Exam questions Flashcards

1
Q

Describe the mechanism of Losartan and explain why it would be prescribed

A

Losartan acts on the renin angiotensin system (RAS). It is an AT1 receptor antagonist, which means that it blocks these receptors.

Normally the RAS produces angiotensin to cause a vasoconstriction and to renally reabsorb more salts, so increasing peripheral resistance and blood pressure.

Since losartan stops angiotensin II from binding to its receptor, bodily systems are not activated as much as normal and so peripheral resistance will decrease, making it easier for the patient’s heart to eject blood.

This will improve the patient’s heart failure symptoms.

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2
Q

Describe the mechanism of Furosemide and explain why it would be prescribed

A

Furosamide is a loop diuretic and is very potent. It inhibits the Na+/K+/2 Cl– symporters in the thick section of the ascending limb of the loop of Henle.

Since this region of the nephron is normally able to reabsorb large quantities of ions, loop diuretics can cause a large diuresis.

Loop diuretics are useful in reducing oedema, which is a common problem in heart failure, thus these drugs will improve patient symptoms.

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3
Q

Describe the mechanism of Bisoprolol and explain why it would be administered

A

Bisproprolol: in heart failure, the heart has been damaged in some way, which causes a reduction in cardiac output.

To compensate for this, the sympathetic autonomic nervous system stimulates cardiac a1-adrenoceptors to increase heart rate and force of contraction, which makes the heart work harder.

Although this may reduce patient symptoms, it does run the risk of causing further damage to the heart. By antagonizing a1-adrenoceptors, bisproprolol protects the failing heart from over stimulation, so the heart is more likely to last for longer.

Bisproprolol can therefore increase patient life expectancy.

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4
Q

Describe the mechanism of Digoxin and explain why it would be administered

A

Digoxin binds to the α-subunit of the Na+/K+ ATPase pump in the membranes of heart cells and decreases its function (it competes with K+ ions).

This causes an increase in the level of sodium ions in the myocytes, which leads to a rise in the level of intracellular calcium ions, since fewer calcium ions are pumped out by the Na+/Ca2+ pump. This raises calcium concentration in myocardiocytes and pacemaker cells.

Increased intracellular calcium lengthens Phase 4 and Phase 0 of the cardiac action potential, which leads to a decrease in heart rate.

Also, increased intracellular concentration of calcium ions causes increased a positive cardiac inotropic effect, so by beating with more force, the heart can eject more blood to reduce heart failure symptoms.

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5
Q

Briefly describe the acute and chronic mechanisms of action of the statin family of drugs and how they can be used to improve plasma cholesterol concentration.

A

High plasma LDL levels are bad for cardiovascular health, as cholesterol will be deposited into arterial walls, which can then develop into atherosclerosis.

Cholesterol can be obtained from the diet, but can also be synthesized by the liver. Statin drugs initially inhibit the enzyme 3-hydroxy-3-methylglutaryl coenzyme A (HMG CoA) reductase, which is involved with cholesterol synthesis.

Therefore circulating cholesterol levels will fall. To compensate for this, the liver will express more HMG CoA reductase, so restoring cholesterol production.

Cholesterol levels in the blood will, however, remain low as the liver also expresses more LDL receptors and is therefore better able to take up LDL cholesterol, so helping to clear it from the blood.

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6
Q

List the side effects of statins

A

Gastrointestinal side effects are commonly encountered, such as constipation or diarrhea, and flatulence.

Feelings of nausea may also occur.

Muscle soreness is a common side effect too

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7
Q

Provide a brief definition of the term “asthma”

A

Asthma is caused by a recurrent, reversible large increase in airway resistance due to stimuli not normally considered to be noxious (would not affect a non-asthmatic subject).

The calibre of a patient’s airways becomes reduced during attacks. Initially this is brought about by a bronchospasm, but can then be followed by inflammatory processes (local vasodilatation, attraction of leucocytes and oedema). Increased mucus secretion will also occur.

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8
Q

Describe the mechanism of action of salbutamol in the treatment of asthma

A

Salbutamol, a b2-adrenoceptor agonist, is most often supplied in a blue inhaler. b2-Adrenoceptor agonists, when used to treat asthma are primarily bronchodilators.

They stimulate b2-adrenoceptors on airway smooth muscle cell membranes to cause relaxation and a bronchodilatation. When b2-adrenoceptors on bronchial smooth muscle cell membranes are stimulated, they activate intracellular adenylate cyclase to convert ATP to cAMP. cAMP then activates protein kinase A, which phosphorylates myosin light chain kinases. When this happens, the cell’s contractile machinery ceases to work, causing relaxation.

Stimulation of b2-adrenoceptors also lowers intracellular concentration of free Ca2+ ions by enhancing calcium intracellular binding and extrusion, so there are less Ca2+ ions available to interact with

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9
Q

What are the likely side effects of salbutamol and why do they occur?

A

Likely side effects of salbutamol include:
• fine muscle tremor, as skeletal muscle b2-adrenoceptors may become stimulated, and
• tachycardia, as salbutamol can stimulate cardiac b1 -adrenoceptors

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10
Q

What advantages are there to administering salbutamol by inhalation?

A

By inhaling salbutamol, the drug is being delivered directly onto its target. Therefore this is a quick route of administration and low doses can be administered, as the drug does not have to be first distributed around the body before it reaches the bronchioles

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11
Q

Insulin binds to tyrosine kinase or type 3 receptors. By means of a labelled diagram describe the main features of this class of receptor, and describe the events that occur following insulin binding

A

The insulin receptor is a complex of two a- and two b- subunits.These are held together by disulphide bridges.
The a-subunits are extracellular. The b-subunits are transmembrane spanning proteins.

The a-subunits form the insulin binding site.
The intracellular portion of the b-units possess tyrosine kinase activity. When insulin binds, the b-subunits autophosphorylate, which enhances the kinase activity of other target proteins.

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