Pharmacology Flashcards
Why aren’t thrombolytics used more regularly?
Because they are associated with increased bleeding risk; the benefits do not always outweigh the harms.
Thrombolytics mechanism
- Catalyses activation of plasminogen into plasmin
- Plasmin breaks down fibrin in clots, thus dissolving them
What are the two main thrombolytic drugs?
- Tenecteplase
- Alteplase
List some conditions which beta blockers can be used to treat
- Heart failure
- Ischaemic heart disease
- Tachycardia
- Essential tremor
Which beta receptors do selective/non-selective beta blockers
Selective: Only block beta 1
Non-selective: Block beta 1 and beta 2
List two beta 1 selective beta blockers
- Atenolol, metoprolol (general)
- Nebivolol and bisoprolol (chronic systolic heart failure)
List four beta 1 selective beta blockers
- Atenolol, metoprolol (general)
- Nebivolol and bisoprolol (chronic systolic heart failure)
List three non-selective beta blockers
- Propanolol (chronic liver disease)
- Carvedilol (chronic heart failure)
- Labetalol (used in hypertension in pregnancy)
Absolute contraindications for beta blockers (think about all effects of beta receptors)
- Hypotension
- Uncontrolled heart failure
- Severe or poorly controlled reversible airways disease
Relative contraindications for beta blockers
- Diabetes (won’t be able to detect hypoglycaemia)
- Peripheral vascular disease (walking distance reduced)
Things to communicate when starting beta blockers
- Dizziness/tiredness
- Do not stop treatment suddenly
For what conditions are calcium channel blockers used?
- Hypertension
- Ischaemic heart disease
- Tachycardia
Effect of calcium channel blockers on vascular smooth muscle
Relaxation
Effect of calcium channel blockers on myocardium
Reduced contractility
Effect of calcium channel blockers on cardiac conduction tissue
Reduced heart rate
Effect of calcium channel blockers on gut
Relaxation of lower oesophagus (reflux) and intestine (constipation)
What are verapamil calcium channel blockers selective for?
Myocardium compared to peripheral vascular tissue
What are dihydropyridine calcium channel blockers selective for?
Peripheral vascular tissue
Which patients should not be prescribed DHP calcium blockers?
- Low HR
- Low BP
- Cardiac conduction defect
- Systolic heart failure
Dihydropyridines (CCB) adverse effects
- Vasodilation: flushing, headache
- Swelling of ankles
How do nitrates work? How do they make it easier for the heart to circulate blood around the body?
- 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
Ace Inhibitor suffix
-pril
Side effects of ACE inhibitors?
- Renal failure
- Bradykinin cough
- Rarely, angioedema
Why aren’t ARBs used all the time instead of ACE inhibitors? After all, they bypass the risk of bradykinin cough…
They aren’t as proven in some situations, and so ACEIs are usually used in the first instance.
ARB suffix
-sartan
What are the two classes of heparin?
- Unfractionated
- Low molecular weight
Why is LMW heparin considered better than unfractionated heparin?
- No antiplatelet effect (no thrombocytopaenia)
- More reliable
- Longer half life
Antiplatelets vs anticoagulants
Antiplatelets: Stop platelets from clumping together
Anticoagulants: Stop clotting factors that produce clots
Heparin suffix
-parin
Recall three types of heparin
- Enoxaparin
- Dalteparin
- Nadroparin
Under what conditions would you not give a patient heparins?
- Active bleeding
- Thrombocytopaenia (in the case of unfractionated heparins)
- Renal failure (drugs are renally cleared)
Describe heparin induced thrombocytopaenia syndrome
IgG antibodies against heparin-platelet complex. Causes platelet aggregation and thrombin generation. Hence, you get thromboses, as well as bleeding due to thrombocytopaenia
What are the main adverse effects of statins?
- Muscle aches (myalgia)
- Mysotisis (inflammation)
- Myopathy (weakness)
- Rhabdomyolysis (muscle death)
What does ARNI stand for?
Angiotensin receptor antagonist + neprolysin inhibitor
What type of enzyme is neprolysin? What does it do?
- In a class of enzymes called neutral endopeptidases
- Breaks down substances such as BNP, angiotensin II, and bradykinin
What is the effect of increased Brain Natriuretic Peptide caused by ARNIs during HF?
- Increased natriuresis
- Decreased sympathetic tone
- Decreased RAAS activation
What is the effect of increased bradkyinin caused by ARNIs during HF?
Angioedema
Why is it that neprolysin inhibitors are combined with angiotensin receptor antagonists in the case of ARNI?
- 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
Suitability issues unique to ARNIs…
- Contraindicated for patients with angioedema
- Can’t be used with ace inhibitor; increased risk of angioedema
Provide a potential mechanism for how SGLT2 inhibitors can help in heart failure
- 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
Ivabradine basic mechanism
- Briefly inhibits flow of ions during cardiac pacemaker current
- Increases length of diastole
- Decreases heart rate
