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Module 6: Mali: Renal > Pharm lectures > Flashcards

Pharm lectures Flashcards

1
Q

what is the drug that is a carbonic anhydrase inhibitor?

A

acetozolamide

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2
Q

what does the carbonic anhydrase do?

A

reversibly blocks carbonic anhydrase in PCT maintaining NaHCO3 in tubule lumen resulting in dieresis

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3
Q

what is important to remember about all diuretics?

A

they can increase concentration of ALL OTHER DRUGS because they cause the loss of water, so the concentration of drugs in the blood become higher!!

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4
Q

what is the most common indication for acetozolamide? what geographical location is this an exception to?

A

used for GLAUCOMA

also used for altitude sickness in the mountains

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5
Q

what are the four thiazide drugs?

A
  1. hydrochorothiadone HCTZ
  2. chlorathiadone
  3. metolazone
  4. indapamide
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6
Q

chlorithiadone is how many more times strong than HCTZ?

A

2x stronger than HCTZ

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7
Q

at what eGFR do HCTZ and chlorthalidone become ineffective?

A

less than 30-40 mL/min

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8
Q

where do the thiazides work their magic in the nephron? what is this important?

A

in DCT

since this medication prevents NaCl reabsorption in DCT its limited effectiveness because ~90% of NaCL is absorbed prior to the DCT, which means that it has a limited effect

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9
Q

what happens if you use thiazides long term?

A

chronic use decreases Ca excretion?

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10
Q

what happens if you use a BB with a either thiazide HCTZ or chlorthialidone?

A

can increase risk for hyperglycemia since BB mask this and these thiazides can cause hyerglycemia

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11
Q

what can all thiazides can cause would increase your risk for gout?

A

increases UA levels or hyperurcemia

increases persons risk for gout!!

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12
Q

for what EGF is metolazone used?

A

any, it doesn’t loose effectiveness with GFR less than 20 ml/min

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13
Q

what is the only drug that metolazone and indapamide interacts with that is different than the other thiazides?

A

bile acid sequestrants

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14
Q

what is the MOA of all thiazides?

A

Na-Cl symporter inhibitor in DCT

this increases Na and Cl excretion

max of 5% of filtered NaCl

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15
Q

what do you need to be really careful about when using metolazone?

A

since this is a very STRONG dieuretic that is usually used as a tag on therapy to give someone a little boost or as SHORT TERM ADJUST

it can cause a large drop in K quickly since it is strong, so you want to monitor this closely

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16
Q

what is the long term thiazide that can be used to decrease HTN in a patient with low GFR?

A

indapdamide

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17
Q

what GFR is indapdamide effective in?

A

all, especially less than 30 ml/min

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18
Q

what thiazide is very potent and is used short term to give a quick burst or as adjust because of its potency?

A

metolazone

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19
Q

what is the indications for all thiazides?

A

HTN

edema in nephrotic syndrome

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20
Q

what is the only loop diuretic that is not sulfa based drug?

A

ethacrynic acid

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21
Q

where do the loop diuretics exert their work?

A

the Thick ascending loop of the loop of henle

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22
Q

what are the two impacts the loop diuretics have on the thick ascending loop of henle?

A
  1. induce prostaglandin-mediated increased renal blood flow

2. increase sodium and water excretion via inhibition of the Na-K-2Cl simporter in the Thick ascending loop of henle

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23
Q

what percent of the filtered Na is excreted by furosemide?

A

25% of filtered Na is reabsorbed, so 75% is excreted…thats a lot!!

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24
Q

what are the four loop diuretics?

A
  1. furosemide
  2. torsemide
  3. ethacrynic acid
  4. bumetanide
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25
what OTC inhibits the mechanism of loop diuretics?
NSAIDS
26
what are two electrolytes you worry about being over excreted in the urine when using loop diuretics?
K and Mg!!
27
all loop diuretics have a ______ dose, which means________
all loop diuretics have a CEILING DOSE which means INCREASING THE DOSING ABOVE THIS AMOUNT WILL NOT HAVE ADDITIONAL IMPACT
28
what do you need to keep in mind can happen in the chronic use of loop diuretics?
you can develop diuretic resistance where there is increase Na reabsorption in the Proximal and distal tubules
29
what are four things you can do to reduce diuretic resistance?
1. increase dose 2. increase frequency of dosing 3. continuous infusion 4. add a thiazide diuretic like metolazone because it is short acting and can give a little extra boost
30
what is the oral bioavalibility of furosemide? what does this mean?
50% it is often used IV to make more effective
31
what loop diuretic do you want to use in a HF patient who is not responding to furosemide? why?
want to use torsemide because it has a 80-100% absorption even when the intestinal mucosa is edematous which happens with HF
32
what is the MOA of all the loop diuretics?
inhibits Na-K-2Cl symporter in thick ascending loop of henle and distal tubule
33
what is the goal target daily weighloss for pt taking diuretic?
2 lbs body weight loss
34
loop duretics can increase the effects of......
HTN MEDS!
35
what are two concentrations you want to check in a pt who is using loop diuretics?
1. glucose HYPERGLYCEMIA | 2. UA (all cause HYPERURCEMIA EXEPT ETHACRYNIC ACID)
36
what is a really strange thing you want to want to monitor when using high dose loop diuretics?
hearing strange!!
37
of the loop diuretics, which one would you want to use in a gout patient and why?
ethacrynic acid because it is the only one that has been shown to decrease UA levels instead of increase them
38
what are the four k+ sparing drugs? of those which are hormones? which two aren't?
Hormones: 1. spirolactone 2. eplenerone Not hormones: 1. amiloride 2. triamterine
39
what is the mechanism of action for the aldosterone antagonist drugs?
competitive antagonists at aldosterone mineralocorticoid receptors in distal convoluted tubule increasing NaCl and water loss but retention of of K
40
of the 4 k sparing dieuretics, which two are aldosterone antagonists?
1. spirolactone | 2. eplenerone
41
of the aldosterone antagonists, which one is at higher risk for causing gyenocomastica?
spirolactone
42
of the two aldosterone antagonists which one is more selective for aldosterone receptors?
eplenerone this is why you don't see gynocomastica
43
of the k sparing diuretics, which two have the added benefit of decreasing myocardial fibrosis?
aldosterone k sparing because increased aldosterone can cause this!! 1. spirolactone 2. eplenerone
44
of the k sparing diuretics...which two are usually used in conjunction with thiazides because they aren't really great diuretics on their own?
1. amiloride | 2. triamterine
45
what can the 4 k sparing diuretics cause?
hyperkalemia...duh good job!
46
what is the osmotic diuretic?
mannitol
47
what is the MOA of mannitol?
osmosis producing increased water loss in proximal convoluted tubule and descending loop of henle
48
what is the indication for mannitol? (3)
reduction of intracranial or intraocclular pressure rhabdomyolysis
49
where is the majority of phosphate found in the body?
bone 80%
50
how is phosphate absorbed in the body?
passive GI uptake although vitamin D stimulates active transport for GI tract
51
what percent of ingested phosphorus is absorbed?
2/3
52
what is phosphates renal excretion mediated by??
PTH
53
what are the 3 ways PTH influences calcium levels?
1. affecting bone formation/reabsorption 2. renal Ca excretion/reabsorption 3. calcitrol synthesis (vitamin D)
54
what is the main function of PTH?
maintain constant Ca concentration in extracellular fluid in response to plasma Ca concentration
55
what are the three functions of PTH in Ca?
1. increase Ca resorption from bone and in proximal renal tubule (increase available levels) 2. decrease phosphorus resorption in proximal renal tubule 3. increase activation of vitamin D which increases the GI absorption of Ca and mobilization of Ca from bone
56
what happens in stage 3 CKD that effects concentration of Ca?
decreased renal phosphorus excretion and decreased vitamin D activation causing decreased GI Ca absorption ultimately left with... elevated serum phosphate concentration and decreased serum Ca concentration
57
if eGFR is below 40 ml/min what is the net effect on Ca and phosphorus? what does this in turn cause?
GFR less than 40 ml/min causes: further decrease in excretion of phosphorus and decreased calcitriol (activated vit D) **so you get low Ca** NET EFFECT: low serum Ca and increased phosphorus......this in turn increases PTH because the Ca is low and causes secondary hyperthyroidism (sPTH) if this continues to happen, you get more and more PTH which causes rapid bone turnover leading to BMMD (less dense bones because its stripping the calcium off)
58
what are the two phosphate binding drugs?
sevelamer | CaCO3
59
where does CaCO3 bind to phosphorus?
in the GI tract and excretes it
60
what is the vitamin D analog?
calcitrol
61
what does calcitrol do to the vitamin D receptors in the GI tract?
it up regulates the vitamin d receptors in the GI tract increasing Ca and Phosphorus absorption
62
what is paricalcitrol?
it is another formulation of calcitrol so a vitamin D analog but it LESS GI RECEPTOR IMPACT SO LESS LIKELY TO CAUSE ANOREXIA AND CONSTIPATION
63
what are two side effects of calcitrol you should be aware of? if a patient developed this what is the alternative that you can give?
anorexia and constipation give paricalcitrol which is another formulation but has less GI receptor impact!!
64
what is the name of the calcimemetic?
cinacalcet
65
what does cinacalcet decrease?
PTH, Ca, Ca-P
66
who do you need to be careful in when giving cinacalcet?
people with seizures!!
67
what regulates the reabsorption of phosphorus? what percent is filtered? reabsorbed?
PTH 90% is filtered, 80% reabsorbed
68
why is there a decrease in erythropoetin in CKD?
because in CKD there is a decrease in the number of functioning nephrons
69
what effect does uremia in CKD stage 5 have on RBC?
shorts the lifespan of RBC from 120 to 60 days by stage 5 CKD
70
what is the indication of erythropoetin?
anemia in CKD
71
what is the MOA of erythropoetin?
stimulates erythroblasts to proliferate and differentiate into normoblasts, then reticulocytes
72
what is the max BP in which you would want to caution using erythropoetin?
caution in very high BP 180/100
73
what is the target Hgb levels when treating a patient with erythropoietin?
10-12....anything more than this is BAD!
74
why do you need to monitor Mg levels very closely?
because serum levels do not reflect intracellular fluid stores
75
if you are going to give someone Mg because they have low Mg, and they have low K too.....what do you do?
treat them both!!!! both need to be raised and they should both be in the normal range for these to work properly
76
at what level of Mg would you use supplement MgCl?
less than 1.5 mg/dl
77
what is important to keep in mind when giving a elderly patient KCl tablet?
it is CAUSTIC TO MUCOSA IN THE ESOPHAGUS so you need to make sure the patient can safely swallow it because if they have dysphagia it can stay in their esophagus
78
who is KCl contraindicated in?
esophageal disorders
79
who should the dose of KCl be decreased in?
elderly since they have decreased renal function
80
the angtiotensin II receptors in the efferent arterioles are more or less sensitive than the afferent arterioles?
more sensitive
81
ACE/ARBs have more of an effect in which arteriole?
EFFERENT because the angiotensin II receptors here are more sensitive
82
what substance dilates the afferent arteriole?
prostaglandin E2
83
what is the substance the constricts the afferent and efferent arteriole? which one does it have a greater effect on?
angtiotensin II...it works more on the efferent than the afferent
84
what can you see with renal artery stenosis, volume depletion, severe CHF, and preexisting renal dysfunction WHEN COMBINED WITH ACE/ARB?
initial bump in creatinine because there is too much dilation of the efferent arteriole (THIS IS TEMPORARY AND HAPPENS NORMALLY) which causes increased blood flow through the glomerulus without adequate time for filtration to occur SO LONG AS CREATININE DOESN'T EXCEED 30% OF THE PREVIOUS SERUM CREATININE IT IS OK AND CONSIDERED ACCEPTIBLE***THIS WEARS OFF IN A COUPLE OF WEEKS!!!
85
why do NSAIDS cause an increase in BP and RAAs activation?
Nsaids block the prostaglandin E2 on the afferent arteriole which leaves the angiotensin II receptor unopposed so that it gets activated and can lead to afferent vasoconstriction and decreased blood flow and activation of the RAAs system with Na and Cl reabsorption
86
what makes a person more susceptible to the effects of NSAIDS? 4
CHF CKD hypovolemia hepatic cirrohsis
87
what can cyclosporine cause?
vasoconstriction and decreased renal function
88
what can ionic contrast material cause?
osmotic diuresis
89
ionic contrast material is _______ in pots with CKD, DM, dehydration, and previous high dose contstrast exposure
ionic contrast material is NEPHROTOXIC in pots with CKD, DM, dehydration, and previous high dose contstrast exposure
90
What agent do you use to decrease the effects of ionic contrast material in patients that have CKD, DM, Dehydration and NEED TO HAVE THE DOSE?
if must use...... use with extracellular volume expansion with isotonic sodium chloride solution to prevent injury with agents
91
ionic contrast material is ____
nephrotoxic!!

Module 6: Mali: Renal (4 decks)

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