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Year 2 Pharmacology > CHD / STROKE Drugs > Flashcards

CHD / STROKE Drugs Flashcards

1
Q

Nitrates (Nitrovasodilators) affect what most?

  • Systemic Arteries
  • Narrow Coronary Arteries
  • Large Veins
  • Cerebral Arteries
A

LARGE VEINS

As there will be less blood returning to the heart because there’s more in the venuos system.
So, heart fills less due to less workload and less O2 demand…

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2
Q

What is the most common Nitrate? (Nitrovasodilator)

A

Glycerin Trinitrate (GTN)

Either- spray, sub lingual tablet, or transdermal patch.

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3
Q

Name common side effects of Nitrovasodilators (Nitrates)?

A 
Dizziness (due to lowered BP)
Throbbing Headache (due to cerebral vasodilation)
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4
Q

What things need to be cautioned when people are on GTN and other Nitrates?

A

That they’re not on anyother BP medication as it can get too low causing fainting and dizziness.

Caution with other drugs acting on same pathway such as:
Viagra (Sildenafil)

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5
Q

What are STATINS in the most basic sence

A

They’re lipid lowering drugs.

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6
Q

What side effect is a big concern if people are on STATINS?

A

Muscle problems such as ‘strange muscle pains’

As this can be a serious sign of myopathy (muscle disease)

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7
Q

Examples of statins…

A

Fluvastatin
Lovastatin
Pravastatin
Simvastatin

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8
Q

Some side effects of STATINS…

A 
GI upset (usually wears off)
Anbormal Liver Tests (usually mild)
Muscle Problems (Myopathy - RARE BUT SERIOUS)
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9
Q

How do STATINS work?

A

They are inhibitors of ‘HMG0Co-A reductase’ a rate-limiting step in cholestral synthesis

So by inhibiting them, you inhibit cholestral synthesis.

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10
Q

True or false:

STATINS can’t work in diabetes

A

FALSE

Statins CAN work in diabetes and also in people at any age and gender.

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11
Q

What’s an MI

A

Myocardial infarction – coronary artery completely blocked, typically by blood clot on ruptured plaque

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12
Q

How do Nitrates work (Nitrovasodilators)?

A

They Produce Nitric Oxide (NO) which increases the production of cGMP in muscle cells. Therefore relaxing muscles and vessles dilate (because there’s a smooth muscle layer in vessles)

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13
Q

Who’s at risk of a stroke?

A 
56 yr old ♂  
smoker  
High BP - 170/110 (Heart overworked)
Total chol - HDL  ratio 5
Ischemic heart pain on exertion
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14
Q

What constitutes a “Cerebrovascular Accident”

A
  • A Blockage; Thromboembolic infarction (~85%) (embolism breaking off from somewhere else in body and travels to the brain)
  • Damage/Bleed; Intracranial Haemorrhage
  • Cerebral, cerebellar and subarachnoid haemorrhage (~15%) - blood leaks into the brain
  • Cerebral Infarction - blood clot stops blood flow to an area of the brain
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15
Q

What drug is an example of Fibrinolysis (Thrombolysis)

A

‘recombinant tissue plasminogen activators’ or ‘r-tPAs’

They activate PLASMIN which is the body’s natural clot busting drug. Turning plasminogen into plasmin!
e.g.
Alteplase® (& other r-tPAs): recombinant HUMAN proteins, so non-antigenic.
Given IVin in stroke units (bleeding risk)
Short-acting.

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16
Q

What is Plasmin

A

It’s the body’s natural clot busting agent. It degrades Fibrin (clots) .

It’s inactivated form is Plasminogen which requires Plasminogen activators to convert it to Plasmin in order to dissolve clots.

17
Q

What are

‘recombinant tissue plasminogen activators’ or ‘r-tPAs’

A

They’re clot busting drugs:

‘Fibrinolysis/ Thrombolysis’ Drugs

eg ALTEPASE

18
Q

Give examples of Anti-platelet drugs

A

Aspirin (Ihnibit COX1 from turning aracadonic acid to thromboxane)
Clopidogrel (Antagonizer on platelett the cell surface)
Dipyridamole (Prevent the conversion of prostaglandin H2 into Thromboxane
Abciximab (Inhibit Fibrinogen)

19
Q

What antiplatelett drugs:

PREVENT AGGREGATION &; CLOT FORMATION by preventing GPIIa/IIIb receptor expression?

A

Aspirin® (acetylsalicylic acid): non steroidal anti-inflammatory drug (NSAIDS)
→ Inhibits cyclo-oxygenase (COX1).
→ Prevents thromboxane formation Dipyridamole
→ Inhibits thromboxane synthase
→ Prevents thromboxane formation Dipyridamole often used in conjunction with Aspirin & Clopidogrel
→antagonize actions of ADP at purinergic (ADP) receptors

20
Q

Which antiplatelett Drugs:

prevent GPIIa/IIIb receptor interaction and Inhibits Fibrinogen

A

Abciximab: Ab to GPIIb/IIIa receptors: prevents linking of platelets to fibres

And inhibits Fibrinogen

21
Q

What triggers the clotting cascade?

A

When blood contacts:

Damaged Tissue and exposed collagen

22
Q

What does Thrombin do?

A

It converts

Fibrinogen –> into Fibrin (an insoluble clot)

23
Q

What is the mechanism of action for Anti- coag drug HEPARIN

A

Heparin (intravenous administration), activates (one of) body’s own anti-clotting molecules, antithrombin III.

Works IMMEDIATELY

24
Q

What is the mechanism of action for Anti-coag drug WARFERIN

A

It is similar to the structure of Vitamin K

Works on the liver to reduce the enzyme:
‘vitamin K reductase’
Which uses vit k to ‘final assemble’ clotting factors.
Which diminished the body’s ability to make clotting factors and therefore the ability to make fibrin.

25
Q

If a patient is on Warferin, what certain things can effect the drug and clotting?

A

diet, drinking, acute illness etc

26
Q

What anticoag/clotting cascade drug is derived from the saliva of the medicinal leech

A

Direct (selective) Inhibition
of steps of clotting cascade

So direct inhibitors of THROMBIN

People on these drugs need less monitoring, less side effects and can be used if warferin isn’t tolerated.

27
Q

What are the 2 types of Heparin?

A
  1. unfractionated heparin.

2. low molecular-weight heparins.

28
Q

True or false…

In haemorrhagic stroke, anticoagulants should be continued.

A

FALSE

  • If haemorrhage confirmed, stop anticoagulating / reverse to establish ‘normal’ clotting (INR!) To prevent the bleed getting worse. Unless good reason to keep on- AF
29
Q

True or false…

There is no evidence to suggest that anticoagulants are effective in the treatment of Acute Ischemic Stroke.

A

TRUE

Meta-analysis of 6 randomized trials (22,000 patients) found: no evidence the use of anticoagulants (unfractionated heparin, low molecular-weight heparins, heparinoids, thrombin inhibitors, or oral anticoagulants) in the acute phase of stroke improves functional outcomes

30
Q

How can you reverse Anti-Coagulant action (like you would in haemorrhagic stroke?

A

If not in hurry, can stop anticoagulant drugs & wait

Vitamin K to reverse warfarin action (still takes a while – why?)

URGENT: give clotting factors

31
Q

How do you treat a long term Ischemic Stroke?

A
  1. Antiplatelet therapy:

Long-term anti-platelet therapy reduces substantially the incidence of further infarction.

Secondary Prevention
e.g. combined aspirin (75 mg day) and dipyridamole (200 mg 2x day)

Year 2 Pharmacology (11 decks)

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