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πŸ”΄ Cardiovascular πŸ”΄ > Pharmacology And Drug Science > Flashcards

Pharmacology And Drug Science Flashcards

1
Q

Why should the physical therapist understand the patient’s drug regimen ?

A

To look out for potential side effects and the drug influence on the outcome of the physical therapy intervention

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2
Q

Cardiovascular disorders are disorders of the heart AND _______________ .

A

Blood vessels

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3
Q

Examples of cardiovascular disorders

A

HTN
Coronary heart disease
MI
PAD
Arrhythmias
HF

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4
Q

What disorders are the number one cause of death globally ?

A

CVDs

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5
Q

What is the term?

  • persistent elevation in systemic blood pressure which is defined as a systolic greater than or equal to 140 mmHg and a diastolic reading greater than or equal to 90 mmHg (140/90)
A

Hypertension

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6
Q

Pathophysiology of hypertension
(Hint:7)

A
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7
Q

What is the RAAS and what organ does it work on?

A

Renin angiotensin aldosterone system

Kidney

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8
Q

Briefly explain how RAAS works .

A

Watch this 2 min video if you don’t know:
https://youtu.be/6EUSEa6Lw8g?si=rNEpQLVigbXyjtF-

Summary
1. Drop in blood volume/pressure (ex: dehydration)
2. Juxtaglomerular cells sense that drop and releases renin into the blood
3. Renin (enzyme) converts angiotensinogen (plasma protein produced by liver) into angiotensin 1.
4. Angiotensin 1 is converted into angiotensin 2 by the ACE enzyme
5. Angiotensin 2 (hormone) binds to angiotensin-2-receptors, stimulating :
- systemic vasoconstriction
- sodium reabsorption in kidneys (water follows)
- promotes aldosterone secretion from adrenal cortex
which leads to sodium and water retention in kidneys
- acts on hypothalamus to stimulate thrist
- acts on posterior pituitary to release ADH for water
retention in kidneys

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9
Q

Chronic activation of RAAS leads to what?

A

Hypertension

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10
Q

Angiotensinogen is produced by what organ?

A

Liver

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11
Q

Renin is produced by what organ?

A

Kidney

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12
Q

What drug groups can be used to treat HTN?

A

Diuretics
ACE-I
ARBs
Ξ² - adrenergic blockers
Calcium channel blockers (CCB)

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13
Q

What are two types of diuretics ?

A

Thiazide diuretics
Loop diuretics

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14
Q

Mechanism of action of thiazide diuretics

A
  1. Increase urinary excretion of Na+ and water BY inhibiting Na+ and Cl- re-absorption in distal renal tubes
  2. Increase urinary excretion of K+ and little bit of bicarbonate
  3. Reducing PVR by DIRECT dilation of arterioles
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15
Q

True or false

Thiazide diuretics can cause hypokalemia

A

True

Due to the increase in urinary excretion of K+

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16
Q

What can happen to urine frequency in general when taking diuretics ?

A

Increases

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17
Q

What happens when NSAIDs are taken with thiazide diuretics ?

A

NSAIDs (ex: Ibuprofen) interact to diminish the anti-hypertensive effects of thiazide diuretics.

So basically it cancels it out .

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18
Q

What can happen when taking thiazide diuretics with antiarrythmic drugs like digoxin or amiodarone ?

A

Thiazide can lead to hypokalemia, which can lead to increased toxicity of digoxin and amiodarone

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19
Q

Thiazide diuretic precaution and monitoring

A
  1. Potassium depletion may require:
    -supplementation
    -↑ dietary intake
    - potassium-sparing diuretics
  2. Hypercalcemia : Calcium levels may increase due to Ca2+ retention
  3. Hyperlipidemia must be evaluated routinely, why?
    - prevent added risk factor for CAD (increase LDL and TG)
  4. Fluid loss must be evaluated to prevent:
    - dehydration
    - postural hypotension
    - hypovolemic shock
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20
Q

Examples of thiazide diuretics

A

Hint: most ends with -thiazide

(Red is the most common ones)

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21
Q

Is atenolol a thiazide diuretic ?

A

NO

It is a Ξ²-blocker

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22
Q

What type of drug is Chlorthalidone

A

Thiazide diuretic

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23
Q

What type of drug is indapamide

A

Thiazide diuretic

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24
Q

Mechanism of action of loop diuretics

A

They act primarily on the loop of Henle to prevent Na+ re-absorption, hence they are called loop diuretics

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25
Q

what happens when we take NSAIDs with loop diuretics

A

NSAIDs diminish the effectiveness of loop diuretics

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26
Q

Precautions/monitoring with loop diuretics

A
  • hypokalemia
  • ↓ Mg2+
  • hyperuricemia
  • hypocalcemia
  • transient deafness
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27
Q

Transient deafness has been reported for which type of diuretic ?

A

Loop diuretic

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28
Q

Which type of diuretic can cause hypercalcemia ?

A

Thiazide diuretics

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29
Q

Which type of diuretic can cause hypocalcemia

A

Loop diuretics

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30
Q

What is type of drug is Tenoretic ?

A

Combination of Atenolol (Ξ² blocker) and Chlorthalidone (thiazide diuretic)

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31
Q

What type of drug is Natrilix SR ?

A

Indapamide (thiazide diuretic)

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32
Q

Examples of loop diuretics

A
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33
Q

What type of drug is Lasix

A

Furosemide (loop diuretics)

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34
Q

Levels of K+ deficiency and their symptoms

A

Mild hypokalemia: often no symptoms

Moderate hypokalemia: 2.5 - 3
- muscular weakness, myalgia, muscle cramps
- constipation

Severe hypokalemia: < 2
- flaccid paralysis
- hyporeflexia
- rhabdomyolysis
- respiratory depression from severe impairment of skeletal muscle function

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35
Q

What is hyperuricemia ?

What are the symptoms in both mild and severe cases?

A

High level of uric acid in blood

Mild cases:
-fatigue
-headaches
-dizziness
-urination problems
-fever

Severe cases:
- gout (swollen, hot, red, stiff, inflamed, and painful)

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36
Q

True or false
NSAIDs dismiss the antihypertensive effect of most of the antihypertensive drugs

A

True

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37
Q

What can be used as alternative options for NSAIDs since they diminish the antihypertensive effect of most antihypertensive drugs?

A

Local anesthetics (creams, ointments), body massage, or acetaminophen

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38
Q

What is a possible consequence that may be seen with an exercising individual that’s on high ceiling agents such as loop diuretics?

A

Hypotension due to volume depletion
Or
Arrhythmia due to electrolyte disturbances

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39
Q

High ceiling VS low ceiling agents ?

Which diuretic type belongs to which agent group?

A

Low ceiling - less effective
Ex: thiazide diuretics

High ceiling - more effective
Ex: loop diuretics

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40
Q

What type of diuretics is best for CHRONIC HTN and which type is best for Heart failure or ascites?

A

Low ceiling - chronic HTN

High ceiling - heart failure, ascites

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41
Q

Transient deafness has been reported with the use of which type of diuretic ?

What drug interaction can result in this?

A

Loop diuretics

ESPECIALLY if patient is on ototoxic drugs
- aminoglycoside antibiotic gentamicin
- chemotherapeutic agent cisplatin

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42
Q

What is the mechanism of action of ACE inhibitors ?

A
  1. Inhibit conversion of Ag1 to Ag2
  2. Indirectly inhibit fluid volume increases by inhibiting Ag2-stimulated release of aldosterone

(so basically inhibiting aldosterone release INDIRECTLY because it DIRECTLY inhibits the formation of Ag2)

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43
Q

Significant interactions with ACE-I

A

NSAIDs diminish the ant-hypertensive effects of ACE-I

K+ sparing diuretics significantly enhance serum K+ levels when used with ACE-I (so serum K+ levels must be monitored)

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44
Q

What symptom can be seen when ACE-I is discontinued ?

A

Dry cough occurs and disappears with few days after discontinuing ACE-I

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45
Q

Precautions and monitoring of K+ is needed with ACE-I . Why?

A

Can cause HYPERkalemia especially in patients with chronic kidney disease or diabetes

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46
Q

Examples of ACE-I

A

Hint: ends with -pril

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47
Q

Lisinopril is what type of drug?

A

ACE-I

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48
Q

Captopril is what type of drug ?

A

ACE-I

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49
Q

What is the mechanism of action for ARBs

A

They block Ag2 receptor subtype 1 receptor that mediates the effects of Ag2

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50
Q

What is the function of Ag2 ?

A

(Hint: 5)

  1. Vasoconstriction
  2. Aldosterone release
  3. Sympathetic activation
  4. Anti-diuretic hormone (ADH) release
  5. Constriction of efferent arterioles of the glomerulus
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51
Q

True or false
Hypokalemia may occur with ARBs use

A

False

Hyperkalemia (similar to ACE-I)

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52
Q

True or false
Cough can occur with ARBs use

A

False

Only with ACE-I

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53
Q

True or false
Both ACE-I and ARBs is contraindicated in pregnancy

A

True

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54
Q

Examples of ARBS

A

Hint: ends with - sartan

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55
Q

What type of drug is Valsartan?

A

ARBs

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56
Q

What type of drug is Losartan ?

A

ARBs

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57
Q

What problems can occur with ARBs use?

A

Hyperkalemia causing :
- if mild: malaise, muscle weakness
- if severe: arrhythmias or death

Dry cough

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58
Q

True or false
All Ξ²-blockers are the same

A

False

There are important pharmodynamic/kinetic differences , however they all lower BP

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59
Q

Due to the different pharmacodynamic properties, Ξ² blockers are split into two groups:
selective agents (cardioselectivity) VS non-selective agents

Provide examples for both.

A

Cardio-selective agents (MAAB):
- Metoprolol
- Atenolol
- Betaxolol
- Bisoprolol

Non-selective agents (PNT):
- propranolol
- nadolol
- timolol

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60
Q

Mechanism of action for cardioselective Ξ² blockers

A

Dismiss cardiac output by reducing HR and contractility thus reducing BP

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61
Q

What happens with Ξ²1 receptor stimulation , and where are these receptors found

A
  • Increase HR
  • Increase contractility
  • Renin release

Receptors found in HEART and KIDNEY

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62
Q

What happens with Ξ²2 receptor stimulation and where are these receptors found

A
  • bronchodilation
  • vasodilation
  • insulin secretion

Receptors found in LIVER, LUNG, PANCREAS, and ARTERIOLE SMOOTH MUSCLE

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63
Q

What can NON-selective Ξ² blockers cause ?

A

BRONCHOCONSTRICTION

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64
Q

What can a and Ξ² blocking activity cause ?

A

BRONCHOCONSTRICTION

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65
Q

What type of drug is Atenolol ?

A

Cardio-selective Ξ² blocker

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66
Q

What type of drug is propranolol

A

Non-selective Ξ² blocker

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67
Q

What type of drug is Metoprolol

A

Cardio-selective Ξ² blockers

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68
Q

Labetalol and Carvedilol are what type of drugs

A

a and Ξ² blockers

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69
Q

What should be monitored when taking Ξ² blockers

A
  1. Cardiac decompensation ( ↓ cardiac output)
    (Especially with cardio-selective agents )
  2. Routine ECG because they can reduce electrical conduction within heart
  3. they may MASK the symptom of hypoglycemia
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70
Q

which drug type can mask the symptoms of hypoglycemia ?

A

Ξ² blockers

You wont be able to see tremor or palpitations related to hypoglycemia, only the sweating is apparent

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71
Q

What are some drug interactions to look out for when using Ξ² blockers

A

Verapamil/Diltiazem - HF, severe bradycardia, heart block

Sympathomimetics (oral decongestants) - decrease anti-hypertensive effects

NSAIDs - decrease anti-hypertensive effects

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72
Q

Mechanism of action of calcium channel blockers, CCB

A

Inhibit the influx of calcium through slow channels in vascular smooth muscle cells and cause relaxation

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73
Q

There are two types of calcium channel blockers CCB

A
  1. Non-dihydropyridine derivatives (cardioselective)
  2. Dihydropyridine derivatives (only a little cardioselective)
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74
Q

What type of drugs are Diltiazem and Verapamil ?
What do they do?
What are their adverse side effects?

A

non-dihydropyridine derivatives calcium channel blockers CCB

  • they ↓ HR and contractility = ↓ BP
  • they slow AV conduction and are used to treat supraventricular tachyarrythmia or atrial fibrillation

Adverse effect:
- bradycardia
- AV block

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75
Q

What is the difference between cardioselective beta blockers and nonselective beta blockers?

A

Nonselective beta blockers can cause bronchoconstriction !

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76
Q

What is the difference between non-dihydropyridine and dihydropyridine calcium channel blockers?

A

Dihydropyridine derivatives can ↑ vasodilatation

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77
Q

Examples of dihydropyridine calcium channel blockers

What do they do?

A

Hint: ends with -dipine

  • greater effect on smooth muscle cells > heart (that’s why it causes vasodilatation)

-Does not alter conduction through AV node (not effective in patients with supraventricular tachyarrhythmia; atrial fibrillation)

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78
Q

True or false
Dihydropyridine derivatives can effectively treat supraventricular arrhythmias or atrial fibrillation

A

False

Non-dihydropyridine derivatives are antiarrhythmic

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79
Q

What is a drug interaction to look out for with calcium channel blockers? And why?

A
  • Grapefruit juice
    (may enhance the effect of CCBs as it delays the breakdown of this medication by the liver enzyme CYP450, leading to toxicity)
  • Decongestants and NSAIDs
    (Diminish antihypertensive effects)
80
Q

What type of drug is verapamil?

A

Non-dihydropyridine CCB

81
Q

What type of drug is diltiazem?

A

Non-dihydropyridine CCB

82
Q

What type of drug is nifedipine?

A

Dihydropyridine CCB

83
Q

What is the general side effect for calcium channel blockers?

A

Bradycardia, which can cause severe symptoms, such as:

  • fainting (syncope)
  • Dizziness
  • Weakness
  • Fatigue
  • Shortness of breath
  • Chest pains
  • Confusion or memory problems
84
Q

What occurs as a side effect of dihydropyridine derivatives CCB specifically?

A

Flushing

  • Which is temporary red dating of the skin, usually the face, and sometimes accompanied by neck or chest .
  • itchy skin, feeling of warmth and sweating
85
Q

True or false

If a patient on beta blocker begins to complain of dyspnea, ankle or extremity edema, orthopnea or other signs of heart failure, the PT must avoid any exercise until the patient’s case is stabilized.

A

True

Also , exercise should begin SLOWLY and patient’s tolerance should be assessed on an ongoing basis

86
Q

When a blood vessel is injured, what physiological mechanisms occur in order to maintain homeostasis?

List them in the correct order

A
  1. Vasoconstriction
  2. Formation of platelet plug (weak and unstable)
  3. Production of a web of fibrin proteins that penetrates and surrounds the platelet plug (strong and stable)
87
Q

What are the two categories of drugs used in coagulation disorders

A

Antiplatelet agents

Antithrombotic agents (anticoagulants)

88
Q

Examples of antiplatelet agents

A
  1. Thromboxane inhibitors
  2. ADP receptor antagonist
  3. Glycoprotein 2b/3a receptor antagonist
89
Q

Examples of antithrombotic agents (anticoagulants)

A
  1. Antithrombins
  2. Factor Xa inhibitors
  3. Direct thrombin inhibitors.
  4. Fibrinolytic agents.
90
Q

Example of thromboxane inhibitors

A

Aspirin (Acetylsalicylic Acid)

91
Q

Aspirin mechanism of action

A
  1. Blocks production of TXA2 by inhibiting cyclooxygenase1 COX1 = reducing :
    - platelet aggregation
    - vasoconstriction mediated by thromboxane
  2. Anti-inflammatory effects due to weak inhibition of COX2 , which produces prostaglandins contributing to inflammatory response
92
Q

True or false
Thromboxane A2 is derived from arachidonic acid

A

True

93
Q

True or false

Aspirin is a strong inhibitor of COX2

A

False

It’s a weak inhibitor hence its anti-inflammatory effect

NSAIDs are the strong inhibitors of COX2

94
Q

What is the adverse effects of aspirin?

A

Gastric irritation with dyspepsia, nausea, ulcerations

95
Q

What Drug interactions should we look out for when using aspirin and why?

A

Warfarin or NSAIDs (↑ risk of bleeding)

Antacids ( ↓ efficacy of aspirin because it alters the pH of the stomach thus altering its absorption)

96
Q

True or false
Low pH is needed to absorb aspirin

A

True

97
Q

What type of drug is aspirin?

A

Thromboxane inhibitor (antiplatelet agent)

98
Q

Example of ADP receptor antagonist

A

Thienopyridines:
- Clopidogrel
- Ticlodipine

99
Q

What type of drug is clopidogrel?

A

ADP receptor antagonist (antiplatelet agent)

100
Q

True or false

Ticlodipine is a calcium channel blocker

A

False

ADP receptor antagonist (antiplatelet agent)

101
Q

ADP receptor antagonists mechanism of action

A

Direct and irreversible inhibition of the P2Y12 receptor for the platelets lifespan, reducing their activation and aggregation

102
Q

Adverse effects of clopidogrel

A

G.I. adverse effects (similar to aspirin)

↑ risk of bleeding when used with other anti-platelet agents (aspirin, NSAIDS) or anticoagulants (warfarin)

103
Q

What drug is Plavix?

A

Clopidogrel (antiplatelet/ ADP receptor antagonist)

104
Q

Unfractionated heparin UFH

  • molecular weight
  • route of administration
  • Mechanism of action
  • Bioavailability
  • half life
  • Dose adjustments
  • Anticoagulant effects
A
  • molecular weight: 3000 to 30,000 (BIG size)
  • route : Intravenous
  • MOA: by accelerating action of antithrombin , it inactivates thrombin, factor 9a, and factor 10a, preventing the production of the fibrin from Fibrinogen AND inhibits Platelet activation by thrombin and vWF
  • bioavailability: less than LMWHs
  • half life: 30 to 60 minutes (less than LMWHs)
  • Dose adjustments: frequent
  • Anticoagulant effects: Factor 10a = 2a
105
Q

Low molecular weight heparin (LMWHs)

  • molecular weight
  • route of administration
  • Mechanism of action
  • Bioavailability
  • half life
  • Dose adjustments
  • Anticoagulant effects
A
  • Molecular weight: 4000-6500 (SMALL size; 1/3 of UFH’s mwt)
  • Route: subcutaneous
  • MOA: accelerates action of antithrombin just like UFH but has less effect on platelet aggregation
  • Bioavailability: more than UFH
  • half life: 120 to 180 minutes (more than UFH)
  • dose adjustment: fixed, weight adjusted
  • Anticoagulant effect: Factor 10a&raquo_space; 2a
106
Q

Which one has more effect on platelet aggregation?
LMWH or UFH?

A

UFH

107
Q

Which one has more effect on factor 10A&raquo_space; 2a?
LMWH or UFH ?

A

LMWH

108
Q

Mechanism of action of warfarin

A

Induces a functional deficiency of vitamin K, preventing the carboxylation of glutamic acid needed for the clotting factors 2, 7, 9, 10

109
Q

What is the major side effect of warfarin?

A

Bleeding

110
Q

What anticoagulant is a teratogenic agent that produces a condition called chondrodysplasia punctata ?

A

Warfarin

111
Q

Warfarin is a teratogenic agent that produces the condition called _________?

A

chondrodysplasia punctata

112
Q

True or false
Care must be taken to avoid situation of soft tissue injury, or potential tissue trauma such as Venipuncture, manual shaving, and resistive exercises when it comes to warfarin use

A

True

113
Q

is there a chance for gastric ulcerations to occur with warfarin use?

A

Yes, especially with aspirin therapy

114
Q

What is the leading cause of death globally, and the most common cause of CAD, PVD, and cerebrovascular disease?

A

Atherosclerosis

115
Q

______________ is a modifiable risk factor for atherosclerosis

A

Dyslipidemia

116
Q

What is dyslipidemia?

A
  1. Elevated blood levels of lipoproteins (cholesterol, triglycerides, phospholipids)
  2. Lipoprotein abnormalities, which include one or more of the following:
    - Elevated total cholesterol TC
    - Elevated low density lipoprotein LDL
    - Elevated triglycerides TG
    - Reduced high density lipoprotein HDL
117
Q

Pathophysiology of atherosclerosis

(Read and understand, its easy)

Key words: MCP-1 and CCR-2)

A

LDLs usually diffuse passively through the endothelial cells to be used in normal cell processes

However if there is damage to the endothelial cells of the arterial wall (which can occur for many reasons like HTN, smoking, hyperglycemia, hypercholesterolemia), this can increase the permeability of the arterial wall, allowing LDLs to enter the tunica intima.

LDL entering the tunica intima isn’t the problem. The problem starts when these LDLs undergo oxidation. That’s why some patients are given anti-oxidants to prevent this step from happening.

This is where the immune system kicks in. But in order for the immune cells to go to the exact place where oxidized LDLs are accumulating, it needs directions. Chemokines/cytokines such as MCP-1 , CCR-2 guide the monocyte in the blood to enter the endothelial tissue to become a macrophage and take it to the oxidized LDLs. Some medications given to these patients work by reducing MCP-1 and CCR-2 action . After that, the macrophage β€œeats” the oxidized LDLs through phagocytosis but they dont have the enzymes to degrade lipids!
ΩŠΨΉΩ†ΩŠ ΨͺΨ§ΩƒΩ„Ω‡Ψ§ وΨͺΨΊΨ΅ ΩΩŠΩ‡Ψ§
فΨͺΨ΅Ψ¨Ψ­ foamy cell
ΩˆΩ…ΨΉ Ψ§Ω„ΩˆΩ‚Ψͺ يءير ΨΉΩ†Ψ―Ω†Ψ§ foamy cell ΨΉΩ„Ω‰ foamy cell
And it all deposits on the inner layer of the artery , with more deposition of cytokines and cellular debris, we get necrosis. That necrotic bulge (gruel) is what clogs the artery

118
Q

How long does it take for atherosclerosis to occlude an artery?

A

30 to 50 years

119
Q

How long does it take for acute coronary syndrome to occlude an artery?

A

Two weeks

120
Q

What are the two main drug categories to treat a patient with atherosclerosis or hyperlipidemia?

A

Statins
Fibrates

121
Q

What type of drug is 3-hydroxy-3-MethylGlutaryl (HMG) CoA reductase inhibitor ?

And what is the mechanism of action?

A

Statin

Reversibly binds to HMG CoA reductase in the liver and inhibits the conversion of HMG CoA β†’ Mevalonate (mevalonic acid), which is the rate limiting step in cholesterol biosynthesis.

122
Q

What are some pleiotropic effects of statins

A
123
Q

Statins are contraindicated in what cases?

A

Pregnancy and lactation

124
Q

Adverse effects of statins

A

Effects can be seen with Liver failure or Rhabdomyolysis - high serum creatinine due to skeletal muscle damage can cause kidney failure

Liver and muscle dysfunction may also occur

125
Q

Examples of statins

A

Hint: ends with -statin

Atrovastatan
Simvastatin
Pravastatin

126
Q

Examples of fibrates

A

Hint: most end with - fibrate
(Except gemfibrozil)

  1. Clofibrate
  2. Gemfibrozil
  3. Bezafibrate
  4. Ciprofibrate
  5. Fenofibrate
127
Q

True or false
Fibrates are anti-inflammatory

A

False

128
Q

Fibrates mechanism of action

A

Acts as agonist of PPARa on hepatocytes leading to change on the gene expression involved in lipoprotein metabolism

129
Q

Side effects of fibrates

A

Myopathy
Elevated liver transaminases
Cholelithiasis
Pancreatitis

130
Q

What type of drug is gemfibrozil?

A

Fibrates

131
Q

True or false

Fibrates are used for ↑ triglycerides and especially for diabetes

A

True

132
Q

Adverse effects of fibrates

A

Rhabdomyolysis in severe cases
- Muscle pain
- Tenderness
- Weakness and swelling of affected muscles

Compartment syndrome - compression of surrounding tissues

133
Q

True or false

It’s safe to take Fibrates while having grapefruit

A

False

134
Q

Which of the following medication can be used for therapeutic management of CHD?

CCB
ARB
ACE-I
Ξ² blockers
Vasodilators
Anticoagulant
Statin/fibrates

A

All of them

135
Q

What drugs can be used to reduce oxygen demands?

A

A. Drugs that ↓ HR and contractility
- beta blockers
- CCB

B. Drugs that ↓ afterload
- CCB
- ACE-I

C. Drug that ↓ preload
- Nitrates (vasodilators)

136
Q

How to maintain or increase oxygen supply

A

Antiplatelet agents

Nitrates

Supplemental oxygen

Revascularization (PCI , CABG)

137
Q

What is the aim of treatment for chronic stable angina

A

↑ myocardial O2 supply

↓ myocardial O2 demand

Treat factors that exacerbate ischemia (HTN, DM, Anemia)

138
Q

Managing chronic stable, angina involves following the
ABCDE approach. Explain what that is.

A
139
Q

What is an alternative if aspirin is contraindicated?

A

Clopidogrel

140
Q

True or false

ACE-I have anti-inflammatory, antithrombotic, anti-proliferative, and antioxidant properties

A

True

141
Q

Most stable angina patients will be on _____________.

A

Statins

142
Q

What do nitrates do?

A

Decrease preload (dilate veins)

Decrease afterload (dilate arteries

Promote coronary artery blood flow

143
Q

Mechanism of action for nitrates

A

Releases nitric oxide NO, which enhances cGMP-production leading to reduction in cytosolic calcium

144
Q

What are the three main nitrates used?

A

Glycerol trinitrate
Isosorbide mononitrate
Isosorbide dinitrate

145
Q

True or false

Nitrates can be administered in several ways

A

True

(IV infusion, conventional or slow release tablets, transdermal patches and ointments, sublingual , sprays, adhesive buccal tablets)

146
Q

Side effects of nitrates

A

Headache
Flushing
Hypotension

147
Q

Can the patient exercise right away after taking sublingual GTN?

A

No, and the patient blood pressure and heart rate should be reevaluated before making a decision to continue treatment

148
Q

Not a question

But these are a few things you should know about nitrate.

A

Nitrate tolerance - continuous administration of nitrates for a long time leads to the loss of its effects on the patient ; higher risk of mortality

GTN should be kept in a dark container

Volatile

Burning sensation when taking the tablet

149
Q

_____________ are useful in preventing angina in exercise because they suppress the rise in blood pressure and resting heart rate

A

Beta blockers

150
Q

True or false
CCB are arterial vasodilators, and have some antiarrhythmic properties

A

True

151
Q

__________ is defined as a progressive clinical syndrome that can result from any disorder that impairs the ability of the ventricle to fill with, and or eject blood, thus rendering the heart unable to pump blood at a rate sufficient to meet the metabolic demands of the body.

A

Heart failure

152
Q

True or false
Diseases that adversely affect ventricular diastole (filling), ventricular systole (contraction), or both can lead to heart failure

A

True

153
Q

In the majority of patients, what two conditions contribute significantly to the development of heart failure?

A

Ischemic heart disease (CAD)
HTN

154
Q

True or false
HF is a largely preventable disorder

A

True

155
Q

Normal stroke volume is around what

A

70 mL

156
Q

The filled ventricles has a normal volume of what

A

130 mL

157
Q

The ejection fraction is over _____ %

A

50%

158
Q

In LVSD, the ejection fraction is reduced to blow _______, and symptoms usually occur when it’s below __________.

A

45 %
35 %

159
Q

Around what percent of ejection fraction is warfarin needed and why

A

When the ejection fraction falls below 10%

Patient will have an added risk of thrombus formation within the ventricle ; therefore warfarin is needed

160
Q

Pathophysiology of heart failure

A

Reduce heart ability to relax or contract, leading to reduce pumping ability

161
Q

What are some compensatory responses if the heart is unable to pump enough blood?

A

Tachycardia and ↑ contractility

Fluid retention and ↑ preload

Vasoconstriction and ↑ afterload

Ventricular hypertrophy and remodeling

162
Q

How does failure of the compensatory responses lead to heart failure

A
163
Q

Read and understand the summary of therapeutic targets of HF

A
164
Q

Mechanism of action of digoxin

A
  1. Inhibits sodium/potassium ATPase which will:
    - ↑ intracellular Na-Ca exchange β†’ ↑ intracellular calcium and therefore = ↑ contractility (positive inotropic effect)
  2. Suppresses AV nodal conduction, and vagal stimulation (therefore is used for atrial fibrillation)
165
Q

True or false

Digoxin can be used for atrial fibrillation

A

True

166
Q

True or false
Digoxin has a negative inotropic effect

A

False

Positive inotropic effect

167
Q

True or false

Digoxin is commonly used for heart failure

A

True

168
Q

Inotropes:

  • examples
  • When do hospitals usually use them?
A

Dopamine
Dobutamine

Acute heart failure

169
Q

Symptoms of digoxin toxicity

A

Hypersalivation
Fatigue
Nausea, vomiting
Changes in heart rate and rhythm
Visual disturbances (yellow/green halos around objects)
Confusion and dizziness

170
Q

What makes digoxin dangerous?

A

It has a low therapeutic index

171
Q

Symptoms of inotropes

A

Headache
Increased heart rate
Shortness of breath
High blood pressure
fainting and dizziness
Mild leg cramps
Tingling sensation

172
Q

____________ is a chronic inflammatory disorder of the airways .

A

Asthma

173
Q

What cells play a big role when it comes to asthma

A

Mast cells
Eosinophils
T-lymphocytes
Macrophages
Neutrophils
Epithelial cells

174
Q

Symptoms during asthmatic episodes

A

Wheezing
Breathlessness
chest tightness
Coughing

175
Q

True or false

The inflammation that occurs with asthma is also associated with existing bronchial hyperresponsiveness BHR to a variety of stimuli; i,e chemicals, allergens, drugs, cold air, exercise, etc.

A

True

176
Q

Pathophysiology of asthma include

A

Inflammatory cells infiltrate
Narrowed lumen
Mucous plugging
Hypertrophy of basement membrane

177
Q

Treatment of asthma includes what medications

A

Ξ²2 agonists

Xanthine drugs (theophylline)

H1 receptor antagonists

178
Q

Mechanism of action for Ξ²2 agonists used for asthma

A
  • Induces Bronchodilation
  • Inhibits mediator, release from muscles and monocytes (TNFa)
  • Increases mucous clearance by the action on cilia
179
Q

Difference between short acting and long, acting inhaled Ξ²2 agonists + examples

A

Short acting inhaled Ξ²2 agonists:
- Most effective/ quick action for ACUTE SEVERE ASTHMA
- Response occurs within 30 minutes of drug administration
Examples: salbutamol, terbutaline

Long acting inhaled Ξ²2 agonists:
- given twice daily as adjuvant therapy in patients whose οΏΌasthma is inadequately controlled by steroids
Ex: salmeterol , formoterol

180
Q

Side effects of Ξ²2 agonists

A

Tremor
Tachycardia
Hypokalemia
Arrhythmia

181
Q

Is this drug a short acting or long acting Ξ²2 agonist?

Salbutamol

A

Short acting

182
Q

Is this drug a short acting or long acting Ξ²2 agonist?

Salmeterol

A

Long-acting

183
Q

Is this drug a short acting or long acting Ξ²2 agonist?

Terbutaline

A

Short acting

184
Q

Is this drug a short acting or long acting Ξ²2 agonist?

Formoterol

A

Long acting

185
Q

Mechanism of action of Xanthine drugs (theophylline) used for asthma

A

Inhibit phosphodiesterase PDE iso-enzymes β†’ increases cAMP/cGMP levels and bronchodilation

186
Q

Theophylline is what type of drug?

A

Xanthine drugs for asthma

187
Q

True or false

Xanthine drugs have a narrow therapeutic index, so overdose can easily happen if not careful

A

True

188
Q

Side effects of Xanthine drugs

A

Arrhythmia
Seizures

189
Q

What are H1 receptor antagonists

A

Antihistamines that are not commonly used to treat asthma, but are used to control acute phase of allergic or exercise-induced asthma

190
Q

side effects of H1 receptor antagonists

A

First generation are non selective so they can cause:
- sedation
- Dizziness
- Blurred vision
- Tremors
Examples: diphenhydramine, chlorpheniramine, cyclizine

2nd and 3rd generation are selective so they are NON-sedative

191
Q

What type of drug is diphenhydramine?

A

H1 receptor antagonist

192
Q

What type of drug is chlorpheniramine?

A

H1 receptor antagonists

193
Q

What type of drug is cyclizine?

A

H1 receptor antagonist

194
Q

True or false
Short/long acting Ξ²2 agonists can cause tremors and hypokalemia (muscle pain)

A

True

195
Q

True or false

Theophylline can cause seizure attacks at high doses

A

True

196
Q

True or false

All FIRST generation H1 blockers can cause dizziness, blurred vision, and tremors

A

True

197
Q

Just read

A

Done

πŸ”΄ Cardiovascular πŸ”΄ (2 decks)

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