Pharmacology Flashcards

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1
Q

Why aren’t thrombolytics used more regularly?

A

Because they are associated with increased bleeding risk; the benefits do not always outweigh the harms.

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2
Q

Thrombolytics mechanism

A
  • Catalyses activation of plasminogen into plasmin
  • Plasmin breaks down fibrin in clots, thus dissolving them
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3
Q

What are the two main thrombolytic drugs?

A
  • Tenecteplase
  • Alteplase
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4
Q

List some conditions which beta blockers can be used to treat

A
  • Heart failure
  • Ischaemic heart disease
  • Tachycardia
  • Essential tremor
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5
Q

Which beta receptors do selective/non-selective beta blockers

A

Selective: Only block beta 1
Non-selective: Block beta 1 and beta 2

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6
Q

List two beta 1 selective beta blockers

A
  • Atenolol, metoprolol (general)
  • Nebivolol and bisoprolol (chronic systolic heart failure)
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7
Q

List four beta 1 selective beta blockers

A
  • Atenolol, metoprolol (general)
  • Nebivolol and bisoprolol (chronic systolic heart failure)
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8
Q

List three non-selective beta blockers

A
  • Propanolol (chronic liver disease)
  • Carvedilol (chronic heart failure)
  • Labetalol (used in hypertension in pregnancy)
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9
Q

Absolute contraindications for beta blockers (think about all effects of beta receptors)

A
  • Hypotension
  • Uncontrolled heart failure
  • Severe or poorly controlled reversible airways disease
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10
Q

Relative contraindications for beta blockers

A
  • Diabetes (won’t be able to detect hypoglycaemia)
  • Peripheral vascular disease (walking distance reduced)
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11
Q

Things to communicate when starting beta blockers

A
  • Dizziness/tiredness
  • Do not stop treatment suddenly
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12
Q

For what conditions are calcium channel blockers used?

A
  • Hypertension
  • Ischaemic heart disease
  • Tachycardia
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13
Q

Effect of calcium channel blockers on vascular smooth muscle

A

Relaxation

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14
Q

Effect of calcium channel blockers on myocardium

A

Reduced contractility

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15
Q

Effect of calcium channel blockers on cardiac conduction tissue

A

Reduced heart rate

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16
Q

Effect of calcium channel blockers on gut

A

Relaxation of lower oesophagus (reflux) and intestine (constipation)

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17
Q

What are verapamil calcium channel blockers selective for?

A

Myocardium compared to peripheral vascular tissue

18
Q

What are dihydropyridine calcium channel blockers selective for?

A

Peripheral vascular tissue

19
Q

Which patients should not be prescribed DHP calcium blockers?

A
  • Low HR
  • Low BP
  • Cardiac conduction defect
  • Systolic heart failure
20
Q

Dihydropyridines (CCB) adverse effects

A
  • Vasodilation: flushing, headache
  • Swelling of ankles
21
Q

How do nitrates work? How do they make it easier for the heart to circulate blood around the body?

A
  • Source of NO
  • Relaxes smooth muscle structures such as veins and arterioles
  • Reduced venous return, reducing preload and work
  • Also, arteriolar dilation, lowering blood pressure and decreasing afterload
22
Q

Ace Inhibitor suffix

A

-pril

23
Q

Side effects of ACE inhibitors?

A
  • Renal failure
  • Bradykinin cough
  • Rarely, angioedema
24
Q

Why aren’t ARBs used all the time instead of ACE inhibitors? After all, they bypass the risk of bradykinin cough…

A

They aren’t as proven in some situations, and so ACEIs are usually used in the first instance.

25
Q

ARB suffix

A

-sartan

26
Q

What are the two classes of heparin?

A
  • Unfractionated
  • Low molecular weight
27
Q

Why is LMW heparin considered better than unfractionated heparin?

A
  • No antiplatelet effect (no thrombocytopaenia)
  • More reliable
  • Longer half life
28
Q

Antiplatelets vs anticoagulants

A

Antiplatelets: Stop platelets from clumping together
Anticoagulants: Stop clotting factors that produce clots

29
Q

Heparin suffix

A

-parin

30
Q

Recall three types of heparin

A
  • Enoxaparin
  • Dalteparin
  • Nadroparin
31
Q

Under what conditions would you not give a patient heparins?

A
  • Active bleeding
  • Thrombocytopaenia (in the case of unfractionated heparins)
  • Renal failure (drugs are renally cleared)
32
Q

Describe heparin induced thrombocytopaenia syndrome

A

IgG antibodies against heparin-platelet complex. Causes platelet aggregation and thrombin generation. Hence, you get thromboses, as well as bleeding due to thrombocytopaenia

33
Q

What are the main adverse effects of statins?

A
  • Muscle aches (myalgia)
  • Mysotisis (inflammation)
  • Myopathy (weakness)
  • Rhabdomyolysis (muscle death)
34
Q

What does ARNI stand for?

A

Angiotensin receptor antagonist + neprolysin inhibitor

35
Q

What type of enzyme is neprolysin? What does it do?

A
  • In a class of enzymes called neutral endopeptidases
  • Breaks down substances such as BNP, angiotensin II, and bradykinin
36
Q

What is the effect of increased Brain Natriuretic Peptide caused by ARNIs during HF?

A
  • Increased natriuresis
  • Decreased sympathetic tone
  • Decreased RAAS activation
37
Q

What is the effect of increased bradkyinin caused by ARNIs during HF?

A

Angioedema

38
Q

Why is it that neprolysin inhibitors are combined with angiotensin receptor antagonists in the case of ARNI?

A
  • Neprolysin breaks down angiotensins I and II and BNP
  • Inhibiting neprolysin increases BNP, which is good, but also increases angiotensin II, which is bad for decreasing blood pressure
  • Therefore, by combining neprolysin inhibitors with ARBs, we get the best of both worlds
39
Q

Suitability issues unique to ARNIs…

A
  • Contraindicated for patients with angioedema
  • Can’t be used with ace inhibitor; increased risk of angioedema
40
Q

Provide a potential mechanism for how SGLT2 inhibitors can help in heart failure

A
  • SGLT2 inhibited in the kidneys
  • Sodium and glucose are not reabsorbed into the bloodstream; remain in filtrate
  • Elevated sodium detected by macula dena
  • Renin release inhibited
  • RAAS inhibited
  • Blood pressure decrease
41
Q

Ivabradine basic mechanism

A
  • Briefly inhibits flow of ions during cardiac pacemaker current
  • Increases length of diastole
  • Decreases heart rate