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Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Statins and Fibrates

A

Anti Cholesterol drugs

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2
Q

Anticoagulant

A

warfarin

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3
Q

Streptokinase tPA

A

Fibrionolytic- used to dissolve a clog which is already there

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4
Q

Aspirin and Clopidogrel

A

antiplatelet drugs

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5
Q

What class of drugs block Na reabsorption in kidneys?

A

diuretics

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6
Q

Furosemide

Bendorfluazide

A
  1. Thiazide diuretics (mild)- hypertension

2. Loop diuretics (stronger)- heart failure

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7
Q

Name some side effects of diuretics

A

K lost from urine- hypokalaemia- tired and arrhythmias

Hyperglycaemia- diabetes

Increased blood sugar levels, increased uric acid- gout

Impotence

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8
Q

Name the 2 classes of beta blockers- which receptors do they block?

A

Cardioselective blocks only B1 receptors

Non selective B blockers blocks B1 and B2

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9
Q

Give an example of each Beta blocker and why they are used

A

B1- atenolol used in angina, hypertension and heart failure

B1+2- used less frequently to block tremor of overactive thyroid

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10
Q

Why should you never use Beta blockers in asthma?

A

Tired,heart failure and cold peripheries

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11
Q

Why are Beta blockers good in long term but not short term?

A

They can worsen heart failure in short term

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12
Q

Name some drugs in Dihyropydrine Ca anatagonists and Rate limiting Ca antagonists

A

Amlodipine

Verapamil, Diltiazem

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13
Q

What does the alpha blockers Doxazosin do and when is it used?

A

blocks alpha adrenoceptors to cause vasodilatation- sed in hpyertension and prostatic hypertrophy but can cause postural hypotension

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14
Q

What is the action of an ACE inhibitor?

A

blocks angiotensin 1 from becoming angiotensin II

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15
Q

Give an example of an ACE inhibitor and what is their typical suffix?

A

Lisinopril and -PRIL

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16
Q

What are the benefits of ACE inhibitors?

A

Hypertension, renal dsyfunction, good for kidneys in diabetic nephtopathy, back for kidneys in renal stenosis

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17
Q

What are the side effects of ACE inhibitors?

A

Dry cough, renal dysfunction, angioneurotic oedema- NEVER GIVE TO A PATIENT WHO HAS HAD LARYNX ODEMA IN PAST

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18
Q

In which patients should ACE inhibitors never be used?

A

Pregnant women and women of child bearing age

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19
Q

What side effect can be avoided by prescribing an Angiotensin Receptor Blocker (ARB) instead of an ACE inhibitor

A

Dry cough

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20
Q

Give an example of an ARB and its generic suffix

A

Losartan -ARTAN

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21
Q

What class of drugs does Isosorbide mononitrate belong to and what is it used it?

A

Nitrates

Angina and ACUTE heart failure

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22
Q

In what class of drugs is tolerance common and how should this be tackled?

A

Nitrates- prescribe during the day but not at night. 8hr periods at a time

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23
Q

What class does these drugs belong to?

A

Aspirin, Clopidogrel, Ticgrelor, Prasugrel

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24
Q

What is the major risk of anti platelet drugs?

A

Haemorrhage

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25
Q

What class is Bezafibrate and what can it be used in?

A

hypertiglyceridaemia, low HDL cholesterol

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26
Q

What are the following drugs used in: Amiodarone, beta blockers, fecainide?

A

Ventricular arthymias

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27
Q

What is digoxin?

A

A cardiac glycoside that increases contractility of the heart

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28
Q

What does Digoxin do to AV conduction?

A

It causes a degree of AV conduction delay

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29
Q

Why is digoxin useful in heart failure?

A

Reduces SV hence reduces CO

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30
Q

Why is digoxin good in AF?

A

It reduces the ventricular rate of beating to half the rate

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31
Q

What does digoxin do to the ventricles?

A

Increases ventricular irritability which produces ventricular arrythmias

32
Q

What is If current and how is it carried?

A

Funny current carried by Na influx- “long current”

33
Q

Name a molecular entity targeted by drugs to decrease heart rate

A

HCN

34
Q

Name an If blocker and what is it useful in?

A

Ivabradine in angina

35
Q

Describe the mechanism of Digoxin

A

3Na is kicked up and 2K goes back in…3Na goes back in and 1 Ca is kicked out

36
Q

What opens HCN channels?

A

cAMP

37
Q

What are the standard limb leads?

A

I- RA-LA
II- RA-LL
III- LA-LL

38
Q

What are the augmented limb leads?

A

aVL, aVR, aVF

39
Q

What are the 7 questions that should be asked in an ECG analysis?

A
  1. Is electrical activity present?
  2. Is the rhythm regular or irregular?
  3. What is the HR?
  4. P waves present?
  5. What is the PR interval (needs to be less than 0.1s)
  6. Is each P wave followed by QRS?
  7. Is QRS duration normal?
40
Q

What does an ECG not include?

A

MI, Intermittent Rhythm Disturbance and stable angina

41
Q

What does HDL do?

A

Reverses cholesterol transport by transporting it back to the liver by “scavenger receptor”

42
Q

What are the components of an arterial thrombus and what occurs as a result?

A

It is a “white thrombus” which is mainly platelets in a fibrin mesh and it detaches from its site of origin e.g. left heart/carotid artery. It can lodge in an artery in the brain causing a stroke

43
Q

What are the components of an venous thrombus and what occurs as a result?

A

Red thrombus: white head and jelly like tail, fibrin rich. If detaches forms an embolus that usually lodges in the lung (PE)

44
Q

Once the endothelial is damaged, what are the 2 main pathways concerned?

A

Platelet reactions and blood coagulation

45
Q

In the blood coagulation cascade, what is the series of events?

A

Platelets release preformed mediators such as ADP or synthesise others such as TXA2 which activate other platelets, causing an activation cascade

46
Q

What pathway activates prothrombin then thrombin

A

X–> Xa–> II–> IIa

47
Q

What does Vitamin K activate?

A

carboxylase enzyme which mediates gamma carboxylation

48
Q

What does Warfarin do pharmacologically?

A

It prevents reduced forms of vitamin K from forming which are needed or the activation cascade

49
Q

Name the glycoprotein precursors

A

VII, IX, X

50
Q

Name the serine proteases

A

VIIa, IXa, Xa

51
Q

What can anticoagulants be used to prevent and treat?

A

Venous thrombosis NOT arterial

52
Q

What can anticoagulants prevent and treat and what is the risk?

A

DVT, post op thrombosis, patients with artificial heart valves, AF
Risk of haemorrhage

53
Q

What factors does Warfarin block?

A

II, VII, IX, X

54
Q

How can the mechanism of warfarin be reversed?

A

Through administration of vitamin K or concentrate clotting factors

55
Q

How can the coagulation cascade be prevented from spinning out of control?

A

By Antithrombin III which along with heparin prevents antithrombin X from becoming Xa and II from becoming IIa

56
Q

What is the mechanism of heparin?

A

IIt binds to antithrombin III and increases its affinity for serine protease clotting factors (Xa and IIa) to increase their rate of deactivation

57
Q

When should low molecular weight heparins not be used and why?

A

In renal failure as elimination occurs via excretion

58
Q

Give 2 examples of LMWH

A

Enoxaparin and dalteparin

59
Q

How is heparin and LMWH given?

A

Heparin- IV or subcubcutaneously

LMWH- subcutaneously

60
Q

What order of kinetics does heparin and LMWH follow?

A

Heparin- zero order

LMWH- first order

61
Q

What are some of the adverse side effects associated with heparin and LMWH?

A

haemorrhage, osteoporosis, hypercalcaemia (hypoalosteronism), hypersensitity reactions

62
Q

What factors drive platelet aggregation and what does it allow?

A

ADP, 5H-T as well as TXA2 from the enzyme cycle-oxygenase (COX)
Allows: fibrinogen to bind and platelets to link

63
Q

What mechanisms do anti platelet drugs block?

A

Clopidogrel blocks ADP on P2Y12 receptor
Tirofiban blocks on GPIIb/IIIa receptor
Aspirin blocks COX- synthesis pathway of TXA2

64
Q

What is Clopidogrel, what is its mechanism and when/how should it be given?

A

Links to P2Y12 by a disulphide bond production irreversible inhibition
More often in patients intolerant of aspirin
Orally
Antiplatelet

65
Q

What is Tirofiban and when/how should it be given?

A

Antiplatelet

Given IV in short term to prevent Mi in high risk patients with unstable angina (with aspirin and heparin)

66
Q

What opposes the coagulation cascade?

A

The Fibrinolytic cascade

67
Q

How is Plasminogen converted into Plasmin?

A

By Streptokinase, alterplase and duptxplase

68
Q

Why are fibrinolytic used?

A

to reopen occluded arteries in acute MI, stroke, venous thrombosis or PE

69
Q

What is the mechanism of clot formation?

A

Plasminogen–> Plasmin–> Fibrin–> Fibrin fragments–> Clot lysis

70
Q

What is Streptokinase and what does it do?

A

A protein extracted from cultures of streptococci
Reduces mortality in MI, but action blocked after 4 days by generation of antibodies and not given after this time
May cause allergic reactions and should not be given to patients with recent Streptococcal infections

71
Q

What are Alteplase and Duteplase and what do they do?

A

Recombinant tissue plasminogen activator (rt-PA)
Effective on fibrin bound plasminogen and are selective for clots
Do not cause allergic reactions
Short HL, given IV

72
Q

What are the major side effects of fibrinolytics and how can it be controlled?

A

Haemorrhage

Controlled by Tranexamic acid which inhibits plasminogen activation

73
Q

What are the classes of drugs used to treat hypertension?

A

diuretics- loop and thiazides, beta blockers, Ca antagonists, ACE, ARB, Peripheral alpha 1 antagonists, central alpha 2 antagonists, direct vasoldilators (rare)

74
Q

What is the first line initial treatment for hypertension in hypertension?

A

Thiazides

75
Q

What is the 1st line treatment for patients with hypertension and diabetes?

A

ACE and angiotensin II receptor blockers

Cardiovascular (8 decks)

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