Term
| Ramipril, Lisinopril, Enalapril, and Captopril are all ACE inhibitors. Broadly, how do ACE inhibitors work? |
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Definition
ACE converts angiotensin I to angiotensin II (ATII). ATII regulates blood pressure and is a key component of the renin-angiotensin-aldosterone system (RAAS). ATII increases blood pressure using a number of mechanisms.
1) Stimulation of secretion of aldosterone from the adrenal cortex
2) Stimulation of Vasopression secretion from the posterior pituitary gland.
3) Through direct arterial vasoconstriction. |
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Term
| How does noradrenaline work as a drug? |
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Definition
| Norepinephrine is a precurser of epinephrine secreted by the adrenal medulla. Norepinephrine is the principal transmitter of most postganglionic sympathetic fibers and of the diffuse projection system in the brain arising from the locus ceruleus. Norepinephrine functions as a peripheral vasoconstrictor by acting on both alpha-1 and a-2 adrenergic receptors. It is also an inotropic stimulator of the heart and dilator of coronary arteries as a result of it's activity at the beta-adrenergic receptors. |
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Term
| Explain the mode of action of Verapamil. |
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Definition
Verapamil inhibits voltage-dependent calcium channels. In the heart it blocks the L-type calcium channels causing a reduction in ionotropy and chronotropy, reducing heart rate and blood pressure.
There are two enantiomers of Verapamil. The R-enantiomer is more effective at reducing blood pressure compared to the S-enantiomer. However, the S-enantiomer is 20 times more potent than the R-enantiomer at prolonging the PR interval in treating arrhythmias.
Verapamil is still used (not commonly) but it can only be given via IV. Diltiazem more common as a non-dihydropyridine Calcium Channel Blocker, but this is not available via IV (although it is in the USA). |
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Term
| Digoxin is a cardiac glycoside NA/K ATPase inhibitor. What the fuck does this mean? :) |
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Definition
Digoxin is used to treat congestive heart failure, and supraventricular arrhythmias.
Its mode of action is via inhibition of the Na-K-ATPase membrane pump, resulting in an increase in intracellular sodium.
This causes in turn the sodium calcium exchanger (NCX) to extrude the sodium and pump in more calcium. This alteration in calcium concentration is thought to promote activation of contractile proteins (e.g., actin, myosin).
Digoxin also acts on the electrical activity of the heart, increasing the slope of phase 4 depolarization, shortening the action potential duration, and decreasing the maximal diastolic potential.
Still used in Atrial Fibrillation, but now very much third line treatment option. Rarely used in heart failure as much better drugs available |
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Term
| Explain the function and uses of Amiodrone. |
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Definition
Amiodarone: An antianginal and antirhythmic agent (A potassium channel blocker)
Amiodarone is a Vaughan-Williams Class III antiarrhythmic agent (lol).
The antiarrhythmic effect of amiodarone may be due to at least two major actions.
1) Prolonging the myocardial cell-action potential (phase 3) duration and refractory period and
2) Acts as a noncompetitive a- and b-adrenergic inhibitor.
It can also have
1) b-blocker activity and calcium channel blocker-like actions on the SA and AV nodes
2) increases the refractory period via sodium- and potassium-channel effects
3) slows intra-cardiac conduction of the cardiac action potential, via sodium-channel effects.
Still used but much less common as defibrillators are now inserted. (makes one wonder why we are learning this then) |
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Term
| Explain the mechanism of action of Warfarin. |
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Definition
Warfarin is used in the prevention and treatment of thromboembolic disease including venous thrombosis, thromboembolism, and pulmonary embolism as well as for the prevention of ischemic stroke in patients with atrial fibrillation (AF). Warfarin can cross the placental barrier during pregnancy resulting in foetal bleeding, spontaneous abortion, and neonatal death.
Warfarin inhibits vitamin K reductase, reducing levels of the reduced form of vitamin K. As vitamin K is required for the production of coagulation factors II, VII, IX, and X and anticoagulant proteins C and S, these levels also drop. Depression of three of the four vitamin K-dependent coagulation factors (factors II, VII, and X) results in decreased prothrombin levels, decreased thrombin generation and reduced ability to form a clot.
Warfarin is declining in use with the advent of non-vitamin K antagonist oral anticoagulants. |
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Term
| Propanolol, Atenolol - who dat? |
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Definition
B -adrenergic antagonists competes with sympathomimetic neurotransmitters such as catecholamines for binding at β1-adrenergic receptors in the heart and vascular smooth muscle. This results in a reduction in resting heart rate, cardiac output, systolic and diastolic blood pressure, and reflex orthostatic hypotension.
Atenolol has similar properties to propranolol and it is a β1-selective antagonist. Higher doses of Atenolol also competitively block β2-adrenergic responses in the bronchial (in asthmatic patients this can cause bronchoconstriction) and vascular smooth muscles. |
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Term
| How does oxygen work as a therapeutic? |
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Definition
| Oxygen levels, or oxygen saturation is a key clinical diagnostic. Healthy individuals should have an Oxygen SAT of greater than 96%. However, patients with lung diseases, such as pneumonia, can have reduced ability to breathe in or transport oxygen effectively, identified in a reduced Oxygen SAT (less than 88%). Therefore, patients with low blood oxygen levels can be treated with additional pure oxygen or air/oxygen mixtures via a mask, nasal cannula, or tracheal intubation. This increased delivery of oxygen should alleviate the symptoms caused by low oxygen levels in the tissues. |
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Term
| Explain the mechanism of action of diamorphine/heroin |
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Definition
Heroin is a mu-opioid agonist. Heroin, targets four endogenous neurotransmitters (beta-endorphin, dynorphin, leu-enkephalin, and met-enkephalin). Heroin reduces (and sometimes stops) production of the endogenous opioids. Endorphins are regularly released in the brain and nerves, attenuating pain.
The onset of heroin's effects is dependent on the method of administration. Taken orally, heroin is totally metabolized in vivo into morphine before crossing the blood-brain barrier; so the effects are the same as oral morphine. Taken by injection, heroin crosses into the brain, where it is rapidly metabolized into morphine by removal of the acetyl groups. It is the morphine molecule that then binds with opioid receptors and produces the subjective effects of the heroin high. |
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