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Pharmacology: Exam 2 > Lecture 8: Vasoactive Peptides > Flashcards

Lecture 8: Vasoactive Peptides Flashcards

1
Q

List the drug classes of Vasoactive Peptides (6)

A
  • Renin Inhibitor
  • Angiotensin-Converting Enzyme Inhibitors (ACEI)
  • Angiotensin Receptor Blockers (ARBs)
  • ET Receptor Antagonist
  • Synthetic BNP Analog
  • ARB+ Neprilysin Inhibitor
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2
Q

Which drug class(es) are the endogenous peptide of Angiotensin II? (3)

A
  • Renin inhibitors
  • ACEI
  • ARBs
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3
Q

Which drug class(es) are the endogenous peptide of Endothelin 1 (1)

A

ET Receptor Antagonist

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4
Q

Which drug class(es) are the endogenous peptide of Natriuretic peptides? (1)

A

Synthethic BNP Analog

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5
Q

Which drug class(es) are the endogenous peptide of Angiotensin II/Natriuretic peptides? (1)

A

ARB + Neprilysin Inhbitor

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6
Q

Which drug(s) are Renin Inhibitor? (1)

A

Aliskiren

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7
Q

Which drug(s) are Angiotensin-Converting Enzyme Inhibitors (ACEI)? (6)

PRIL=ACEI

A
  • Captopril
  • Benazepril
  • Enalapril
  • Lisinopril
  • Quinapril
  • Ramipril
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8
Q

Which drug(s) are Angiotensin Receptors Blockers (ARBs)? (4)

Sartan=ARBs

A
  • Candesartan
  • Irbesartan
  • Losartan
  • Valsartan
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9
Q

Which drug(s) are ET Receptor Antagonist? (1)

A

Bosentan

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10
Q

Which drug(s) are Synthetic BNP Analog? (1)

A

Nesiritide
(Never use terrible side effects)

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11
Q

Which drug(s) are ARB+Neprilysin Inhibitor? (2)

A

Sacubitril and Valsartan

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12
Q

List some natural substances in our bodies that cause vasocontriction? (3)

A
  • Endothelin
  • Vasopressin
  • Angiotensin II
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13
Q

List some natural substances in our bodies that cause vasodilation? (2)

A
  • Bradykinin
  • Natriuretic Peptides
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14
Q

How to vasoactive peptide drugs target vasoconstrictors and vasodilators in our body?

A
  • Vasoconstrictors: Drugs BLOCK them to ↑ dilation
  • Vasodilators: Drugs PROMOTE these to ↑ dilation

Vasoconstrictiors: Endothelin, Vasopressin, Angiotensin II
Vasodilators: Bradykinin, Natriuretic Peptides

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15
Q

Using the image below explain what occurs in the heart after hypertension, heart attack, etc that eventually leads to Heart Failure

A
  • When a pt has HTN or heart attack the heart goes through remodeling (e.g. fiber tissue issues or RV issues)
  • D/t remodeling the heart ability to get blood into the system is decreased
  • The body believes the BP is low, so it activates the short term (baroreceptors) and long term (RAAS) feedback loops to help increase BP
  • The effects occur (e.g. fluid retention by the RAAS pathway) but d/t remodeling the heart is not working properly
  • These causes the feedback systems to activate again and again w/ the heart getting worst and eventually leading to worsening Heart Failure

RAAS pathway includes Renin, Angiotension and Aldosterone

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16
Q

What are the biological effects of Angiotensin II? (4)

A

When Angiotensin II is released:

  • ↓ Natriuresis (Na+ in urine), ↑H2O reabsorption (d/t ↑ Aldosterone & Vasopressin (ADH))-Volume Expansion
  • Release of Vasoconstrictors→Direct Vasconstriction
  • ↑ Symphathetic Tone
  • Cell Proliferation (Heart remodeling), Migration and Hypertrophy
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17
Q

Explain the short term and long term changes that occur d/t the release of Angiotensin II

A
  • Short term: Release Ca2+ which causes contraction and excitation→Vasoconstriction
  • Long-term: Activates Jak2 which causes Mitogenic effect→Genetic changes: Remodeling
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18
Q

What step in the Angiotensin II release pathway does the drug Aliskiren affect?

A
  • Aliskiren is a renin inhibitor so it STOPS Angiotensinogen (secreted by liver) from turining into Angiotensin I

Angotensinogen is the first step of the RAAS pathway

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19
Q

What step in the Angiotensin II release pathway does ACEI affect?

-PRIL=ACE inhibitors

A
  • STOPS Angiotensin I from converting to Angiotensin II by inhibiting ACE
  • STOPS the breakdown of Bradykinin into compounds (PGE2, PGI2, NO, EDHF) that cause dilation by inhibiting ACE
  • ACE= Angiotensin-Converting Enzyme
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20
Q

Which steps in the Angiotensin II release pathway does ARBs affect?

-Sartan= ARBs

A
  • Blocks the Angiotensin II recptors that normally causes vasoconstriction and aldosterone secretion
  • Vasoconstriction→↑ peripheral vascular resistance→↑BP
  • Aldosterone secretion→↑Na+ secretion and H2O retention→↑BP
  • ARBs block the receptors that cause the normal mechanism of increasing BP BUT do NOT affect Angiotensin II levels

ARBs= Angiotension Receptor Blockers

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21
Q

What are the Vascular effects of ACE-I and ARBs?

-PRIL: ACE-I
-Sartan: ARBs

A
  • Vasorelaxation
  • Decrease in arterial resistance
  • Progressive reduction in BP (NO reflex tachy)
  • Reverese hypertrophy
  • Augument vascular distensibility
  • Decrease oxidative stress (injury to blood vessels)
  • Improved endothelial function
  • Antiplatelet effect (ACE-I greater)
  • Stabilizes Plaque
  • ↓ Neutrophils and monocular cells Proliferation (Remodeling)
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22
Q

What are the Cardic effects of ACE-I and ARBs?

-PRIL: ACE-I
-Sartan: ARBs

A
  • Decreased preload and afterload
  • NO change, or an increase, in cardic ouput
  • ↓ Aldosterone→ ↓BP; ↓ Angiotesin II→↓ remodeling: Reverse Hypertrophy
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23
Q

What are the Renal Effects of ACE-I and ARBs?

-PRIL: ACE-I
-Sartan: ARBs

A
  • Renoprotective
  • Decrease proteinuria (less kidney damage)
  • Increase renal blood flow
  • Decreased kaliuresis that may result in HYPERKALMIA
  • Reduces intraglomerular pressure(perferential dilation of efferent arterioles)

Kailuresis: amount of K+ that leaves w/ urine

24
Q

TRUE or FALSE. ACE-I and ARBs are used together for treatment

A

FALSE
* ACE-I and ARBs have the same effect, if added together lead to hyper-K+

25
Q

List other effects of ACE-I and ARBs

-PRIL: ACE-I
-Sartan: ARBs

A
  • ↓ Pulmonary vascular resistance
  • ↓ Pulmonary capillary wedge pressure (preload)
  • ↓ Sympathetic outflow
  • ↓ Aldosterone production
  • Improves insulin sensitivity (can use if diabetic)
26
Q

A 67-year-old Cucasian man with chronic kidney disease is prescribed losartan. Which of the following is an effect of losartan that will improve outcomes in this patient?
a. Decrease intraglomerular pressure
b. Decrease K+ wasting
c. Increased ADH
d. Increased glomerular filtration
e. Inhibiton of angiotensin converting enzyme

A

a. Decrease intraglomerular pressure

27
Q

What are the clinical use(s) of ACE Inhibitor drugs?

-PRIL: ACEI

A
  • Hypertension
  • Heart Failure
28
Q

What is the clincial use(s) of ARBs drugs?

-Sartan: ARBs

A

Hypertension

29
Q

What does it mean that the blood pressure lowering effects of ACE-I and thiazide-type drugs have an ADDITIVE effect?

A

It means they can be used together in most instances

30
Q

What does it mean that the blood pressure lowering effects of ACE-I and β-blockers or ACE-I and ARBs have LESS THAN ADDITIVE effect?

A

It means that they can only be used together if the pt has a history of MI

31
Q

What group of people respond less favorable to ACEIs at low [ACEI] monotherapy?

A

Low renin producers (e.g. African Americans)

32
Q

What are the systolic and diastolic numbers of the Hypertension Stages?

  • Normal
  • Elevated
  • Stage 1
  • Stage 2
A
  • Normal=S: <120 mmHg, D: <80 mmHg
  • Elevated= S:120-129 mmHg, D:<80 mmHg
  • Stage 1= S: 130-139 mmHg, D: 80-90 mmHg
  • Stage 2= S: ≥140 mmHg, D: ≥90 mmHg
33
Q

Which drug class(es) are the first line treatment of adults with systolic/diastolic hypertension (w/ out other compelling indicators)?

Target: <130/80 mmHg

A
  1. Thiazide/thiazide-like
  2. ACEI
  3. ARB
  4. CCB
34
Q

What is the common type of therapy used when treating systolic/diastolic hypertension?

A
  • Dual Therapy or Triple/Quadruple therapy
  • Mixing drugs from the four 1st line classes together for treatment
  • Rarely ever do monotherapy b/c it does not work
35
Q

What are the Preferred antihypertensive combinations? (3)

HIGH yield

A
  • ACE-I or ARB + Thiazide
  • ACE-I or ARB + CCB
  • CCB + Thiazide (black population)
36
Q

What are the Acceptable antihypertensive combinations?

HIGH yield

A
  • CCB + Thiazide (nonblack population)
  • β-blocker + DHP CCB or thiazide
  • Thiazide + K sparing diuretic
  • Aliskiren + Thiazide or CCB
37
Q

What are the NOT preferred antihypertensive combinations?

LOW yield

A
  • ACEI + ARB
  • β-blockers + ACEI or ARB (preferred only post-MI or HF)
  • β-blocker + Non-DHF CCB
  • β-blocker + central acting (i.e. clonidine, etc)
38
Q

Which drug class(es) are the first line treatment of adults with systolic ONLY hypertension (w/ out other compelling indicators)?

Target: <130 mmHg

A
  1. Thiazide/thiazide-like
  2. ARB
  3. CCB
39
Q

When are ACE-I and ARBs first line therapy for hypertension?

A
  • Ischemic Heart Disease
  • Recent STEMI or non-STEMI
  • Left Ventricular Systolic Dysfunction
  • With Cerebrovascular Disease
  • Left Ventricular Hypertrophy
  • Non-Diabetic Chronic Kidney Disease (Caution with arterial stenosis)
  • Diabetes +/- CKD

Help w/ Remodeling

40
Q

What are the adverse effects and contrindications/interactions of ACE-I?

-PRIL: ACE-I

A

Adverse Effects

  • Dry cough
  • Angioedema
  • Hypotension
  • Hyperkalemia

Contraindications/Interactions

  • Bilateral renal arter stenosis
  • K+ sparing diuretics
  • ARBs
  • NSAIDs
  • Pregnancy
41
Q

What are the adverse effects and contrindications/interactions of ARBs?

-Sartan: ARBs

A

Adverse Effects
​
* Dry cough
* Angioedema
* Hypotension
* Hyperkalemia
​
Contraindications/Interactions
​
* Bilateral renal artery stenosis
* K+ sparing diuretics
* ACE-I
* NSAIDs
* Pregnancy

42
Q

True or False. Abrupy withdrawal of ACE-I and ARBs have been associated with a rapid increase in blood pressure

A

False

43
Q

Explain why bilateral renal stenosis is a contraindication for ACE-I and ARBs

A
  • Both arteries are affected and need constriction to maintain pressure.
  • If ACE-I/ARB are used the efferent artert will be dilated
  • If dilated it won’t filter and rentain waste
  • Unilater renal stenosis is not affected d/t other kidney making up for damaged kidney
44
Q

What are the Clinical use(s), Side effects/adverse effects of Aliskiren?

Renin Inhibitor

A

Clinical Use:

  • Hypertension

Side Effects/Adverse effects:

  • Dizziness
  • Headache
  • Hyperkalemia
  • Hypotension
  • Renal impairment
  • Category D (Pregnancy/lactation)
45
Q

What are the physical actions of Natruretic Peptides (ANP)?

A
  • Decrease renin secretion
  • Vasodilation
  • Decrease BP
  • Increase endothelial premeability
  • Decrease Hypertrophy
  • Decrease Fibrosis
  • Decrease Sympathetic outflow

Opposite of Angiotension II

46
Q

What is the clinical use(s), side effects/adverse effect of Nesiritide (ANP)?

NOTE: DRUG IS NEVER USED D/T HORRIBLE SIDE EFFECTS

LOW Yield

A

Clinical use:

  • Acutely decompensated congestive failure

Side Effects:

  • Hypotension
  • Tachycardia
  • Headache
  • Abdominal Pain
  • Insomnia
  • Dizziness
  • Anxiety
  • Nausea
  • Vomiting
  • Category C (pregnancy/lactation)
47
Q

After the horrible side effects of Nesiritide, what to drugs where made to target Angiitensin II/Natriuretic peptides?

HIGH yield

A
  • Sacurbitril (increase Endogenous NPs)
  • Valsartan (block ANGII)
48
Q

What was the outcome of the drug combination of Sacibitril and Valsartan?

HIGH yield

ARB + Neprilysin Inhibitor

A

First 2 drugs to double life expectancy for patients with heart failure

49
Q

List the physiology/pathophysical effects of Endothelian? (5)

A
  • Vasoconstriction
  • Mitogenesis
  • Positive inotropic and chronotropic effects
  • Decreased glomerular filtration rate
  • Decreased sodium and water excretion
50
Q

What disease tends to have increased endothelin in patients?

A

Pulmonary hypertension

51
Q

What are the clincial use(s), side effects/adverse effects of Bosentan?

ET Receptor Antagonist (Endothelin)

A

Clincial use:

  • Pulmonary hypertension

Side Effects:

  • Potential liver injury
  • Decrease in hemoglobin and hematocrit
52
Q

What does inhibition of endothelian receptors cause?

A

A decrease in pulmonary vascular resistance

53
Q

A patient with hypertension and no comorbidity presents and is found to have blood pressure of 150/92 mmHg. He is currently being treated with lisinopril. Which of the following medications would be contraindicated in this patient?
a. Amlodipine
b. Chlorthalidone
c. Digoxin
d. Metoprolol
e. Prazosin
f. Valsartan

A

f. Valsartan

54
Q

A 32 year-old woman presents for annual physical and is found to have hypertension, which is confirmed by home blood pressure monitoring. In which of the following conditions would ramipril be contraindicated in this patient?
a. Asthma
b. Low plasma K+
c. Heart failure
d. Patient being treated with metoprolol
e. Pregnancy
f. Severe hypertension

A

e. Pregnancy

55
Q
  1. Which of the following drugs is a contraindication when taking Candesartan?
    a. Lisinopril
    b. Metoprolol
    c. Verapamil
    d. Amlodipine
A

a. Lisinopril

56
Q
  1. Which of the following drugs has no effects on angiotensin II levels?
    a. Lisinopril
    b. Losartan
    c. Aliskiren
    d. Ramipril
A

b. Losartan

57
Q
  1. Which of the following is NOT a contraindication/interaction with Enalapril?
    a. Losartan
    b. NSAIDs
    c. Spironolactone
    d. Propranolol
A

d. Propranolol

Pharmacology: Exam 2 (10 decks)

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