Brainscape's Knowledge GenomeTM

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


See full index

OS2 - Cardio > Pharm - All drugs > Flashcards

Pharm - All drugs Flashcards

1
Q

Statins

A

inhibit HMG CoA reductase (RLS of cholesterol synthesis in hepatocytes), upregulate LDL receptors; fecal 60%/renal 20% elimination; AEs include mild GI & sleep disturbance, increased liver enzymes, myalgia/myositis, rhabdomyolysis, teratogenic (CatX)

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

Lovastatin

A

CYP3A4. lipid soluble. intermediate potency. 20-40mg.

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

Simvastatin

A

CYP3A4. lipid soluble. 10-40mg.

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

Pravastatin

A

water soluble. low potency. 10-80mg.

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

Atorvastatin

A

CYP3A4. active as given and long half life. high potency.

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

Rosuvastatin

A

CYP2C9 (minimal). active as given.

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

Fluvastatin

A

CYP 2C9.

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

Bile acid resins/sequestrants

A

these bind bile acids in GI lumen and prevent reuptake/reuse of the cholesterol in the bile acid; fecal elimination; AEs include GI disturbance (bloating, constipation, nausea, flatulence), also fecal impaction and paradoxical HTG; can prevent uptake of other drugs. Includes Colestipol, Cholestyramine, Colesevelam.

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

Cholesterol Absorption Inhibitor(s)

A

acts at the epithelial brush border in the small intestine to prevent uptake of cholesterol from the diet, also upregulates LDL receptor expression in hepatocytes. Only one in class is Ezetimibe.

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

Nicotinic acid

A 
inhibits FFA mobilization from adipocytes and thereby reduces hepatic VLDL synthesis, enhances LPL and thereby promotes VLDL-->LDL conversion; AEs include cutaneous flushing, elevated transaminases, hepatitis, liver failure, GI disturbance (nausea, peptic ulcers), hyperurecemia/gout, conjunctivitis, cystoid macular edema, retinal detachment, myositis, dry skin, pruritis, insulin resistance, teratogenic (catC); available in immediate and extended release forms.
Only one in class is Niacin.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Fibrates/Fibric acid derivatives

A

serves as ligand for nuclear receptor PPARalpha in hepatocytes; reduces synthesis of VLDL and raises synthesis of HLDL

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

Gemfibrozil

A

UGT1A1. safe in renal disease. don’t co-administer with statins (UGT enzyme interference).

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

Fenofibrate

A

hepatic metabolism. renal elimination. don’t administer in renal disease (can accumulate).

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

N-3 Fatty acids

A

ligand for PPARalpha nuclear receptor in hepatocytes; reduces TG synthesis by increased FA oxidation. Best source is fish oil.

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

Common mechanism of cholesterol lowering drugs:

A

increased expression of LDL receptors and increased LDL uptake

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

MOA of Beta-blockers

A

Blocks beta-1 (NE, heart and kidneys) and/or beta-2 (NE, lungs; Epi, skeletal muscle vessels) receptors.
When blocked:
Beta-1:
- inhibit stimulation of SA/AV node/ectopic pacemakers –> dec. HR
- inhibit myocytes –> dec. contractility
- inhibit juxtaglomerular cells –> don’t release renin
Beta-2:
- inhibit skeletal muscle vessels –> vasodilation
Altogether treats HTN.

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

MOA of alpha-2 antagonists

A

Block the alpha-2 receptor, which is a NE autoregulatory receptor. Stimulating alpha-2 inhibits NE release, blocking it promotes NE release. Central effects outweigh the local (vessel) effects.

18
Q

When do you want to use CCBs?

A

DHPs - together with beta-blockers for vasodilation and reduced afterload in sinus bradycardia, SA/AV block, or valvular insufficiency
Non-DHPs - in asthma/bronchospastic COPD, severe PVD, and labile (variable glu levels) IDDM

19
Q

MOA of Ranolazine.

Clinical uses and contraindications.

A

A novel metabolic modulator that is a partial FA oxidase inhibitor, which increases glucose oxidation and efficiency of O2 utilization in the heart. Also inhibits the late Na current. No effect on HR/BP or cardiac event prevention.
Used for chronic stable angina together with amlodapine, BB, or nitrates when refractory to these.
Contraindicated in concurrent CYP3A4 inhibitors (or hepatic impairment), tricyclic antidepressants, or existing long-QT.

20
Q

Hierarchy of drug choice in agina

A
  1. Beta-blockers (unless vasospastic angina, then these are ineffective)
  2. CCBs (DHP+BB)
21
Q

MOA of Nitrates

A

enter smooth muscle cell and undergoes denitration to release NO, which induces relaxation by activating GC and increasing cGMP. Dilation of coronaries increases flow to myocardium, and venodilation results in decreased preload which reduces wall stress: so the subendocardial blood vessels have less resistance (heart wall has less pressure on it) and there is less O2 demand. Beware of tolerance - don’t dose at night.

22
Q

MOA of Ranolazine.

Clinical uses and contraindications.

A

A novel metabolic modulator that is a partial FA oxidase inhibitor, which increases glucose oxidation and efficiency of O2 utilization in the heart. Also inhibits the late Na current. No effect on HR/BP or cardiac event prevention.
Used for chronic stable angina together with amlodapine, BB, or nitrates when refractory to these.
Contraindicated in concurrent CYP3A4 inhibitors (or hepatic impairment), tricyclic antidepressants, or existing long-QT.

23
Q

What meds are used to prevent MI and CHD death in patients with angina?

A

Preventing CHD death: Beta-blockers work best. CCBs do sometimes. Nitrates dondo not.
ASA reduces reinfarction, CHD death, and stroke.
ACEIs increase survival in pts post-MI with LV dysfunction; reduces MI in high-risk pts.
Thrombolysis reduces first year mortality following MI.
Statins reduce recurrent MI.; HDL raisers reduce recurrent MI/CHD death

24
Q

MOA of Ca channel blockers

A

CCBs bind L-type Ca channels (specific to the CV system; not N- and P-type in neurons) and increase the time they are closed, thereby prevent Ca entry into the cell (cardiac myocytes and [more so arterial] vascular smooth muscle cells). Closing the channels prevents Ca entry and contraction (normally Ca will bind troponin and release inhibition of actin-myosin cross bridges, allowing contraction). Result is vasodilation, reduced afterload, reduced inotropy, slowed AV conduction. DHPs are selective vasodilators and non-DHPs are equipotent for cardiac tissue (myocytes, SA&AV nodes) and vasculature.

25
Q

Clinical effect of Nitrates on angina; contraindications.

A
  1. venodilation - dec. preload and diastolic pressure –> inc. subendocardial BF
  2. vasodilation - dec. R in coronaries, prevent spasm
  3. BP - same/slight dec.
  4. HR - same/slight inc.
  5. Pulm resistance - dec.
  6. CO - slight dec.
    Contraindications: don’t use together with PDE inhibitors, remove at night to avoid tolerance, beware extreme hypotension, don’t abruptly stop or else vasospasm.
26
Q

Clinical effect of DHP CCBs on angina, best situations for use.

A

Vasodilator (selective, esp. coronaries–prevent spasm), reduces afterload, may see reflex cardiac stimulation therefore only use together with beta-blocker.
Use to vasodilate and reduce afterload in sinus bradycardia, SA/AV block, or valvular insufficiency.
Highly effective for exertional and variant angina, but they don’t reduce CHD death or re-infarction and inc. M&M in LV dysfunction; extensive first-pass and hepatic metabolism so lower dose in liver disease.

27
Q

Clinical effect of non-DHP CCBs on angina, best situations for use

A

CCB for both vascular sm. muscle and cardiac tissue = Direct lowering of heart work/demand by dec. HR, contractility, slow AV conduction, and coronary vasodilation.
Use in asthma, bronchospastic COPD, severe PVD, and labile (variable glu levels) IDDM.
Highly effective for exertional and variant angina, but they don’t reduce CHD death or re-infarction and inc. M&M in LV dysfunction; extensive first-pass and hepatic metabolism so lower dose in liver disease. Verapamil really inhibits CYP3A4.

28
Q

Beta blockers that are

  • highly lipid soluble
  • moderately lipid soluble
A

High: Propanolol
Moderate: Metoprolol, Carvedilol, Betaxolol, Timolol (low-mod)

29
Q

Beta blockers that have good MSA and ISA.

A 
MSA = CAP - Propanolol, Acebutelol, Carvedilol
ISA = PA - Pindolol, Acebutelol
30
Q 
Beta blockers: 
1st generation, non-selective
2nd generation, B-1 selective
3rd generation plus, non-selective
4th generation plus, B-1 selective
A 
1st: PPTN
Propranolol, Pindolol, Timolol, Nadolol
2nd: EAMA
Esmolol, Acebutolol, Metoprolol, Atenolol
3rd: LC
Labetalol, Carvedilol
4th: BN
Betaxolol, Nebivolol
31
Q

Which B-blocker has the longest half life?

Shortest?

A 
Longest = Nebivolol (11-30hr) or maybe Nadolol (20-24hr)
Shortest = Esmolol (0.15hr)
32
Q

Which beta blockers have good intrinsic sympathomimetic activity (ISA)?
When are they useful/not useful?

A

These are the partial agonists: Pindolol, Acebutelol
Useful in avoiding profound bradycardia/negative inotropy in a resting heart. However the partial agonism may be disadvantageous in secondary MI prevention.

33
Q

Which B-blockers have the best membrane stabilizing activity, and what is MSA?

A

“membrane stabilizing CAP”: Carvedilol, Acebutolol, Propranolol.
Others but only at higher doses.
MSA means that (in addition to their beta-receptor block) these drugs bind to fast sodium channels and delay phase 0 of the cell depolarization (cell = non-nodal, cardiac myocytes and Purkinje fiber), decrease the slope of phase 0 which also leads to decrease in AP amplitude.

34
Q

Beta-blockers with extended actions; name their extended actions

A

NO = N
A-1 block = CL
Ca entry block = CB
Antioxidant = CN
Details:
- Nitric Oxide production stimulated by Nebivolol; NO stimulates GC, which increased cGMP, vasodilation.
- Alpha-1 Antagonism: CL; blocking alpha 1 receptors means no VC, causes vasodilation
- Ca Entry Blockade: CB, blocks Ca entry through channels, prevents contraction
- Antioxidant Activity: CN; blocks ROS from promoting LDL oxidation, lipid peroxidation, endothelial dysfunction, and apoptosis

35
Q

Overdose of Beta-blockers

A

MSA is more and will further depress contractility/conduction. This may be associated with V-tachyarrhythmias. Beta receptor specificity is lost at high doses, therefore causes lots of problems (think off-target effects, amplified).
For beta-blockers with extended actions, direct vasodilation can contribute extreme hypotension. Treat overdose with high dose insulin/glucose or glucagon.

36
Q

Off-target effects of Beta-blockers

A

Pulm: blocks beta-2 receptors, bronchoconstriction
CNS: (esp with more lipophilic) CNS depression, mental disorders, fatigue, vivid dreams
Glucose: blocks beta-2 on pancreas (which would stimulate hepatic glycogenolysis and release glucagon), hypoglycemia; decreases HR which in diabetic would otherwise signal insulin-induced hypoglycemia
Lipids: blocks beta receptors which mediate lipolysis, increase TGs and dec HDLs (inc TGs is esp bad for CHF pts)

37
Q

Stimulation of:

  • muscarinic receptors (overall)
  • M2
  • M3/M5
A

Muscarinic stimulation inhibits AC, decreases cAMP, no contraction.
M2 (HEART: Gi, blocks AC, hyperpolarizes cell): in SA node - dec HR by activating inward K channels and inhibiting VGCC, hyperpolarizes cells; in AV node - dec conduction velocity; in atrial* cardiac myocytes - inc ERP, dec contraction; in peripheral nerves - dec ganglionic transmission by inhibiting auto-/heteroreceptors
M3/M5 (VESSELS: Gs, stimulates AC, excites cell): located in endothelium of heart/brain/viscera vessels - vasodilating via EDRF synthesis and release (NO is best known EDRF)
*NOT MUCH PSNS innervation of ventricles at all. Main effects are supraventricular.

38
Q

Mediators that regulate the release of ACh from PSNS nerve terminals

A
  1. M2 and M4 autoreceptors (ACh)
  2. non adrenergic, non cholinergic (NANC) factors released along with ACh: adenosine A1, histamine H3, and opioid receptors
  3. local substances, like NO
  4. heteroreceptors where inhibition of one ANS by the other can take place
39
Q

Effects of ACh on the CV System (4)

A
  1. vasodilation (via NO release)
  2. dec HR (via activation of inward K channels at SA node)
  3. dec AV node conduction velocity (via inhibition of VGCC)
  4. dec contractility (inc refractory period with more K and less Ca)
    * remember, effects may all be obscured by CV reflexes
    * *ACh also inhibits release of NE from SNS nerves (M receptors on sympathetic nerves)
40
Q

Effects of IV ACh

A

Following administration there will be a transient decrease in BP because ACh binds endothelial cell M3 receptors, which stimulates release of NO/vasodilation. This is followed by reflex tachycardia.
If endothelium is damage, ACh binds M3 on exposed vascular smooth muscle and directly induces vasoconstriction.

41
Q

Atropine

A

Muscarinic antagonist
Low doses: inhibits presynaptic M1 autoreceptors which inc ACh release from PS nerves and causes transient slight HR decrease.
High doses: progressive tachycardia due to blocking SA node cells (PSNS can’t slow SA node) which inc resting HR but doesn’t affect max HR.
Vasculature: counteracts vasodilation BUT remember, most vessels are not parasympathetically innervated, so there is not a huge effect.
Atropine can raise temp because it inhibits sweating, and cutaneous vasodilation/flushing may occur as a compensatory reaction.

42
Q

What is atropine used for?

A

To abolish reflexive vagal cardiac slowing or asystole (from things like irritant vapors, carotid sinus stimulation, eye pressure, others).
To abolish bradycardia or asystole from parasympathomimetic drugs; cardiac arrest from vagal stimulation.
To facilitates AV conduction (shortens ERP of AV node because PSNS not there to increase it) which helps pts with AV block or nodal bradycardia, especially in setting of inferior/posterior wall MI.

OS2 - Cardio (6 decks)

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