Cardiology: Clinical Flashcards
Sodium Nitroprusside
- Main indications
- MoA
- Relevant pharmacology
- Side effects/Contraindications
- Other considerations
Indications: Smooth muscle relaxant, used for treatment of acute severe hypertension and CHF
MoA: provides the smooth muscle cell with nitric oxide. It significantly decreases total peripheral resistance.
Side effects: mainly hypotension. Can also cause irritation at injection sites and extraversion should be avoided
Nitroglycerin
- Main indications
- MoA
- Relevant pharmacology
- Side effects/Contraindications
- Other considerations
Indications: CHF or hypertension
MoA: venodilator therefore reducing preload, myocardial oxygen demand, Essentially it is broken down into nitric oxide
Side effects: rash and headaches, hypotension.
Other: tolerance will develop within 48-72 hours.
What receptors does dobutamine work on?
What is its advantage over dopamine?
Predominantly beta-1
It also has a mild beta 2 and alpha 1 effect - these tend to cancer each other out.
Dopamine leads to a release of endogenous norepinephrine whereas dobutamine does not.
Digoxin
- Main indications
- MoA
- Relevant pharmacology
- Side effects/Contraindications
- Other considerations
Indications: supraventricular arrhythmias (mainly AFib).
MoA:
- Increases myocardial contractility
- Decreases conduction velocity through the AVN
These are thought to result from increased calcium availability to myofibrils and inhibition of Na/KATPase.
Relevant pharmacology: really excreted, careful with MDR1
Side effects:
- Do not extravase
- Arrythmias
- Gastrointestinal upset
Amiodarone
- Main indications
- MoA
- Relevant pharmacology
- Side effects/Contraindications
- Other considerations
Indications: can be used for most arrhythmia but due to the side-effects it is usually a last-line treatment.
- MoA: primarily potassium blockade but also has beta and calcium channel blocking effects.
- Side Effects/Contraindications:
- Don’t use in thyroidal disease patients
- GI, hepatotoxicity, neutropenia, thrombocytopenia, keratopathy
- Skin effects
Pimobendan
- Main indications
- MoA
- Relevant pharmacology
- Side effects/Contraindications
- Other considerations
Indications: heart diesease
MoA:
Positive inotrope, vasodilation, indirect negative chronotrope.
Inhibition of PDEIII and increase in calcium sensitivity of contractile apparatus without changing intracellular calcium concentrations. PDEIII inhibition increases cAMP which increases cardiac contraction but inhibits it in vascular smooth muscle (I think!).
What does PDE III do?
It converts cAMP to AMP.
MoA of aspirin?
COX-1 inhibition through acetylation of the enzyme.
MoA of heparin
Enhances the activity of AT III.
This results in inhibition of thrombin (IIa), Xa, IXa and XIIa.
At higher doses it prevents thrombin from activating V and VIII.
MoA of urokinase/streptokinase
Convert plasminogen to plasmin
MoA Warfarin
Inhibits vitamin K epoxide reductase (so vitamin K epoxide cannot be refreshed into vitamin K to be used in carboxylation of II, IV, VII, IX, X).
It also inhibits the production of protein C and S so can cause an initial hypercoaguable state.
Clopidogrel effects
The membrane ADP(2Y12) receptor on platelets which prevents platelet activation. Altering this receptor prevents membrane complex IIB/IIIA forming fully which prevents release of vasoactive compounds such as ADP and serotonin and also prevents binding to fibrin and vWF. This alteration is permanent throughout the life of the platelet.
What are the main types of heart failure?
Diastolic failure
Volume overload (or reduced ability to pump e.g. DCM, MMVD, shunts)
Increased afterload (e.g. valvular stenosis)
Arrhythmia related
What are the main neurohormonal alterations in heart failure?
Sympathetic stimulation
RAAS activation
ANP and BNP over secretion
Increased adrenomedullin, endothelia and AVP
Increase in pro-inflammatory cytokines such as TNF-a, IL-1 and IL-6.
Which enzyme is present in the adrenal medulla that allows the conversion of nEP to EP?
Phenyletholamine N-methyltransferase (PNM)
CNP - what does it do, where is it produced?
It is produced in the vasculature and may relax vessels.
What are the receptors and functions that AVP can act on?
V1A = increases inotropy and causes vasoconstriction V2 = renal reabsorption of H20 V2r = baroreceptors to augment the baroreceptor reflex
Why is AVP thought to be released in heart failure?
Probably due to a reduced cardiac output, as otherwise the state is one of low osmolality.