Brainscape's Knowledge GenomeTM

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


See full index

Renal II > Drugs > Flashcards

Drugs Flashcards

1
Q

How to change Mean arterial pressure

A

Change Cardiac output or change TPR

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

Hydralazine

A

Increase NO release
dilated arteries. not veins
first line treatment for hypertension pregnancy with methyldopa.

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

Carbonic anhydraze inhibitor

A

acetazolamide

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

Loop diuretics

A

ethacrynic acid (not a sulfonamide)

Furosemide

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

thiazide diuretics

A

chlorothalidone
hydrochlorothiazide (HCTZ)
Chlorothiazide

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

K sparing diuretics

aldosterone antagonists

A

Spironolactone

Eplerenone

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

K sparring diuretics

Na sodium channel blockers

A

Amiloride -> not metabolized by liver

triamterene -> metabolized by liver

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

oncotic diutetics

A

mannitol

isosorbide

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

ADH antagonists

A

Conivaptan

tolovaptan

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Acetazolamide

A

inhibits carbonic anhydrase

will cause a decrease in body pH but a increase in urine pH

increasing diuresis and Na, HCO3 in the lumin.

used for altitude sickness, metabolic alkalosis, and glaucoma.

adverse effects: sulfonamide hypersensitivity, renal stones, paresthesias with high doses.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

loop diuretics induce what type of synthesis

A

prostaglandin which increases blood flow.

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

loop diuretic effects

A

decrease intracellular Na, K, Cl

OTOTOXICITY

decrease reabsorption of Mg and Ca.

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

Ototoxicity

A

occurs from using loop diuretics.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

ethacrynic acid

A

a loop diuretic that can be used in people that are allergic to sulfa drugs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

drugs that cause sulfa reactions

A

Furosemide, bumetanide, torsemide

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

Hydrochlorothizaide (HCTZ)

A

a thiazide diuretic

Enhances the reabsorption of Ca in both the DCT and PCT.

used for nephrolithiasis, mild heart failure, and hypertension

More hyponatremic effects than loop diuretics (you lose more Na)

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

Spironolactone

A

K sparing drug that works by inhibiting the aldosterone receptor

only drug that doesn’t have to go into the lumin to have an effect.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

amiloride

A

K sparing diuretic. acts by inhibiting the ENaC channel.

use in lithium induced nephrogenic diabetes insipidus.

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

ACE inhibitors

A

-pril
Captopril
Enalapril
Lisinopril

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

ARBs

A

-sartans
Losartan
valsartan

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

renin secretion blockers

A

Clonidine

propranolol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

renin inhibitors

A

Aliskiren

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

angiotensin II effects

A

Kidney: increase Na r and H2O retention

Brain: release of corticotropin and adiuretin, thirst

Adrenals: increase aldosterone production

Blood vessels: vasoconstriction.

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

Captopril

A

ACEI

not a active metabolite

converts the formation of Angiotensin II. will have a backup of angiotensin I

Importantly will prevent the break down of bradykinin.

used in hypertension, heart failure, Prophylaxis for future cardiovascular events and nephropathy,

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Lisinopril

A

ACEI that doesn’t have a active metabolite.

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

ACEI that are excreted via liver and kidney

A

Fosinopril and tradolapril

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

Enalapril

A

ACEI

Enalaprilat is the IV version.

converts the formation of Angiotensin II. will have a backup of angiotensin I

Importantly will prevent the break down of bradykinin.

used in hypertension, heart failure, Prophylaxis for future cardiovascular events and nephropathy,

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

Drug to use in diabetic patients with HTN

A

ACEI

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

Adverse effects of ACEI

A

Cough from bradykinin accumulation.

hyperkalemia -> avoid K sparing diuretics

angioedema
Fetopathic potential (teratogen)

can cause a rapid decrease in GFR leading to acute renal failure. (happens in renal artery stenosis)

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

ACEI effects on the vessels

A

causes vasodilation of the efferent arterioles more than the afferent

will lead to less protein expression because we decrease the pressure in the glomerulus.

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

Angiotensin II receptors

A

AT1: major subtype. causes a activation of Gq, causes a increase of IP3 and DAG leading to increased Ca -> smooth muscle constriction.

AT2: activates production of NO and Bradykinin -> causes smooth muscle dilation.

32
Q

ARB effect

A

Angiotensin II receptor blocker

blocks AT1 that will cause a decrease in Gq stimulation leading to decrease in [Ca] -> less smooth muscle contraction.

No Effect on Bradykinin metabolism -> less cough.

33
Q

aliskiren

A

Direct renin inhibitor

blocks the conversion of Angiotensinogen to Ang I

No increase of Bradykinin.

34
Q

direct renin inhibitor effects concentrations

A

increase in Plasma [renin]

decrease in renin activity, Ang I, Ang II

ACE, Bradykinin, AT1 and 2 receptors are not effected

35
Q

ACE inhibitor effects on Concentrations

A

increase in plasma [renin], PR activity, Ang-I, Bradykinin

decrease in Ang II, ACE

AT-I and 2 receptors are not effected

36
Q

ARB effects on concentrations

A

Increase [PR] and activity, Ang-I and II

no effect on ACE and bradykinin

inhibition of AT-1

Stimulation of AT-2

37
Q

Diuretics effects on Concentrations

A

Increase [PR] and activity, Ang-I and II

38
Q

Ca channel blockers effects on concentrations

A

No effect on anything

39
Q

Beta-blockers effect on concentrations

A

decreases [PR] and activity, Ang-I and II

40
Q

Ca channel blocker types

A

Dihydropyridines (DHP)

Non-dihydropyridines

41
Q

Dihydropyridines (DHP)

A

-Pine

Amlodipine

Nifedipine

42
Q

Non-DHP (non-dihydropyridines)

A

Diltiazem

verapamil

43
Q

K channel openers

A

Diazoxide

Minoxidil

44
Q

Dopamine agonist

A

Fenoldopam

45
Q

NO donors

A

hydralazine

Nitroprusside (nitropress)

46
Q

Non-DHP effects

A

block L-type Ca channels which causes prominent cardiac effects (suppression of contractility as well as suppressing the SA and AV node) as well as acting on vascular tissues -> vasodilation.

47
Q

DHP effects

A

Predominantly arteriolar vasodilation even though it still block L-type Ca channels.

48
Q

L type Ca channels

A

type of Ca channels in cardiac myocytes, SA and AV nodal cells.

49
Q

Diltiazem and verapamil contraindications

A

Non-DHP Ca channel blockers.

Not to be used with Beta-blockers -> can lead to AV blocks.

also don’t use in patients with ventricular dysfunction and systolic

50
Q

Amlodipine

A

Ca channel blocker (DHP type).

can be used in hypertension (especially when combined with a Beta blocker “to contract reflex tachycardia”), hypertensive emergencies, angina (reduces demand of 02 on the heart)

51
Q

Nifedipine

A

Ca channel blocker (DHP type).

can be used in hypertension (especially when combined with a Beta blocker “to contract reflex tachycardia”), hypertensive emergencies, angina (reduces demand of 02 on the heart)

52
Q

Potassium channel openers action

A

cause increase permeability of K which will stabilize the resting membrane potential reducing the probability of contraction.

53
Q

Diazoxide

A

K channel opener

can cause excessive hypotension and cause stroke & MI

known to cause hyperglycemia.

54
Q

Minoxidil

A

K channel opener
causes arteriolar vasodilation

used in sever hypertension and baldness (topical)

Causes reflex tachycardia and edema. must be used with Beta blocker and diuretic.

55
Q

Minoxidil required other drugs

A

Beta blocker and Diuretic. this is needed because the K channel opener causes edema and reflex tachycardia.

56
Q

fenoldopam

A

D1 receptor agonist.

renal affarent vessels contain d1 receptors

used in hypertensive emergencies and post operative HTN

57
Q

fenoldopam adverse effects

A

D1 receptor agonist

can cause tachycardia, headache, and flushing.

Don’t use in glaucoma due to increase in interocular pressure

58
Q

Hydralazine

A

NO modulator

causes dilation of arterioles but not veins.

first line oral therapy in pregnancy with methyldopa.

combine with Nitrates for patients in heart failure.

cause cause fluid and Na retention, reflex tachycardia, lupus like syndrome

59
Q

nitroprusside

A

NO modulator

causes dilation of both the art. and Veins -> decreases TPR

decreased both preload and after load.

mainly relaxes large veins which decreases preload.

minor effects on after load.

can cause excessive hypotension and cyanide poisoning.

60
Q

Labetalol

A

nonselective Beta and alpha-1 blocker

partial agonist at Beta 2

causes vasodialaition
used for sever hypertension and hypertension during pregnancy

61
Q

carvedilol

A

non-selective beta and alpha-1 blocker

causes vasodilation
has antioxidant properties

62
Q

nebivolol

A

Beta-3 partial agonist.

causes vasodilation

63
Q

Propranolol

A

non selective beta blocker

64
Q

metoprolol

A

Beta 1 selective blocker

65
Q

atenolol

A

Beta 1 selective blocker

66
Q

Beta blockers predispose you to what

A

Diabetes especially when combined with Thiazide diuretics.

67
Q

esmolol

A

very rapid onset beta-1 blocker

used via IV infusion.

used in electroconvulsive therapy

68
Q

Prazosin

A

a Alpha-1 blocker that will cause the dilation

69
Q

Clonidine

A

alpha-2 agonist
will cause a decrease in sympathetic effect.

IV: causes increase BP (peripheral alpha2B) followed by decreased BP (central Alpha 2A recptors)

Oral and patch: decreased BP (decrease C.O., preload)

used in essential hypertension, adjunct for narcotic, alcohol, and tobacco withdrawal.

Side effects: Sudden withdrawal causes hypertensive crisis.

70
Q

Methyldopa

A

a false neurotransmitter. gets converted to methyl-NE and is stored and released. acts on central Alpha-2 receptors -> decreases BP

side effects, sedation, dry mouth, sexual dysfunction, postural hypotension, anemia

Used to treat hypertension in pregnancy

71
Q

Beta blockers used for MI

A

Metoprolol, carvedilol, & bisoprolol

72
Q

Chlorothiazide

A

the only thiazide diuretic that can be given via parenteral administration.

73
Q

Eplerenone

A

K sparing androgen inhibitor that is more receptor sensitive and has less anti-androgen effect that spironolactone

74
Q

triamterene

A

potassium sparing diuretic that can cause the formation of kidney stones

75
Q

Nitroglycerin

A

A NO acting drug.

used in a patient that has MI or unstable angina you will want to give Nitroglycerin because it dilates veins more than arteriole

Renal II (1 decks)

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