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Year 1 Systems (JBR) > Cardiology Non-Clinical Pharmacology > Flashcards

Cardiology Non-Clinical Pharmacology Flashcards

1
Q

Electrical activity yin the heart spreads via?

A

Gap junctions

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2
Q

The P wave on ECG represents?

A

AP upstroke through atrial muscle (0.08-0.10)

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3
Q

The QRS complex on ECG represents?

A

AP upstroke through ventricular muscle (<0.10)

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4
Q

What does the T wave on ECG represent?

A

Ventricular depolarisation

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5
Q

What does the PR interval on ECG represent?

A

Largely AV node delay (0.12-0.20)

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6
Q

What does the ST segment on ECG represent?

A

maintained ventricular depolarisation (systole)

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7
Q

What does the TP interval on ECG represent?

A

Diastole

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8
Q

What does the S wave on ECG represent?

A

Depolarisation of the ventricles at base of hear moving away from recording electrode

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9
Q

What does the R wave on ECG represent?

A

Depolarisation of the main ventricular mass moving towards the recording electrode

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10
Q

A large box on ECG paper represents?

A

0.2 seconds

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11
Q

A small box on ECG paper represents?

A

0.04 seconds

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12
Q

How can the HR be calculated from ECG paper?

A

300 / Number of large boxes between beats

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13
Q

In the heart, sympathetic (noradrenalin + adrenaline) activate beta-1-adrenoceptors in nodal and myocardial cells causing…?

A

Activation of adenylyl cyclase to increase cAMP

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14
Q

Sympathetic influences increases contractility (positive inotropic response) due to?

A

Increase in plateau phase in ventricular/atrial myocytes + enhanced calcium influx and sensitisation of contractile proteins to Ca

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15
Q

Sympathetic influences increases HR (positive chronotropic response) due to?

A

Increase in pacemaker potential caused by enhanced funny and calcium current + reduction in threshold for Ap initiation caused by enhanced calcium
Mediated by SA node

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16
Q

Why may sympathetic influence cause arrhythmia in atria?

A

Decreased AP duration and refractory period predispose to re-entrant arrhythmias

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17
Q

Vagal manoeuvres increase parasympathetic output may be used in ________ to suppress impulse conduction via AVN?

A

atrial tachycardia

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18
Q

Vagal manoeuvres like carotid artery bifurcation massage activate?

A

baroreceptors (aorta or carotid sinus)

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19
Q

Hyper-polarisation activates cation selective HCN channels in SA node facilitation?

A

Slow phase 4 depolarisation

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20
Q

Block of HCN channels decreases the slope of _______ and reduce _____?

A

pacemaker potential

Reduce heart rate

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21
Q

What is an example of a HCN channel blocker?

A

Ivabradine

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22
Q

Outline the mechanism of cardiac muscle contraction.

A

Ventricular AP
Open voltage-gated Ca-channels
Ca influx into cytoplasm
CICR from SR (via ryanodine Type 2 channel)
C binds to troponin C & shift tropomyosin out of the actin cleft
Cross-bridge between actin & myosin
Contraction via sliding filament mechanism

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23
Q

Outline the mechanism of cardiac muscle relaxation.

A

Depolarisation
Ca channels close
Ca influxx stops and calcium efflux occurs via NCX1
Ca release from SR stops and active sequestration via Ca-ATPase from cytoplasm beings
Ca dissociates from troponin C
Cross bridges between actin and myosin break
Relaxation

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24
Q

What is the mechanism of Levosimendan? (calcium sensitiser)

A

Binds to troponin C in cardiac muscle sensitising it to Ca-action
Opens K-ATP channels in vascular smooth muscle causing vasodilation (decrease after load and cardiac work)

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25
Q

Levosimendan is used in the treatment of?

A

Acute decompensated heart failure

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26
Q

What are functions of lipids?

A

Membrane biogenesis
Integrity and energy source
Precursor for hormones
Signalling molecules

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27
Q

Non-polar lipids are transported within?

A

Lipoproteins

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28
Q

What are lipoproteins?

A

Spherical particle consisting of a hydrophobic core and hydrophilic coat

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29
Q

What determines the target/pathway of the lipoprotein and stabilises the outer shell?

A

Apoproteins

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30
Q

Apo-B-containing lipoproteins deliver _____ to _____ for ATP synthesis and _____ for storage

A

Triglycerides
Muscle

Adipocytes

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31
Q

Where are chylomicrons formed?

A

Intestinal cells

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32
Q

Chylomicrons transport?

A

Dietary triglycerides via exogenous pathway) to muscle and adipocytes

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33
Q

VLDL are synthesised in?

A

Hepatocytes

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34
Q

VLDL transport _____ synthesised de-novo in that organ via the ______ pathway

A

triglycerides

endogenous

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35
Q

What are the (3) stages of the life cycle of App-B-containing Lipoproteins?

A

Assembly
Intravascular Metabolism (involves metabolism of triglyceride core)
Receptor-mediated clearance

36
Q

How do triglyceride enter the systemic circulation?

A 
Absorbed 
Coalesce into triglyceride droplets 
Apo-B protein produced by ribosomes
Mature chylomicron formed
Add 2nd apoprotein (Apo-A1)
Enters lymphatic system
Enters systemic circulation via thoracic duct
37
Q

VLDL is assembled in hepatocytes using ____ from adipose tissue and de-novo synthesis

A

fatty acids

38
Q

MTP lipidases apoB100 forming new VLDL coalesce with?

A

Triglyceride droplets

39
Q

How does chylomicron and VLDL activation occur?

A

Transfer of apo-C2 from HDL particles

40
Q

How does intravascular metabolism of ApoB-containing Lipoproteins occur?

A

Bind to chylomicrons and VLDL (facilitated by Apo-C2) and the core triglycerides are hydrolysed
Free fatty acids and glycerol enter tissues

41
Q

How are Apo-B-Containing Lipoproteins cleared?

A

LPL causes VLDL and chylomicrons to become relatively enriched with cholesterol due to triglyceride metbaolism
Chylomicrons and LDL dissociate from LPL
ApoC2 transferred to HDL particles in exchange for ApoE
VLDL & Chylomyicrons now remnants
Return to liver and further metabolised by hepatic lipase

42
Q

Lipoprotein clearance is highly dependent on?

A

LDL receptors expressed by liver (main) and other tissues

43
Q

How is LDL take up by cells?

A

Receptor-mediated endocytosis

44
Q

What is the rate-limiting enzyme in de-novo cholesterol synthesis?

A

HMG-CoA-reductase

45
Q

In the cell cholesterol is released from cholesteryl ester by?

A

Hydrolysis

46
Q

Released cholesterol causes _________ inhibition causing down regulation of LDL receptors and esterification of stored cholesterol

A

HMG-CoA reductase

47
Q

HDL accepts excess cholesterol from the plasma membrane of cells and removes it by transporting it to the?

A

Liver

48
Q

Where is HDL mainly formed?

A

In the liver

49
Q

The precursor of HDL is?

A

Pre-beta-HDL

Apo-A1 in association with small amount of surface phospholipid and unesterified cholesterol

50
Q

Where des pre-beta HDL mature into spherical alpha-HDL?

Meanwhile cholesterol is converted to?

A

In the plasma

cholesterol ester that migrates into the core of the particles

51
Q

In the liver, HDL interacts with _____- receptor which allow cholesterol and cholesterol ester transport into hepatocytes

A

Scavenger

52
Q

In lasma cholesterol ester transfer protein (CETP) mediates cholesteryl ester transfer from _____-to _____-

A

HDL

VLDL and LDL

53
Q

Fibrates (lipid lowering drug) such as bezafibrate or gemfibrozil act as an agonist of ______ to enhance gene transcription including LPL

A

nuclear receptor

54
Q

Adverse effects of fibres?

A 
Rarely myositis (don't combine with statin)
Avoid in alcoholics
55
Q

Bile salt resins like colestyraminase, colestipol and colsevelam cause _______ resulting in more cholesterol being converted to ___ via enterohepatic recycling

A

Bile salt

Bile salts

56
Q

Bile salt resins cause?

A

Decreased triglyceride absorption

Increased LDL receptor expression

57
Q

What are adverse effects of bile salt resins?

A

Gi tract irritation

58
Q

Fibrates act to?

A

Decrease triglycerides and LDL

Increase HDL

59
Q

Ezetimibe reduces absorption of cholesterol by inhibiting?

A

Niemann-Pick-C1 like 1 transport protein in enterocytes of the duodenum

60
Q

Ezetimibe is used if?

A

Statin doesn’t give sufficient result

61
Q

Ezetimibes and Bile acid resins are administered?

A

PO

62
Q

Ezetimibe undergoes what kind of metabolism?

A

Enterohepatic recycling

63
Q

What are adverse effects of ezetimibe?

A

Diarrhoea
Abdominal pain
Headache

64
Q

Ezetimibe is contraindicated in?

A

Breast feeding females because neonates need cholesterol for normal development

65
Q

In normal sinus rhythm the origin of electrical signal is the _______ and the major point of delay is the _______

A

SA node

AV node

66
Q

Physiological electrical dysfunction results in modulation of the _______ by the ___

A

SA node

ANS

67
Q

Pathological electrical dysfunction results when a __________ subverts the SA node’s function

A

latent pacemaker

68
Q

Pathologically low SA firing rate (or impaired conduction) results in?

A

Escaped beats

69
Q

A series of escaped beats is known as an?

A

Escape rhythm

70
Q

If the latent pacemaker beats faster than the SA node it results in?

A

Ectopic beats

71
Q

A series of ectopic beats is known as an?

A

Ectopic rhythm

72
Q

What are causes of an ectopic rhythm?

A

Ischaemia
Hypokalaemia
Increased sympathetic activity
Fibre stretch

73
Q

Early afterdepolarisation occurs during which phase(s) of the action potential?

A 
Phase II (mediated by calcium channels) 
Phase II (mediated by sodium channels)
74
Q

EAD is associated with?

A

Prolonged APs and drugs that prolong the QT interval

75
Q

Which drugs are known to prolong the QT interval?

A

Sotalol
CCB
B-blocker

76
Q

How is reentrant (aka ‘circus’) circuit established?

A

Self-sustaining circuit stimulates an area of the myocardium repeatedly allowing retrograde conduction

77
Q

In some patients, there are pathways (like the pathway of Kent) that bypass the AV node. These are known as?

A

Accessory pathways

78
Q

In the pathway of Kent impulses are sent faster than via the AV node - the ventricles impulses from both the normal and accessory pathways
This can set up a condition for a ________ predisposing to?

A

Re-entrant loop

tachyarrythmias

79
Q

What mediates gamma-carboxylation of factor II, VII, IX and X (required for subsequent prodcutio not active forms)

A

Vitamin K

80
Q

What are the sources of Vitamin K?

A

Diet

Intestinal flora

81
Q

Which enzyme allow the conversion of reduced vitamin K (hydroquinone) to oxidised vitamin K (exposed)?

A

Vitamin K reductase

82
Q

Outline the mechanism of vascular smooth muscle contraction.

A

Calcium induced calcium release
Ca binds to Calmodulin (caM)
Ca-CaM phosphorylates myosin light chain leading to contraction

83
Q

Outline the mechanism of vascular smooth muscle relaxation?

A

Myosin-LC-phosphate is activated by protein kinase G and then dephosphorylated to Myosin-LC leading to relaxation

84
Q

How do vasodilation substances cause relaxation of vascular smooth muscle?

A

Simulate guanylase cyclase which converts GTP to cGMP increasing protein kinase G
Also stimulate Ca-dependent-K-channels causing hyperpolarising K-efflux

85
Q

How do adrenaline, angiotensin II, ADH, etc lead to contraction?

A

Increase gene expression to produce endothelium I via precursor in endothelial cells via ET-A-Receptor in smooth muscle cells causing increased Ca leading to contraction

86
Q

What are antagonist of ET-A-receptor that can be used to treat pulmonary hypertension?

A

Basentan

Ambrisetan

87
Q

Renin inhibitors should not be combined with?

A

ARBS or Ace inhibitors

Year 1 Systems (JBR) (21 decks)

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