Brainscape's Knowledge GenomeTM

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


See full index

Pharmacology > Exam 2 Review > Flashcards

Exam 2 Review Flashcards

1
Q

Afterload

A

Resistance to flow in the aorta and arteries (peripheral vascular resistance)

Also, the work required to opn the aortic valve

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

Preload

A

Venous return from the upper and lower body to the right atrium

Blood volume/ventricular filling

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

Where is angiotensinogen produced/released from?

A

Liver

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

Where is renin produced/release from?

A

Kidney

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

Which drug class for hypertension did we learn about that has a sideffect of a slight cough? Why? What would you substitute?

A

ACE inhibitors (-prils)

-Because there is decreased bradykinin breakdown (more of them present)

Substitute with ARBs

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

Which drug is the cornerstone of CHF (congestive heart failure)?

A

ACE inhibitors (-prils)

  • Reduced pre- and after-loads
  • Inhibits cardiac and vascular remodeling

Angioedema is a rare but lifethreatening side-effect

Contraindicated in pregnancy and K-sparing diurectics (spironolactone) due to decrease in aldosterone secretion

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

ARBs

A
  • artans
  • Reduced pre- and after-loads
  • Also inhibit cardiac and vascular remodeling
  • valsartan approved for post-MI usage like ACE inhibitors; others aren’t
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

How do the ARBs and ACE inhibitors reduce pre- and after-loads?

A

Dilate veins and arteries by down-regulating the amount of Angiotensin II in circulation

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

What is the Triple Whammy Crisis?

A

ACE inhibitors, NSAIDs, and Diuretics

Efferent arteriole dilation, block prostaglandin production (afferent arteriole constricted), and decreased plasma volume

Combined, they lead to severe Renal failure crisis

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

Cardiac Glycosides (digoxin and digitalis)

A

Inotropic drug

Primary use is for CHF but never the first drug (or only drug) used

Secondary use is for atrial tachycardia, flutter, and fibrillation

MOE is to block Na/K ATPase, leading to a buildup of intracellular Ca++

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

Pharmacokinetics of digoxin

A

25% plasma protein bound

36 hour half-life

Antibiotic treatment can lead to a sudden increase in digoxin availability and toxicity!

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

Digoxin Toxicity

A

Low therapeutic index (narrow safety margin)

Side-effects: Visual disturbances, disorientation, and confusion; various stages of heart block, ectopic systoles of ventricular origin and arrythmia

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

What is the best treatment for Digoxin toxicity?

A

digoxin specific antibodies (Digoxin Immune Fab [Digibind]) has a rapid response in less than a minute

lidocaine is used for ventricular arrhythmias

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

Digoxin Drug Interactions

A

Adrenergic agonists (epinephrine)

Antibiotics

Anticholinergics (antisialologues) : via antagonism with vagus nerve cholinergic effect of digoxin

Antacids

Diuretics (K depleting)

Prolonged corticosteroid therapy

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

Therapy Approaches for CHF

A

Decreased Preload pressure

Increased contractility

Decreased Afterload pressure

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

Arrythmia

A

Any abnormality of firing rate, regularity or site of origin of cardiac impulse or disturbance of conduction that alters normal sequence of activity of atria and ventricles

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

Definitions:

Flutter

Tachycardia

Bradycardia

Fibrillation

A

Flutter: very rapid but regular contractions

increased rate

decreased rate

fibrillation: disorganized contractile activity

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

Atrial Fibrillation increases the risk for what?

A

Blood clots

Stroke

Heart failure (in the long term)

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

What is a non-invasive method of treatment for a-fib?

A

Catheter ablation

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

Atrioventricular Nodal Reentry Tachycardia (AVNRT)

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

AVRT

A

There’s an abnormal electrical pathway involved (ablation can help)

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

Premature Ventricular Contraction

A

1 area in the ventricles producing abnormal signals

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

Ventricular fibrillation

A

Multiple areas in both ventricles producing abnormal signals

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

What are 3 principles to keep in mind about anti-arrythmic agents?

A
  1. Every antiarrythmic drug can be pro-arrythmic
  2. Therapeutic range of drug levels is empirically-derived
  3. Caution needs to be taken, especially with high-risk patients like the elderly, pregnancy, hepatic/renal insufficiency or failure, and patients on multiple drugs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

What are the 4 main classes and 3 subclasses of Antiarrythmic drugs?

A

1: Na+ Channel blockers

1a: Quinidine/Procainamide
1b: Lidocaine
1c: Flecainide/Propafenone
2: Beta blockers (Propanolol)
3: K+ Channel blockers (sotalol and amiodarone)
4: Ca++ Channel blockers (verapamil)

*note sotalol is also a beta blocker

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

Class 1a Antiarrythmic Drugs

A

Quinidine

  • Actions opposite to digitalis (anti-cholinergic effect leading to increased heart rate)
  • Negative inotropic effect and diarrhea side-effect

Procainamide

  • More commonly used but short term due to higher incidence of adverse reactions
  • Common choice for ventricular arrythmias associated with acute MIs (more effective than lidocaine)
  • Increased antinuclear antibody titer with long-term use that resembles Lupus Erythematosus!
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Class 1b Antiarrythmic drugs

A

Lidocaine

-Very low toxicity with good therapeutic index but rarely used today

Little effect on atria function or vagus nerve

-Primary target is ventricular function (treatment of ventricular tachycardia of digoxin toxicity and ventricular ectopic rhythms)

28
Q

Class 1c Antiarrythmic drugs

A

Flecainide (Tambocor)

-Associated with significant mortality and use limited to a last resort

29
Q

Na Channel Blockade Strength

A

1C > 1A > 1B

30
Q

Class 1 ERP Ranking

A

1A > 1C > 1B

1C is a last resort

31
Q

Class 2 Antiarrythmic drugs

A

Beta Blockers

  • Slow AV conduction
  • Prolong AV refractory period
  • Suppress automaticity

*Treatment for Pheochromocytoma and Thyroid disorders

32
Q

Class 2 Antiarrythmic drugs Toxicities

A

Will worsen congestive heart failure

SA and/or AV block

Sudden withdrawal may worsen angina and arrythmias due to receptor upregulation

-Bronchospasm, sedation, insomnia, and depression

33
Q

Class 3 Antiarrythmic Drug Action

A

Primary anti-arrythmic action is through blockade of rapid component of the delayed rectifier outward potassium current; this action prolongs the the ERP (effective refractory period) of mycocardial cells

34
Q

Class 3 Antiarrythmic Drugs

A

Sotalol

  • Also a beta blocker on top of being a K-blocker
  • Atrial flutter and fibrillation

Amiodarone

-High incidence of adverse effects including: potentially fatal pulmonary toxicity (fibrosis) and thyroid dysfunction; many drug-drug interactions due to metabolism by CYP3A4 and CYP2C8

35
Q

Class 4 Antiarrythmic Drugs

A

Ca blocking agents

-First choice with adenosine for SVT (supraven. tac.) due to AVNRT

Examples: non-dihydropyridine Ca blockers => verapamil and diltiazem

36
Q

What are the important considerations for treating arrythmias?

A

Class 1-3 are used for ventricular conditions while supraventricular is Class 4

Acute: Adenosine (1), Digoxin (cadiac glycoside), Amiodarone (3), Procainamide (1a), Sotalol (2)

Chronic: beta blocker (2), Ca blocker (4), Amiodarone (3), Sotalol (3), Flecainide (1c)

37
Q

End of Drug Arrythmias and CHF drugs

A
38
Q

3 Types of Angina pectoris

A
  1. Chronic Stable: classic angina of effort; presence of atheromatous obstruction in coronary arteries; therapeutic goal is to increase myocardium perfusion/decrease O2 demand
  2. Variant: coronary vasospasm (goal is to prevent vasospasm)
  3. Unstable: presence of transient thrombi near atherosclerotic plaque (goal is to correct tendency to form thrombi)
39
Q

Classifications of Drugs Used to Treat Angina Pectoris

A
  1. Negative inotropic vasodilators
    - Nitrates (nitroglycerine) and nitrites
    - dipyridamole
  2. Other
    - beta blocker (propranolol)
    - Ca channel blocker (nicardipine)
    - ACE inhibitor (-pril)
    - ARB (-artan)
40
Q

How do negative inotropic vasodilators treat Angina Pectoris?

A

Via dilation of nearly all vascular beds

may also relax non-vascular smooth muscles (GI, bronchi)

41
Q

What is the primary action of Angina Pectoris drugs?

A

To decrease preload and/or afterload blood pressure

-This leads to increased efficiency in oxygen utilisation by myocardium and decreases oxygen demand

Increased Oxygen Supply/Demand ratio

42
Q

What is the MOA for Nitrates such as nitroglycerin?

A

To produce NO (nitric oxide) in vascular smooth muscle

Dephosphorylation of myosin results in relaxation, vasodilation, and hyperpolarization

43
Q

Which is affected more significantly by nitrates like nitroglycerin: venous dilation or arterial dilation?

A

Venous dilation is more significantly impacted:

  • Decreased venous return, ventricular preload pressue, mechanical work and O2 consumption
  • Increased exercise tolerance
44
Q

What are some other effects of nitrates (nitroglycerin)?

A

Cardiac muscle: may initiate reflex tachycardia

Relaxation of other smooth muscles: bronchi, GI

Platelet aggregation may decrease

*No direct effect on skeletal muscle

45
Q

What is the primary route of administration for nitrates (nitroglycerin)?

A

Sublingual because oral is avoided to circumvent the 1st pass effect (exception is dinitrites)

46
Q

What are some of the adverse reactions/precautions for nitrates?

A

Throbbing vascular headaches

Face flushing

Fainting, hypotension, reflex tachycardia (palpitations), methemoglobulinemia

47
Q

What occurs after long-term nitrate administration?

A

Decrease in guanylyl cyclase activation

ANS compensatory mechanism

Salt and water retention

*reversed by stopping administration for 8 hours

48
Q

Beta 1 Blocker Function for Treating Angina Pectoris

A

Reduces myocardial O2 demands

Negative chronotropism and inotropism

propranolol and metoprolol

49
Q

Ca Blockers MOA for Angina Pectoris

A

-Relaxant effect on vascular smooth muscle

-Arterial dilation in coronary and systemic beds

Blockage of L-type Ca channel

nifedipine, amlodipine, and nicardipine

50
Q

Section: Anticoagulants

A
51
Q

Heparin

A

-Extreme negative charge

Unfractionated heparin has activity on thrombin and factor Xa

Low weight heparin just binds Xa (Lovenox and Arixtra)

Antagonized by protamine sulfate

Adverse Effects: bleeding, thrombocytopenia, headache

52
Q

warfarin (Coumadin)

A

past oral anticoagulant of choice (now been replaced by Xarelto, etc.)

-Antagonizes the utilization of Vitamin K (factors 7, 9, and 10 require this as a cofactor)

-Highly bound to plasma protein (99%)

-Metabolized by CYP2C9 and 3A4

-36-72 hour lag in onset

53
Q

Coumadin Dosing

A

Pharmacogenetics may explain large response differences in the population

-Polymorphism in CYP2C9 AND VKORC1

54
Q

Coumadin Adverse Effects

A

Fatal bleeding (black box warning)

55
Q

What is the antidote for warfarin (Coumadin)?

A

phytonadione (Mephyton)

Emergency: fresh plasma transfusion as antidote may take up to 25 hours or longer

56
Q

warfarin (Coumadin) Drug-Drug Interactions

A
57
Q

What are the newer oral anticoagulants?

A

Direct Factor Xa inhibitors: Xarelto, Eliquis

Direct Thrombin inhinitors: Pradaxa

Antidote for Pradaxa –> Idarucizumab

Antidote for Xarelto/Eliquis –> Andexanet

58
Q

Anticoagulant Factor Xa Inhibitors

A
  • xaban
  • Metabolism by CYP3A4

Rivaroxaban (Xarelto)

Apixaban (Eliquis)

Edoxaban (Savaysa)

59
Q

Guide to Anticoagulatant use (photo)

A

*Heparin can be used in pregnancy but is not administered orally

*Warfarin (Coumadin) has a delayed onset

60
Q

Section: Thrombolytics

A
61
Q

What is the primary use of thrombolytic enzymes/drugs? What are 4 examples?

A

For treatment of post-MI and stroke patients (not hemhorragic strokes though?)

  1. Tissue Plasminogen Activator (t-PA)
    - alteplase (Activase) is most common and binds to fibrin and activates fibrin-bound plasminogen better than free plasminogen to break clots
  2. Tenecteplase (TNKase)
  3. Urokinase (Abbokinase)
  4. Streptokinase (Streptase)
62
Q

How quickly must thrombolytics be administered to be useful in post-MI and stroke patients?

A

post-MI must occur within 6 hours

Stroke therapy must occur within 3 hours of onset of symptoms

63
Q

MOA of Thrombolytic Agents

A
64
Q

What are the antidotes for the thrombolytic agents?

A

Amino caproic acid (Amicar)

Tranexamic acid (Cyklokapron)

They act by blocking the binding site of plasminogen to prevent fibrinolysis

65
Q

Platelet Inhibitors Section

A
66
Q
A

Pharmacology (7 decks)

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