts in tubules can indicate what
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chronic pyelonephritis
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what disease can present with blunted calyx and corticomedullary scarring
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chronic pyelonephritis
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5 drugs that can cause drug-induced interstitial nephritis
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aspirin, sulfonamides, penicillin derviatives, rifampin
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drug-induced nephritis, symptoms occur how long after administration, presentation
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1-2 weeks
eosinophilic pyuria and azotemia (can also have rash, fever, CVA tenderness, hematuria) |
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with things such as septic shock and obstetric catastrophies (like abruptio placenta), there can be acute cortical necrosis of kidneys. This is probably caused by both
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vasospasm and DIC
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what is most common cause of acute renal failure in hospitals?
reversible? characteristic finding? |
Acute Tubular Necrosis
reversible if treated, but fatal if not characteristic finding= granular brown casts in urine |
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3 stages of acute tubular necrosis, and how long is usual timecourse
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inciting event
maintenance (oliguria) recovery (usually takes about 2-3 weeks) |
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3 causes of acute tubular necrosis
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ischemia (septic shock, etc)
myoglobinuria (from crush injury) toxins |
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most common cause of microscopic hematuria in adult males
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BPH
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urine dipstick measures
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albumin
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2 conditions with increased Creatinine clearance
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pregnancy
early diabetic nephropathy |
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what is gold standard to evaluate renal disease
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urinalysis
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Diffuse segmental glomerulonephropathy has association with what disease
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HBsAg
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renal papillary necrosis may present after what?
4 associations |
presents with gross heamturia and proteinuria
may be after recent infection/immunologic stimulus DM acute pyelonephritis phenacetin use sickle cell anemia |
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Prerenal Azotemia (acute renal failure) cause
changes in: osmolarity FEna Serum BUN/Cr |
hypotension
osmolarity >500 FEna <1% Serum BUN/Cr >20 (normal 15) |
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Renal Azotemia (acute renal failure) cause
changes in: osmolarity FEna Serum BUN/Cr |
kidney disease (ATN, ischemia, crescentic glomerulonephritis, toxins)
osmolarity <350 FEna >2% Serum BUN/Cr <15 |
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Postrenal Azotemia (acute renal failure) cause
changes in: osmolarity FEna Serum BUN/Cr |
bilateral obstruction (BPH, stones, congenital anomalies)
osmolarity <350 FEna >4% Serum BUN/Cr >15 |
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platelet dysfunction, encephalopathy, pericarditis can all be caused by
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uremia
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Renal osteodystrophy caused by:
and changes seen |
renal failure
decreased reabsorption of Ca2+ and excretion of PO4- causes secondary hyperparathyroidism (calcium levels low until end stage when GFR too low to excrete calcium) |
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can dyslipidemia result from renal failure?
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yes, especially increased TGs
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what changes seen in renal failure? (8)
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Na/H20 retention
hyperkalemia acidosis uremia anemia (decreased Epo) dyslipidemia (especially increased TGs) Renal Osteodystrophy growth retardation |
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what is most common genetic cause of renal failure in adults, and genes involved?
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AD polycystic kidney disease
APKD1 or APKD2 |
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Multiple large bilateral kidney cysts in adult with progressive kidney disease is what? death usually due to what (2)
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ADPCKD (progressive destruction of parenchyma)
due to complications from chronic kidney disease, or HTN (may secrete renin) |
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AD polycystic Kidney Disease associations (3)
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Berry aneurysms
Polycystic liver disease Mitral valve prolapse |
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AR polycystic kidney disease:
association in utero congenital association 3 adult associations |
utero- Potter's
congenital - hepatic fibrosis adult- portal HTN, HTN, renal insufficiency |
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can long-standing dialysis result in renal cysts?
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yes, both medullary and cortical
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thin, non-enhancing, cortical, fluid filled simple cyst in adult is
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simple cyst, benign and common
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Medullary sponge kidney get cysts where, complication
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in medullary collecting tubules
can get kidney stones |
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Medullary cystic disease
get cysts where, complication |
corticomedullary cysts that cause fibrosis and progressive renal insufficiency, US shows small kidney
poor prognosis |
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2 places in nephron mannitol works as diuretic
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thin loop of henle
CCT |