pharm: 10-1 Vasoactive Peptides Flashcards by Brian McCalister

Captopril

A: MOA

B: Route of Administration

C: Indication

D: Contraindication

A: ACEk2 Inhibitor

B: Oral

C: HTN

D: Contraindicated in [Septic HTN pts]

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Enalapril

A: MOA

B: Route of Administration

C: Indication

D: Contraindication

A: ACEk2 Inhibitor

B: Oral

C: HTN

D: Contraindicated in [Septic HTN pts]

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Losartan

A: MOA

B: Route of Administration

C: Indication (2)

A: ARB - Angiotensin Receptor BLOCKER

B: Oral

C: HTN and [Septic HTN]

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Valsartan

A: MOA

B: Route of Administration

C: Indication (2)

A: ARB - Angiotensin Receptor BLOCKER

B: Oral

C: HTN and [Septic HTN]

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IcaTibant

A: MOA

B: Route of Administration

C: Indication (2)

A: [Bradykinin B2 Receptor BLOCKER]

B: Oral

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

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Aprotonin

A: MOA

B: Route of Administration

C: Indication

A: Kallikrein inhibitor that is NO LONGER USED CLINICALLY

B: IV

C: Inflammation

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Desmopressin (dDAVP)

A: MOA

B: Route of Administration (2)

C: Indications (3)

A: Vasopressin Arginine analogue

B: IV or intranasal

C: D8S

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

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Bosentan

A: MOA

B: Route of Administration (2)

C: Indication

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

B: Oral and IV

C: [Pulmonary Arterial HTN]

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Captopril

Side Effects ( 3 )

Severe Abd Pain
Chest Pain
Allergic Rxn

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Enalapril

Side Effects ( 2 )

Severe Abd Pain
hypOtension

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Losartan

Side Effects ( 3 )

DIN*
Diarrhea
Insomnia
Nasal Congestion

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Valsartan

Side Effects ( 2 )

Abd Pain
Nausea

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IcaTibant

Side Effects ( 2 )

Abd Pain
Nausea

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Aprotonin

Side Effects ( 3 )

MI
Stroke
Renal Failure

THIS DRUG IS NO LONGER CLINICALLY USED

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Desmopressin (DDAVP)

Side Effects ( 3 )

Abd Pain
Nausea
HA

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Bosentan

Side Effects ( 3 )

Abd Pain
Hepatotoxicity
Nausea

General MOA for Vasoactive Peptides

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

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

(Plasma or Tissue) Aminopeptidase

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

Corticosteroids
Estrogen
Thyroid Hormones
[ACTIVE Angiotensin 2]
Pregnancy Related HTN

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: 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

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

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

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

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?

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]

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?

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

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

[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

A: Where are [Plasma preKallikrein] produced?

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

A: Liver, but then disseminates everywhere

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

A: Relation of Kallikreins to [DIC associated hypOtension]? B: How are Kallikreins activated in the Pancreas?

A: ## Footnote Many patients with consumption coagulapathy (DIC) develop hypotension due to increased kallikrein production B: **Trypsin**

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: 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]

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: 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]

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

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**

A: [**VIP** -*Vasoactive Intestinal Peptide*] is a \_\_(#) amino acid ______ related to ______ and \_\_\_\_\_\_. B: Vasoconstriction or VasoDilation?

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

A: Substance P belongs to the ______ family (which includes _________ ). B: Vasoconstriction or VasoDilation

A: Substance P belongs to the tachykinin family (which includes [Decapeptides Neurokinin]). B: VasoDilation by stimulating NO release

A: Neurotensin is made in association with *\_\_\_\_\_\_* B: In **peripheral circulation** it causes what 4 things?

A: Neurotensin is made in association with *neuromodulin N*. In **peripheral circulation** it causes: " **HIVV**" - vasoDilation - vascular permeability - Hyperglycemia - Inhibition of gastric motility

A: Where is **CGRP** present in large amounts? B: Side Effects of [IV **CGRP**] (2)

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

A: Adrenomodulin is a _____ distributed _____ that mediates _____ responses B: Adrenomodulin INCREASES during what events? (4)

A: Adrenomodulin is a widely distributed peptide that mediates hypothyroid responses and will INCREASE during: - intense exercise - HTN - Renal Failure - Septic shock

A: ______ is one of the most abundant neuropeptides in both the central and peripheral nervous system B: 3 Functions

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

**Urotensin** ## Footnote A: Vasoconstrictor or VasoDilator? B: In what Disease does it levels increase? C: What's unique about its makeup

A: [**Arterial Bed** POTENT Vasoconstrictor] B: Levels INC in pts with [End Stage Heart Failure] C: Contains a conserved cyclic HeptaPeptide sequence

Name the 5 Phosphodiesterase Inhibitors

"**I**ntimate **M**oments **D**emand **V**iagra and **C**ondoms" 1. **I**milironone 2. **M**ilironone 3. **D**ipyridamole 4. **V**iagra 5. **C**ilastazol