Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
202 Cards in this Set
- Front
- 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
|
