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Pharmacology > Cardiovascular, Pulmonary, and Coagulation Medications > Flashcards

Cardiovascular, Pulmonary, and Coagulation Medications Flashcards

1
Q

What are the reasons for HTN?

A

Excess vascular volume
low vasculature compliance
Increased RAS activity

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2
Q

What does Renin do ?

A

Proteolytic enzyme that is released by the kidneys when:

  1. sympa nerve activity acts on Beta1 adrenoceptors
  2. renal artery Hypotension
  3. decreased NA delivery to distal kidney tubules

Renin is released when the kidneys are hypoprofused and vasoconstricts vessels, by allowing angiotensinogen to convert Ang I > Ang II (Important MOA for ACE inhibitors)

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3
Q

Essential Vs Secondary HTN

A

Essential HTN has no clear cause
Secondary HTN may be sue to head trauma, cancer, kidney/ endocrine disease.
Often more than 1 drug is needed to control BP; use 1 depending on initial readings, then multiple for different MOAs and changes doses

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4
Q

Blood pressure target

A

<140/90

130/80 is the new recommendation

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5
Q

First line medication classes for HTN

A
  • Thiazide diuretics
  • ACE inhibitors
  • Angiotensin receptor blockers (ARBs)
  • Calcium channel blockers (CCBs)
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6
Q

Second line meds for HTN

A
  • Beta-blockers
  • Aldosterone antagonists
  • Loop diuretics
  • Direct vasodilators, alpha-1 blockers, alpha-2 blockers (will not be discussed today)
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7
Q

What are the Basic Targets for Treating Hypertension?

A

• Decrease Heart rate (HR), contractility, conductivity
by Direct Cardiac Agents

  • Peripheral resistance, decrease pre-load, vascular health, vasodilation by Peripheral Vascular agents
  • Decrease Fluid volume, metabolites by Renal Agents
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8
Q

Which drugs act on the heart to control HR, contractility and conductivity?

A
  • Beta Blockers

* Calcium Channel Blockers

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9
Q

Which drugs act on the peripheral system for resistance, pre/after load

A
  • Hydralazine
  • Alpha 1 Antagonists
  • Alpha 2 Agonists
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10
Q

Which drugs act on the renal system for fluid volume control

A
  • ACE Inhibitors
  • Angiotensin2 Inhibitors
  • Diuretics
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11
Q

What do Thiazide diuretics do?

A

Antihypertensives Impact fluid volume and decrease fluid retention. 1st line.
Can also help with HTN by Inhibition of Sodium/Cl reuptake
- 1st line of defense for HTN
- moderate diuretic and afterload reduction

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12
Q

What are the targets of loop diuretics?

A
  • Inhibit Na, K, Ca, Mg reabsorption in the loop of Henle
  • Powerful diuresis and volume reduction
  • Decreased afterload
  • Not used much for BP reduction
  • Useful in patients with edema and heart failure
  • Most common is furosemide (Lasix)
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13
Q

What are the targets of loop diuretics? Potassium Sparing Diuretics –Aldosterone Antagonists

A 
- Created bc. pts werent absorbing K and were becoming hypokalemic 
•Used for resistant hypertension
•Inhibits aldosterone by inhibiting sodium-potassium exchange site in the distal tubule
       .–Excretes sodium
       .–Excretes water
       .–Retains potassium
•Also used to treat heart failure
•Aldosterone antagonists
–Spironolactone (Aldactone )
–Eplerenone
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14
Q

What do ACE inhibitors do?

A

Antihypertensives Renal agent that Impact fluid volume and metabolites (decr fluid volume). 1st line.
•Inhibition of Angiotensin Converting Enzyme (ACE)
–Inhibition of the conversion of Angiotensin I to Angiotensin II
•Peripheral Vasodilation
–ATII causes peripheral vasoconstriction
•Reduced Antidiuretic Hormone (ADH) Production
–Reduced fluid volume
•Reduced Aldosterone Production–Reduced fluid volume

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15
Q

What do ARBs do? (Angiotensin Receptor Blockers)

A

Anti-HTN, Renal agent to decrease fluid. 1st line.
•Inhibition of Angiotensin II receptor
–Action of angiotensin II is blocked despite its production

•Peripheral Vasodilation
–ATII causes peripheral vasoconstriction

•Reduced Antidiuretic Hormone (ADH) Production
–Reduced fluid volume

•Reduced Aldosterone Production
–Reduced fluid volume

•First line option
–Should not be combined with ACE inhibitors Anti hypertensive same results as ACE inhibitor just diff MOA

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16
Q

what do calcium Channel Blockers do?

A

Anti HTN: Cardiac agent, decreases contractility. 1st line.
•Inhibition of sympathetic simulation of vascular smooth muscle
–That means reduced afterload, but also reduced cardiac muscle contractility!

•Mechanism is by blocking calcium re-entry–Reduced contractility, reduced HR
–Preserve renal function in those with HTN-related renal disease
•Vasodilation of vasculature
•↓BP
•Alleviate chest pain/spasm

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17
Q

What do Sympatholytics Beta 1 Blockers do?

A
  • inhibit the SA node
  • Inhibit rennin secretion
  • Cardioselctive
  • “LOLs”
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18
Q

What do Sympatholytics Beta 2 Blockers do?

A

–Beta 2 receptors inhibit smooth muscle contractions in the lungs and GI tract
–Beta 2 blockade is useful for restricting hepatic blood flow for patient with Liver Cirrhosis, but generally not a therapeutic effect for CVD
–Beta 2 blockade may cause bronchospasm

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19
Q

What are Beta blocker considerations in PT ?

A
  • blunts HR response
  • can decrease ex tolerance
  • 2nd line for HTN when 1st line is already optimized
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20
Q

What do Combined alpha and nonselective beta-blockers do?

A
  • Alpha 1blockade causes peripheral vasodilation

- Combined alpha and nonselective beta-blockers lower blood pressure more than beta-blockers without alpha blockade

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21
Q

How does HTN impact PT?

A

-Provide pt. education on med compliance and remind
them of the “silent killer”
-Beta-Blockers and Calcium Channel Blockers can cause decreased CV response during Ex
- postural related hypertension with position changes (Sit>stand ), therefore we should watch for: •Orthostasis, Hypotension, Dizziness, Fatigue
•Use caution when doing activities that may cause vasodilation and further drops in blood pressure (heat)
•Be aware of the patient’s ability to exercise
•Help with compliance (pharm and non-pharm)

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22
Q

What are non pharma approaches to HTN ?

A
  • Diet modification
  • Low fat
  • Low sodium
  • Omega-3 fatty acids
  • Exercise
  • Limit alcohol
  • Smoking cessation
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23
Q

What is Ischemic Heart Disease in 30 seconds ?

A

cardiac muscle has decreased O2 possible due to block or plaque. O2 input

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24
Q

How do you treat angina?

A

-•Organic Nitrates•Beta Blockers•Calcium Channel Blockers•Ranolazine

Beta blockers and nitrates will decrease o2 demand
Ca channel blockers decrease demand and increase supply
- decreasing ca decreases heart contractility and therefore decreases cardiac load and work ultimately decreasing angina
-these drugs help restore the balance btwn o2 need and supply

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25
Q

What are the 3 types of angina?

A

Stable angina- demand is greater than supply; seen with excretion

Prinzmetal’s angina (variant)- can occur at rest with vasospasm which decr o2

unstable angina - atherosclerotic plaque rupture causes decreased o2 suplly with increased demand

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26
Q

What is the first line of defense for stable angina

A

Beta blockers- limits the max HR that can be achieved, limiting how much O2 is needed. Decr morbidity and mortality (death and symptoms)

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27
Q

What role do organic nitrates play in cardiovascular Rx mgmt ?

A

promotes NO release in vessels for vasodialation and decr preload
•Short acting first line for Angina Attacks (nitroglycerin)
•Long acing second line after Beta Blockers for Symptom Relief

28
Q

What do Ca channel blocker do for angina issues?

A

Used prophetically but not after MI

-Reduced contractility, reduced HR

29
Q

What does Ranolazine do to angina ?

A

2nd line defense
MOA not really known - blocks Na channels
does not affect BP/HR

30
Q

what are Non-pharmacological Management methods of Angina?

A 
•Underlying disease state needs to be addressed
 such as Hypertension CAD CHF Anemia
•Weight loss 
•Smoking cessation
•Stress reduction
•PCI/CABG
31
Q

What are PT implication for angina ?

A
  • make sure drug is near by during rehabilitation sessions (nirtoglycerin)
  • Avoid over-challenging the heart during sessions
  • Pt may have artificial increase in tolerance to exercise 2/2 nitrates
  • Guard against orthostatic hypotension
32
Q

What medications would you expect a patient post MI to be on and what education should you provide to them?

A 
Aspirin
•P2Y12inhibitor for at least 12 months
•Beta blocker
•Statin
•+/-ACE inhibitor

Tell them about weight loss, smoking exercise

33
Q

What are Special Considerations for a Physical Therapist with a patient with MI

A

look for:
•Diaphoresis
•Chest pain (often radiates to jaw or arm)
•Shortness of breath (not necessarily with exertion)

what should you do:
•Call 911
•Administer nitro if patient uses
•Administer 325mg of aspirin –chew and swallow
•Administer O2 via NC if O2sat is <90% if able
•Hospital acronym: MONA morphine, O2 nitrates asprin

34
Q

Explain heart failure in 30 seconds

A
  • Chronic overwork of the heart muscle causes hypertrophic remodeling
  • Reduced cardiac output
  • Fluid retention
35
Q

What is the treatment strategy for Heart failure ?

A 
•Decrease cardiac load
•Decrease resistance
•Increase contractility
Meds:
Cardiac Glycocides
ACE Inhibitors
Beta Blockers
Aldosterone Antagonists
Vasodialtors 
Diurectics
36
Q

what are Cardiac Glycoside (Digoxin)?

A 
• used for CHF
Positive inotropes that increase contractility 
•Narrow therapeutic index medication
•Signs/symptoms of toxicity
•Visual disturbances
•Bradycardia and heart block
•Anorexia
•Nausea and vomiting
37
Q

what are Special Considerations for a Physical Therapist: Heart Failure?

A

•Know signs of CHF exacerbation
Dyspnea/ Cough
•Be aware of medication side effects, especially digoxin V.V.B.BA.N
•Be aware of hypotension and dizziness
•Use caution when doing activities that may cause vasodilation and further drops in blood pressure

38
Q

How are arythmias managed?

A

Arrhythmias are irregular heart rhythms that can be tachy or brady, supra ventricular or ventricular

Many antiarrhythmic drugs can produce side effects including increased arrhythmias. For this reason, non pharmaceutical management of arrhythmias is common.

Devices/ procedures: Ablation, AICD , Pacemakers

39
Q

What are Special Considerations for a Physical Therapist: Arrhythmias

A
  • Be aware of medication side effects
  • Especially dizziness and syncope
  • Assess rate & rhythm by checking pulse
  • Help with compliance
40
Q

here are the key points :)

A
  • Organic nitrates, beta blockers, and calcium channel blockers are the primary drugs to treat angina
  • Antianginal drugs used alone or in combination to treat or prevent the various forms of angina
  • Sodium channel blockers, beta blockers, and calcium channel blockers can prolong the cardiac action potential to treat arrhythmias.
  • ACE inhibitors and beta blockers treat congestive heart failure by decreasing the counterproductive changes that increase cardiac workload in heart failure.
  • Rehabilitation providers need to monitor these patients closely during exercise and help educate patients on cardiac risk factors and symptoms related to CV disease
41
Q

What are two main complaints of respiratory illnesses and what causes them?

A

Congestion : Common Cold, Allergies, Bronchitis, Various Resp. infections

Obstruction: Asthma,+COPD,+Emphysema

42
Q

How are the 2 main respiratory complaints treated:

A

Congestion: Antitussives, Decongestants, Expectorants, Mucolytics, Antihistamines
Obstruction: Bronchodilators, Glucocorticoids & other anti-inflammatory agents

43
Q

What are Antitussives, and what are they used for?

A
  • congestion med
    •Used to suppress coughing, often with Acetaminophen •Shortterm use
    •questionable Efficacy esp for non Rx products
  • coughing a mechanism to get rid of phlegm consider with you would want to prevent the body from doing this
44
Q

What are Decongestants and what are they used for?

A

congestion med
-•Stimulate nasal vasoconstriction inorder to decr congestion
•Can cause CNS excitation HA, dizziness, nervousness, HTN, palpitations
•May cause rebound congestion with long term use

45
Q

What are Antihistamines and what are they used for?

A

congestion med
•Histamine: regulates normal function: gastric secretion, CNS activities
allergies
•Block H1 receptors 4
•Decreases nasal congestion, mucosal irritation, discharge rhinitis, sinusitis , conjunctivitis
•Able to cross BBB and cause sedation
•Newer generation is improves with less sedative effects

46
Q

What are Beta-Adrenergic Agonists and what are they used for?

A
  • Bronchodilators
  • act on beta 2 receptrs for smooth muscle relaxation and bronchodilation
  • admin route: inhalation via metered dose inhalers, dry powder or nebulizer
  • adverse effects: airway irritation, nervousness, restlessness, tremor, increased HR
  • shouldnt be used frequently
47
Q

What Bronchodilators and anti inflamtory classes of drugs for obstruction complaints for repiratory illnesses

A

Bronchodilators
•Beta-Adrenergic Agonists
•Anti-cholinergics
•Xanthine Derivatives

Anti-inflammatory
•Glucocorticoids (corticosteroids)
•Cromones
•Leukotriene Inhibitors

48
Q

What are Anti-cholinergics and what are they used for?

A

Bronchodilators
lungs have extensive parasympa innervation via vagus nerve
- blocking muscarinic receptors to prevent ACH induced bronchspasm
- drug of choice for COPD, chronic bronchitis
- Adverse effects: dry mouth, constipation, urinary retention, confusion, blurred vission

49
Q

What are Xanthine Derivatives and what are they used for?

A

Bronchodilators

  • CNS stimulant for reversible airway obstruction such as bronchitis, emphysema
  • not used frequently
50
Q

What are Glucocorticoids and what are they used for?

A

Anti-inflammatory
- most effective for controlling asthma
-prodice anti- inflamatory effects by inhibiting proinflamatory proteins
- decr. Se if inhaled (besides thrush)
- avoid prolonged oral use
Adverse SE: thrush, catabolic effect on support tissues osteoporosis, skin, muscle wasting , aggravation of diabetes , HTN

51
Q

What are Cromones and what are they used for?

A

Anti-inflammatory

  • Can be used prophylactically to prevent asthma, esp in children
  • inhibit infamatory mediators
  • virtually no SE !
  • not really used however 2/2 no prevention of bronchospasm in asthma seen in leukotrienes
52
Q

What are Leukotriene Inhibitorsand what are they used for?

A

Anti-inflammatory
- mediate airway inflamation
- inhibit lipoxygenase enzyme
- combo with glucocorticoids for optimal COPD and asthma mgmt
few adverse effects; mild liver impairment

53
Q

What is asthma ? and how is it mgmt long term?

A

Dual components of inflammation and bronchospasm

  • shifting to anti-inflam drugs like glucocorticoids and bronchodialator combo
  • long acting B blockers shouldn’t be used alone
  • use a rescue inhaler
54
Q

COPD mgmt philosophy

A
  • prevent airflow restriction and maintain airway by Anticholinergics and beta adrenergic blockers

short term mgmt: oral glucocorticoids

55
Q

What are PT implications for Respiratory Pharmacology?

A

Exercise can exacerbate asthma

  • bring rescue inhaler to sessions
  • be aware pf SE of bronchodialators; HR Arrhythmias, Nervousness, confusion signs of toxicity
  • adjust tissue loading if pt is on glucocorticoids
56
Q

What are types of clotting disorders and which promote clotting vs. not?

A

hemophilia - Factor 2,7,8,9 deff.
inherited hyper coagulate state - loves clotting
acquired hyper coagulate state - loves clotting

57
Q

what is a DVT and a PE ?

A

•DVT-–deep-vein-thrombosis-•Clot-in-the-venous-system,-generally-the-legs-due-to-poor-flow•PE-–pulmonary-embolism•Clot-in-the-pulmonary-veins,-commonly-emboli-from-a-DVT

58
Q

What are the 4 types of coagulation medications ?

A

anti thrombotic agents -inhibit platelet function AND prevent thrombus formation

anti-platelet agents-inhibit platelet function

anti coagulation agents-alter clotting factors and prevent thrombus formation

thrombolytic agents - break down a thrombus thats already formed in order to restore flow

59
Q

Heparin Induced Thrombocytopenia?

A

After heparin use, a dramatic decrease in platelets that causes thrombocytopenia

  • must stop all heparin products
  • High rate of thrombus formation > amputation/death?
60
Q

If a patient has liver damage, what effect would this have on their ability to clot?

A

The liver produces platelets, a vitamin K deficiency would result in a more clotting system

61
Q

How do Statins work?

A
  • Decrease cholesterold production in teh liver
  • up regulate LDL surface receptors so LDL breakdown can be increased
  • VLDL production is lowered so LDL production can be lowered
  • other benefits include plauq reduction, antioxidant effects and antithombotic effects
  • bloacks the HMG-CoA reductase pathway which makes cholesterol
62
Q

Fibric Acid derivatives, what do the do?

A
  • Primarily used for hypertriglyceridemia

- increase lipoprotein lipase enzyme > decrease TG levels and increase VLDL breakdown

63
Q

What are the otehr Other Lipid Lowering Agents?

A

*Nicotinic Acid (Niacin®)
Vitamin B3
decrease LDL synthesis
May cause flushing

  • *Bile acid sequesterants
  • Cholestyramine: Questran
  • *Ezetimibe: Zetia
  • *= decreased GI absorption and increase TG (Statins, Fibrics, nicotinic acid decreases the total, decr LDL/TG and increase HDL )
64
Q

What are Special Considerations for anticoagulant medications and lipid meds?

A

•Be aware of the increased risk of bleeding in patients on anticoagulant medications
-Especially post-­‐hip/knee surgery

  • Be aware of patients with hemophilia
  • Watch out for myopathies secondary to lipid lowering agents
  • Help with compliance (pharm and non-­‐pharm)
65
Q

Key Points of anti-coags and lipids

A
  • Normal hemostasis is a balance between excessive and inadequate blood clotting.
  • Thrombus formation and occlusion can occur with overactive blood clotting.
  • Anticoagulant drugs (heparin & warfarin) and platelet inhibitors (aspirin) are used to treat venous thrombus formation and arterial thrombogenesis, respectively.
  • Conditions such as hemophilia by need vitamin K to improve clotting factors or antifibrinolyticagents to inhibit clot breakdown.
  • Hyperlipidemia drugs focus on minimizing atherosclerotic plaque formation.

Pharmacology (5 decks)

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