Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Module 6: Mali: Renal > Pharm lectures > Flashcards

Pharm lectures Flashcards

1
Q

what is the drug that is a carbonic anhydrase inhibitor?

A

acetozolamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what does the carbonic anhydrase do?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what are the four thiazide drugs?

A
  1. hydrochorothiadone HCTZ
  2. chlorathiadone
  3. metolazone
  4. indapamide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

chlorithiadone is how many more times strong than HCTZ?

A

2x stronger than HCTZ

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

at what eGFR do HCTZ and chlorthalidone become ineffective?

A

less than 30-40 mL/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what happens if you use thiazides long term?

A

chronic use decreases Ca excretion?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

for what EGF is metolazone used?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

bile acid sequestrants

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

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

A

indapdamide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what GFR is indapdamide effective in?

A

all, especially less than 30 ml/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

what is the indications for all thiazides?

A

HTN

edema in nephrotic syndrome

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

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

A

ethacrynic acid

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

where do the loop diuretics exert their work?

A

the Thick ascending loop of the loop of henle

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the four loop diuretics?

A
  1. furosemide
  2. torsemide
  3. ethacrynic acid
  4. bumetanide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what OTC inhibits the mechanism of loop diuretics?

A

NSAIDS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what are two electrolytes you worry about being over excreted in the urine when using loop diuretics?

A

K and Mg!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

all loop diuretics have a ______ dose, which means________

A

all loop diuretics have a CEILING DOSE which means INCREASING THE DOSING ABOVE THIS AMOUNT WILL NOT HAVE ADDITIONAL IMPACT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what do you need to keep in mind can happen in the chronic use of loop diuretics?

A

you can develop diuretic resistance where there is increase Na reabsorption in the Proximal and distal tubules

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

what are four things you can do to reduce diuretic resistance?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

what is the oral bioavalibility of furosemide? what does this mean?

A

50%

it is often used IV to make more effective

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

what loop diuretic do you want to use in a HF patient who is not responding to furosemide? why?

A

want to use torsemide because it has a 80-100% absorption even when the intestinal mucosa is edematous which happens with HF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the MOA of all the loop diuretics?

A

inhibits Na-K-2Cl symporter in thick ascending loop of henle and distal tubule

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

what is the goal target daily weighloss for pt taking diuretic?

A

2 lbs body weight loss

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

loop duretics can increase the effects of……

A

HTN MEDS!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

what are two concentrations you want to check in a pt who is using loop diuretics?

A
  1. glucose HYPERGLYCEMIA

2. UA (all cause HYPERURCEMIA EXEPT ETHACRYNIC ACID)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what is a really strange thing you want to want to monitor when using high dose loop diuretics?

A

hearing

strange!!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

of the loop diuretics, which one would you want to use in a gout patient and why?

A

ethacrynic acid because it is the only one that has been shown to decrease UA levels instead of increase them

38
Q

what are the four k+ sparing drugs? of those which are hormones? which two aren’t?

A

Hormones:

  1. spirolactone
  2. eplenerone

Not hormones:

  1. amiloride
  2. triamterine
39
Q

what is the mechanism of action for the aldosterone antagonist drugs?

A

competitive antagonists at aldosterone mineralocorticoid receptors in distal convoluted tubule increasing NaCl and water loss but retention of of K

40
Q

of the 4 k sparing dieuretics, which two are aldosterone antagonists?

A
  1. spirolactone

2. eplenerone

41
Q

of the aldosterone antagonists, which one is at higher risk for causing gyenocomastica?

A

spirolactone

42
Q

of the two aldosterone antagonists which one is more selective for aldosterone receptors?

A

eplenerone

this is why you don’t see gynocomastica

43
Q

of the k sparing diuretics, which two have the added benefit of decreasing myocardial fibrosis?

A

aldosterone k sparing because increased aldosterone can cause this!!

  1. spirolactone
  2. eplenerone
44
Q

of the k sparing diuretics…which two are usually used in conjunction with thiazides because they aren’t really great diuretics on their own?

A
  1. amiloride

2. triamterine

45
Q

what can the 4 k sparing diuretics cause?

A

hyperkalemia…duh

good job!

46
Q

what is the osmotic diuretic?

A

mannitol

47
Q

what is the MOA of mannitol?

A

osmosis producing increased water loss in proximal convoluted tubule and descending loop of henle

48
Q

what is the indication for mannitol? (3)

A

reduction of intracranial or intraocclular pressure

rhabdomyolysis

49
Q

where is the majority of phosphate found in the body?

A

bone 80%

50
Q

how is phosphate absorbed in the body?

A

passive GI uptake although vitamin D stimulates active transport for GI tract

51
Q

what percent of ingested phosphorus is absorbed?

A

2/3

52
Q

what is phosphates renal excretion mediated by??

A

PTH

53
Q

what are the 3 ways PTH influences calcium levels?

A
  1. affecting bone formation/reabsorption
  2. renal Ca excretion/reabsorption
  3. calcitrol synthesis (vitamin D)
54
Q

what is the main function of PTH?

A

maintain constant Ca concentration in extracellular fluid in response to plasma Ca concentration

55
Q

what are the three functions of PTH in Ca?

A
  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
Q

what happens in stage 3 CKD that effects concentration of Ca?

A

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
Q

if eGFR is below 40 ml/min what is the net effect on Ca and phosphorus? what does this in turn cause?

A

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
Q

what are the two phosphate binding drugs?

A

sevelamer

CaCO3

59
Q

where does CaCO3 bind to phosphorus?

A

in the GI tract and excretes it

60
Q

what is the vitamin D analog?

A

calcitrol

61
Q

what does calcitrol do to the vitamin D receptors in the GI tract?

A

it up regulates the vitamin d receptors in the GI tract increasing Ca and Phosphorus absorption

62
Q

what is paricalcitrol?

A

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
Q

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?

A

anorexia and constipation

give paricalcitrol which is another formulation but has less GI receptor impact!!

64
Q

what is the name of the calcimemetic?

A

cinacalcet

65
Q

what does cinacalcet decrease?

A

PTH, Ca, Ca-P

66
Q

who do you need to be careful in when giving cinacalcet?

A

people with seizures!!

67
Q

what regulates the reabsorption of phosphorus?

what percent is filtered? reabsorbed?

A

PTH

90% is filtered, 80% reabsorbed

68
Q

why is there a decrease in erythropoetin in CKD?

A

because in CKD there is a decrease in the number of functioning nephrons

69
Q

what effect does uremia in CKD stage 5 have on RBC?

A

shorts the lifespan of RBC from 120 to 60 days by stage 5 CKD

70
Q

what is the indication of erythropoetin?

A

anemia in CKD

71
Q

what is the MOA of erythropoetin?

A

stimulates erythroblasts to proliferate and differentiate into normoblasts, then reticulocytes

72
Q

what is the max BP in which you would want to caution using erythropoetin?

A

caution in very high BP 180/100

73
Q

what is the target Hgb levels when treating a patient with erythropoietin?

A

10-12….anything more than this is BAD!

74
Q

why do you need to monitor Mg levels very closely?

A

because serum levels do not reflect intracellular fluid stores

75
Q

if you are going to give someone Mg because they have low Mg, and they have low K too…..what do you do?

A

treat them both!!!! both need to be raised and they should both be in the normal range for these to work properly

76
Q

at what level of Mg would you use supplement MgCl?

A

less than 1.5 mg/dl

77
Q

what is important to keep in mind when giving a elderly patient KCl tablet?

A

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
Q

who is KCl contraindicated in?

A

esophageal disorders

79
Q

who should the dose of KCl be decreased in?

A

elderly since they have decreased renal function

80
Q

the angtiotensin II receptors in the efferent arterioles are more or less sensitive than the afferent arterioles?

A

more sensitive

81
Q

ACE/ARBs have more of an effect in which arteriole?

A

EFFERENT because the angiotensin II receptors here are more sensitive

82
Q

what substance dilates the afferent arteriole?

A

prostaglandin E2

83
Q

what is the substance the constricts the afferent and efferent arteriole? which one does it have a greater effect on?

A

angtiotensin II…it works more on the efferent than the afferent

84
Q

what can you see with renal artery stenosis, volume depletion, severe CHF, and preexisting renal dysfunction WHEN COMBINED WITH ACE/ARB?

A

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
Q

why do NSAIDS cause an increase in BP and RAAs activation?

A

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
Q

what makes a person more susceptible to the effects of NSAIDS? 4

A

CHF
CKD
hypovolemia
hepatic cirrohsis

87
Q

what can cyclosporine cause?

A

vasoconstriction and decreased renal function

88
Q

what can ionic contrast material cause?

A

osmotic diuresis

89
Q

ionic contrast material is _______ in pots with CKD, DM, dehydration, and previous high dose contstrast exposure

A

ionic contrast material is NEPHROTOXIC in pots with CKD, DM, dehydration, and previous high dose contstrast exposure

90
Q

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?

A

if must use……

use with extracellular volume expansion with isotonic sodium chloride solution to prevent injury with agents

91
Q

ionic contrast material is ____

A

nephrotoxic!!

Module 6: Mali: Renal (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions