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Pharm - conceptual Flashcards

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0
Q

1st line therapy for STABLE angina

A

Beta blockers!
decrease HR & contractile force, increase efficiency
- esp. B1 blockers –> increase coronary perfusion
* only helpful as prophylaxis, not for acute episode.

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1
Q

purpose of anti-anginal drugs

A

= to treat/manage symptoms, increase exertional capacity;
NOT proven to reduce mortality or MI.
ie: beta blockers, nitrates, Ca2+ channel blockers

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2
Q

adverse effects of beta blockers

A

all: mask hyperglycemia/worsen glycemic control;
also fatigue, depression, impotence
B1 –> heart failure, bradycardia, AV block
B2 –> bronchospasm, Reynauld’s, periph. vascular disease

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3
Q

mech of action of nitrates

A
  1. Decrease cardiac work (relax smooth muscle –> venous/vasodilation) => decrease preload (#1) and afterload,
  2. Increase O2 to heart (vasodilate, decrease preload)
  3. Decrease platelet aggregation
    = for acute angina symptoms, does NOT decrease mortality.
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4
Q

common side effects of organic nitrates

A

reflex tachycardia, flushing, syncope;
headache, dizziness, postural hypOtension.
* effects = dose related (proportional to size of dose)
** do NOT take w/in 24 hrs of PDE-5 inhibitors (ie: sildenafil/viagra) –> severe hypotension **

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5
Q

Mechanism of action of Ca2+ channels blockers (“VOCC”)

A
  • L-type blockers: (oral, liver metabolism)
  • relax arteriolar sm muscle cells –> vasodilation
  • block myocytes, SA & AV node tissues –> reduced inotropic effect.
    (= 3rd line agents, BUT great for asthmatics!)
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6
Q

Adverse effects of VOCCs (Ca2+ channel blockers)

A
  • do NOT take w. beta blockers! => severe/compounded bradycardia.
    Also: headache, nausea, flushing.
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7
Q

List of MI-prevention drugs (for angina pts)

A

(to prevent adverse outcomes)
Primary (#1): aspirin, statins
Secondary: beta blockers (post-MI), or ACE Inhibitors (if DMII or LV dysfunction)

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8
Q

Combo therapy strategy for asthma/COPD

A

use 2 different classes of drugs to manage different parts of disease:

  1. bronchodilators = symptom management (acute Sx Tx)
  2. anti-inflammatories = prevent lung damage (“controller” Tx)
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9
Q

Contraction mechanism in Asthma

A
  • blocked w/ meds for Sx management*
    1. CysLT Rs and M3 ACh Rs = activated (by PNS)
  • -> signal cascade
    2. increase intracellular Ca2+
    3. => smooth muscle contraction
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10
Q

Relaxation mechanism in asthma

A
  • stimulated by drugs to manage symptoms *
    1. Beta-2 Rs activated by circulating catecholamines
    2. increase cAMP –> activate PDE
    3. relax bronchial smooth muscle
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11
Q

classes of bronchodilators used for asthma

A
  1. Beta-adrenoceptor agonists (increase relaxation)
    • Beta-2 = most potent bronchodilators
  2. CysLT R antagonists (inhibit contraction)
    • also anti-inflammatory
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12
Q

drugs used as anti-inflammatories for asthma

A

–>decrease inflammation = limit damage to lungs, NOT for Sxs
#1. glucocorticoids - highly effective
2. cromones - weak, poorly understood
3. anti-IgE antibodies - if specific allergic trigger

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13
Q

drug treatment for COPD

A
  • can’t reverse damage, so no need for anti-inflammatories
    #1. bronchodilators - esp. anticholinergics, …or beta agonists
    2. PDE-5 inhibitors - for combo Tx, decrease chronic inflammation
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14
Q

strategy for combinatorial therapy for asthma

A

1st (mild): inhaled corticosteroid (“ICS”) for exacerbations
*try increasing dose of ICS before add meds;
2nd (moderate): ICS + daily oral long-acting beta agonist (“LABA”)
*can use LOW dose of ICS when add LABA
3rd (severe): high dose ICS + LABA + oral corticosteriod

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15
Q

types & potencies of inhaled glucocorticosteroids (ICS)

A

1. Fluticasone (highest potency)

2. Budesonide (~high potency
3. Beclomethasone (lower potency)
4. Flunisolide (low potency)
5. Prednisone = oral)

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16
Q

most effective approach to treating CHF

A 
block AngII and aldosterone, (& NE)
=> decrease:
- fluid retention (decrease afterload)
- tissue remodeling
- neurohormonal/reflex compensation
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17
Q

inotropic agent

A

substance that increases cardiac contractility (inotropic effect)

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18
Q

2 main mechanisms of ACE Inhibitors

A

by blocking ACE activity:
1. block AngI –> AngII
2. increase bradykinin levels (=> increase endogenous NO, prostacyclins –> vasodilation and anti-proliferative effects)
==> increase survival.

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19
Q

Major effects of ACE Inhibitors and ARBs

A
  1. vasodilation –> decrease TPR and afterload, increase CO; decrease PCWP and preload (a little);
  2. diuresis & natriuresis
    * 3. NO direct change to HR or contractility
    * ** no tolerance dvpt! ***
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20
Q

list of ARBs

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A

(= Angiotensin I Receptor Blockers)
“-sartan”
Losartan, valsartan, irbesartan, telmisartan.

21
Q

orthostatic hypotension = SE for…

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A

any drugs that dilate veins.

  • only venous: organic nitrates
  • mixed a/v: nitroprusside, PDE-Is, ACEIs, ARBs, nesirtide
22
Q

Hemodynamic effects of Nitrates/NO donors

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A
  • arteriolar dilation: decrease afterload
    • coronary vasodilation: increase cardiac perfusion
  • venodilation: decrease preload & pulmonary congestion
23
Q

Clinical uses for nitrates

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A

1: chronic/acute CHF…w/ MI, pulmonary edema

Also:
pulmonary congestion, orthopnea, paroxysmal nocturnal dyspnea

24
Contraindications/Risks w/ nitrates
Contraindications: mitral stenosis, increased ICP (intracranial P), anemia SE: tolerance, headache, syncope,
25
Function of diuretics
(ie: thiazides/Loop diuretics) decrease Na+ retention --> decrease plasma volume; => decrease preload & congestion, usually no effect on CO. Used *short term* for CHF w/ pulmonary congestion (decrease morbidity/mortality, increase exercise capacity)
26
Concerns about diuretics
1. can activate neurohormonal systems --> stimulate NE & AngII 2. Hypokalemia (may dangerously alter electrolyte levels) - -> do NOT use w/ Digoxin! 3. may develop diuretic resistance
27
risk of electrolyte changes w/ diuretics
With all diuretics (thiazides AND Loop): decrease Na+, K+ --> metabolic alkalosis only w/ Loop diuretics: decrease Mg2+, Ca2+
28
Concerns about aldosterone antagonists (diuretics)
- hyperkalemia (esp. if use w/ ACE Inh. or ARB) | - gynecomastia (just Spironolactone bc steroidal structure)
29
Why use Beta-adrenergic R antagonists ("BARX") for CHF?
- antiHTN, anti-anginal, anti-arrhythmic - decrease neurohormonal activation - decrease sudden death & hypokalemia - anti-proliferative & decrease myocyte apoptosis
30
Inotropic drugs
For end-stage CHF, no effect on survival (may Increase mortality)! - cardiac glycosides (digoxin) - Beta adrenergic R agonists (dobutamine) - PDE-3 Inhibitors (inamrinone)
31
Hemodynamic effects of Digoxin
- increase CO & renal f(x) - increase LV ejection fraction & decrease LV End-diastolic P - increase exercise tolerance - increase renal BF and natriuresis
32
neurohormonal effects of digoxin
- increase vagal tone - decrease cardiac and peripheral SNS activity - decrease Renin/AngII/Ald activity * normalizes arterial baroRs
33
Digoxin Toxicity
* very narrow therapeutic range! renal clearance... - ventricular/supraventricular arrhythmias - SA node/AV node blocks - GI: nausea, vomiting, diarrhea; NS: depression, paresthesia, - blurry vision/color changes, hyperestrogenism...
34
factors influencing Digoxin toxicity
Toxicity Increased by: - hypOkalemia (Dig binds to K+) - Hypothyroidism - renal failure - drugs that decrease clearance Toxicity Decreased by: - hyperthyroidism - in infants
35
classes of anti-arrhythmic drugs
``` class I: Na channel blockers (delay depolarization) class II: Beta blockers (slow HR... - via pacemaker potential, plateau, & repol. phases) class III: K+ channel blockers (delay repolarization) class IV: Ca channel blockers (prolong plateau & repol. phases) ```
36
Na+ channel blocking drugs (6)
``` (used as anti-arrhythmics) 1A: (prolong AP) Disopyramide, Procainamide, Quinidine 1B: (shorten AP) Lidocaine 1C: Flecainide, Propafenome (delay AP peak, no change in duration) ```
37
K+ blocking drugs (4)
(used as anti-arrhythmics) | Amiodarone, Drondearone, Bretylium, Sotalol
38
Ca2+ channel blocking drugs (2)
(used as anti-arrhythmics) | Diltiazem & Verapamil
39
Mech of action for Class 1 anti-arrhythmic drugs
Block voltage-dep. Na+ channels --> delay depolarization. * higher affinity for active channels, so selectively target damaged regions of heart. Use: V-fib., sustained ventricular tachycardia SE: CNS effects & long-term = pro-arrhythmic
40
Use of beta blockers for arrhythmias
Mech: block B1 receptors @ SA & AV nodes -> prolong recovery time. Use: atrial flutter, A-fib, AV nodal reentry *use w/ Ca channel blockers for A-fib.* Why? prevent transmission of rapid atrial beats through AV node
41
Mech for Class III anti-arrhythmic drugs
Mech: K+ channel blockers, prolong repolarization Use: V-fib., long-term for ventricular tachycardia SE: bradycardia, prolonged QT interval/torsades de pointe, long term pro-arrhythmic
42
Drug classes best used for supraventricular arrhythmias
Class II and IV II - beta blockers (propanolol) IV - verapamil/diltiazem
43
Drug classes best used for ventricular arrhythmias
Classes I and III I - Lidocaine (also Disopryramide, Procainamide, Quinidine; Flecainide) III - Sotalol, *digoxin (also Amiodarone, Bretylium, Dronedarone)
44
3 parts to medical management of atrial fibrillation
1. Anti-thrombotics (to decrease risk of stroke) 2. Ventricular rate control (beta or Ca2+ channel blockers) 3. Control any other co-existing heart problems - optional: anti-arrhythmics, cardioversion
45
Why use anti-thrombotics for A-fib treatment?
= only treatment shown to decrease mortality w/ A-fib. | * anti-platelet drugs (ie: warfarin) = more effective than anti-coag. (ie: Aspirin)
46
Use of cardiac glycosides in A-fib
(ie: digoxin) Can be ventricular rate control and CHF, BUT: only work at rest, so okay for elderly if inactive. * narrow therapeutic range!
47
Drug-drug interactions for Warfarin: | -- DEcrease effect
- P450 Inducers: barbiturates, rifampin, carbemazine, phentoin. - Alter GI absorption: cholestyramine - Alter binding: excess K+ consumption, hypothyroidism
48
Drug-drug interactions for warfarin: | -- INcrease effect
- Decrease metabolism: cimetidine, trimethoprim - Alter plasma: high albumin, aspirin - Hypokalemia: acute intoxication, some antibiotics - Coag. factor deficit: hepatic dysfunction, hyperthyroidism
49
antidotes to warfarin overdose
``` #1: fresh frozen plasma (IV, immediate) 2. vitamin K (oral/IV, has lag time) ```

HD 1 (9 decks)

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