Pharm Exam 3 Flashcards

1
Q

Use: HTN
MOA: Adrenergic transmitter depleter
AE: Depletes NE in SNS=depression
Notes: Crosses BBB; long acting

A

Reserpine

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

Use: HTN
MOA: Adreneergic transmitter depleter
AE: Orthostatic hypotension
Notes: Depletes NE peripherally at nerve terminal

A

Guanethidine

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

Use: HTN, drug and nicotine withdrawal
MOA: Central alpha-2a agonist
AE: Dry mouth, sedation, decr libido, rebound HTN
Notes:Reduced LVH and total cholesterol

A

Clonidine

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

Use: HTN
MOA: Central alpha-2a agonist
AE: dry mouth, + Coombs test, dry mouth
Notes: Good during pregnancy!!

A

Alpha-methyl-DOPA

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

Use: Smooth musc vasodilator for HTN
MOA: Incr NO and K+ permeability
AE: tachycardia, HA, edema, nausea
Notes:Lupus-like syndrome

A

Hydralazine

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

Use: Smooth musc vasodilator in HTN
MOA: Incr K+ channel opening
AE: Hair growth, tachy, HA, edema, nausea

A

Minoxidil (Rogain)

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

Use: Smooth musc vasodilator in HTN
MOA: Metab to NO
AE: HA and nausea
Notes: IV; given in HTN crisis

A

Nitroprusside

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

Thiazied diuretics incr what macromolecules?

A

Cholesterol and triglycerides

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

Use: Mild diuretic effect
MOA: Reduce Na+ in VSM to reduce contractility
AE: High Na+ intake can reverse effect, hypokalemia, hyperglycemia, hyperuricemia
Notes: Anti-HTN effect is mild, ceiling effect=maxed out at 15mmHg

A

HCTZ

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

Use: **
MOA: K+ sparing, aldosterone antagonist
AE: hyperkalemia, gynecomastia
Notes: **Can preserve K+ in combo w/ other diuretic and get anti-HTN effect

A

Spironolactone

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

Use: **
MOA: K+ sparing
AE: Hyperkalemia
Notes: **Can preserve K+ in combo w/ other diuretic to get anti-HTN effect

A

Amiloride

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

Do Beta-blockers (incr/decr) (HDL/LDL)?

A

Decr HDL

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

Beta-blockers have what effect on triglycerides?

A

Increase triglycerides

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

What is a main drug interaction of beta-blockers?

A

NSAIDs=may reduce or even block anti-HTN effects

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

Use: HTN
MOA: Decr renin, CO, and block presynaptic beta-receptor
AE: Asthma, DM, cardiac depression
Notes: Not as good as preventing strokes as ACEIs, ARBs, or CCBs

A

Beta Blockers

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

What is a non-selective beta-blocking drug used to treat A-fib and flutter, and post-MI arrhythmias?

A

Propranolol and Labetolol

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

What is a selective beta1-receptor drug used to treat HTN and angina?

A

Atenolol

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

What drugs decr total cholesterol but have NO EFFECT on HDL levels?

A

Alpha-1-antagonists

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

What drug is selective for antagonizing alpha-1 and alpha-2 receptors, is used to tx HTN, may cause syncope, and has the potential to cause sudden death secondary to cardiac arrhythmias?

A

Prazosin

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

What drugs are used to prevent the conversion of Angiotensin I to Angiotensin II?

A

ACE inhibitors

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

What are some SEs of ACE-Is?

A

Cough, bronchospasm, renal complications, hypotension (w/ volume depletion), detal mortality (2nd and 3rd trimesters), and birth defects (1st trimester)

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

What are some drug interactions of ACE-Is?

A
  • Dangerous hyperkalemia if combined w/ K+ apring diuretic
  • Oral contraceptives incr Angiotensin I levels
  • NSAIDs can reduce anti-HTN effects and may incr kidney problems
  • Incr Lithium retention (Bipolar pts)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What class of drugs do Captopril, Enalapril, and Fosinopril fall under?

A

ACE-Is

24
Q

What is the main advantage that Angiotensin II antagonists (or ARBs=Angiotensin Receptor Blocker) have over ACE-Is?

A

A2 antagonists do not cause cough

25
Q

In what pt population are ACE-Is and ARB not as effective in?

A

African American populations

26
Q

What class of drugs to Losartan and Valsartan fall under?

A

ARBs

27
Q

What is the MOA of renin inhibitors?

A

Binds renin to prevent the conversion of renin to Angiotensinogen–>Angiotensin

28
Q

What is Aliskrein?

A
  • It is a Renin inhibitor

- Does not cause cough (similar to ARB) and CANNOT use in pregnant pts

29
Q

How do CCBs tx high BP?

A

Reduce VSM tone to decrease peripheral resistance

30
Q

Use: HTN, SVT, vasospastic angina
MOA: L-type CCB
AE: Sudden death; myocardial depression; heart block; constipation
Notes: negative inotrope=signif reflex tachy; AA populations respond well

A

Nifedipine

31
Q

Use: HTN, suppress SA & AV nodal reentry
MOA: L-type CCB; inhibits phase 0 in nodal tissue and phase 2 in muscle tissue
AE: little reflex tachy, but dose cause cardiac depression
Notes: Constipation, AA pop responds well, negative inotrope

A

Verapamil

32
Q

What drug is similar to verapamil but is less severe?

A

Diltizaem

33
Q

How to Nitrovasodilators work?

A
  • Agents are denitrated releasing NO
  • NO stim guanyl cycylase–>cGMP
  • cGMP promotes dephos of myosin light chains
  • Results in smooth musc relaxation/vasodilation
34
Q

In what ways is Nitric Oxide synthesized?

A
  • In the brain (nNOS)
  • Via cytokines (iNOS)
  • Regulated by vasomotor tone (eNOS)
35
Q

What is the general mechanism of Nitrates?

A

They decr preload and afterload; decr the amount of work the hear has to do

36
Q

When is NTG indicated?

A
  • Stable angina (symptomatic use)
  • Variant angina (in conjuction w/ a CCB)
  • Pulmonary congestion w/ CHF
37
Q

What are the adverse effects of NTG?

A
  • HA (almost always due to vasodilation of vessels in brain=messes w/ pressure)
  • Nitrate syncope
  • Decr coronary perfusion w/ excessive hypotension
38
Q

What orally administered nitrate:

  • is liver metab
  • has a long onset of action (30 min)
  • is indicated for chronic stable angina
  • is combined w/ hydralazine for CHF
  • causes methemoglobinemia when OD’d
A

Isodorbide diniatrate

39
Q

What is the drug of choice for a tonic-clonic (grand-mal) seizure?

A

Valproate

40
Q

What is/are the drug/s of choice for a partial (also secondarily generalized) seizure?

A
  • Valproate

- Lamotrigine

41
Q

What is/are the drug/s of choice for a generalized absence seizure?

A
  • Valproate
  • Ethosuximide
  • Lamotrigine
42
Q

What is the drug of choice for a myoclonic, atonic seizure?

A

Valproate

43
Q

What is an alternative drug for partial onset seizures?

A

Topiramate (also phenytoin)

44
Q

What are common drug interactions of certain anti-epileptic drugs?

A

Macrolide abx and azole antifungals. These drugs cause elevated levels of:

  • Carbamazepine
  • Phenytoin
  • Valproate
  • Zonisamide
45
Q

What is the recommended procedure for treating Status Epilepticus?

A
  1. Lorazepam or diazepam IV
  2. Phenytoin or phenobarbital
  3. Anesthetic (if needed)
46
Q

Do low potency, typical antipsychotics have more or less sedation?

A

More sedation (“Less is More”)

47
Q

Do high potency, typical antipsychotics have more or less sedation?

A

Less sedation, but MORE extrapyramidal (EPS) effects

48
Q

What is Neuroleptic Malignant Syndrome a/w?

A

Hyperthermia, diffuse muscular rigidity, autonomic dysfxn, and fluctuating levels of consciousness

49
Q

What types of drugs usually (but rarely) cause Neuroleptic Malignant Syndrome?

A

Parenterally administered high-potency anti-psychotic agents

50
Q

What is the ‘Label Warning’ for Atypical antipsychotics?

A

Incr risk of:

  • Weight gain
  • DM
  • Hyperlipidemia
51
Q

Many antipsychotics block alpha-receptors. Why is this important?

A
  • Bc they have the potential to cause CNS, respiratory, and CV depression
  • They also competitively inhibit CYP2D6 and 3A4
52
Q

Which class/type of antipsychotic drug induces EPS effects and elevates [prolactin]?

A

Typical antipsychotics

53
Q

Atypical antipsychotic drugs don’t normally affect serum [prolactin], however, there is one that does. Which one?

A

Risperidone

54
Q

What are they atypical antipsychotic drugs?

A
  • Risperidone
  • Olanzapine
  • Aripiprazole
  • Clozapine
55
Q

What are the high potency, typical antipsychotic drugs?

A
  • Fluphenazine

- Haloperidol

56
Q

What are the low potency, typical antipsychotic drugs?

A

Chlorpromazine