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Cardiovascular > Pharmacology > Flashcards

Pharmacology Flashcards

1
Q

Where is the fast response action potential present in?

It is _____ dependent

A
  • atrial and ventricular muscles

- sodium dependent

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2
Q

Explain phases 0-4 action potentials FAST RESPONSE

A

Phase 4 - outward flux of K is dominant
Phase 0 - upstroke, inward flux of Na+ is dominant
Phase 1 - early repolarisation, outward flux of K+ is dominant
Phase 2 - plateau, inward flux of Ca2+ balanced by outward flux of K+
Phase 3 - final depolarisation, outward flux of K+ is dominant

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3
Q

Where is the slow response action potential present in?

It is _____ dependent

A
  • SA, AV node

- calcium dependent

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4
Q

Explain phases 0-4 action potentials SLOW RESPONSE

A

Phase 4 - outward flux of K+, reduced by inward flux of Na+ and Ca+
Phase 0 - opening of L-type Ca2+ channels
Phase 3 - opening of delayed rectifier K+ channels

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5
Q

Sympathetic system effect on the heart
? post ganglionic transmitter
? receptor
? coupled protein

A
  • NA
  • B1 adrenoreceptor
    -Gs coupled protein
    Increase the intracellular cAMP
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6
Q

Parasympathetic system effect on the heart
? post ganglionic transmitter
? receptor
? coupled protein

A
  • Ach
  • M2 muscarinic receptor
  • Gi coupled
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7
Q

Meaning of inotropic?

A

Heart contractility

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8
Q

Meaning of chronotropic?

A

Heart rate

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9
Q

Meaning of dromotropic?

A

conduction velocity in AV node

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10
Q

What does “If” represent

A
  • Funny current

- depolarising current

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11
Q

Explain the funny current

A
  • If
  • depolarising current
  • Na+ current
  • hyperpolarising activates HCN channels in SA node
  • Blocking HCN channels –> decreased HR
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12
Q

What is drug is used as an HCN blocker?

A
  • Ivabradine
  • Block HCN
  • Decreases HR
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13
Q

Explain the action of a beta 1 adrenoceptor agonist

A
  • activates Gs coupled receptor
  • ATP converted into cAMP by adenylyl cyclase
  • activates protein kinase A
  • this phosporylates Ca2+ channels
  • increased Ca2+ –> increased contracility
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14
Q

Examples of b adrenocepetor agonists

A
  • dobutamine
  • adrenaline
  • noradrenaline
  • all examples of catecholamines
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15
Q

What pharmacokinetics does b adrenoceptor agonists have?

A
  • increased force, rate and cardiac output

- decreased efficency

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16
Q

What is adrenaline used in?

A
  • b adrenoceptor agonist
  • cardiac arrest
  • anaphylactic shock
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17
Q

What is dobutamine used in?

A
  • acute potentialy reversible heart failure
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18
Q

b adrenoceptor antagonists examples and their pharmacokinetics

A

May be selective or non-selective beta blockers.
non selective - propranolol
selective - atenolol, bisoprolol

Pharmakinetics: little effect at rest, but during exercise stress, force, CO are depressed

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19
Q

Uses of b adrenoceptor antagonists (beta blockers)

A

treatment of disturbances of cardiac rhythm
treatment of angina
treatment of heart failure
treatment of hypertension

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20
Q

Adverse effects of beta blockers?

A
  • bronchospasm (asthmatics)
  • aggravation of cardiac failure
  • bradycardia
  • hypoglycaemia
  • cold extremities
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21
Q

What would a non-selective muscarinic ACh receptor antagonist be used for?

A
  • bradycardia when the heart rate is lower than 60bmp
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22
Q

What is an example of a muscarinic ACh antagonist?

A

Atropine

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23
Q

What is digoxin used for?

A

it is a cardiac glycoside that increases contractility of the heart
Example of an inotropic drug (causes a leftward shift in the SV, EDV curve)

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24
Q

What does digoxin inhibit to increase contractility?

A

It inhibits the sarcolemma ATPase

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25
Q

Lipids are _____ in water

a) insoluble
b) soluble

A

a) insoluble

26
Q

How are non-polar lipids transported in blood

A

They are transported within lipoproteins

27
Q

What are the 2 types of lipoproteins

A
  • High Density Lipoproteins (HDL)
  • Low Desnsity Lipoproteins (LDL)
  • VLDL
  • Chylomicrons
28
Q

CVD is associated with elevated _______ Density Lipoproteins levels and decreased ________Density Lipoproteins

A
  • Elevated LDL

- Decreased HDL

29
Q

Explain the structure of a lipoprotein

A
  • hydrophobic core

- hydrophillic coat

30
Q

Explain the makeup of the hydrophobic core of a lipoprotein

A
  • esterified cholestrol and triacyglycerols
31
Q

Explain the makeup of the hydrophilic coat of a lipoprotein

A
  • monolayer of amphiatic cholestrol, phospholipids and apoproteins
32
Q

What are apoproteins

A
  • recgonised by receptors in the liver and other tissues, allowing lipoproteins to bind to cells
33
Q

4 classes of lipoproteins and their carrier apoprotein

A
  • HDL particles (apoA-1 + apoA-2)
  • LDL particles (ApoB-100)
  • VLDL particles (ApoB-100)
  • chylomicrons (ApoB-48)
34
Q

What Apoprotein is associated with LDL

A

apoB-100

35
Q

What Apoprotein is associated with Chylomicrons

A

apoB-48

36
Q

What Apoprotein is associated with HDL

A

apoA-1 + apoA-2

37
Q

What do ApoB lipoproteins do?

A
  • deliver TAGs to muscle for ATP biogensis

- adipocytes for storage

38
Q

Where are chylomicrons formed and what is their pathway

A
  • formed in interstinal cells

- exogenous pathway

39
Q

Where are LDL formed and what is their pathway

A
  • formed in the liver

- endogenous pathway

40
Q

How are chylomicrons and VLDL particles activated?

A
  • activated by the transfer of apoC-II from HDL particles
41
Q

What apoprotein is involved in the metabolism of apoB lipoproteins

A

apoE

which is a high affinity ligand for receptor mediated clearance –> remnants

42
Q

What is the definition of haemostasis?

A
  • arrest of blood loss from a damaged vessel at the site of injury
43
Q

What are the 3 main processes of haemostasis?

A
  • vascular wall damage
  • primary haemostasis
  • activation of blood clotting
44
Q

Explain what part vascular wall damage plays in haemostasis

A
  • injury to vascular wall
  • collagen exposed
  • platelets bind to the collagen and become activated
  • activated platelets releases thromboxane A2 (TXA2)
45
Q

What does TXA2 do in haemostasis?

A
  • TXA2 binds to TXA2 GPCR receptors, releasing 5-HT (Serotonin) and ADP
46
Q

What is serotonin role in haemostasis

A

causes vasoconstriction

47
Q

What is ADP role in haemostasis

A
  • released from TXA2 GPCR
  • binds to purine receptors (P2Y12)
  • Activates further platelets
  • expresses acidic phoshoplipid to form a solid clot
48
Q

Explain the coagulation cascade

A 
X --> activates IX and VIII
II --> activates X and V
Produces thrombin (IIa)
thrombin cleaves fibrinogen --> fibrin
fibrin --> solid clot
49
Q

What cleaves fibrinogen to fibrin?

A

thrombin

50
Q

What is thrombosis?

A
  • pathological haemostasis

- forms a haematological plug in abscence of bleeding

51
Q

What colour are arterial thrombus?

A
  • white
52
Q

What colour are venous thrombus?

A
  • red
53
Q

How do you treat arterial thrombus?

A
  • anti-platelet

- asprin

54
Q

How do you treat venous thrombus?

A
  • anti-coagulant

- warfarin

55
Q

What are the risks of anti-coagulants

A
  • haemorrhage
56
Q

What factors does Warfarin block?

A

II, VII, IX , X

57
Q

What does heparin bind to?

A
  • antithrombin III
58
Q

Name 2 low molecular weight heparins?

A
  • dalteparin

- enoxaprin

59
Q

What factor does LMWH act on?

A

Xa

60
Q

How do anti-platelet drugs work?

A
  • prevents TXA2 synthesis
61
Q

How do fibrinolytics work?

A
  • fibrin broken down to firbin fragments

- reopens occluded arteries

Cardiovascular (26 decks)

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