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Pharm Y2S1 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

Give examples of the functional responses of alpha-1 adrenoceptors.

A

Vasoconstriction
Increased blood pressure
Contraction of visceral smooth muscle
Relaxation of GI tract

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2
Q

Give examples of the functional responses of alpha-2 adrenoceptors.

A

Reduced transmitter and insulin release

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3
Q

Give examples of the functional responses of beta-1 adrenoceptors.

A 
Increase SA node firing
Lower AV refractory period
Increase myocardium force
Renin release from juxtaglomerular
Relaxation of GI muscle
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4
Q

Give examples of the functional responses of beta-2 adrenoceptors.

A

Bronchodilation
Nitric Oxide release
Reduce histamine
Stimulate glycogenolysis

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5
Q

Describe the mechanism of acetylcholine.

A

Calcium stimulates fusion of ACh containing vesicles to the presynaptic membrane, releasing ACh into the synapse. This then binds to receptors on the post synaptic membrane

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6
Q

How is the cholinergic mechanism halted?

A

AChE cleaves the ester bond in ACh and the remaining choline is taken up into the nerve terminal to be converted back to ACh.

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7
Q

Describe the structure of a muscarinic acetylcholine receptor.

A

Slow G protein coupled receptor, monomeric with 5 subtypes, each with varying tissue distribution. Contains 1 G protein binding site and one ACh binding site

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8
Q

Describe the structure of a nicotinic acetylcholine receptor.

A

Pentameric ligand gated channel with 5 subunits (2 alpha, beta, epsilon and delta). Each has two ACh binding sites.

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9
Q

Define stable angina.

A

Chest pain occurring on exertion and alleviated by rest. Occurs due to partial occlusion of coronary arteries.

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10
Q

Define unstable/brittle angina.

A

Chest pain occurring at rest due to disruption of atherosclerotic plaque in coronary artery.

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11
Q

What is variant angina?

A

Chest pain due to reflex spasm of coronary arteries.

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12
Q

Describe the mechanism of stable angina.

A

Occurs upon release of bradykinin adenosine from muscles during exercise. Can result in maximal dilation of vessels thus release of potassium and hydrogen ions to sensory nerve terminals resulting in pain due to the inability to maintain oxygen supply.

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13
Q

What is the role of phosphodiesterase?

A

Breakdown of cGMP and cAMP

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14
Q

Describe the process of vascular smooth muscle contraction involving calcium.

A

Adrenaline binding to alpha-1 receptors activates phospholipidase C, catalysing formation of inositol triphosphate. This causes calcium ion release from the sarcoplasmic reticulum within the cell, leading to the opening of calcium sensitive chloride channels. The efflux of chloride causing depolarisation causes the opening of L-tpe calcium channels, calcium influx causes binding to calmodulin which activates myosin causing contraction.

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15
Q

Describe the roles of cholesterol in the body.

A

Essential in plasma membranes

Precursor for steroid hormones, bile acid and vitamin D3.

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16
Q

What is the main role of triglycerides within the body?

A

Fat storage

17
Q

Describe the features of chylomicron.

A

Large, low density lipoprotein with high TG levels. Made in the gut and transported via lacteals into the lymph.

18
Q

Describe the features of very low density lipoproteins.

A

30-80nm in length with high TG levels. Made in the liver and transports lipids to tissues.

19
Q

Describe the features of low density lipoproteins.

A

20-30nm in length, low TG levels. Accounts for most blood cholesterol, transports lipids into tissues.

20
Q

Describe the features of high density lipoproteins.

A

7-20nm in length with low TG levels. Scavenge cholesterol from tissues and transfer it to vLDL/LDL via cholesteryl ester transferase.

21
Q

What is dyslipidaemia?

A

Abnormally low lipid levels, especially HDL.

22
Q

Describe the classifications (I-V) of hyperlipidaemia.

A

Type I: chylomicrons elevated (no increased risk of atherosclerosis)
Type IIa: LDL elevated (high risk of atherosclerosis)
Type IIb: LDL + VLDL elevated (high risk)
Type III: IDL elevated (moderate risk)
Type IV: VLDL elevated (moderate risk)
Type V: chylomicrons + VLDL elevated (no increased risk of atherosclerosis)

23
Q

What is the role of lipoprotein lipase?

A

Breaks down TG in lipoproteins to release fatty acids for energy production. Converts vLDL, LDL, chylomicrons to a remnant version.

24
Q

How do LDLs negatively impact the body?

A

LDL accumulates and is oxidised at sites of endothelial damage forming fatty streaks, promoting atherosclerosis. Fibrinolysis is inhibited, promotes platelet aggregation and thrombosis.

25
Q

How to HDLs positively impact the body?

A

They remove cholesterol from plaques within blood vessels and promote prostacyclin to work, inhibiting platelet aggregation and acting as a vasodilator.

26
Q

What are the ideal cholesterol levels within the blood?

A 
Total <5mmol/L
LDL <3mmol/L
HDL >1mmol/L
TG <1.7mmol/L
Ratio total:HDL <4
27
Q

Describe the pacemaker action potential.

A

Rapid depolarisation occurs due to opening of fast sodium channels. Sodium channels close causing minor repolarisation. Potassium channels close and slow calcium channels open causing a plateau in mV. Repolarisation occurs when potassium channels reopen and slow calcium channels close. At this point, all sodium and calcium channels are closed and potassium channels are open re-establishing -90mV resting potential.

28
Q

Describe the structure of calcium channels.

A

Has an alpha and beta subunit. Alpha subunit has 6 transmembrane domains in each of 4 pseudosubunits. There is a membrane dipping domain between the fifth and sixth domain that forms the lining. The 4th TM acts as the voltage sensor, opening and closing the channel.

29
Q

What is myasthenia gravis?

A

Autoimmune disease of the skeletal muscle that is the result of the attacking of the nicotinic receptors on the muscle membrane, compromising the ability of muscle to contract.

30
Q

Give examples of treatments available for myasthenia gravis.

A

Removal of the thymus gland
Acetylcholinesterase inhibitors
Immunosuppressants
Plasmapheresis to remove autoantibodies from circulation

31
Q

What drugs would restore enzymatic activity of AChE following exposure to sarin?

A

Pralidoxime

Pharm Y2S1 (8 decks)

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