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Mandies Pharm III > Renal I-III > Flashcards

Renal I-III Flashcards

1
Q

single nephron glomerular filtration rate

A

K(change in pressure - pi)
k = ultrafiltration coefficient
pi is difference in osmotic pressure

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2
Q

proximal tubule

-What absorbed?

A

65% H20; most K; 65% Na+, 65% bicarb
urine here is iso-osmotic w blood
organic acids and bases are secreted actively into urine, esp highly PRO bound small molecules–2nd point of entry. Imp for renal elim of drugs
-driving force is the Na/K ATPase in basolateral surface of membranes

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3
Q

loop of Henle

-What is absorbed?

A

H20 25%; no NaCl, no urea = thin descending limb

no H20, no urea, NaCl out = ascending limb

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4
Q

vasa recta

A

descending absorbs NaCl from ascending loop of Henle

ascending absorbs H20 from descending loop of Henle

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5
Q

macula

A

-specialized epithelial cells at the distal end of the ascending thick limb
-sense osmolality of urine
-if NaCl is too high, sends signal to afferent arteriole to reduce BF, drops GFR (tubuloglomerular feedback)
Na diuresis is self-limiting due to TGF

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6
Q

distal convoluted tubule

A

actively transports out NaCl but not H20

fluid here is hypotonic urine, even when dehydrated

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7
Q

collecting tubules

A

H20 out only if ADH present, highly dependent on NaCl concentration in medulla.
-urea out of distal collecting duct only, adds to medullary salt gradient

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8
Q

diuretic

A

increases solute excretion to increase volume of urine

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9
Q

aquaretic

A

increases excretion of h20 but not of solutes (dilute urine)

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10
Q

natriuretic

A

inc. excretion of Na and CL ions

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11
Q

saluretic

A

increases excretion of Na and Cl iones

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12
Q

Kaliurietic

A

incr excretion of potassium

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13
Q

acetazolamide

A
  • carbonic anhydrase inhibitor
  • acts on CA in lumen and cells of prox tubule (distal collecting duct is a secondary site of ax where acid secretion in inhibited)
  • proximal tubule is the major site of bicarb reabsorption and acidification (net result: drives sodium bicarb out of urine, inhibitors leave na bicarb in urine)
  • luminal pH increases, less H+ delivery to lumen.
  • sulfanilamide drug
  • K wasting due to high Na delivery to distal nephron
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14
Q 
acetazolamide effects on excretion:
Na
K
H
Ca/Mg
Cl
HCO3
H2P04
A 
Na: inc (5%)
K: incr x 2
H+: decrease
Ca/Mg no effect
Cl: NA
HCo3/h2po4: increased x 2
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15
Q

any mechanism that increases ______ to distal tubules increases K excretion

A

Na delivery

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16
Q

indications for rx with acetazolamide

A

CA inhibitor

  • open angle glaucomea
  • pre surg relief of glaucoma pressure
  • altitude sickness relieved temporarily by lower Co2 in blood/brain and metabolic acidosis
  • counteracting diuretic induced metabolic alkalosis (low eff as a single agent diuretic)
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17
Q

adverse reactions to acetazolamide

A

CA inhibitor

  • allergies (sulta drugs)
  • metabolic acidosis
  • diversion of renal ammonia into cirulation that can worsen hepatic encephalopathy (d/t alkaline urine, ammonia not secreted)
  • kidney stones from alkaline urine
  • BM depression, paresthesias, tingling
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18
Q

gylerin action

A
  • act on tissues by drawing water into blood
  • act on kidney by inc renal BF (by decreasing viscosity, inc rate passing through glomerulus) and washing out medullary salt gradient
  • primary site of action in loop of henle
  • secondary site is prox convoluted tubule where water efflux is inhibited by osmotic gradient
  • K wasting diurectics
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19
Q 
osmotic diuretic effect on:
Na
K 
Ca 
Mg 
H 
Cl 
HC03 
h2p04 
uric acid
A 
glycerin effect on:
Na incr x 2
K increased
Ca inc
Mg inc x 2
H NA
Cl inc
HC03 inc
h2p04 inc
uric acid inc
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20
Q

mannitol action

A
  • act on tissues by drawing water into blood
  • act on kidney by inc renal BF (by decreasing viscosity, inc rate passing through glomerulus) and washing out medullary salt gradient
  • primary site of action in loop of henle
  • secondary site is prox convoluted tubule where water efflux is inhibited by osmotic gradient
  • K wasting diurectics
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21
Q

indications for osmotic diuretics

A

(mannitol, glycerin)

  • ARF
  • ATN
  • dialysis disequilibrium syndrome resulting from too rapid removal of solutes during dialysis
  • acute glaucoma to reduce IOP
  • mannitol and urea are used pre-op and post op for neurosur to reduce brain swelling (contraindicated in bleed, will worsen swelling)
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22
Q

osmotic diuretics adverse reactions

A

glycerin, mannitol

  • can convert pulmonary congestion to pulm edema
  • hyponatremia
  • hyponatremia and dehydration
  • contraindicated in anuria, impaired liver fxn (can’t get rid of it)
  • mannitol/urea contraindicated in active intracranial bleed
  • glycerin is metabolized and could cause hyperglycemia
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23
Q

furosemide action

A
  • inhibits Na/K/2Cl symporter in ascending loop of henle
  • enters urine via organic ion transporters in proximal tubules (anything that interferes with process with inhibit efficacy)
  • K wasting
  • Na, Cl, K stay in the thick ascending limb tubule, h20 stays with ions, medullary ion gradient diminishes
  • urine flow is increased and urine is more concentrated bc salts are not removed
  • furosemide is also a weak CA inhibitor and sulfa moiety
  • furosemide acutely incr systemic venous capacitance (relaxes vasculature)
  • glucuronidated in kidney, not liver
  • all are high ceiling diuretics
  • block Na transport into macula, not limited by TGF
24
Q

bumetanide action

A
  • inhibits Na/K/2Cl symporter in ascending loop of henle
  • enters urine via organic ion transporters in proximal tubules (anything that interferes with process with inhibit efficacy)
  • K wasting
  • Na, Cl, K stay in the thick ascending limb tubule, h20 stays with ions, medullary ion gradient diminishes
  • urine flow is increased and urine is more concentrated bc salts are not removed
  • all are high ceiling diuretics
  • block Na transport into macula, not limited by TGF
  • mostly renal excretion, rest is metabolized
25
Q

ethacrynic acid action

A
  • inhibits Na/K/2Cl symporter in ascending loop of henle
  • enters urine via organic ion transporters in proximal tubules (anything that interferes with process with inhibit efficacy)
  • K wasting
  • Na, Cl, K stay in the thick ascending limb tubule, h20 stays with ions, medullary ion gradient diminishes
  • urine flow is increased and urine is more concentrated bc salts are not removed
  • all are high ceiling diuretics
  • block Na transport into macula, not limited by TGF
  • mostly renal excretion, rest is metabolized
26
Q

torsemide action

A
  • inhibits Na/K/2Cl symporter in ascending loop of henle
  • enters urine via organic ion transporters in proximal tubules (anything that interferes with process with inhibit efficacy)
  • K wasting
  • Na, Cl, K stay in the thick ascending limb tubule, h20 stays with ions, medullary ion gradient diminishes
  • urine flow is increased and urine is more concentrated bc salts are not removed
  • all are high ceiling diuretics
  • block Na transport into macula, not limited by TGF
  • mostly metabolizes, small amt renal excretion
27
Q 
effect of loop diuretics on:
Na
K
H
Ca/Mg
Cl
bicarb
phos
uric acid
A 
torsemide, furosemide, bumetanide, ethacrynic acid
na inc x 2
K inc x 2
H inc
ca/mg inc x 2
cl inc x 2
bicarb inc
phos inc
uric increased acutely, decreased chronic d/t decr circulating volume
28
Q

indications for loop diuretics

A
  • tosemide, furosemide, bumatanide, ethacrynic acid
  • acute pulm edema
  • CHF
  • HTN (thiazides preferred)
  • nephrotic syndrome
  • edema and ascites of cirrhosis (may induce hepatorenal syndrome)
  • CRF
29
Q

loop diuretics adverse effects

A

furosemide, torsemide, bumetanide, ethacrynic acid
-few unrelated
to diuretic activity
-hyponatremia
-hypokalemia (arrhythmias)
-volume depletion (contraindicated with hypovolemia)
-ADH will not work
-metabolic alkalosis
-hyperuricemia (bad for gouty types)
-ototoxicity d/t inhibitiion of same symporter in the inner ear
-contraindicated with sulfonamide sensitivity
-NSAIDs reduce diuretic response
-probenecid may increase effective dose (blocks ion channels)
-interacts with anticoags, propanolol, lithium, sulonylurea, cisplatin, amphotericin B

30
Q

hydrochlorothiazide action

A

-sulfonamide analog but not CA inhib
-blocks Na/Cl symport but not K
-enter urine via organic ion transporters in porximal tubules, like loop diuretics-act on distal convoluted tubule-commonly used
-potassium wasting
-different transporter than loop diuretics, but energy is still from basolateral NaK antiporter
shorter 1/2 life, better for acute diuresis

31
Q

chlorothiazide action

A

-sulfonamide analog but not CA inhib
-blocks Na/Cl symport but not K
-enter urine via organic ion transporters in porximal tubules, like loop diuretics-act on distal convoluted tubule-commonly used
-potassium wasting
-different transporter than loop diuretics, but energy is still from basolateral NaK antiporter
-only moderately efficacious bc 90% of na already absorbed before DCT
-but, acti distal to the macula, so not limited by TGF
-secondary effect of some thiazides on CA
-inc Ca with chornic use
-medullary salt conc not affected so h20 retention during dehydration is preserved
shorter 1/2 life, better for acute diuresis

32
Q

metolazone action

A
  • sulfonamide analog but not CA inhib; thiazide LIKE diuretic
  • blocks Na/Cl symport but not K
  • enter urine via organic ion transporters in porximal tubules, like loop diuretics-act on distal convoluted tubule-commonly used
  • potassium wasting
  • different transporter than loop diuretics, but energy is still from basolateral NaK antiporter
  • only moderately efficacious bc 90% of na already absorbed before DCT
  • but, acti distal to the macula, so not limited by TGF
  • secondary effect of some thiazides on CA
  • inc Ca with chornic use
  • medullary salt conc not affected so h20 retention during dehydration is preserved
  • longer 1/2 life, good for HTN
33
Q 
thiazide effects of:
Na
K
H
Ca
Mg
Cl
bicarb
phos
uric acid
A

metolaxone, chlorothiazide, hydrochlorothiazide
Na inc
K incr x 2
H inc
Ca dec
mag inc
cl inc
bicarb inc (bc of weak ca inihib, doesn’t inhib H elimination)
phos inc
uric acid inc acutely, decreased chronically

34
Q

indications for thiazide diuretics

A

HTN bc do not risk hypovolemia

  • edema from CHF
  • daily dosing
  • considering safe although there is a small risk of sudden death and renal ca
  • bc ca reabsorption in increased, these can be used to treat calcium nephrolithiasis and aid in rx of osteoporosis
  • treats nephrogenic DI, reducing urine volume 50%. unknown mech
35
Q

adverse effects of thiazide diuretics

A

chlorothiazide, hydrochlorothiazide, metolazone

  • hypotension, hypokalemia, hyponatremia, metabolic alkalosis
  • corticosteroids and amphotericin B inc risk of hypokalemia and arrhythmias
  • hypercalcemia, hyperuricemia
  • contraindicated with sulfa allergy
  • NSAID reduce diuresis
  • probenecid may increase effective dose
  • may decrease glucose tolerace and unmask latent diabetes
  • rare CNS and GI effects, erectile dysfxn
36
Q

amiloride

A

in the late distal tubule, Na channel depolarizes the luminal membrane but not he basolateral membrane, thus driving K secretion, blocking Na channel drops K secretion, inhibits proton secretion by raising intra luminal positive potential

  • block uptake of lithium by na channels in collecting duc
  • used for lithium induced DI (reverse lithium OD)
37
Q

triamterene

A

in the late distal tubule, Na channel depolarizes the luminal membrane but not he basolateral membrane, thus driving K secretion, blocking Na channel drops K secretion, inhibits proton secretion by raising intra luminal positive potential

38
Q 
inhibitors of renal Na channels effects on excretion
Na
K
H
Ca
Mg
Cl
A 
amiloride (renal excretion) triamterene (metabolized)
Na inc
K dec
ca dec (chronic)
mg dec (chronic)
Cl inc
39
Q

indications for renal na Channel inhibitors

A

amiloride, triamterene
-only slighly increased na excretion as most na is reabsorbed proximally
strongly increases K reabsorbtion, can result in hyperkalemia
-typically co admin w thiazide or loop diuretics to enhance effects and reduce K loss
-rx for liddle’s syndrom (genetic d/o w stabilization of Na channel)
-%5 AA have a polymorphism in the ENaC beta subunit (target for drug), makes them potent for reducing HTN in this group
-used as aerosol in cystic fibrosis to clear mucous

40
Q

adverse reactions of renal Na inhibitors

A

amiloride, triamterene
-hyperkalemia (arrhythmias/death)
-will interact with other potassium sparing diuretics (spironolactone), ACE inhib, NSAIDs, K dietary supplements
-AIDS patients with pneumocystis carinii rx w pantamidine and trimethoprim wich are also ENaC inhib will get hyperkalemia
-triamterene is a folate antagonist and may lead to megaloblastic anemia in cirrhosis
-some diffuse CNS, GI, derm, hematological effects
NSAIDS may decrease efficiency

41
Q

spironolactone action

A

competitiely binds mineralocorticoid receptor, blocks fxn
-mineralocorticoids are secreted by the adrenal glands and cuase retention of salt/water, while increasing excretion of K and protons
sites of activity are mineralocorticoid receptors in the distal convoluted tubule and collecting duct

42
Q

eplerenone action

A

competitiely binds mineralocorticoid receptor, blocks fxn
-mineralocorticoids are secreted by the adrenal glands and cuase retention of salt/water, while increasing excretion of K and protons
sites of activity are mineralocorticoid receptors in the distal convoluted tubule and collecting duct

43
Q

action of aldosterone

A

acts in the nucleus to change DNA expression of aldosterone induced proteins, which activate previously silent Na channels and pumps, promoting increased Na and water reabsorption

  • induced in response to dehydration
  • Na channels increase rep on membrane, Na/K atpase increases in activity
44
Q 
effects of mileralocoritcoid antagonists on secretion:
Na
K
H
Ca
Mg
Cl
A 
eplerenone, spironolactone
na inc
k dec
H decrease
ca dec
mg dec
cl inc
45
Q

mineralocorticoid antagonists indications

A

eplerenone, spironolactone

  • coadmin w thiazides or loops diuretics for K sparing action
  • spironolactone used to rx primary hyperaldosteronism in adrenal adeomas/hyperplasia
  • spironolactone used w secondary hyperaldosteronism from cardiac failure, cirrhosis, nephrotic syndrome, severe ascities
  • spironolactone is rx o choice for ascites and edema assoc w cirrosis (primarily driven by inc in aldosterone)
46
Q

adverse effects of mineralocorticoid antagonists

A

eplerenone, spironolactone
kyperkalemia
NSAIDs may decrease diuretic efficiency
cross rxn w other steroid receptors (antiandrogen = feminization, antiprogesterone = menstrual irreg)
diarrhea, gastritis, gastric bleeding, contraindicated with peptic ulcers
CNS symp and rash
eplerenone clearance rate sig decreased by inhibitors of CYP3A4
possible malignancies from spironolactone chronic use

47
Q

vasopressin

A

antidiuretic morphone

-binds V1/V2 receptors, increases H20 reabsorption from collecting ducts via aquaporins

48
Q

desmopressin action, indication

A

synthetic analog of vasopressin
little V1 activity, primary effeccts via V2 receptors
indication: DI (not nephrogenic DI)

49
Q

V1 effects

A

in vasculature

-reduce medullary BF, thus increasing medullary salt gradient and reabsorption of h20

50
Q

v2 effects

A

stimulate water reab in distal tubule and collecting duct by stimulating production of aquaporins in epithelim, more aquaporins in apical membrane due to increased recycling

  • more perm of distal duct to urea
  • incr activity of Na/K/2Cl symporter in thick ascending limb
51
Q

adverse effects of desmopressin

A

coronary artery constriction, water intox

52
Q

chlorpropamide action

A

sulfonylurea previously used for DM II. increase adh section

53
Q

gout

A

painful inflammatory response to the presence of urate crystal in tissues and joints, precipitated by hyperuricemia

54
Q

allopurinol

A

inhibits xanthine oxidase (converts xanthine to uric acid)

55
Q

colchicine

A

reduces neutrophil activity (not understood by works for gout)

56
Q

probenecid

A

uricosuric agent, increases renal excretion of uric acid

  • biphasic effect: 1) causes decreased excretion of UA by blocking acid transport into the tubular lumen (proximal tubule)
    2) once in the lumen, urance reabsoprtion is inhibited, resulting in increaed urate excretion
57
Q

adverse effects of probenecid

A

well tolerated
increased risk for renal stones
interferes with renal excretion of many drugs
interfere with diuretics (loop/thiazide) by preventing transport into the tubular lumen

Mandies Pharm III (10 decks)

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