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Cardio-resp > Pharmacology > Flashcards

Pharmacology Flashcards

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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
ADH
Water reabsorption in collecting duct
26
Loop diuretics
Inhibit sodium-potassium-chloride co-transporter in the thick ascending limb- leads to water loss and sodium loss FRUSEMIDE
27
Thiazide diuretics
Do the same thing but in the distal tubule HYDROCHLOROTHIAZIDE INDAPAMIDE
28
K+ sparing diuretics
Antagonise action of aldosterone (aldosterone receptor antagonists) EPLERENONE
29
Potency of diuretics
The diuretics that act earlier on prevent more reabsorption compared to the ones that act later on
30
K+ wasting diuretics
Both loop and thiazide diuretics that act directly on the channels lead to increased K+ excretion
31
Initial treatment of hypertension
- Thiazide diuretic with ACE-I or AT1 blocker | - Then add Ca2+ channel blocker
32
Exogenous and endogenous pathway of lipid transport
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
Reverse cholesterol transport
Process by which cholesterol is removed from the tissues HDL is the main particle here
34
Statins
Reduce the synthesis of hepatically produced cholesterol | Upregulate LDL receptors of hepatocytes
35
Mechanism of statins
They inhibit HMG CoA reductase which eventually also increases the LDL receptors
36
Side-effects of statins
Hepatic- increase transaminase Cognitive- memory loss Diabetes Myositis
37
Ezetimibe
Inhibits interaction of NPC1/L1 with clathrin/AP2- preventing endocytosis of cholesterol complex in the small intestine
38
PCSK9 inhibitors
Prevent recycling of LDL and mark it for degradation | PSCK9 MABS
39
PSCK9 side-effects
``` URTI GI Hypertension Neurocognitive Muscle (myositis) ```
40
Fibrates
Increases FFA B-oxidation
41
Niacin
Reduces synthesis of TG via hepatic DGAT reduction
42
GLP1
Glucagon like peptide 1 | Reduces TGs
43
DPP-4
Prolongs activity of GLP1
44
Thiazolidinediones
PPARy antagonist
45
Classes of drugs for heart failure
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
Three areas where the HF drugs work
1) Failing pump 2) Cardiac remodelling 3) Salt and water retention 4) Peripheral vasoconstriction
47
What is one abnormality in heart failure
Aldosterone over-production leasing to salt and H2O retention and vasoconstriction
48
B1 blocker adverse effects
- Bronchospasms - Bradycardia - Acute worsening heart failure - Reduced exercise tolerance
49
Digoxin
Competes with K+ blocking Na/K ATPase Less efficient Na/K exchange Effects: Slower SA node rate Slower AV conduction **INCREASES VAGAL TONE
50
Digoxin toxicity
Not enough K+ can leave- increases RMP Greater risk of arrhythmias Serious arrhythmias Nausea Confusion Visual Hypokalaemia brings digoxin toxicity
51
What happens to preload in HF?
It increases
52
How can you make the heart work less harder?
1) Reduce heart rate 2) Reduce contractility 3) Reduce afterload
53
GTN
Glyceryl trinitrate- broken down into NO which reduces afterload
54
Early drug management for ACS
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
Goals of asthma therapy
1) Prevent bronchoconstriction 2) Suppress inflammation 3) Prevent mucus hypersecretion
56
Two short-acting bronchodilators (B2 receptor agonists)
Salbutamol | Terbutaline
57
Long acting bronchodilators
Eformoterol | Salmetrol (not a good reliever)
58
ICS + LABA
E.g. seretide
59
Ipratropium bromide
Muscarinic cholinoceptor antagonists
60
ICS
Inhaled corticosteroids Reduce inflammation in asthmatic airways #1 controllers Fluticasone
61
Leukotriene receptor antagonists
Montelukast | Zafirlukast
62
Anti-IgE antibodies
OMALIZUMAB Subcutaneous injections and expensive
63
Other controllers
Cromolyns Theophylline **Weak efficacies- good for children
64
Three things that happen to the airways in asthma
1) Increased thickness of airway wall 2) Increased mucus secretion 3) Increased constriction

Cardio-resp (4 decks)

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