Pharmacology And Drug Science Flashcards

(197 cards)

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
β - 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 β-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
what happens when we take NSAIDs with loop diuretics
NSAIDs diminish the effectiveness of loop diuretics
26
Precautions/monitoring with loop diuretics
- hypokalemia - ↓ Mg2+ - hyperuricemia - hypocalcemia - transient deafness
27
Transient deafness has been reported for which type of diuretic ?
Loop diuretic
28
Which type of diuretic can cause hypercalcemia ?
Thiazide diuretics
29
Which type of diuretic can cause hypocalcemia
Loop diuretics
30
What is type of drug is Tenoretic ?
Combination of Atenolol (β blocker) and Chlorthalidone (thiazide diuretic)
31
What type of drug is Natrilix SR ?
Indapamide (thiazide diuretic)
32
Examples of loop diuretics
33
What type of drug is Lasix
Furosemide (loop diuretics)
34
Levels of K+ deficiency and their symptoms
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
35
What is hyperuricemia ? What are the symptoms in both mild and severe cases?
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)
36
True or false NSAIDs dismiss the antihypertensive effect of most of the antihypertensive drugs
True
37
What can be used as alternative options for NSAIDs since they diminish the antihypertensive effect of most antihypertensive drugs?
Local anesthetics (creams, ointments), body massage, or acetaminophen
38
What is a possible consequence that may be seen with an exercising individual that’s on high ceiling agents such as loop diuretics?
Hypotension due to volume depletion Or Arrhythmia due to electrolyte disturbances
39
High ceiling VS low ceiling agents ? Which diuretic type belongs to which agent group?
Low ceiling - less effective Ex: thiazide diuretics High ceiling - more effective Ex: loop diuretics
40
What type of diuretics is best for CHRONIC HTN and which type is best for Heart failure or ascites?
Low ceiling - chronic HTN High ceiling - heart failure, ascites
41
Transient deafness has been reported with the use of which type of diuretic ? What drug interaction can result in this?
Loop diuretics ESPECIALLY if patient is on ototoxic drugs - aminoglycoside antibiotic gentamicin - chemotherapeutic agent cisplatin
42
What is the mechanism of action of ACE inhibitors ?
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)
43
Significant interactions with ACE-I
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)
44
What symptom can be seen when ACE-I is discontinued ?
Dry cough occurs and disappears with few days after discontinuing ACE-I
45
Precautions and monitoring of K+ is needed with ACE-I . Why?
Can cause HYPERkalemia especially in patients with chronic kidney disease or diabetes
46
Examples of ACE-I
Hint: ends with -pril
47
Lisinopril is what type of drug?
ACE-I
48
Captopril is what type of drug ?
ACE-I
49
What is the mechanism of action for ARBs
They block Ag2 receptor subtype 1 receptor that mediates the effects of Ag2
50
What is the function of Ag2 ?
(Hint: 5) 1. Vasoconstriction 2. Aldosterone release 3. Sympathetic activation 4. Anti-diuretic hormone (ADH) release 5. Constriction of efferent arterioles of the glomerulus
51
True or false Hypokalemia may occur with ARBs use
False Hyperkalemia (similar to ACE-I)
52
True or false Cough can occur with ARBs use
False Only with ACE-I
53
True or false Both ACE-I and ARBs is contraindicated in pregnancy
True
54
Examples of ARBS
Hint: ends with - sartan
55
What type of drug is Valsartan?
ARBs
56
What type of drug is Losartan ?
ARBs
57
What problems can occur with ARBs use?
Hyperkalemia causing : - if mild: malaise, muscle weakness - if severe: arrhythmias or death Dry cough
58
True or false All β-blockers are the same
False There are important pharmodynamic/kinetic differences , however they all lower BP
59
Due to the different pharmacodynamic properties, β blockers are split into two groups: selective agents (cardioselectivity) VS non-selective agents Provide examples for both.
Cardio-selective agents (MAAB): - Metoprolol - Atenolol - Betaxolol - Bisoprolol Non-selective agents (PNT): - propranolol - nadolol - timolol
60
Mechanism of action for cardioselective β blockers
Dismiss cardiac output by reducing HR and contractility thus reducing BP
61
What happens with β1 receptor stimulation , and where are these receptors found
- Increase HR - Increase contractility - Renin release Receptors found in HEART and KIDNEY
62
What happens with β2 receptor stimulation and where are these receptors found
- bronchodilation - vasodilation - insulin secretion Receptors found in LIVER, LUNG, PANCREAS, and ARTERIOLE SMOOTH MUSCLE
63
What can NON-selective β blockers cause ?
BRONCHOCONSTRICTION
64
What can a and β blocking activity cause ?
BRONCHOCONSTRICTION
65
What type of drug is Atenolol ?
Cardio-selective β blocker
66
What type of drug is propranolol
Non-selective β blocker
67
What type of drug is Metoprolol
Cardio-selective β blockers
68
Labetalol and Carvedilol are what type of drugs
a and β blockers
69
What should be monitored when taking β blockers
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
70
which drug type can mask the symptoms of hypoglycemia ?
β blockers You wont be able to see tremor or palpitations related to hypoglycemia, only the sweating is apparent
71
What are some drug interactions to look out for when using β blockers
Verapamil/Diltiazem - HF, severe bradycardia, heart block Sympathomimetics (oral decongestants) - decrease anti-hypertensive effects NSAIDs - decrease anti-hypertensive effects
72
Mechanism of action of calcium channel blockers, CCB
Inhibit the influx of calcium through slow channels in vascular smooth muscle cells and cause relaxation
73
There are two types of calcium channel blockers CCB
1. Non-dihydropyridine derivatives (cardioselective) 2. Dihydropyridine derivatives (only a little cardioselective)
74
What type of drugs are Diltiazem and Verapamil ? What do they do? What are their adverse side effects?
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
75
What is the difference between cardioselective beta blockers and nonselective beta blockers?
Nonselective beta blockers can cause bronchoconstriction !
76
What is the difference between non-dihydropyridine and dihydropyridine calcium channel blockers?
Dihydropyridine derivatives can ↑ vasodilatation
77
Examples of dihydropyridine calcium channel blockers What do they do?
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)
78
True or false Dihydropyridine derivatives can effectively treat supraventricular arrhythmias or atrial fibrillation
False Non-dihydropyridine derivatives are antiarrhythmic
79
What is a drug interaction to look out for with calcium channel blockers? And why?
- 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
What type of drug is verapamil?
Non-dihydropyridine CCB
81
What type of drug is diltiazem?
Non-dihydropyridine CCB
82
What type of drug is nifedipine?
Dihydropyridine CCB
83
What is the general side effect for calcium channel blockers?
Bradycardia, which can cause severe symptoms, such as: - fainting (syncope) - Dizziness - Weakness - Fatigue - Shortness of breath - Chest pains - Confusion or memory problems
84
What occurs as a side effect of dihydropyridine derivatives CCB specifically?
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
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.
True Also , exercise should begin SLOWLY and patient’s tolerance should be assessed on an ongoing basis
86
When a blood vessel is injured, what physiological mechanisms occur in order to maintain homeostasis? List them in the correct order
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
What are the two categories of drugs used in coagulation disorders
Antiplatelet agents Antithrombotic agents (anticoagulants)
88
Examples of antiplatelet agents
1. Thromboxane inhibitors 2. ADP receptor antagonist 3. Glycoprotein 2b/3a receptor antagonist
89
Examples of antithrombotic agents (anticoagulants)
1. Antithrombins 2. Factor Xa inhibitors 3. Direct thrombin inhibitors. 4. Fibrinolytic agents.
90
Example of thromboxane inhibitors
Aspirin (Acetylsalicylic Acid)
91
Aspirin mechanism of action
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
True or false Thromboxane A2 is derived from arachidonic acid
True
93
True or false Aspirin is a strong inhibitor of COX2
False It’s a weak inhibitor hence its anti-inflammatory effect NSAIDs are the strong inhibitors of COX2
94
What is the adverse effects of aspirin?
Gastric irritation with dyspepsia, nausea, ulcerations
95
What Drug interactions should we look out for when using aspirin and why?
Warfarin or NSAIDs (↑ risk of bleeding) Antacids ( ↓ efficacy of aspirin because it alters the pH of the stomach thus altering its absorption)
96
True or false Low pH is needed to absorb aspirin
True
97
What type of drug is aspirin?
Thromboxane inhibitor (antiplatelet agent)
98
Example of ADP receptor antagonist
Thienopyridines: - Clopidogrel - Ticlodipine
99
What type of drug is clopidogrel?
ADP receptor antagonist (antiplatelet agent)
100
True or false Ticlodipine is a calcium channel blocker
False ADP receptor antagonist (antiplatelet agent)
101
ADP receptor antagonists mechanism of action
Direct and irreversible inhibition of the P2Y12 receptor for the platelets lifespan, reducing their activation and aggregation
102
Adverse effects of clopidogrel
G.I. adverse effects (similar to aspirin) ↑ risk of bleeding when used with other anti-platelet agents (aspirin, NSAIDS) or anticoagulants (warfarin)
103
What drug is Plavix?
Clopidogrel (antiplatelet/ ADP receptor antagonist)
104
Unfractionated heparin UFH - molecular weight - route of administration - Mechanism of action - Bioavailability - half life - Dose adjustments - Anticoagulant effects
- 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
Low molecular weight heparin (LMWHs) - molecular weight - route of administration - Mechanism of action - Bioavailability - half life - Dose adjustments - Anticoagulant effects
- 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 >> 2a
106
Which one has more effect on platelet aggregation? LMWH or UFH?
UFH
107
Which one has more effect on factor 10A >> 2a? LMWH or UFH ?
LMWH
108
Mechanism of action of warfarin
Induces a functional deficiency of vitamin K, preventing the carboxylation of glutamic acid needed for the clotting factors 2, 7, 9, 10
109
What is the major side effect of warfarin?
Bleeding
110
What anticoagulant is a teratogenic agent that produces a condition called chondrodysplasia punctata ?
Warfarin
111
Warfarin is a teratogenic agent that produces the condition called _________?
chondrodysplasia punctata
112
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
True
113
is there a chance for gastric ulcerations to occur with warfarin use?
Yes, especially with aspirin therapy
114
What is the leading cause of death globally, and the most common cause of CAD, PVD, and cerebrovascular disease?
Atherosclerosis
115
______________ is a modifiable risk factor for atherosclerosis
Dyslipidemia
116
What is dyslipidemia?
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
Pathophysiology of atherosclerosis (Read and understand, its easy) Key words: MCP-1 and CCR-2)
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 “eats” the oxidized LDLs through phagocytosis but they dont have the enzymes to degrade lipids! يعني تاكلها وتغص فيها فتصبح foamy cell ومع الوقت يصير عندنا foamy cell على 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
How long does it take for atherosclerosis to occlude an artery?
30 to 50 years
119
How long does it take for acute coronary syndrome to occlude an artery?
Two weeks
120
What are the two main drug categories to treat a patient with atherosclerosis or hyperlipidemia?
Statins Fibrates
121
What type of drug is 3-hydroxy-3-MethylGlutaryl (HMG) CoA reductase inhibitor ? And what is the mechanism of action?
Statin Reversibly binds to HMG CoA reductase in the liver and inhibits the conversion of HMG CoA → Mevalonate (mevalonic acid), which is the rate limiting step in cholesterol biosynthesis.
122
What are some pleiotropic effects of statins
123
Statins are contraindicated in what cases?
Pregnancy and lactation
124
Adverse effects of statins
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
Examples of statins
Hint: ends with -statin Atrovastatan Simvastatin Pravastatin
126
Examples of fibrates
Hint: most end with - fibrate (Except gemfibrozil) 1. Clofibrate 2. Gemfibrozil 3. Bezafibrate 4. Ciprofibrate 5. Fenofibrate
127
True or false Fibrates are anti-inflammatory
False
128
Fibrates mechanism of action
Acts as agonist of PPARa on hepatocytes leading to change on the gene expression involved in lipoprotein metabolism
129
Side effects of fibrates
Myopathy Elevated liver transaminases Cholelithiasis Pancreatitis
130
What type of drug is gemfibrozil?
Fibrates
131
True or false Fibrates are used for ↑ triglycerides and especially for diabetes
True
132
Adverse effects of fibrates
Rhabdomyolysis in severe cases - Muscle pain - Tenderness - Weakness and swelling of affected muscles Compartment syndrome - compression of surrounding tissues
133
True or false It’s safe to take Fibrates while having grapefruit
False
134
Which of the following medication can be used for therapeutic management of CHD? CCB ARB ACE-I β blockers Vasodilators Anticoagulant Statin/fibrates
All of them
135
What drugs can be used to reduce oxygen demands?
A. Drugs that ↓ HR and contractility - beta blockers - CCB B. Drugs that ↓ afterload - CCB - ACE-I C. Drug that ↓ preload - Nitrates (vasodilators)
136
How to maintain or increase oxygen supply
Antiplatelet agents Nitrates Supplemental oxygen Revascularization (PCI , CABG)
137
What is the aim of treatment for chronic stable angina
↑ myocardial O2 supply ↓ myocardial O2 demand Treat factors that exacerbate ischemia (HTN, DM, Anemia)
138
Managing chronic stable, angina involves following the ABCDE approach. Explain what that is.
139
What is an alternative if aspirin is contraindicated?
Clopidogrel
140
True or false ACE-I have anti-inflammatory, antithrombotic, anti-proliferative, and antioxidant properties
True
141
Most stable angina patients will be on _____________.
Statins
142
What do nitrates do?
Decrease preload (dilate veins) Decrease afterload (dilate arteries Promote coronary artery blood flow
143
Mechanism of action for nitrates
Releases nitric oxide NO, which enhances cGMP-production leading to reduction in cytosolic calcium
144
What are the three main nitrates used?
Glycerol trinitrate Isosorbide mononitrate Isosorbide dinitrate
145
True or false Nitrates can be administered in several ways
True (IV infusion, conventional or slow release tablets, transdermal patches and ointments, sublingual , sprays, adhesive buccal tablets)
146
Side effects of nitrates
Headache Flushing Hypotension
147
Can the patient exercise right away after taking sublingual GTN?
No, and the patient blood pressure and heart rate should be reevaluated before making a decision to continue treatment
148
Not a question But these are a few things you should know about nitrate.
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
_____________ are useful in preventing angina in exercise because they suppress the rise in blood pressure and resting heart rate
Beta blockers
150
True or false CCB are arterial vasodilators, and have some antiarrhythmic properties
True
151
__________ 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.
Heart failure
152
True or false Diseases that adversely affect ventricular diastole (filling), ventricular systole (contraction), or both can lead to heart failure
True
153
In the majority of patients, what two conditions contribute significantly to the development of heart failure?
Ischemic heart disease (CAD) HTN
154
True or false HF is a largely preventable disorder
True
155
Normal stroke volume is around what
70 mL
156
The filled ventricles has a normal volume of what
130 mL
157
The ejection fraction is over _____ %
50%
158
In LVSD, the ejection fraction is reduced to blow _______, and symptoms usually occur when it’s below __________.
45 % 35 %
159
Around what percent of ejection fraction is warfarin needed and why
When the ejection fraction falls below 10% Patient will have an added risk of thrombus formation within the ventricle ; therefore warfarin is needed
160
Pathophysiology of heart failure
Reduce heart ability to relax or contract, leading to reduce pumping ability
161
What are some compensatory responses if the heart is unable to pump enough blood?
Tachycardia and ↑ contractility Fluid retention and ↑ preload Vasoconstriction and ↑ afterload Ventricular hypertrophy and remodeling
162
How does failure of the compensatory responses lead to heart failure
163
Read and understand the summary of therapeutic targets of HF
164
Mechanism of action of digoxin
1. Inhibits sodium/potassium ATPase which will: - ↑ intracellular Na-Ca exchange → ↑ intracellular calcium and therefore = ↑ contractility (positive inotropic effect) 2. Suppresses AV nodal conduction, and vagal stimulation (therefore is used for atrial fibrillation)
165
True or false Digoxin can be used for atrial fibrillation
True
166
True or false Digoxin has a negative inotropic effect
False Positive inotropic effect
167
True or false Digoxin is commonly used for heart failure
True
168
Inotropes: - examples - When do hospitals usually use them?
Dopamine Dobutamine Acute heart failure
169
Symptoms of digoxin toxicity
Hypersalivation Fatigue Nausea, vomiting Changes in heart rate and rhythm Visual disturbances (yellow/green halos around objects) Confusion and dizziness
170
What makes digoxin dangerous?
It has a low therapeutic index
171
Symptoms of inotropes
Headache Increased heart rate Shortness of breath High blood pressure fainting and dizziness Mild leg cramps Tingling sensation
172
____________ is a chronic inflammatory disorder of the airways .
Asthma
173
What cells play a big role when it comes to asthma
Mast cells Eosinophils T-lymphocytes Macrophages Neutrophils Epithelial cells
174
Symptoms during asthmatic episodes
Wheezing Breathlessness chest tightness Coughing
175
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.
True
176
Pathophysiology of asthma include
Inflammatory cells infiltrate Narrowed lumen Mucous plugging Hypertrophy of basement membrane
177
Treatment of asthma includes what medications
β2 agonists Xanthine drugs (theophylline) H1 receptor antagonists
178
Mechanism of action for β2 agonists used for asthma
- Induces Bronchodilation - Inhibits mediator, release from muscles and monocytes (TNFa) - Increases mucous clearance by the action on cilia
179
Difference between short acting and long, acting inhaled β2 agonists + examples
Short acting inhaled β2 agonists: - Most effective/ quick action for ACUTE SEVERE ASTHMA - Response occurs within 30 minutes of drug administration Examples: salbutamol, terbutaline Long acting inhaled β2 agonists: - given twice daily as adjuvant therapy in patients whose asthma is inadequately controlled by steroids Ex: salmeterol , formoterol
180
Side effects of β2 agonists
Tremor Tachycardia Hypokalemia Arrhythmia
181
Is this drug a short acting or long acting β2 agonist? Salbutamol
Short acting
182
Is this drug a short acting or long acting β2 agonist? Salmeterol
Long-acting
183
Is this drug a short acting or long acting β2 agonist? Terbutaline
Short acting
184
Is this drug a short acting or long acting β2 agonist? Formoterol
Long acting
185
Mechanism of action of Xanthine drugs (theophylline) used for asthma
Inhibit phosphodiesterase PDE iso-enzymes → increases cAMP/cGMP levels and bronchodilation
186
Theophylline is what type of drug?
Xanthine drugs for asthma
187
True or false Xanthine drugs have a narrow therapeutic index, so overdose can easily happen if not careful
True
188
Side effects of Xanthine drugs
Arrhythmia Seizures
189
What are H1 receptor antagonists
Antihistamines that are not commonly used to treat asthma, but are used to control acute phase of allergic or exercise-induced asthma
190
side effects of H1 receptor antagonists
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
What type of drug is diphenhydramine?
H1 receptor antagonist
192
What type of drug is chlorpheniramine?
H1 receptor antagonists
193
What type of drug is cyclizine?
H1 receptor antagonist
194
True or false Short/long acting β2 agonists can cause tremors and hypokalemia (muscle pain)
True
195
True or false Theophylline can cause seizure attacks at high doses
True
196
True or false All FIRST generation H1 blockers can cause dizziness, blurred vision, and tremors
True
197
Just read
Done