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202 Cards in this Set

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  • Back
which kidney is typically used to renal transplants and why
the left kidney is typically used for renal transplants because it has a longer renal vein
what is the relationship of the ureter to the uterine artery and ductus deferens
the ureter passes UNDER both the ureter and uterine artery ("water under the bridge")
inulin is used to measure which fluid volume
extracellular volume (ECF)
radiolabeled albumin is used to measure which fluid volume
plasma volume
which fluid compartment can NOT be directly measured
intracellular fluid (ICF)
normal osmolarity of body's fluid/serum
290 mOsm
what is the "60-40-20" rule of body weight
the body is composed of 60% fluid-- of this 60%, 40% is the ICF and 20% is the ECF
3 layers of the glomerulus
1. fenestrated capillary endothelium
2. basement membrane fused with heparan sulfate (negative charge)
3. epithelial layer with podocyte foot processes
is the basement membrane of the glomerulus positively or negatively charged, and what molecule creates this charge
the BM is negatively charged due to heparan sulfate (this charge is disrupted in nephrotic syndrome)
equation for renal clearance of a substance
C= (urine concentration x urine flow rate) / plasma concentration
what substance is used to best calculate GFR and why
inulin because it's freely filtered and neither reabsorbed nor secreted
normal GFR
100mL/min
effective renal plasma flow can be "estimated" via what measurement
PAH clearance

(usually within 10% of actual RPF)
what's the filtration fraction equation and what's a normal filtration fraction
FF = GFR/RPF

normal FF is 20%
pathway of renal blood flow starting with the renal artery to the renal vein
renal a. -> interlobar a. -> interlobular a. -> afferent arterioles -> glomerulus -> efferent arterioles -> vasa recta -> interlobular v. -> interlobar v. -> renal v.
effect of prostaglandins on renal blood flow
dilates the afferent arterioles (which will increase GFR and RPF, with the FF remaining the same)

**note that since NSAIDs inhibit prostaglandins, they will indirectly constrict the afferent arterioles thus decreasing the GFR and RPF
effect of angiotensin II on renal blood flow
angiotensin II constricts efferent arterioles (which will increase GFR but decrease RPF, so FF increases)

**note that since ACE inhibitors will inhibit the formation of angiotension II, they will indirectly dilate the efferent arterioles, thus decreasing GFR, increasing RPF, and decreasing FF
effects of afferent arteriole dilation and constriction
dilation of the afferents: increase GFR, increase RPF, FF stays the same

constriction of the afferents: decrease GFR. decrease RPF, FF stays the same
effects of efferent arteriole dilation and constriction
dilation of the efferents: decrease GFR, increase RPF, decrease FF

constriction of the efferents: increase GFR, decrease RPF, increase FF
plasma protein concentration effects on the GFR
increased plasma protein concentration: decreases GFR (no change in RPF, thus decrease FF)

decreased plasma protein concentration: increases GFR (no change in RPF, thus increase FF)
how does constriction/obstruction of the ureter affect the GFR
constriction/obstruction of the ureter decreases the GFR (RPF stays the same, thus FF decreases)
glucose is reabsorbed completely in the kidney via cotransport with what ion
sodium
even minor glucosuria is suggestive of what disease
diabetes mellitus
what's the threshold concentration for glucose in the kidney, in which trace amounts start being excreted in the urine
160-200
what's the concentration in which all glucose transporters in the kidney are fully saturated (Tm), thus ALL glucose is excreted in the urine
350
all glucose, all amino acids, and most of the HCO3, Na, Cl, and H2O are reabsorbed in what part of the nephron
early PCT
ammonia is generated and secreted by what part of the nephron
early PCT
what is the effect of parathyroid hormone (PTH) on the early PCT
PTH inhibits sodium/phosphate cotransport, thus phosphate is NOT reabsorbed and is excreted
what is the effect of angiotensin II on the early PCT
angiotensin II stimulates Na+/H+ exchange, thus sodium and water are reabsorbed

**note that angiotensin also leads to the formation of aldosterone which also reabsorbs sodium and water, but this takes place in the collecting tubules, NOT the early PCT
small amounts of Na, K, Cl, Mg, and Ca are reabsorbed in which part of the nephron
thick ascending loop of henle
which part of the loop of henle is permeable to water, and which part is impermeable to water
the descending loop is permeable to water, and the thick ascending loop is impermeable to water
which part of the nephron reabsorbs only small amounts of Na and Cl; it's known as the diluting segment of the nephron
early DCT
what is the effect of parathyroid hormone (PTH) on the early DCT
PTH increases the Ca/Na exchange, thus leading to the reabsorption of calcium
what 2 cells make up the collecting tubules
principal cells and intercalated cells
ADH and aldosterone exert their effects on which cells of the collecting tubules
principal cells
ADH acts on which portion of the nephron and what receptors does it activate
exerts its effects in the collecting tubules at the V2 receptors (activates aquaporins)
where is angiotensinogen formed
liver
where is renin formed
JG cells of the kidney
where is the majority of ACE formed
lung (small amounts in kidney as well)
renin promotes what enzymatic reaction
angiotensinogen -> angiontensin 1
ACE promotes what enzymatic reaction
angiotensin I -> angiotensin II
what cells of the kidney sense decreases in BP and thus activate the renin-angiotensin-aldosterone system
JG cells
what are the 6 effects of angiotensin II
1. activates angiotensin II receptors on vascular smooth muscle causing vasoconstriction (thus increasing BP)
2. constricts the efferent arterioles thus increasing GFR, decreasing RPF, and increasing FF which will preserve renal function-> important in shock)
3. causes the release of aldosterone from the zona glomerulosa of the adrenal cortex which causes reabsorption of sodium and water in the CT
4. causes the posterior pituitary to secrete ADH thus increasing water reabsorption in the CT
5. increases the Na+/H+ exchange in the early PCT thus leading to sodium and water reabsorption
6. causes the hypothalamus to trigger thirst
what is ANP, and what are its effects on the kidneys
ANP (atrial natriuretic peptide) is a hormone released from the atria in response to increased volume and high BP

It relaxes smooth muscle via cGMP leading to increased GFR and decreased renin (thus BP and volume decrease)
what makes up the juxtaglomerular apparatus
made up of JG cells (in the afferent arterioles) and the macula densa (sodium sensor in the early DCT)
what structure mediates sodium concentration in the early DCT
macula densa
what do JG cells secrete
renin
hormone released by the kidneys in response to hypoxia
erythropoietin
what is the kidney's effect on vitamin D
in the PCT, 25-OH vitamin D is converted into 1,25(OH)2 vitamin D via the enzyme 1alpha-hydroxylase

**note, that PTH upregulates 1alpha-hydroxylase, thus increasing the formation of active vitamin D in order to increase calcium reabsorption in the intestines
negative physiologic effect of aldosterone
increases potassium excretion (can eventually lead to hypokalemia)
what causes potassium to shift OUT of the cell (causing hyperkalemia)
1. insulin deficiency (decreases Na+/K+ ATPase)
2. B-adrenergic antagonists (decreases Na+/K+ ATPase)
3. acidosis
4. exercise (increases K+/H+ exchange)
5. hyperosmolarity
6. digitalis
7. cell lysis
what causes potassium to shift INTO the cell (causing hypokalemia)
1. insulin (increases Na+K+ ATPase)
2. B-adrenergic agonists (increases Na+K+ ATPase)
3. alkalosis (increases K+H+ exchange)
4. hypoosmolarity
you need to check the anion gap for which acid/base disturbance
metabolic acidosis
what's the equation for the anion gap
anion gap = Na - (Cl + HCO3)
does renal tubular acidosis have a normal or increased anion gap
normal anion gap
what are the different types of renal tubular acidosis
type 1: defect in DCT (can't excrete H+, leads to hypokalemia and kidney stones)
type 2: defect in PCT (can't reabsorb HCO3, associated with hypokalemia and rickets)
type 3: defect in CT (doesn't respond to aldosterone, associated with hyperkalemia)
RBC casts in the urine suggests what
ischemia, malignant HTN, glomerulonephritis (nephritic)
what casts are found in the urine in acute tubular necrosis
granular ("muddy brown") casts
symptoms of nephritic syndrome
hematuria, RBC casts, azotemia, oliguria, HTN, proteinuria (<3.5)
acute post-streptococcal glomerulonephritis is most commonly seen in what age group
children
which kidney diseases cause nephritic syndrome (5)
acute poststreptococcal glomerulonephritis
rapdily progressive glomerulonephritis
diffuse proliferative glomerulonephritis
Berger's disease
Alport's disease
in this kidney disease, the glomerulus takes on a crescent-moon shape and consists of fibrin, plasma proteins (C3b), parietal cells, monocytes, and macrophages
rapidly progressive glomerulonephritis
3 common diseases that can cause rapidly progressive glomerulonephritis
Goodpasture's syndrome, Wegener's granulomatosis, and microscopic polyangiitis
2 MAIN symptoms of Goodpasture's syndrome
hematuria and hemoptysis
what are the antibodies directed against in Goodpasture's syndrome
antibodies against type IV collagen (alpha3 domain) of the basement membrane of the kidney and lungs
what type of hypersensitivity is Goodpasture's syndrome
type II
Wegener's granulomatosis has antibodies directed against what
c-ANCA
Microscopic polyangiitis has antibodies directed against what
p-ANCA
In this kidney condition, light microscopy of what glomerular pathology will show "wire-looping" of the capillaries, subendothelial DNA-anti-DNA immune complexes
diffuse proliferative glomerulonephritis
SLE is most commonly associated with what glomerular pathology
diffuse proliferative glomerulonephritis
this glomerular pathology is characterized by an increased synthesis of IgA leading to deposits in the mesangium
Berger's disease (IgA glomerulopathy)
what 2 conditions can precipitate Berger's disease
acute gastroenteritis and upper respiratory infections
this disease is characterized by mutations in type IV collagen creating a split basement membrane
Alport syndrome
X-linked dominant disease characterized by nerve disorders, ocular disorders, and deafness; if left untreated or undetected, it will lead to death
Alport syndrome
what diseases cause nephrotic syndrome
diffuse membranous glomerulonephritis
minimal change disease
amyloidosis
diabetic glomerulonephropathy
focal segmental glomerulosclerosis
membranoproliferative glomerulonephritis
what are the symptoms of nephrotic syndrome
massive proteinuria (>3.5g), frothy urine, hyperlipidemia, fatty casts, edema
MOST common cause of nephrotic syndrome in adults
diffuse membranous glomerulonephritis
MOST common cause of nephrotic syndrome in children
minimal change disease
characterized by a diffuse capillary thickening of the glomerular basement membrane; it takes on a "spike and dome" pattern with subepithelial deposits
diffuse membranous glomerulonephritis
glomerular pathology associated with a Congo red stain with apple-green birefringence
amyloidosis
3 MOST common diseases associated with amyloidosis affecting the kidney
multiple myeloma, TB, and RA
how does diabetes affect the glomerulus
untreated diabetes leads to nonenzymatic glycosylation of the glomerular basement membrane causing increased permeability and thickening
NEG also occurs in the efferent arterioles which increases GFR
name of the lesions in the glomerulus seen in diabetic glomerulonephropathy
Kimmelstiel-Wilson lesions
what kidney pathology is MOST common in HIV patients
focal segmental glomerulosclerosis
what kidney pathology is MOST common in hepatitis patients (HBV and HCV)
membranoproliferative glomerulonephritis type 1
which glomerular pathology can cause BOTH nephrotic and nephritic syndrome
membranoproliferative glomerulonephropathy (MPGN)
what is the only type of kidney stone that will show up as radiolucent on an xray
kidney stone made from uric acid
kidney stones are MOST commonly made from what
calcium
which type of kidney stones are associated with urease positive organisms (such as Klebsiella and Proteus), as well as S. aureus
ammonium, magnesium, phosphate kidney stones
an elder presents with hematuria, flank pain, fever, and weight loss; labs reveal polycythemia; there is a palpable mass in one of the kidneys; the patients is overweight and a smoker; what's the MOST likely diagnosis
renal cell carcinoma
renal cell carcinomas are associated with what genetic disease
von Hippel-Lindau
2 MOST common locations for metastasis of renal cell carcinoma
lung and bone
MOST common renal malignancy in children
Wilms' tumor
what gene (on what chromosome) is linked to Wilms' tumor
WT1 gene on chromosome 11
transitional cell carcinoma (i.e. in the renal pelvis, ureters, bladder etc.) is linked to toxic exposures to what substances
aniline dyes, cyclophosphamide, and phenacetin (smoking is also a major risk factor)
Female presents with fever, flank pain at the CVA, and vomiting; what's the MOST likely diagnosis
pyelonephritis
what type of casts are associated with pyelonephritis
white cell casts

(if condition is chronic, there may also be eosinophilic casts)
associated with pyuria and azotemia after starting a new medication
drug-induced interstitial nephritis
5 drugs commonly linked to drug-induced interstitial nephritis
diuretics, NSAIDs, penicillins, sulfonamides, and rifampin
MOST common cause of acute renal failure in the hospital
acute tubular necrosis
is acute tubular necrosis reversible
yes
causes of acute tubular necrosis
renal ischemia (from shock, sepsis, malignant hypertension), crush injuries (leading to release of myoglobin), and toxins
where is the nephron does acute tubular necrosis usually affect
Straight portion of the PCT and ascending loop of henle
African american patient with diabetes and sickle cell presents with gross hematuria and massive proteinuria after a recent infection; what's the MOST likely diagnosis
renal papillary necrosis
in a normal nephron, is BUN reabsorbed
yes
in a normal nephron, is creatinine reabsorbed
no
3 types of acute renal failure
1. prerenal azotemia (via hypotension)
2. intrinsic renal (via acute tubular necrosis, toxins, or ischemia)
3. post-renal (kidney stones, BPH, neoplasia)
MOST common type of acute renal failure
prerenal azotemia
2 classes of drugs that most commonly cause acute renal failure
NSAIDs and ACE inhibitors
how does the BUN/Cr ratio change in the different types of acute renal failure
1. prerenal azotemia: greatly increased, >20
2. intrinsic renal: greatly decreased, <15
3. postrenal: between 15-20
which type of acute renal failure will have an extremely high urine osmolarity
prerenal azotemia (>500)
which type of acute renal failure will have an very high urine Na concentration as well as a large increases in Fe(Na)
post-renal
patient presents with CHF, pulmonary edema, and HTN; labs reveal hyperkalemia, metabolic acidosis, uremia, anemia, secondary hyperparathyroidism, and dyslipidemia; what's the MOST common diagnosis
acute renal failure
5 clinical symptoms of uremia
anorexia, pericarditis, asterixis, encephalopathy, and platelet dysfunction
how genetic transmission differ in adult PKD versus child PKD
adult PKD is autosomal dominant
child PKD is autosomal recessive
3 conditions associated with adult PKD
polycystic liver disease, berry aneurysms, and mitral valve prolapse
young child presents with hepatic fibrosis, Potter's disease, HTN, and renal insufficiency; what's the MOST likely diagnosis
child PKD (autosomal recessive)
patient presents with progressive renal insufficiency; ultrasound reveals very small kidneys with cysts located inside the cortex; what's the MOST likely diagnosis
medullary cystic disease
osmotic diuretic used for increased intracranial pressure
mannitol
MOA of acetazolamide
inhibits carbonic anhydrase
SE of acetazolamide
hyperchloremic metabolic acidosis, peripheral neuropathy, NH3 toxicity, and sulfa allergy
MOA of furosemide
inhibits the cotransport of Na+/K+/2Cl- in the ascending limb of the loop of henle
which diuretic causes a baroreceptor-mediated increase in sympathetics by increasing renin which will increase aldosterone
furosemide
SE of furosemide
ototoxicity, hypokalemia, dehydration, interstitial nephritis, gout, and sulfa allergy
diuretic used in glaucoma and altitude sickness
acetazolamide
furosemide's effect on calcium
increases calcium excretion (thus can treat hypercalcemia)
diuretic DOC for people with sulfa allergy
ethacrynic acid (same MOA as furosemide)
MOA of hydrochlorothiazide
inhibits NaCl reabsorption in the early DCT
effect on hydrochlorothiazide on calcium
decreases calcium excretion (thus can cause hypercalcemia)
SE of hydrochlorothiazide
sulfa allergy, hypokalemic metabolic alkalosis, hyperglycemia, hyperlipidemia, hyperuricemia, and hypercalcemia
diuretic used to treat nephrogenic diabetes insipidus
hydrochlorothiazide
MOA of spironolactone
competitive antagonist at the aldosterone receptors in the CT
MOA of triamterene and amiloride
blocks Na+ channels in the CT
which diuretics are potassium-sparing
spironolactone, eplerenone, triamterene, and amiloride
SE of spironolactone
gynecomastia, hyperkalemia, and impotence
which diuretics lower blood pH (acidemia)
acetazolamide and K+ sparing diuretics
which diuretics raise blood pH (alkalemia)
furosemide and hydrochlorothiazide
MAJOR SE of ACE inhibitors and the physiologic mechanism behind it
dry cough due to failed inactivation of the bradykinin normally inactivated by ACE
if patient is on ACE inhibitor and develops a severe dry cough, you switch them to this drug that has a similar MOA but doesn't cause a dry cough
Losartan
MOA of losartan
angiotensin II receptor antagonist
MOST common cause of UTI
E.coli
patient has a UTI and their urine is very basic (>8.0); whats the MOST likely cause
proteus (produces ammonia)
what diet should you place someone on who has renal failure
high carbs
moderate fats
low proteins
restricted fluids
only portion of the nephron that has a brush border
PCT
how much fluid is lost from drinking 1L of seawater
0.5L is lost for every 1L of seawater
maximum concentrating ability of the kidney is what osmolarity
1200
minimum concentrating ability of the kidney is what osmolarity
50
in maximum concentrated urine, urea must account for how much of the osmolarity
half (600 of the 1200 mOsm)
Condition characterized by eosinophilia, asthma, and renal insufficiency
Churg-Strauss syndrome
MOST important regulator in plasma sodium concentration
ADH-thirst mechanism
what is azotemia
elevation of BUN and creatinine
cause of secondary hyperparathyroidism
renal failure
casts found in the urine in chronic renal failure
waxy casts
MOST common organism linked to post-streptococcal glomerulonephritis
S. pyogenes
glomeruli have a "lumpy-bumpy" appearance with subepithelial immune complex humps
acute post-streptococcal glomerulonephritis
how are the antibodies organized in Goodpasture's syndrome
linear
child presents with purpura on the extremities and butt; he also complains of vomiting with blood in the vomit; UA reveals mild proteinuria and hematuria; biopsy shows IgA deposits
Henoch-Schonlein purpura
what casts are seen in nephrotic syndromes
fatty casts (oval fat bodies)
why is nephrotic syndrome associated with hypercoagulability and thromboembolism
loss of antithrombin III production
mutated protein in the hereditary form of minimal change disease
nephrin
kidney pathology linked to Hodgkin's lymphoma
minimal change disease
initial symptoms of diabetic glomerulonephropathy
microalbuminuria
what causes the osmotic damage to the glomerular capillary endothelial cells in diabetic nephropathy
sorbitol
kidney biopsy shows splitting of BM secondary to mesangial ingrowth
MPGN type 1
Hartnup disease is characterized by the inability to reabsorb what amino acid
tryptophan
Fanconi syndrome is characterized by the inability to reabsorb what
glucose
patient has HTN; bruits can be heard over one of the renal arteries
renal artery stenosis
patient presents with HTN, hematuria, hematemesis, and melena after a GI infection
hemolytic-uremic syndrome
kidney pathology occuring after an obstretics emergency (most commonly abruptio placentae)
diffuse cortical necrosis
horseshoe kidneys trap which vessel
IMA
"swiss-cheese" appearance of the kidneys
medullary sponge kidney
composition of struvite stones
magnesium ammonia
where in the kidney is erythropoietin produced
interstitial cells of the peritubular capillaries
muscle that empties the bladder
detrusor muscle
innervation to external urethral sphincter
pudendal nerve
sympathetic innervation to the bladder is via what nerve
hypogastric n. (L2)
where is the micturition center
pons
ratio of cortical vs. juxtamedullary nephrons
3:1
about how many times each day does the body recycle its fluid volumes
60x per day
how do sympathetic agents affect GFR
they decrease GFR (by constricting the afferent arterioles)
equation for RBF
RBF = (renal a. pressure - renal v. pressure) / total renal vascular resistance
glucose gets reabsorbed from the lumen into the tubular cells through what transporters in the kidney
SGLT2 (90%) and SGLT1 (10%)
glucose dissolves from the tubular cells into the interstitial fluid through what transporters in the kidney
GLUT2
where in the nephron are amino acids reabsorbed
PCT
major regulator of aldosterone
K+ concentration
ADH binds to what receptors and activates what aquaporins
binds to V2 receptors and activates aquaporin2
normal osmolarity throughout the nephron
PCT- 300
Loop of Henle- 600
DCT- 100
constant osmotic gradient between the loop of henle and the medulla
200 mOsm
urea is reabsorbed in the CT via what receptors
UT-A3
difference between central vs. nephrogenic diabetes insipidus
central: pituitary doesn't produce ADH
nephrogenic: kidney doesnt respond to ADH
which drug can cause diabetes insipidus as a SE
lithium
where in the hypothalamus is ADH synthesized
AV3V region of the anterior hypothalamus
Of the following, which ones increase ADH and which ones decrease ADH: nausea, alcohol, clonidine, hypoxia, nicotine, morphine, haloperidol, cyclophosphamide
INCREASE ADH: nausea, hypoxia, nicotine, morphine, cyclophosphamide

DECREASE ADH: alcohol, clonidine, haloperidol
paracellular reabsorption of calcium is coupled with what other ion
magnesium
death will ensue shortly after urine output drops below what value unless lifesaving measures are taken
<0.5L per day
The 4 conditions that have a NORMAL anion gap metabolic acidosis
diarrhea
glue sniffinf
renal tubular acidosis
hyperchloremia

(*note that diarrhea causes a hyperchloremic form of metabolic acidosis)
what drugs can you NOT combine with loop diuretics
aminoglycosides (increases ototoxicity) and NSAIDs (decreases efficacy of loop diuretics)
which diuretics cause alkalosis and which cause acidosis
acetazolamide and K+ sparing cause acidosis

Loops and HCT cause alkalosis
what serum levels does HCT increase
increases serum glucose, lipids, uric acid, and calcium
DOC to treat calcium kidney stones
HCT
how will the pressure in the glomerular arterioles compared to systemic arterioles
higher in the glomerular arterioles
absolute contraindication for ACE inhibitors
pregnancy