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

Cardiology Non-Clinical Pharmacology Flashcards

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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
Levosimendan is used in the treatment of?
Acute decompensated heart failure
26
What are functions of lipids?
Membrane biogenesis Integrity and energy source Precursor for hormones Signalling molecules
27
Non-polar lipids are transported within?
Lipoproteins
28
What are lipoproteins?
Spherical particle consisting of a hydrophobic core and hydrophilic coat
29
What determines the target/pathway of the lipoprotein and stabilises the outer shell?
Apoproteins
30
Apo-B-containing lipoproteins deliver _____ to _____ for ATP synthesis and _____ for storage
Triglycerides Muscle Adipocytes
31
Where are chylomicrons formed?
Intestinal cells
32
Chylomicrons transport?
Dietary triglycerides via exogenous pathway) to muscle and adipocytes
33
VLDL are synthesised in?
Hepatocytes
34
VLDL transport _____ synthesised de-novo in that organ via the ______ pathway
triglycerides | endogenous
35
What are the (3) stages of the life cycle of App-B-containing Lipoproteins?
Assembly Intravascular Metabolism (involves metabolism of triglyceride core) Receptor-mediated clearance
36
How do triglyceride enter the systemic circulation?
``` 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
VLDL is assembled in hepatocytes using ____ from adipose tissue and de-novo synthesis
fatty acids
38
MTP lipidases apoB100 forming new VLDL coalesce with?
Triglyceride droplets
39
How does chylomicron and VLDL activation occur?
Transfer of apo-C2 from HDL particles
40
How does intravascular metabolism of ApoB-containing Lipoproteins occur?
Bind to chylomicrons and VLDL (facilitated by Apo-C2) and the core triglycerides are hydrolysed Free fatty acids and glycerol enter tissues
41
How are Apo-B-Containing Lipoproteins cleared?
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
Lipoprotein clearance is highly dependent on?
LDL receptors expressed by liver (main) and other tissues
43
How is LDL take up by cells?
Receptor-mediated endocytosis
44
What is the rate-limiting enzyme in de-novo cholesterol synthesis?
HMG-CoA-reductase
45
In the cell cholesterol is released from cholesteryl ester by?
Hydrolysis
46
Released cholesterol causes _________ inhibition causing down regulation of LDL receptors and esterification of stored cholesterol
HMG-CoA reductase
47
HDL accepts excess cholesterol from the plasma membrane of cells and removes it by transporting it to the?
Liver
48
Where is HDL mainly formed?
In the liver
49
The precursor of HDL is?
Pre-beta-HDL | Apo-A1 in association with small amount of surface phospholipid and unesterified cholesterol
50
Where des pre-beta HDL mature into spherical alpha-HDL? | Meanwhile cholesterol is converted to?
In the plasma | cholesterol ester that migrates into the core of the particles
51
In the liver, HDL interacts with _____- receptor which allow cholesterol and cholesterol ester transport into hepatocytes
Scavenger
52
In lasma cholesterol ester transfer protein (CETP) mediates cholesteryl ester transfer from _____-to _____-
HDL | VLDL and LDL
53
Fibrates (lipid lowering drug) such as bezafibrate or gemfibrozil act as an agonist of ______ to enhance gene transcription including LPL
nuclear receptor
54
Adverse effects of fibres?
``` Rarely myositis (don't combine with statin) Avoid in alcoholics ```
55
Bile salt resins like colestyraminase, colestipol and colsevelam cause _______ resulting in more cholesterol being converted to ___ via enterohepatic recycling
Bile salt | Bile salts
56
Bile salt resins cause?
Decreased triglyceride absorption | Increased LDL receptor expression
57
What are adverse effects of bile salt resins?
Gi tract irritation
58
Fibrates act to?
Decrease triglycerides and LDL | Increase HDL
59
Ezetimibe reduces absorption of cholesterol by inhibiting?
Niemann-Pick-C1 like 1 transport protein in enterocytes of the duodenum
60
Ezetimibe is used if?
Statin doesn't give sufficient result
61
Ezetimibes and Bile acid resins are administered?
PO
62
Ezetimibe undergoes what kind of metabolism?
Enterohepatic recycling
63
What are adverse effects of ezetimibe?
Diarrhoea Abdominal pain Headache
64
Ezetimibe is contraindicated in?
Breast feeding females because neonates need cholesterol for normal development
65
In normal sinus rhythm the origin of electrical signal is the _______ and the major point of delay is the _______
SA node | AV node
66
Physiological electrical dysfunction results in modulation of the _______ by the ___
SA node | ANS
67
Pathological electrical dysfunction results when a __________ subverts the SA node's function
latent pacemaker
68
Pathologically low SA firing rate (or impaired conduction) results in?
Escaped beats
69
A series of escaped beats is known as an?
Escape rhythm
70
If the latent pacemaker beats faster than the SA node it results in?
Ectopic beats
71
A series of ectopic beats is known as an?
Ectopic rhythm
72
What are causes of an ectopic rhythm?
Ischaemia Hypokalaemia Increased sympathetic activity Fibre stretch
73
Early afterdepolarisation occurs during which phase(s) of the action potential?
``` Phase II (mediated by calcium channels) Phase II (mediated by sodium channels) ```
74
EAD is associated with?
Prolonged APs and drugs that prolong the QT interval
75
Which drugs are known to prolong the QT interval?
Sotalol CCB B-blocker
76
How is reentrant (aka 'circus') circuit established?
Self-sustaining circuit stimulates an area of the myocardium repeatedly allowing retrograde conduction
77
In some patients, there are pathways (like the pathway of Kent) that bypass the AV node. These are known as?
Accessory pathways
78
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?
Re-entrant loop | tachyarrythmias
79
What mediates gamma-carboxylation of factor II, VII, IX and X (required for subsequent prodcutio not active forms)
Vitamin K
80
What are the sources of Vitamin K?
Diet | Intestinal flora
81
Which enzyme allow the conversion of reduced vitamin K (hydroquinone) to oxidised vitamin K (exposed)?
Vitamin K reductase
82
Outline the mechanism of vascular smooth muscle contraction.
Calcium induced calcium release Ca binds to Calmodulin (caM) Ca-CaM phosphorylates myosin light chain leading to contraction
83
Outline the mechanism of vascular smooth muscle relaxation?
Myosin-LC-phosphate is activated by protein kinase G and then dephosphorylated to Myosin-LC leading to relaxation
84
How do vasodilation substances cause relaxation of vascular smooth muscle?
Simulate guanylase cyclase which converts GTP to cGMP increasing protein kinase G Also stimulate Ca-dependent-K-channels causing hyperpolarising K-efflux
85
How do adrenaline, angiotensin II, ADH, etc lead to contraction?
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
What are antagonist of ET-A-receptor that can be used to treat pulmonary hypertension?
Basentan | Ambrisetan
87
Renin inhibitors should not be combined with?
ARBS or Ace inhibitors

Year 1 Systems (JBR) (21 decks)

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