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Cardio-resp > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

ERP

A

Effective refractory period

The length of time a cell in its normal condition would remain refractory before responding to a cell next to it

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2
Q

Arrhythmias classification

A
  • Bradyarrhythmia (atrioventricular block)

- Tachyarrhythmia (ectopic beats, tachycardia, fibrillation)

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3
Q

Can conduction blocks cause tachycardia

A

Yes, as well as bradycardia they can also cause tachycardia- through re-entry arrhythmias

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4
Q

What two things are critical for re-entry arrhytmia to occur

A

Timing

Refractory state

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5
Q

Classes of anti-arrhythmic drugs

A

1) Na+ channel blockers
2) B blockers
3) Prolong ERP
4) Ca2+ channel blockers

Adenosine
Digoxin

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6
Q

Effects of anti-arrhythmic drugs

A

1) Suppress enhanced automaticity (II and IV)
2) Prolong ERP (III)
3) Slow conduction rate (I and II)
4) Depress RMP (adenosine)

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7
Q

Na+ channel blockers

A

Slow conduction time (reduce conduction velocity) by blocking fast Na+ channels

Lignocaine
Flecainide

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8
Q

Adverse effects of Na+ channel blockers

A

1) Enhanced risk of arrhythmia

2) More chance of a fatal arrhythmia

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9
Q

B-blockers

A

B receptors cause increased HR as well as increase sino-atrial automaticity

These drugs reduce automaticity and conduction velocity

“olols”

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10
Q

Prolong ERP drugs (K+ channel blockers)

A

K+ channel blockers
Delay repolarosation

Amiodarone
Sotalol

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11
Q

Ca2+ channel blockers

A

Reduce conduction velocity

Suppress automaticity

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12
Q

Three classes of CCBs

A

1) Dihyropyridines (Verapamil and Diltiazem)

2) Non-dihydropyridines

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13
Q

Side effects of amiodarone

A

Hypothyroidism
Hyperthyroidism
Pulmonary fibrosis

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14
Q

Adenosine

A

Adenosine receptors are linked to K+ receptors,

they reduce RMP so that stimulus can’t raise it above the threshold

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15
Q

Three ways to treat hypertension

A

1) Reduce blood volume
2) Reduce SVR
3) Reduce CO by depressing HR and SV

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16
Q

What does angiotensin II do?

A

Raises BP

Increases retention of salt and water (through ADH)

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17
Q

What do anti-hypertensives act on in RAS system?

A

Angiotensin II

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18
Q

What are the classes of drugs- two actions on the renin-angiotensin system?

A

1) ACE inhibitors (“prils”)

2) Angiotensin receptor blockers (ARBs) (“sartans”)

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19
Q

Side-effects of angiotensin blockers?

A

Sudden drop in BP
Renal failure (fall in glomerular perfusion pressure)
ACE inhibitor cough (as bradykinin is broken down by ACE in the lungs)
Angioneurotic oedema

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20
Q

All anti-hypertensive drug classes

A

1) Angiotensin blockers
2) B-receptor blockers
3) a-receptor blockers
4) Ca2+ channel blockers
5) Volume reduction diuretics

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21
Q

B-receptor blockers

A

Work by reducing CO (decrease HR and contractility)

**Can’t work in the periphery

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22
Q

a-receptor blockers

A

Prazosin
Blocking causes reduced SVR and vasodilation

**If you block a-receptors on their own, body tries to compensate and reflex tachycardia may occur

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23
Q

Ca2+ channel blockers

A

Two classes:

  • Cardio-selective (Veramapil)
  • Cardio and vascular (Diltiazem)
  • Vascular selective (Dihydropyridines)
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24
Q

What is the mechanism of action of volume reduction diuretics?

A

1) Na+: prevent absorption in loop and DCT

**Aldosterone stimulates reabsorption of sodium

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25
Q

ADH

A

Water reabsorption in collecting duct

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26
Q

Loop diuretics

A

Inhibit sodium-potassium-chloride co-transporter in the thick ascending limb- leads to water loss and sodium loss

FRUSEMIDE

27
Q

Thiazide diuretics

A

Do the same thing but in the distal tubule

HYDROCHLOROTHIAZIDE
INDAPAMIDE

28
Q

K+ sparing diuretics

A

Antagonise action of aldosterone (aldosterone receptor antagonists)

EPLERENONE

29
Q

Potency of diuretics

A

The diuretics that act earlier on prevent more reabsorption compared to the ones that act later on

30
Q

K+ wasting diuretics

A

Both loop and thiazide diuretics that act directly on the channels lead to increased K+ excretion

31
Q

Initial treatment of hypertension

A
  • Thiazide diuretic with ACE-I or AT1 blocker

- Then add Ca2+ channel blocker

32
Q

Exogenous and endogenous pathway of lipid transport

A

Exogenous:

Absorption from diet —-> TG and cholesterol packaged in CM —-> CM circulate around and release TG —-> LDL hydrolyses TG and FFA are released —> CM repackaged and remnant CM removed by liver

Endogenous

TG synthesised by the liver packed into VLDL —-> Processed by LPL in tissues —-> FA taken up by muscles for energy —-> Either become IDL or LDL and go to the LDL receptor on the liver

33
Q

Reverse cholesterol transport

A

Process by which cholesterol is removed from the tissues

HDL is the main particle here

34
Q

Statins

A

Reduce the synthesis of hepatically produced cholesterol

Upregulate LDL receptors of hepatocytes

35
Q

Mechanism of statins

A

They inhibit HMG CoA reductase which eventually also increases the LDL receptors

36
Q

Side-effects of statins

A

Hepatic- increase transaminase
Cognitive- memory loss
Diabetes
Myositis

37
Q

Ezetimibe

A

Inhibits interaction of NPC1/L1 with clathrin/AP2- preventing endocytosis of cholesterol complex in the small intestine

38
Q

PCSK9 inhibitors

A

Prevent recycling of LDL and mark it for degradation

PSCK9 MABS

39
Q

PSCK9 side-effects

A 
URTI
GI
Hypertension
Neurocognitive
Muscle (myositis)
40
Q

Fibrates

A

Increases FFA B-oxidation

41
Q

Niacin

A

Reduces synthesis of TG via hepatic DGAT reduction

42
Q

GLP1

A

Glucagon like peptide 1

Reduces TGs

43
Q

DPP-4

A

Prolongs activity of GLP1

44
Q

Thiazolidinediones

A

PPARy antagonist

45
Q

Classes of drugs for heart failure

A

1) Sympathetic NS activation (B-blockers)
2) Failing pump (Digoxin)
3) Salt and water retention (Diuretics)
4) Cardiac remodelling (RAS inhibitors)
5) Peripheral vasoconstriction (Nitrate)

6) Peripheral vascular resistance (ACE inhibitor)
7) Aldosterone driven remodelling (Aldosterone antagonist)

46
Q

Three areas where the HF drugs work

A

1) Failing pump
2) Cardiac remodelling
3) Salt and water retention
4) Peripheral vasoconstriction

47
Q

What is one abnormality in heart failure

A

Aldosterone over-production leasing to salt and H2O retention and vasoconstriction

48
Q

B1 blocker adverse effects

A
  • Bronchospasms
  • Bradycardia
  • Acute worsening heart failure
  • Reduced exercise tolerance
49
Q

Digoxin

A

Competes with K+ blocking Na/K ATPase
Less efficient Na/K exchange

Effects:
Slower SA node rate
Slower AV conduction

**INCREASES VAGAL TONE

50
Q

Digoxin toxicity

A

Not enough K+ can leave- increases RMP
Greater risk of arrhythmias

Serious arrhythmias
Nausea
Confusion
Visual

Hypokalaemia brings digoxin toxicity

51
Q

What happens to preload in HF?

A

It increases

52
Q

How can you make the heart work less harder?

A

1) Reduce heart rate
2) Reduce contractility
3) Reduce afterload

53
Q

GTN

A

Glyceryl trinitrate- broken down into NO which reduces afterload

54
Q

Early drug management for ACS

A

1) Analgesia
2) Limitation of infarct size (coronary thrombolysis)
3) Management of arrhythmias
4) Anti-platelet and anti-coagulant therapy
5) Management of acute heart failure

55
Q

Goals of asthma therapy

A

1) Prevent bronchoconstriction
2) Suppress inflammation
3) Prevent mucus hypersecretion

56
Q

Two short-acting bronchodilators (B2 receptor agonists)

A

Salbutamol

Terbutaline

57
Q

Long acting bronchodilators

A

Eformoterol

Salmetrol (not a good reliever)

58
Q

ICS + LABA

A

E.g. seretide

59
Q

Ipratropium bromide

A

Muscarinic cholinoceptor antagonists

60
Q

ICS

A

Inhaled corticosteroids
Reduce inflammation in asthmatic airways
#1 controllers

Fluticasone

61
Q

Leukotriene receptor antagonists

A

Montelukast

Zafirlukast

62
Q

Anti-IgE antibodies

A

OMALIZUMAB

Subcutaneous injections and expensive

63
Q

Other controllers

A

Cromolyns
Theophylline

**Weak efficacies- good for children

64
Q

Three things that happen to the airways in asthma

A

1) Increased thickness of airway wall
2) Increased mucus secretion
3) Increased constriction

Cardio-resp (4 decks)

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