Brainscape's Knowledge GenomeTM

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


See full index

(D) Pharmacology > T3- CV Part 1 > Flashcards

T3- CV Part 1 Flashcards

1
Q

Where does angiotensinogen come from?

A

Liver

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

Where does renin come from?

A

Kidneys

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

What converts angiotensinogen to angiotensin 1?

A

Renin

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

What convert angiotensin 1 to angiotensin 2?

A

ACE from kidneys and lungs.
Angiotensin converting enzyme

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

What does angiotensin II do?

A

Increased sympathetic activity
Na+ Cl- absorption, K+ excretion, H2O retention
Increased aldosterone secretion
Arteriolar vasoconstriction
ADH secretion

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

What can cause increased angiotensinogen production?

A

Corticosteroids, estrogens, thyroid hormones, pregnancy.

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

Is ANG 1 as potent as ANG II?

A

No. ANG 1 has little to no biologic effect.

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

What are the two AT receptors and their effects?

A

AT1:
Vasoconstriction
Sympathetic activation
Cell growth
Sodium/fluid retention.

AT2:
Vasodilation
Inhibition of Cell growth
Embryonal development
Apoptosis

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

What drugs can inhibit the RAAS?

A

Renin inhibitors
ACE inhibitors
ARBs
Aldosterone antagonists

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

What do ACEI do in RAAS?

A

Block ACE, which prevents the conversion of ANG 1 to ANG 2. Also prevents breakdown of bradykinin, which causes extra vasodilation.

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

What do all ACE inhibitors end in?

A

pril!

Common:
BenazePRIL
CaptoPRIL
EnalaPRIL
LisinoPRIL
RamiPRIL

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

What are the PK considerations for an ACE inhibitor?

A

Hepatic conversion to active metabolite. Exceptions are captopril and lisinopril.

Kidney elimination. Exception is fosinopril.

Enalaprilat is the only IV ACE inhibitor. All others are oral.

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

What 3 things do we use ACE inhibitors for?

A

First line antiHTN.
Cardioprotective (patients with systolic HF and pts with HTN and at risk for CAD)
Renal protective (slow diabetic nephropathy)

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

What does an ACE inhibitor do to arterioles in the kidney?

A

It dilates the efferent arteriole, dropping intraglomerular pressure and reducing filtration.

Note: Normally, AT2 constricts efferent arterioles much more than afferent.

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

What are the common symptoms of an ACE inhibitor?

A

Dry, hacking cough (5-20%, not dose-related, due to bradykinin)
Hypotension
Hyperkalemia (reduces aldosterone, which excretes K+)

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

What are the adverse effects of an ACE inhibitor?

A

Angioedema (usually occurs within 1 week)
Acute Renal Failure

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

What are the contraindications of an ACE inhibitor?

A

Pregnancy (Category D)
Hypersensitivity to ACE inhibitors
Hx of angioedema
Coadministration with renin inhibitor in patient with DM or renal impairment.

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

What do ACE inhibitors interact with?

A

Potassium supplements, potassium-sparing diuretics, mineralcorticoid receptor antagonists, or ARBs, all of which can cause hyperkalemia.

NSAIDs.

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

What are some clinical pearls regarding ACE inhibitors?

A

Adequate BP control as monotherapy. (start low and go slow)

One is usually not better than the other.

Intermediate durations of actions, QD dosing.
(Exception is captopril, TID/ER required)

Monitor potassium and serum creatinine levels.

Warn patients about cough and angioedema.

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

What does ARB stand for?

A

Angiotensin receptor blocker.

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

What do all ARBs end in?

A

artan!

Candesartan
Irbesartan
Losartan
Olmesartan
Telmisartan
Valsartan

22
Q

What is the key difference between ARBs and ACE inhibitors?

A

ARBs do not affect bradykinin levels.
No cough, but less vasodilation.

23
Q

What is the PK of an ARB?

A

Oral admin.
Intermediate durations
(Exception is valsartan, TID/ER)

24
Q

What is a renin inhibitor?

A

Inhibits the action of renin, which is to convert angiotensinogen to Angiotensin 1.

25
Q

What renin inhibitor did we learn?

A

Aliskiren, AKA tekturna.

26
Q

What are renin inhibitors for?

A

ONLY HTN.

27
Q

What are some safety/contraindications of renin inhibitors?

A

Cough and angioedema
Diarrhea at high doses
Cautious when combining with ACE inhibitor or ARB
Pregnancy category D

Metabolized by CYP3A4.

28
Q

What is an aldosterone antagonist also known as?

A

Mineralcorticoid receptor antagonist

29
Q

What do aldosterone antagonists end in?

A

one.

Spironolactone (Aldactone)
Eplerenone (Inspra)

30
Q

What do aldosterone antagonists do?

A

Antagonize aldosterone at intracellular receptor sites, preventing Na/K exchange of collecting tubule.

Increases Na+ and water excretion, retains K+.

31
Q

What are the key differences between spironolactone and eplerenone?

A

Spironolactone is a synthetic steroid. Slow onset, takes days for full effect.

Eplerenone is a spironolactone analog. High sensitivity for just aldosterone receptor. Small effect on androgen and progesterone receptors.

32
Q

When is an aldosterone antagonist indicated?

A

Primary hypersecretion (Conn’s syndrome, ectopic adrenocorticotropic hormone production)

Secondary hyperaldosteronism (HF, hepatic cirrhosis, nephrotic syndrome, conditions associated with diminished effective intravascular volume)

Diuretic (first-line in hepatic cirrhosis), weaker than other diuretics.

Systolic HF

Resistant HTN (already on 3 or more anti HTNs)

Polycystic ovary syndrome (OFF-LABEL USE), only for spironolactone.

33
Q

What is the PK of an aldosterone antagonist?

A

Oral

Metabolized by liver into ACTIVE.

Spironolactone is a p-gp inhibitor.

Eplerenone metabolized by 3A4

NSAIDs can reduce effectiveness.

34
Q

What are the aldosterone antagonist contraindications?

A

BLACK BOX WARNING: tumor growth (for existing)

Hypersensitivity reaction
anuria
severe renal impairment
acute renal insufficiency

35
Q

What are the aldosterone antagonist adverse effects?

A

Pregnancy Category C

Avoid use in pts with renal impairment

Avoid concomitant K-sparing diuretics, esp. in renal impairment.

Inhibiting H+ secretion in parallel with K+ secretion can cause hyperchloremic metabolic acidosis.

36
Q

What are some specific spironolactone side effects?

A

Spironolactone can cause gynecomastia, impotence, and menstrual irregularities.

GI upset/nausea

Note:
Eplerenone is more selective for just aldosterone receptors, so no hormonal effect.

37
Q

What should I monitor in aldosterone antagonists?

A

K and serum creatinine levels.

38
Q

What are the vasodilators we learned?

A

Hydralazine
Minoxidil
Nitroprusside/Nipride

39
Q

What are the indications for hydralazine?

A

Relaxes arteries and arterioles only (no veins).
Decreased TPR, producing reflex stimulation of heart, increased contractility, HR, and O2 consumption.

Treating resistant HTN, in combo.

Increases plasma renin levels, including sodium and water retention.

40
Q

What is the PK of Hydralazine?

A

Well absorbed and metabolized via liver.

2-3 times dosing, minimal half life of 1.5-3 hrs but effect last longer.

Oral/injection

CAN USE FOR PREGNANCY HTN

41
Q

What are the common side effects of hydralazine?

A

HA, nausea, anorexia, palps, sweating and flushing.

42
Q

What are some uncommon side effects of hydralazine?

A

Periphal neuropathy, drug fever.
DILE (drug induced lupus erythematosus). Usually at high doses >200 mg/day

43
Q

What is minoxidil for?

A

Dilation of only arterioles.
Very efficacious orally active vasodilator, opening K+ channels in smooth muscle membranes.

44
Q

What does minoxidil have to be used with often?

A

Beta blocker and LOOP diuretic.

It causes reflex sympathetic stimulation and sodium/fluid retention.

45
Q

What are some effects of minoxidil?

A

Tachycardia, palps, angina, and edema if beta blocker and diuretic dosage is insufficient.

HA, sweating, and hypertrichosis.

46
Q

What else can minoxidil be used for?

A

Topical minoxidil, known as Rogaine.

Stimulant for hair growth.

47
Q

What is nitroprusside for?

A

Paraenteral Vasodilator

Treats HTN emergenices and severe HF.
Dilates all blood vessels (arteries and veins)

Activation of guanylyl cyclase, increasing intracellular cGMP, relaxing vascular smooth muscle.

48
Q

What is nitroprusside made of?

A

Iron, cyanide, and nitroso moeity.

Metabolized by RBCs, which release NO and cyanide.

Cyanide is converted to thiocyanate (less toxic)

49
Q

What is the PK of nitroprusside?

A

Rapid lowering of BP, stops after 1-10 minutes.

0.5mcg/kg/min is starting dose.

IV infusion only, requires A-line BP monitoring.

50
Q

What is the black box warning for nitroprusside?

A

Hypotension, irreversible ischemic injury, metabolic acidosis, arrhythmias, and death

51
Q

What is used to counter cyanide poisoning from nitroprusside?

A

Sodium thiosulfate or hydroxocobalamin

52
Q

What does thiocyanate poisoning present as?

A

Weakness, disorientation, psychosis, muscle spasms, and convulsions. Can cause delayed hypothyroidism.

Found in renal insufficient pts.

(D) Pharmacology (18 decks)

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