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🄼💊 CARDIO PATH/RX > pharm: 10-1 Vasoactive Peptides > Flashcards

pharm: 10-1 Vasoactive Peptides Flashcards

1
Q

Captopril

A: MOA

B: Route of Administration

C: Indication

D: Contraindication

A

A: ACEk2 Inhibitor

B: Oral

C: HTN

D: Contraindicated in [Septic HTN pts]

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2
Q

Enalapril

A: MOA

B: Route of Administration

C: Indication

D: Contraindication

A

A: ACEk2 Inhibitor

B: Oral

C: HTN

D: Contraindicated in [Septic HTN pts]

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3
Q

Losartan

A: MOA

B: Route of Administration

C: Indication (2)

A

A: ARB - Angiotensin Receptor BLOCKER

B: Oral

C: HTN and [Septic HTN]

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4
Q

Valsartan

A: MOA

B: Route of Administration

C: Indication (2)

A

A: ARB - Angiotensin Receptor BLOCKER

B: Oral

C: HTN and [Septic HTN]

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5
Q

IcaTibant

A: MOA

B: Route of Administration

C: Indication (2)

A

A: [Bradykinin B2 Receptor BLOCKER]

B: Oral

C:

  • Inflammatory Responses
  • Adjunct with C1 estrase inhibitor for [Angioneurotic Edema] in Europe
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6
Q

Aprotonin

A: MOA

B: Route of Administration

C: Indication

A

A: Kallikrein inhibitor that is NO LONGER USED CLINICALLY

B: IV

C: Inflammation

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7
Q

Desmopressin (dDAVP)

A: MOA

B: Route of Administration (2)

C: Indications (3)

A

A: Vasopressin Arginine analogue

B: IV or intranasal

C: D8S

  1. Diabetes Inspidius (initial purpose)
  2. INC [Factor 8] and [Von Willebrand factor] in [mild hemophilia] / [Von Willebrand Dz] / [Plasma donor blood]
  3. Surgical bleeding Controller
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8
Q

Bosentan

A: MOA

B: Route of Administration (2)

C: Indication

A

A: [General Endothelin receptor BLOCKER] (blocks both ETa and ETb)

B: Oral and IV

C: [Pulmonary Arterial HTN]

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9
Q

Captopril

Side Effects ( 3 )

A
  • Severe Abd Pain
  • Chest Pain
  • Allergic Rxn
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10
Q

Enalapril

Side Effects ( 2 )

A
  • Severe Abd Pain
  • hypOtension
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11
Q

Losartan

Side Effects ( 3 )

A
  • DIN*
  • Diarrhea
  • Insomnia
  • Nasal Congestion
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12
Q

Valsartan

Side Effects ( 2 )

A
  • Abd Pain
  • Nausea
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13
Q

IcaTibant

Side Effects ( 2 )

A
  • Abd Pain
  • Nausea
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14
Q

Aprotonin

Side Effects ( 3 )

A
  • MI
  • Stroke
  • Renal Failure

THIS DRUG IS NO LONGER CLINICALLY USED

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15
Q

Desmopressin (DDAVP)

Side Effects ( 3 )

A
  • Abd Pain
  • Nausea
  • HA
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16
Q

Bosentan

Side Effects ( 3 )

A
  • Abd Pain
  • Hepatotoxicity
  • Nausea
17
Q

General MOA for Vasoactive Peptides

A

act on cell surface [G protein-coupled receptors] and cause production of second messengers and opening of ion channels.

18
Q

Which enzyme converts [ACTIVE Angiotensin 2] —> [inactive Angiotensin 3]?

A

(Plasma or Tissue) Aminopeptidase

19
Q

A: What Factors INC circulating plasma level of Angiotensinogen (5)

A
  1. Corticosteroids
  2. Estrogen
  3. Thyroid Hormones
  4. [ACTIVE Angiotensin 2]
  5. Pregnancy Related HTN
20
Q

A: ACEk2 (Angiotensin Converting Enzyme-Kininase 2) works by cleaving [inactive Angiotensin 1] on its ______ terminal —> [ACTIVE Angiotensin 2]. This enzyme is also known as ___ or ____

B: Which enzymes hydrolyze Angiotensin 2 and 3 into small inactive fragments?

A

A: ACEk2 (Angiotensin Converting Enzyme-Kininase 2) works by cleaving [inactive Angiotensin 1] on its CARBOXYL terminal —> [ACTIVE Angiotensin 2]. This enzyme is also known as:

    • Peptidyl dipeptidase*
    • Kininase 2****

B: Angiotensinases

21
Q

[ACTIVE Angiotensin 2]​ is __ times more potent than NorEpi.

B: Name all 6 functions of [ACTIVE Angiotensin 2]

A

A: [ACTIVE Angiotensin 2]​ is 40 x more potent than NorEpi Has other functions other than vasoconstriction:

” [Angiotensin 2] GAVE [Cardiac Hypertrophy] “

  • Stimulates Autonomic ganglion and Facilitates Autonomic Transmissions
  • INC release of Epi and NorEpi from Adrenal Medulla
  • Aldosterone secretion from Adrenal Cortex
  • [Cardiac Hypertrophy] as a potent mitogenic agent (can be inhibited by [ACEk2 inhibitors] )
  • Stimulates Glucocorticoids biosynthesis at HIGH CONCENTRATION
22
Q

A: ACEk2 inhibitors not only block conversion
of [angiotensin 1] but also inhibit degradation of other vasopeptides such as: (3)

B: Side Effects of ACEk2 inhibitors (3)

C: ACEk2 inhibitors are contraindicated in what type of pt?

A

A:

  • bradykinin
  • Substance P
  • enkephalin

B: Side Effects include

(x) hypOtensive Shock (from inhibiting bradykinin degradation)
(x) Angioedema
(x) cough

C: Don’t give ACEk2 inhibitors to [Septic Hypertensive pt]

23
Q

A: What are the Steps for producing Bradykinin (2)

B: How are Bradykinin and Kallidin inactivated?

C: Are the Kinin family Vasoconstrictors or VasoDilators?

D: How is this related to insect bites?

A

A:

1st - [THK - Trypsin / [Hageman Factor] / Kallikrein] all convert [Plasma preKallikrein] —> [Plasma Kallikrein]

2nd: [Plasma Kallikrein] converts [HMWKF (HMW Kininogen Fitzgerald)] —> Bradykinin

OR

[Tissue Kallikreins] converts [LMW Kininogen] –> Kallidin —(via Aminopeptidases)—> Bradykinin

B: Bradykinin AND Kallidin are both inactivated by [Kininases 1 and 2]

C: Kinin are VasoDilator Peptides

D: Insect can release [Kinin generating enzymes] in their bite

24
Q

A: Where are [Plasma preKallikrein] produced?

B: This enzyme is AKA ____ and can be activated by ___

A

A: Liver, but then disseminates everywhere

B: AKA Fletcher Factor – Activated by [Factor 12A Hageman]

25
Q

A: Relation of Kallikreins to [DIC associated hypOtension]?

B: How are Kallikreins activated in the Pancreas?

A

A:

Many patients with consumption coagulapathy (DIC) develop hypotension due to increased kallikrein production

B: Trypsin

26
Q

A: List the 3 Kinins and where they come from?

B: MOA of Kinins (3)

C: Which Kinin enters blood circulation to contribute to localized hypOtension and inflammation?

D: Which [Kinin Receptors] do drugs target to block?

A

A:

1) Bradykinin comes from [Plasma Kallikrein]
2) Lysyl Bradykinin comes from [Pancreas-Kidney glandular Kallikrein]
3) Meth-Lysyl Bradykinin comes from [pepsin/pepsin-like enzymes]

B:

  • Stimulate release of [nitric oxide]/ PGE2 and PGi2].
  • Promote water/solution passage resulting in edema
  • Produce pain via [nociceptive skin/viscera afferents]

C: Lysyl Bradykinin

D: [less predominant B2 Receptors]

27
Q

A: Natriuretic Peptides have _____ half-lives but can _____ and INC _____ Excretion –> prevents _____

B: What is the significance of BNP (___ natriuretic peptide) in CHF

C: How are Natriuretic Peptides broken down? How is this circumvented pharmacologically?

A

A: Natriuretic Peptides have short half-lives but can vasoDilate and INC [Sodium Renal Excretion] –> prevents HTN

B: BNP (Brain Natriuretic Peptide) Improves Hemodynamics and [Sodium Renal excretion] in CHF pts

C: Natriuretic Peptides are broken down by Metaloproteases. Drugs INHIBIT Metaloproteases–> [INC Natriuretic Peptides]

28
Q

1) Endothelins produce a _____ dependent vascular _____ in most vascular beds via _____.
2) What are the Two Receptor subtypes? Which Drug Blocks both?

A

1) Endothelins (3 isoforms possible) produce a dose dependent vascular constriction in most vascular beds via [signal transduction].
2) Two Receptor subtypes - ETa and ETb –> BOTH CAN BE BLOCKED BY Bosentan

29
Q

A: [VIP -Vasoactive Intestinal Peptide] is a __(#) amino acid ______ related to ______ and ______.

B: Vasoconstriction or VasoDilation?

A

A: [VIP -Vasoactive Intestinal Peptide] is a 28 amino acid Neuromodulator related to secretin and glucagon.

B: VasoDilation

30
Q

A: Substance P belongs to the ______ family (which includes _________ ).

B: Vasoconstriction or VasoDilation

A

A: Substance P belongs to the tachykinin family (which includes [Decapeptides Neurokinin]).

B: VasoDilation by stimulating NO release

31
Q

A: Neurotensin is made in association with ______

B: In peripheral circulation it causes what 4 things?

A

A: Neurotensin is made in association with neuromodulin N. In peripheral circulation it causes: “ HIVV”

  • vasoDilation
  • vascular permeability
  • Hyperglycemia
  • Inhibition of gastric motility
32
Q

A: Where is CGRP present in large amounts?

B: Side Effects of [IV CGRP] (2)

A

A: [CGRP - (Calcitonin Gene Related Peptide)] present in large amounts within the Thyroid gland (but also in CNS and GI tract with Substance P)

B: [IV CGRP] can cause hypOtension and tachycardia

33
Q

A: Adrenomodulin is a _____ distributed _____ that mediates _____ responses

B: Adrenomodulin INCREASES during what events? (4)

A

A: Adrenomodulin is a widely distributed peptide that mediates hypothyroid responses and will INCREASE during:

  • intense exercise
  • HTN
  • Renal Failure
  • Septic shock
34
Q

A: ______ is one of the most abundant neuropeptides in both the central and peripheral nervous system

B: 3 Functions

A

A: [Neuropeptide Y] is one of the most abundant neuropeptides in both the central and peripheral nervous system

B:

  • vasoconstriction
  • mediates Hypertensive responses
  • CNS effect
35
Q

Urotensin

A: Vasoconstrictor or VasoDilator?

B: In what Disease does it levels increase?

C: What’s unique about its makeup

A

A: [Arterial Bed POTENT Vasoconstrictor]

B: Levels INC in pts with [End Stage Heart Failure]

C: Contains a conserved cyclic HeptaPeptide sequence

36
Q

Name the 5 Phosphodiesterase Inhibitors

A

“Intimate Moments Demand Viagra and Condoms”

  1. Imilironone
  2. Milironone
  3. Dipyridamole
  4. Viagra
  5. Cilastazol

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