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HD 1 > Pharm - conceptual > Flashcards

Pharm - conceptual Flashcards

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

A

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

21
Q

orthostatic hypotension = SE for…

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

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

Clinical uses for nitrates

A

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

Also:
pulmonary congestion, orthopnea, paroxysmal nocturnal dyspnea

24
Q

Contraindications/Risks w/ nitrates

A

Contraindications:
mitral stenosis, increased ICP (intracranial P), anemia

SE: tolerance, headache, syncope,

25
Q

Function of diuretics

A

(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
Q

Concerns about diuretics

A
  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
Q

risk of electrolyte changes w/ diuretics

A

With all diuretics (thiazides AND Loop): decrease Na+, K+
–> metabolic alkalosis
only w/ Loop diuretics: decrease Mg2+, Ca2+

28
Q

Concerns about aldosterone antagonists (diuretics)

A
  • hyperkalemia (esp. if use w/ ACE Inh. or ARB)

- gynecomastia (just Spironolactone bc steroidal structure)

29
Q

Why use Beta-adrenergic R antagonists (“BARX”) for CHF?

A
  • antiHTN, anti-anginal, anti-arrhythmic
  • decrease neurohormonal activation
  • decrease sudden death & hypokalemia
  • anti-proliferative & decrease myocyte apoptosis
30
Q

Inotropic drugs

A

For end-stage CHF, no effect on survival (may Increase mortality)!

  • cardiac glycosides (digoxin)
  • Beta adrenergic R agonists (dobutamine)
  • PDE-3 Inhibitors (inamrinone)
31
Q

Hemodynamic effects of Digoxin

A
  • increase CO & renal f(x)
  • increase LV ejection fraction & decrease LV End-diastolic P
  • increase exercise tolerance
  • increase renal BF and natriuresis
32
Q

neurohormonal effects of digoxin

A
  • increase vagal tone
  • decrease cardiac and peripheral SNS activity
  • decrease Renin/AngII/Ald activity
  • normalizes arterial baroRs
33
Q

Digoxin Toxicity

A
  • 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
Q

factors influencing Digoxin toxicity

A

Toxicity Increased by:

  • hypOkalemia (Dig binds to K+)
  • Hypothyroidism - renal failure
  • drugs that decrease clearance

Toxicity Decreased by: - hyperthyroidism - in infants

35
Q

classes of anti-arrhythmic drugs

A 
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
Q

Na+ channel blocking drugs (6)

A 
(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
Q

K+ blocking drugs (4)

A

(used as anti-arrhythmics)

Amiodarone, Drondearone, Bretylium, Sotalol

38
Q

Ca2+ channel blocking drugs (2)

A

(used as anti-arrhythmics)

Diltiazem & Verapamil

39
Q

Mech of action for Class 1 anti-arrhythmic drugs

A

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
Q

Use of beta blockers for arrhythmias

A

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
Q

Mech for Class III anti-arrhythmic drugs

A

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
Q

Drug classes best used for supraventricular arrhythmias

A

Class II and IV
II - beta blockers (propanolol)
IV - verapamil/diltiazem

43
Q

Drug classes best used for ventricular arrhythmias

A

Classes I and III
I - Lidocaine
(also Disopryramide, Procainamide, Quinidine; Flecainide)
III - Sotalol, *digoxin
(also Amiodarone, Bretylium, Dronedarone)

44
Q

3 parts to medical management of atrial fibrillation

A
  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
Q

Why use anti-thrombotics for A-fib treatment?

A

= only treatment shown to decrease mortality w/ A-fib.

* anti-platelet drugs (ie: warfarin) = more effective than anti-coag. (ie: Aspirin)

46
Q

Use of cardiac glycosides in A-fib

A

(ie: digoxin) Can be ventricular rate control and CHF,
BUT: only work at rest, so okay for elderly if inactive.
* narrow therapeutic range!

47
Q

Drug-drug interactions for Warfarin:

– DEcrease effect

A
  • P450 Inducers: barbiturates, rifampin, carbemazine, phentoin.
  • Alter GI absorption: cholestyramine
  • Alter binding: excess K+ consumption, hypothyroidism
48
Q

Drug-drug interactions for warfarin:

– INcrease effect

A
  • Decrease metabolism: cimetidine, trimethoprim
  • Alter plasma: high albumin, aspirin
  • Hypokalemia: acute intoxication, some antibiotics
  • Coag. factor deficit: hepatic dysfunction, hyperthyroidism
49
Q

antidotes to warfarin overdose

A 
#1: fresh frozen plasma (IV, immediate)
2. vitamin K (oral/IV, has lag time)

HD 1 (9 decks)

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