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Cardiopulmonary PT > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

What is goal of pharmacology?

A

Prescribe appropriate meds for patient’s needs.
Medication delivered to site of action.
Elicit and appropriate clinical response.

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2
Q

What are types of drug administration?

A

Parenteral, enteral,

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3
Q

What are categories of parenteral drug administration?

A

Injection, intravenous, intramuscular, subcutaneous, intrathecal, sublingual, inhalational

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4
Q

What are characteristics of parental administration?

A

No GI absorption, fast acting, high concentration of drug quickly, valuable during emergency, pain at injection site,

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5
Q

Which parental administrations has quick delivery?

A

Inhalation: quick delivery to bronchi or alveoli for local effect.
Gaseous anesthetic, vaporizes quickly

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6
Q

Which type of drug administration is convenient, most common, effective absorption, and is the most economical?

A

Enteral by mouth (p.o.)- tablets, capsules, sustained release, chewable, liquid

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7
Q

What are effects of rectal administration?

A

Local or systemic effects, effective if GI tract is upset

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8
Q

What are effects of transdermal administration?

A

Slowly absorbed, prolongs blood levels

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9
Q

What are different terms for pharmokinetics?

A 
Bioavailability
Distribution
Clearance
Half-life
Dosage
Administered
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10
Q

What is bioavailability?

A

Route of administration with goal of getting into bloodstream.
IM, sublingual, by mouth, or transdermal

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11
Q

What is definition for distribution?

A

Drug passes through body via circulatory system

General or restricted: depends on permeability, drugs bind to proteins but now drug unavailable to bind to receptor site

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12
Q

What is clearance and what accomplishes it?

A

Rate of elimination by all routes relative to concentration of drug in biological fluid.

Kidneys are most important route for clearance.

Inadequate body system or circulatory system may hamper clearance: drug toxicity

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13
Q

What is half-life?

A

Time needed for drug to be reduced by 50% in plasma concentration.
The length of time the effects of drug will last.
Medications taken at regular intervals

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14
Q

T/F: the longer the half life, the longer effect of drugs?

A

True

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15
Q

Who determines dosage?

A

Physician

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16
Q

What must be considered with dosage of drugs?

A

Amount to be administered at one time.
Route of administration
Interval between doses
Period of time over which drug administration is to be continued

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17
Q

What are characteristics of pharmacokinetics: administered?

A

Continuous input: sustained release, IV, subcutaneous

Intermittent doses: meds given at certain times during day

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18
Q

What are parts of pharmacodynamics?

A 
Drugs don't have isolated effects on tissues.
Digitalis and generalized effects.
Selectivity
Agonist vs antagonist
Receptors
Autonomic nervous system
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19
Q

How can drugs effect tissue?

A

Can affect any receptor specific to drug’s structure.

Person’s tolerance to drug is related to drug’s primary effect, secondary effects, or side effects

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20
Q

What does digitalis do?

A

Works at sodium potassium pump.
Primary target is AV node (decrease conduction)
Increased myocardial activity
Affects blood chemistry: hypokalemia

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21
Q

What is drug selectivity?

A

Certain concentrations of drug exists, drug is preferentially attracted on one group of receptors.
Atenolol targets B1 receptors
Propanolol targets B1 and B2 (non selective)

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22
Q

T/F: atenolol targets B2 receptors?

A

False: targets B1

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23
Q

What does propranolol target?

A

B1 and B2 receptors (non selective)

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24
Q

What are pharmacodynamics of the autonomic nervous system?

A

Cholinergic (PNS)
Adrenergic (SNS): alpha and beta receptors sensitive to catecholamines, epinephrine in adrenal medulla, norepinephrine in local level from sympathetic postganglionic fibers

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25
Q

What are goals of medical management of cardiopulmonary disease?

A

Acute vs long term treatment of CAD and symptoms
Treatment directed toward preventing myocardial ischemia and infarction
Want to maximize and improve existing cardiac function

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26
Q

What are nitrates used to treat?

A

Angina symptoms from myocardial ischemia.

Heart failure, acute MI, HTN

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27
Q

How do nitrates work?

A

They vasodilate by relaxing smooth muscle in coronary and peripheral arteries, veins, bronchioles, GI tract, and uterus

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28
Q

What does the vasodilation result in (nitrates)?

A

Peripheral vasodilation results in venous pooling, decreased venous return to heart (decreased preload).

Decreased preload reduces ventricular dimensions and diastolic filling pressures.

Decreased resistance decreases afterload

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29
Q

What is result of decreased afterload (nitrates)?

A

Reduces myocardial demand

Relieves or delays onset of angina

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30
Q

What are contraindications and side effects for nitrates?

A

Reflex tachycardia, orthostatic hypotension, flushing headache

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31
Q

What is effect of nitrates on exercise in CAD?

A

Nitrates prior to exercise reduces cardiac workload and improves exercise performance.
Increased tolerance for activity before onset of angina pain

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32
Q

What must we as PTs consider when our patient is on nitrates?

A

Obtain BP before they take them.
Have them lie down before administration.
If pain not relieved by 3 doses of nitro (one tablet every 5 minutes) call 911

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33
Q

T/F: if chest pain is not relieved in your patient after 3 doses of nitro tell them to take another one.

A

False: call 911 if in home health, if in hospital activate protocol,

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34
Q

T/F: beta blockers reduce myocardial oxygen requirements

A

True

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35
Q

What is primary mechanism for beta blockers?

A

Responsible for diminishing actions of SNS (catecholamine release) on beta receptors

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36
Q

How do beta blockers reduce myocardial oxygen requirements?

A

Decrease HR, BP, myocardial contractility (rest and exercise).
Decreased HR= prolong diastole (increased blood supply to myocardium)

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37
Q

What are the steps of beta blocker drugs effects?

A

Compete with catecholamines for beta receptor sites in heart and other tissues
Causes inhibition of adrenergic stimuli to Beta 1 and Beta 2 receptor sites

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38
Q

Where are beta 1 found? Where are beta 2 found?

A

1: found in heart. Inhibition decreases HR, conduction through AV node, decrease contractility
2: found in periphery, lungs, and body. Inhibition causes bronchoconstriction, vasoconstriction of vessel beds

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39
Q

What normally happens at beta receptor sites?

A

Catecholamines bind with beta receptors sites

Which initiates responses to SNS adrenergic stimulation

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40
Q

What are beta blockers used for?

A

After acute MI they can be used to salvage ischemic myocardium: decreased myocardial demand
Treatment of mild HTN, atrial/ventricular arrhythmias

41
Q

How do beta blockers help atrial/ventricular arrhythmias?

A

Decrease automaticity of myocardial cells

Slow conduction through AV node

42
Q

How does beta blockers help with therapy?

A

Increased exercise tolerance and aerobic capacity.
Decreased resting and submaximal HR, BP, RPP.
Higher levels of activity before the individuals threshold is reached and angina pain or ECG changes occur.

43
Q

What are side effects of beta blockers?

A

Bradycardia, hypotension, bronchospasm, AV block, nausea, fatigue, depression, and sleep disorders.
Stopping suddenly may bring on recurrence of angina pain, or AMI, arrhthymias, or sudden death

44
Q

What are considerations for taking beta blockers?

A

Don’t stop abruptly (unless bronchospasm)
Increases to HR normally seen with exercise are decreased.
Changes in meds may need repeated GXT and reassessment of exercise prescription.
Observe patients for changes in respiratory effort or dyspnea

45
Q

What is calcium important for? What inhibits flow of calcium ions?

A

Myocardial contractility, vascomotor tone, cardiac electrical activity.

Membranes or myocardial and vascular smooth muscle inhibits flow

46
Q

What are the 4 groups of Ca channel blockers?

A

Type 1: myocardial and electrophysiologic effects
Type 2: predominant vascular effects
Type 3: selective vascular properties
Type 4: complex pharmacologic properties

47
Q

How does type 1 calcium channel blockers work on heart?

A

Decreased myocardial oxygen demand by: decreasing HR, decreasing contractility, decreasing afterload through peripheral vasodilation

2 drugs: verapamil, diltiazem

48
Q

What are type 1 Ca channel blockers used to treat?

A

HTN, angina, arrhythmias (supraventricular tachy)

49
Q

What are type 2 Ca channel blockers used for?

A

Treat HTN
Used in combination with nitrates to treat angina
Used in combination with beta blockers
No effect on treating AMI

50
Q

How do type 2 Ca channel blockers work on heart?

A

Dihydropryridines are strong peripheral dilators: difedipine has strongest effect

Decrease afterload by peripheral vasodilation
No direct effect on HR or as an antiarrhythmic properties

51
Q

What are contraindications for calcium channel blockers?

A

Moderate to severe CHF
Hypotension
Aortic stenosis
Sick sinus syndrome

52
Q

What are side effects of calcium channel blockers (including CNS and GI tract)?

A 
Headache
Hypotension
Flushing
Peripheral edema
Worsening of sinus node dysfunction
CNS side effects: tremors, mood changes, fatigue, reflex tachycardia
GI: distress
53
Q

What are effects of Ca channel blockers on exercise and CAD?

A

Decrease myocardial oxygen demand
Improve myocardial blood supply
Enhance tolerance for activity

54
Q

What are considerations when someone is on calcium channel blockers?

A

Observe for postural hypotension
Monitor BP and cardiac rhythm changes
Potential aggravation of myocardial ischemia with these drugs secondary to hypotension and decreased coronary perfusion

55
Q

What is digitalis used to treat?

A

Treatment of CHF

Prevention of supraventricular arrhythmias especially with CHF

56
Q

How does digitalis work?

A

Increase Ca influx into myocardial cell (increased contractility)
Alter electrochemical properties of cell by effecting active transport of Na and K

57
Q

How does digitalis help the heart?

A

Increasing contractility improves oxygen delivery to all tissues

Increases renal perfusion : decreases circulating blood volume

Increasing myocardial contractility: increases Q, decreases preload, cardiac workload, and myocardial oxygen demand

Reduces clinical effects of CHF

Possess electrophysiologic effects: decrease conduction velocity through AV node, decrease ventricular response to SVT (Afib, Aflutter), alters conduction/refractory period for AV node

58
Q

What are contraindications and side effects of digitalis (cardiac glycosides)?

A

Low margin of safety (therapeutic and toxic range)
EKG changes
Toxicity can precipitate any arrhythmia
Vomiting, nausea, fatigue, drowsiness, confusion, visual disturbances

59
Q

What are effects of cardiac glycosides on exercise in people with CAD?

A

Increased exercise tolerance: increased efficiency of ventricular function and oxygen utilization

Can observe ST and T wave changes similar to ischemia in those taking digitoxin: compare resting with exercise

60
Q

What are considerations for cardiac glycosides?

A

sagging ST segment may be mistaken for ST depression in ischemia
Arrhythmias associated with cardiac glycosides may be precipitated by exercise.
Educate patients to take peripheral pulses daily and report significant brady/tachy cardia
Classic signs of toxicity are nausea, vomiting, anorexia, and visual disturbances
Maintenance doses of 0.125 to 0.25 mg AD

61
Q

What are causes of arrhythmias?

A

Electrolyte imbalance, drug toxicity, excessive nicotine or caffeine, emotional stress, hyperthyroidism

62
Q

What is an arrhythmia?

A

Condition where disturbances in pacemaker impulse formation, contraction impulse conduction, combination of the two

Results in rate and/or timing of contraction of heart muscle that is insufficient to maintain normal cardiac output

63
Q

What is most common cause of sudden death?

A

Ventricular arrhythmia.

Majority occurs in people with neither a previously known heart disease nor history of VA

64
Q

What are mechanisms of cardia arrhythmias?

A

Cardiac ischemia
Excessive discharge or sensitivity to autonomic transmitters
Exposure to toxic substances
Unknown etiology

65
Q

What are disorders of impulse formation?

A

No signal from pace maker site.
Development of ectopic pacemaker: may arise from conduction cells (capable of spontaneous activity), usually under control of SA node (if it slows down too much conduction cells could become dominant), often result of other injury (ischemia, hypoxia)

66
Q

T/F: antiarrhythmics can cause arrhythmia?

A

True

67
Q

What are class 1 anti arrhythmic?

A 
Blockers of fast Na channels
Subclass IA, IB, IC
68
Q

How does subclass 1A anti arrhythmic work?

A

Prolong repolarization

Increased duration of action potential

69
Q

What is quinidine?

A

Class 1A
1st antiarrhythmic used
Treat both atrial and ventricular arrhythmias
Increases refractory period

70
Q

What is procainamide?

A

Class 1 A

increases refractory period but side effects

71
Q

What is disopyramide?

A

Class 1 A
Extended duration of action
Used only to treat ventricular arrthymias

72
Q

How doe class 1B anti arrythmics work?

A

Weak phase 0 depression
Shortened depolarization
Increased action potential duration

73
Q

WHat are class 1 B anti arrhytmics?

A

Lidocane (also acts as local anesthetic) – blocks Na+ channels mostly in ventricular cells, also good for digitalis-associated arrhythmias
Mexiletine - oral lidocaine derivative, similar activity
Phenytoin – anticonvulsant that also works as antiarrhythmic similar to lidocane

Lidocane
Mexiletine
Phenytoin

74
Q

What do class 1C do to help arrhythmias?

A

Strong phase 0 depression
No effect of depolarization
No effect on action potential duration

75
Q

What are the types of class 1C drugs?

A

Flecainide (initially developed as a local anesthetic)
Slows conduction in all parts of heart,
Also inhibits abnormal automaticity

Propafenone
Also slows conduction
Weak β – blocker
Also some Ca2+ channel blockade

76
Q

What are actions of Class 2 antiarrhythmics?

A

Beta adrenergic blockers
2 major actions: blockade of myocardial beta adrenergic receptors, direct membrane stabilizing effects related to Na channel blockade

77
Q

What the different class 2 anti arrhythmic drugs?

A

Propranolol: causes both myocardial β–adrenergic blockade and membrane-stabilizing effects, slows SA node and ectopic pacemaking, can block arrhythmias induced by exercise or apprehension,
other β–adrenergic blockers have similar therapeutic effect
Metoprolol
Nadolol
Atenolol
Acebutolol
Stalol

78
Q

How does class 3 anti arrhythmic work?

A

Potassium channel blockers

Cause delay in repolarization and prolonged refractory period

Developed because patients negatively sensitive to Na channel blockers

79
Q

What are the types of class 3 anti arrhythmic?

A

Amiodarone – prolongs action potential by delaying K+ efflux but many other effects characteristic of other classes
Ibutilide – slows inward movement of Na+ in addition to delaying K + influx.
Bretylium – first developed to treat hypertension but found to also suppress ventricular fibrillation associated with myocardial infarction
Dofetilide - prolongs action potential by delaying K+ efflux with no other effects

80
Q

How do class 4 anti arrhythmic work?

A

Calcium channel blockers

Slow rate of AV conduction in patients with atrial fibrillation

81
Q

What are the types of class 4 anti arrhythmic drugs?

A

Verapamil: blocks Na channels in addition to Ca, also slows SA node in tachycardia
Diltiazem

82
Q

What structures detect changes in BP?

A

Carotid baroreceptors
Kidney sensors

Trigger appropriate alterations in Q and peripheral vascular resistance: maintains normotension

83
Q

Alterations in BP are regulated at what 4 sites?

A

Arterioles
Post capillary venules
Heart
Kidney: control BP by regulating intravascular volume (cardiac preload)

SNS also regulates by the renin angiotensin aldosterone system

84
Q

WHat is the problem with anti hypertensive therapy?

A

Threshold of baroreceptors and renal blood volume- pressure control is “set” too high

85
Q

T/F: classification of anti hypertensive drugs is related to primary receptor site and mode of action

A

True

86
Q

What are types of anti hypertensive drugs?

A

Diuretics
Drugs that limit SNS activity
Vasodilators
Act on renin angiotensin aldosterone system at kidney

No drugs are safe and effective in directly affecting baroreceptor activity
Some are combination of diuretic and beta blocker

87
Q

How to diuretics work?

A

Reduce circulating volume and lower BP.
Act along renal tube or Henley’s loop.
Alter reabsorption of sodium= directly affects water

88
Q

What are the diuretics that are usually prescribed?

A

Lasix (greatest effect)

Thiazides (most frequently prescribed)

89
Q

What are clinical considerations when prescribing diuretics?

A

Caution with pts taking diuretics and participating in aerobic exercise.
Volume reduction and electrolyte disturbance place pt at risk for hypotension or arrhythmias and hypokalemia

90
Q

How do drugs alter SNS activity to control BP?

A

Central NS acting to reduce neural transmission from vasopressor cetners in brainstem.

Inhibit vasoconstriction via norepi release inhibition.
Block alpha adrenoceptors in arterioles and venules.
Block beta adrenoreceptors in heart responsible for renin release:

91
Q

What happens when alpha and beta receptors gets blocked?

A

Alpha: prevents vasoconstriction, peripheral resistance reduced

Beta: limits Q and vasoconstriction

92
Q

What are factors that affect release of renin?

A

Decrease in renal artery pressure
SNS stimulation
Na reduction

93
Q

What are steps of angiotensin system?

A

Renin reacts to form angiotensin 1.

Angiotension converting enzyme turns angio 1 to angio 2

94
Q

What is function of angiotensin 2?

A

potent vasoconstrictor(?) that influences aldosterone production and sodium retention.

Results in increased BP

95
Q

What is the BP drug that affect the renin angiotension system?

A

ACE inhibitors effective at controlling BP.

Reduces formation of angiotension 2

96
Q

When is pharmacologic intervention recommended to manage lipids?

A

Recommended after 3-6 months of dietary and/or exercise interventions

Goal is to decrease LDL through diet, exercise, meds

97
Q

What do the statins do?

A

Decrease LDL by inhibiting cholesterol synthesis; increases HDL

98
Q

What does niacin do? What about fish oil>

A

Niacin: decreases LDL, triglycerides, increases HDL

Fish oil: omega 3 fatty acids, decreased triglycerides

99
Q

What is oxygen therapy used for?

A

Hypoxemia: pulmonary edema, CHF (hinder oxygen diffusion in periphery)

Conditions of reduced hemoglobin concentrations: reduces desaturation

Cardiopulmonary PT (19 decks)

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