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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

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2
Q

Preload

A

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

Blood volume/ventricular filling

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3
Q

Where is angiotensinogen produced/released from?

A

Liver

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4
Q

Where is renin produced/release from?

A

Kidney

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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

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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

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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
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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

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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

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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++

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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!

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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

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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

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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

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15
Q

Therapy Approaches for CHF

A

Decreased Preload pressure

Increased contractility

Decreased Afterload pressure

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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

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17
Q

Definitions:

Flutter

Tachycardia

Bradycardia

Fibrillation

A

Flutter: very rapid but regular contractions

increased rate

decreased rate

fibrillation: disorganized contractile activity

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18
Q

Atrial Fibrillation increases the risk for what?

A

Blood clots

Stroke

Heart failure (in the long term)

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19
Q

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

A

Catheter ablation

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20
Q

Atrioventricular Nodal Reentry Tachycardia (AVNRT)

A
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21
Q

AVRT

A

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

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22
Q

Premature Ventricular Contraction

A

1 area in the ventricles producing abnormal signals

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23
Q

Ventricular fibrillation

A

Multiple areas in both ventricles producing abnormal signals

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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
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25
What are the 4 main classes and 3 subclasses of Antiarrythmic drugs?
1: **Na+ Channel blockers** ## Footnote 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
26
Class 1a Antiarrythmic Drugs
**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!
27
Class 1b Antiarrythmic drugs
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
Class 1c Antiarrythmic drugs
Flecainide (Tambocor) ## Footnote -Associated with **significant mortality** and use limited to a last resort
29
Na Channel Blockade Strength
1C \> 1A \> 1B
30
Class 1 ERP Ranking
1A \> 1C \> 1B 1C is a last resort
31
Class 2 Antiarrythmic drugs
Beta Blockers - Slow AV conduction - Prolong AV refractory period - Suppress automaticity \*Treatment for Pheochromocytoma and Thyroid disorders
32
Class 2 Antiarrythmic drugs Toxicities
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
Class 3 Antiarrythmic Drug Action
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
Class 3 Antiarrythmic Drugs
**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
Class 4 Antiarrythmic Drugs
Ca blocking agents -**First choice** _with adenosine_ for **SVT** (supraven. tac.) due to **AVNRT** Examples: non-dihydropyridine Ca blockers =\> **verapamil and diltiazem**
36
What are the important considerations for treating arrythmias?
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
End of Drug Arrythmias and CHF drugs
38
3 Types of Angina pectoris
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
Classifications of Drugs Used to Treat Angina Pectoris
1. Negative inotropic vasodilators - Nitrates (nitroglycerine) and nitrites - dipyridamole 2. Other - beta blocker (propranolol) - Ca channel blocker (nicardipine) - ACE inhibitor (-pril) - ARB (-artan)
40
How do negative inotropic vasodilators treat Angina Pectoris?
Via **dilation of nearly all vascular beds** may also relax non-vascular smooth muscles (GI, bronchi)
41
What is the primary action of Angina Pectoris drugs?
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
What is the MOA for Nitrates such as nitroglycerin?
To **produce NO** (nitric oxide) in _vascular smooth muscle_ Dephosphorylation of myosin results in **relaxation, vasodilation, and hyperpolarization**
43
Which is affected more significantly by nitrates like nitroglycerin: venous dilation or arterial dilation?
**Venous dilation** is more significantly impacted: - Decreased _venous return_, _ventricular preload pressue_, _mechanical work and O2 consumption_ - Increased exercise tolerance
44
What are some other effects of nitrates (nitroglycerin)?
Cardiac muscle: may initiate _reflex tachycardia_ Relaxation of other smooth muscles: _bronchi, GI_ **Platelet aggregation** may **decrease** \*No direct effect on skeletal muscle
45
What is the primary route of administration for nitrates (nitroglycerin)?
**Sublingual** because oral is avoided to circumvent the 1st pass effect (exception is dinitrites)
46
What are some of the adverse reactions/precautions for nitrates?
**Throbbing vascular headaches** **Face flushing** Fainting, hypotension, reflex tachycardia (palpitations), methemoglobulinemia
47
What occurs after long-term nitrate administration?
Decrease in guanylyl cyclase activation ANS compensatory mechanism Salt and water retention \*reversed by stopping administration for 8 hours
48
Beta 1 Blocker Function for Treating Angina Pectoris
**Reduces myocardial O2 demands** Negative chronotropism and inotropism propranolol and metoprolol
49
Ca Blockers MOA for Angina Pectoris
**-Relaxant effect on vascular smooth muscle** **-Arterial dilation** _in coronary and systemic beds_ Blockage of **L-type** Ca channel *nifedipine, amlodipine, and nicardipine*
50
Section: Anticoagulants
51
Heparin
-_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
warfarin (Coumadin)
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 CYP***_2C9 and 3A4_*** **-36-72 hour lag in onset**
53
Coumadin Dosing
**Pharmacogenetics** may explain large response differences in the population -Polymorphism in CYP**2C9** AND **VKORC1**
54
Coumadin Adverse Effects
**Fatal bleeding** (black box warning)
55
What is the antidote for warfarin (Coumadin)?
phytonadione (**Mephyton**) Emergency: fresh plasma transfusion as antidote may take up to 25 hours or longer
56
warfarin (Coumadin) Drug-Drug Interactions
57
What are the newer oral anticoagulants?
Direct _Factor Xa_ inhibitors: **Xarelto, Eliquis** Direct _Thrombin_ inhinitors: **Pradaxa** Antidote for Pradaxa --\> _Idarucizumab_ Antidote for Xarelto/Eliquis --\> _Andexanet_
58
Anticoagulant Factor Xa Inhibitors
- xaban - Metabolism by CYP**3A4** Rivaroxaban (Xarelto) Apixaban (Eliquis) Edoxaban (Savaysa)
59
Guide to Anticoagulatant use (photo)
\*Heparin can be used in pregnancy but is not administered orally \*Warfarin (Coumadin) has a delayed onset
60
Section: Thrombolytics
61
What is the primary use of thrombolytic enzymes/drugs? What are 4 examples?
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
How quickly must thrombolytics be administered to be useful in post-MI and stroke patients?
post-MI must occur within **6 hours** Stroke therapy must occur within **3 hours** of onset of symptoms
63
MOA of Thrombolytic Agents
64
What are the antidotes for the thrombolytic agents?
Amino caproic acid (**Amicar)** **Tranexamic acid** (Cyklokapron) They act by **blocking the binding site of plasminogen** to prevent fibrinolysis
65
Platelet Inhibitors Section
66

Pharmacology (7 decks)

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