Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

IMCP I > Exam 4 > Flashcards

Exam 4 Flashcards

(98 cards)

Start Studying
1
Q

Hydralazine and minoxidil MOA?

A

Opens K+ channels –> hyperpolarization of membrane and inhibition of calcium entry into smooth muscle –> Art VD –> (-) PVR AND (-) afterload pressure.

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

What are the Adverse Effects of sodium nitroprusside?

A

profound hypotension, Profound hypotension, reflex tachycardia. **Cyanide vs thiocyanate toxicity • Liver impairment (↑CN), or renal impairment (↑thiocyanate)

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

What are the Adverse Effects of hydralazine?

A

Reflex tachycardia, edema. Systemic lupus erythematosus-like syndrome- esp. in slow-acetylators

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

What are the Adverse Effects of minoxidil?

A

Reflex tachycardia, edema, more potent vasodilator. Therefore, it has the potential to precipitate angina and congestive heart failure.
Hirsutism.

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

PK of hydralazine?

A

t1/2 ~ 2-4 hrs.

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

PK of minoxidil?

A

Pro-drug - Activated by hepatic sulfotransferase.
last over 24 hrs (2-5 days).

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

What is the MOA of sodium nitroprusside?

A

vascular metabolism/ activation to NO by RBCs (heme) , NO then diffuses into the blood vessel ↑ cGMP –> smooth muscle relaxation, Opens K+ channels –> hyperpolarization and inhibition of calcium entry. Venous and Arterial Vasodilation)à Drop in Preload and Afterload

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

PK of sodium nitroprusside?

A

BP reduction < 2 minutes. Short-acting: Duration: 1-10 minutes.

Metabolism:
Blood Nitroprusside → cyanide (CN) ions. Liver CN → thiocyanate by rhodanase mitochondrial enzyme. Rate limiting step is the availability of thiosulfate donors. Kidney Thiocyanate slowly eliminated.

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

What is special about minoxidil?

A

Hirsutism.

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

What is special about sodium nitroprusside?

A

Methemoglobinemia, Photosensitive

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

What are the DHP CCBs?

A

Nicardipine, Nifedipine, Amlodipine

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

What is the MOA of DHPs?

A

Block L-type vg-calcium channels in arterial VSM –> (+) Ca2+ influx –> Arterial vasodilation

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

PK of nicardipine?

A

IV: 10 min.

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

PK nifedipine?

A

t1/2 = 2 hrs (IR). ER has biphasic peaks first at 2 hrs and at 6-12 hrs (ER).

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

PK of amlodipine?

A

Duration of action ~ 18-24 hrs; t1/2 = 30-50 hrs.

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

Adverse effects of DHPs?

A

Reflex tachycardia, edema and Hypotension.

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

DDIs of DHPs?

A

CYP 3A4 substrates, inhibitors / inducers.

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

What is special about nicardipine?

A

Indication: acute hypertensive crisis.
Has less negative inotropic effects than nifedipine.

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

What is special about nifedipine?

A

Short-acting is associated with an increased risk for MI or mortality. Long-acting CCB’s are preferred in chronic treatment of HTN.

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

What is special about amlodipine?

A

amlodipine is administered once daily in its standard formulation

(immediate release).

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

What are the Non-DHPs?

A

Verapamil, diltiazem

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

MOA of Non-DHPs?

A

inhibit calcium influx in myocardium and VSM.

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

Verapamil PK?

A

Metabolism: CYP 3A4 (N-demethylation) –> active (~20%) metabolite (norverapamil t1/2: 6-10 hrs).CYP 2D6 (O-demethylation) to inactive metabolite.

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

Diltiazem PK?

A

Deacetylation (major route) –> active metabolite (~25-50%). CYP 3A4 (N-demethylation) and CYP 2D6 (O- demethylation).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
AEs of Non-DHPs?
Edema, Hypotension, HF, Arrhythmias, AV block, bradycardia.
26
DDIs of Non-DHPs?
CYP 2D6 & 3A4 substrates, inducers, inhibitors. an inhibitor of P-gp and CYP 3A4. inhibits Pgp efflux → ↑[digoxin] → digoxin toxicity (verapamil?).
27
Verapamil special?
Indication: atrial fibrillation, angina, HTN. (Negative chronotrope, Moderate negative inotrope. Can precipitate heart failure esp. in patients with limited cardiac reserve.
28
Special diltiazem?
Mild negative inotropic effects. Intermediate affinity to cardiac cells. **safer than verapamil.**
29
DDI barbituates and felodipine, nifedipine, and verapamil?
Decreased effects of CCBs
30
DDI Beta-blockers and CCBs?
Additive or synergistic (more verapamil and diltiazem); inhibition of beta-blocker metabolism
31
DDI cimetidine and CCBs?
Increased 1,4 DHP levels
32
DDI digoxin and nifedipine, diltiazem, and verapamil?
Increased digoxin levels
33
DDI HMG CoA reductase inhibitors and diltiazem, verapamil?
Increased levels of HMG CoA reductase inhibitors
34
DDI phenytoin and CCBs?
Decreased effectiveness of CCBs due to induction
35
DDI rifamin and diltiazem, nifedipine, nisoldipine, verapamil?
Decreased levels of CCB
36
Angiotensin II on blood vasculature?
Direct rapid vasoconstriction
37
Angiotensin II on kidneys?
Increased Na+ reabsorption, increased vasocontriction
38
Angiotensin II on heart?
Increased HR
39
MOA of ACE inhibitors?
Reversible inhibition of ACE. (block angiotensin --\> VD, No aldosterone releaseàno Na and Water retention, block hydrolysis of bradykinin).
40
Lisinopril PK?
No activation required o t1/2 = ~ 12 hrs.
41
Captopril PK?
Poor bioavailability with food
42
Benazipril PK?
Metabolism by liver esterase to active benazeprilat
43
Enalapril PK?
Metabolism via liver esterase to active drug, enalaprilat. Enalaprilat is available in IV formulation for HTNsive crisis
44
Quinapril PK?
Metabolism via liver esterase to active drug, quinaprilat
45
Fosinopril PK?
Metabolism via liver esterase to active drug, fosinoprilat.
46
AEs of ACEIs?
1. Angioedema 2. Hypotension – first dose effect 3. Chronic dry cough 4. Hyperkalemia. **contraindicated in pregnancy.**
47
DDIs of ACEIs?
Digoxin: increase or decrease digoxin plasma level. K preps.: hyperkalemia. NSAIDs: decrease hypotensive effect.
48
Indications for all ACEIs?
1. Hypertension 2. Heart failure 3. Myocardial infarctions 4. Left ventricular dysfunction 5. Diabetic nephropathy.
49
Captoril special?
AE: rashes and taste disturbance due to sulfhydryl group.
50
AT1 recptor activation?
Gaq --------\> vasocontriction
51
AT2 recptor activation?
Balance AT1, vasodilation
52
What are the ARBs?
Losartan, olmesartan, candesartan, irbesartan, telmisartan, valsartan, azilsartan
53
MOA of ARBs?
Selective AT1–R antagonist to inhibit constriction of VSM in arterial and venous.
54
What is special about the MOA of azilsartan?
Highly selective.
55
PK olmesartan?
(Pro-Drug). t1/2=10–15hrs.
56
Special PK candesartan?
Ester prodrug.
57
Special PK valsartan?
Food markedly decreases absorption. Metabolism by non-CYP mechanism. Elimination is primarily via hepatic elimination.
58
DDIs of ARBs?
Digoxin: increase or decrease digoxin plasma level. K preps.: hyperkalemia. NSAIDs: decrease hypotensive effect.
59
Special ARBs?
Contraindicated in pregnancy.
60
What are the NItrates?
NTG, isosorbide di, isodorbide mono
61
MOA of Nitrates?
**VSM relaxation. Nitroglycerin is denitrated by glutathione S- transferase which releases the free nitrite ion.** A second enzymatic reaction releases free radical nitric oxide (NO). NO in turn causes direct **activation of guanylyl cyclase --\> Increased levels of cGMP --\> activate a Myosin Light Chain Phosphatase --\> VSM Relaxation.**
62
PK NTG?
t1/2: 1-3 mins.
63
PK isosorbide di?
sublingual route. t1/2: 45 mins Active metabolites have much longer half-life ~ 3-6 hrs
64
PK Isosorbide mono?
No first pass effects. t1/2: 3-6 hrs. Metabolism via glucuronidation
65
AE Nitrates?
Headache, Orthostatic hypotension, Reflex tachycardia. Serious: Syncope, Methemoglobinemia. Tolerance due to frequent dosing.
66
NTG special?
Fastest
67
Isosorbide di special?
Slowest
68
Isosorbide mono
Slower than NTG
69
Special all Nitrates?
have more impact on preload than afterload
70
DDI nitrates?
Phosphodiesterase-5 inhibitors (PDE5-I).
71
What are the diuretics?
Acetazolamide, Mannitol, Furosemide, Bumetanide, Torsemide, Ethacrynic
72
Loop diurectic site of action?
TALH
73
MOA Loop?
74
**Inhibition of Na/K/2Cl co-transporter** in luminal renal epithelium of TALH. **Most potent class**. (Fast action and short duration).
75
PK furosemide?
t1/2 ~ 2 hrs.
76
PK bumetanide?
1/2 =1 - 3 hrs.
77
PK torsemide?
t1/2 = 2-4 hrs.
78
PK ethacrynic?
t1/2 1-4 hr.
79
AE Loop?
hyponatremia, hypokalemia, hypochloremia, hypocalcemia and hypomagnesemia. ## Footnote **Orthostatic hypotension, Hyperuricemia.**
80
DDI Loop?
Decrease lithium clearance à lithium toxicity. Digoxin toxicity. hypokalemia and hypomagnesemia enhance Na-K-ATPase inhibition by (digoxin).
81
Special Acetazolamide?
Indication: Acute mountain sickness. Glaucoma.
82
What are the thiazide and thiazide-like diuretics?
HCTZ, chlorthalidone, metolazone
83
Site of Action thiazide and thiazide-like diuretics?
Na/Cl co-transporter at DCT.
84
MOA of thiazide and thiazide-like?
Inhibition of Na/Cl co-transporter in DCT.
85
PK HCTZ?
t1/2 = 6-15 hrs.
86
PK chlorthalidone?
t1/2 = 40-60 hrs.
87
PK metolazone?
t1/2 = 8-14 hrs. duration of action ~ 12-24 hrs.
88
AE thiazide and thiazide-like?
Hyponatremia, hypokalemia, hypomagnesemia, hypophosphatemia, hypochloremia alkalosis. Hypercalcemia, hyperuricemia, hyperlipidemia, Hyperglycemia.
89
DDI thiazide and thiazide-like?
Decrease lithium clearance --\> lithium toxicity. Digoxin toxicity. hypokalemia and hypomagnesemia enhance Na-K-ATPase inhibition by (digoxin).
90
Thiazide and thiazide-like special?
Sulfonamide group (Rash). Chlorthalidone most potent.
91
What are the ENaC Inhibitors?
Triamtrene, amiloride
92
SIte of action triamtrene, amiloride?
ENac at CD & CT
93
ENaC Inhibitor MOA?
Inhibits (ENaC) --\> (-) Na reabsorption and K secretion.
94
Triamtrene PK?
t1/2 = 1 – 3 hrs. duration of action ~ 8-10 hrs.
95
Special triamtrene?
Used in combination with Thiazide or loop.
96
Aldosterone Receptor Antagonists (K sparing) antagonist?
Spironolactone
97
Spironolactone Site of Action?
Aldosterone Receptor at CD&CT.
98
Spironolactone special?
(pro-Drug) not potent antihypertensive/diuretic by itself. **Contraindicated: acute renal insufficiency, concomitant ENaCI, hyperkalemia.**

IMCP I (32 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions