pharm: 10-1 Vasoactive Peptides Flashcards
Captopril
A: MOA
B: Route of Administration
C: Indication
D: Contraindication
A: ACEk2 Inhibitor
B: Oral
C: HTN
D: Contraindicated in [Septic HTN pts]
Enalapril
A: MOA
B: Route of Administration
C: Indication
D: Contraindication
A: ACEk2 Inhibitor
B: Oral
C: HTN
D: Contraindicated in [Septic HTN pts]
Losartan
A: MOA
B: Route of Administration
C: Indication (2)
A: ARB - Angiotensin Receptor BLOCKER
B: Oral
C: HTN and [Septic HTN]
Valsartan
A: MOA
B: Route of Administration
C: Indication (2)
A: ARB - Angiotensin Receptor BLOCKER
B: Oral
C: HTN and [Septic HTN]
IcaTibant
A: MOA
B: Route of Administration
C: Indication (2)
A: [Bradykinin B2 Receptor BLOCKER]
B: Oral
C:
- Inflammatory Responses
- Adjunct with C1 estrase inhibitor for [Angioneurotic Edema] in Europe
Aprotonin
A: MOA
B: Route of Administration
C: Indication
A: Kallikrein inhibitor that is NO LONGER USED CLINICALLY
B: IV
C: Inflammation
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
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]
Captopril
Side Effects ( 3 )
- Severe Abd Pain
- Chest Pain
- Allergic Rxn
Enalapril
Side Effects ( 2 )
- Severe Abd Pain
- hypOtension
Losartan
Side Effects ( 3 )
- DIN*
- Diarrhea
- Insomnia
- Nasal Congestion
Valsartan
Side Effects ( 2 )
- Abd Pain
- Nausea
IcaTibant
Side Effects ( 2 )
- Abd Pain
- Nausea
Aprotonin
Side Effects ( 3 )
- MI
- Stroke
- Renal Failure
THIS DRUG IS NO LONGER CLINICALLY USED
Desmopressin (DDAVP)
Side Effects ( 3 )
- Abd Pain
- Nausea
- HA
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] β> [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 β> [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 β> [ACTIVE Angiotensin 2]. This enzyme is also known as:
- Peptidyl dipeptidase*
- Kininase 2****
B: Angiotensinases
[ACTIVE Angiotensin 2]β is __ times more potent than NorEpi.
B: Name all 6 functions of [ACTIVE Angiotensin 2]
A: [ACTIVE Angiotensin 2]β is 40 x more potent than NorEpi Has other functions other than vasoconstriction:
β [Angiotensin 2] GAVE [Cardiac Hypertrophy] β
- 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?
A:
- bradykinin
- Substance P
- enkephalin
B: Side Effects include
(x) hypOtensive Shock (from inhibiting bradykinin degradation)
(x) Angioedema
(x) cough
C: Donβt 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?
A:
1st - [THK - Trypsin / [Hageman Factor] / Kallikrein] all convert [Plasma preKallikrein] β> [Plasma Kallikrein]
2nd: [Plasma Kallikrein] converts [HMWKF (HMW Kininogen Fitzgerald)] β> Bradykinin
OR
[Tissue Kallikreins] converts [LMW Kininogen] β> Kallidin β(via Aminopeptidases)β> 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 β Activated by [Factor 12A Hageman]
A: Relation of Kallikreins to [DIC associated hypOtension]?
B: How are Kallikreins activated in the Pancreas?
A:
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 β> 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] β> 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 Metaloproteasesβ> [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 β> 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: β HIVVβ
- 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
A: Vasoconstrictor or VasoDilator?
B: In what Disease does it levels increase?
C: Whatβs 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
βIntimate Moments Demand Viagra and Condomsβ
- Imilironone
- Milironone
- Dipyridamole
- Viagra
- Cilastazol