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1
Q

Cardiac channel blockers

What are the two types?

  • mechanism of each
  • adverse effects
A

Cardioselective; or vascular selective

mechanism
- block L-type Ca2+ channels in cells -> slow the entry of Ca into the cell

Cardioselective (verapamil) -
slow entry of Ca -> decreases heart rate -> increases time for perfusion of cardiac muscle - decreases cardiac contractility -> decrease SV and CO -> decreasing demand for O2; increasing perfusion of muscle

adverse effects:

  • flushing; headache (overdilation)
  • oedema
  • bradycardia
vascular selective (nifedipine): 
- L-type channels block -> arterial dilation -> reduces afterload on heart -> less O2 demand   
adverse effects:
 - flushing; headache; 
oedema 
- hypotension 
- reflex tachycardia 
- AV block
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2
Q

cholesterol

  • biochemical structure
  • how many carbons
  • rough structure
  • hydrophilic/phobic?
  • what part of molecules is cleaved off in derivatives?
A
  • C27
  • 4 fused rings
  • ABCD + YvY tail
  • amphiphilic
  • has a hydroxy group at C3; rest of molecule is hydrophobic
  • at C17 have YVY tail
  • this is cleaved off

cholesterol is a greasy solid; insoluble in water -> forms gallstones

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3
Q

Cholesterol is a precursor for..

A
  • steroid hormonse
  • bile salts
  • vitamin D
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4
Q

cholesterol synthesis pathway

A

acetyl CoA (mitochondria) -> moves out as citrate (oxaloacetate + acetyl CoA = citrate) -> back to acetyl coa in cytosol

acetyl CoA + acetyl Coa -> acetoacetyl CoA + acetyl CoA -> HMG CoA

HMG CoA -> when in cytosol will form cholesterol (in mitochondria; forms ketone bodies)

HMG CoA -> via HMG reductase + 2 NADPH -> mevalonic acid

mevalonic acid (5c) -> isoprene (5c) -> squalene (30C) -> cholesterol (27C)

-> need 6 mevalonic acid molecules for cholesterol

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5
Q

Complications of MI

  • immediate/within hours (2)
  • days (6)
  • months/years (4)
A

immediate

(1) arrhythmias (VT; VF; asystole; AF..) - often within an hour
(2) acute cardiac failure - LV fails -> decreased CO; if severe enough - acute pulmonary oedema

days
(1) progressive cardiac failure
(2) rupture: 1-10 days (before scar tissue) - generally in free wall; papillary muscle; IV septum
(3) -> rupture may cause mitral incompetece; left-to-right shunt; tamponade
=> LV mural thrombus formation
(4) arrhythmias
(5) infarct expansion
(6) fibrinous pericarditis - acute inflammation in underlying muscle - sharp; well-localised pain

months/years

(1) ongoing caridac failure
(2) arrhythmias
(3) papilary muscle dysfunction
(4) ventricular aneurysm

  • usually no rupture but can lead to: thrombus; arrhythmias; heart failure
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6
Q

Definition of cardiac failure

Is it usually a systolic or a diastolic failure?

A

when cardiac output < body needs

usually systolic failure - contractility is lessened - can’t pump out the blood

may be diastolic failure (reduced LV compliance; so have an increased LVEDP that is required to maintain the same SV)

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7
Q

Describe lipoprotein movement around the body

A
  1. meal: lipases break down fats; gut mucosa takes them up and repackages as chylomicrons -> lymph -> plasma
  2. cells with ApoC-II (chylomicron etc) receptors - activate lipoprotein lipase -> cells take up free fatty acids from chylomicrons; form chylomicron remnannts
  3. remnants end up in liver -> repackaged as VLDL (formation uses ACAT)
  4. VLDL circulates plasma; taken up by liver again; or mature in plasma to become LDL (lose ApoC-II; retain ApoB-100)
  5. LDL circulates and donates cholesterol to tissues - cells that recognise ApoB-100 take up cholesterol
  6. HDL - formed in plasma from precursors (with LCAT) - has ApoA-1 protein -> scavenges cholesterol from membranes and cells
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8
Q

Difference between arterial and venous thrombus - how they form - how they look

A

Arterial thrombus formation - endothelial damage is very important

  • tend to be pale: mesh of platelets; fibrin; RBC; leukocytes
  • grow in retrograde direction from pt of attachment
  • mostly due to atherosclerosis

Venous thrombus formation - hypercoagulability + blood stasis is more important

  • tend to be red: formed in stasis - more RBCs along with fibrin; platelets
  • extend in direction of blood flow
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9
Q

ECG findings in cardiac tamponade

A

QRS complexes are seen; but there is no cardiac output -> pulseless electrical activity

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10
Q

general structure of chylomicrons + HDL + LDL

A

inside: triacylglycerols + cholesteryl esters
outside: phospholipid monolayers - single layer because the interior is hydrophobic

outside: has Apolipoproteins - fit different receptors
- diff types have diff proteins -> gives protein different functions + target cells

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11
Q

Histology of infarcts what do you see at - up to 12hrs - 1-2 days - 1-2 weeks - 6-8 weeks

A

Infarcts demonstrate coagulative necrosis (except brain: liquefactive)

  • hypereosinophilic - still have outline
  • fading nuclei
  • loss of detail of cytoplasm

6-12hrs - no change
1-2 days - acute inflammation - lots of neutrophils
1-2 weels - granulation tissue (macrophages; capillaries; fibroblasts; lymphocytes)
6-8 weeks - scar tissue

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12
Q

How do beta-adrenoceptor agonists work to help symptoms of acute heart failure? Example adverse effects

A

examples: noradrenaline; adrenaline; dobutamine (selective for b1)

increase activation of a- and b-adrenoceptors -> increase contractility

adverse effects

  • increase cardiac work; and therefore O2 demand -> problem in heart failure
  • may cause arrhythmias
  • in long run - decrease receptor expression -> reduced sensitivity and sympathetic drive
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13
Q

How do beta-blockers help symptoms in ischaemic heart disease?

A
  • block the effects of the SNS
  • > decrease HR (in SA; AV nodes) -> increase time for perfusion of cardiac muscle
  • > decrease contractility in muscle; decrease SV -> decrease CO so decrease demand for O2
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14
Q

how do beta-blockers work in heart failure? examples

A

beta-blockers have negative ionotropic effects and effects on heart rate -> should be harmful in heart failure - but experiments show an increased stroke volume

  • also reduce renin release -> subsequent angII effects -> reduce afterload

b1 blockers - metoprolol b1 and a1 blockade - vascular only: carvedilol -> vasodilation

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15
Q

How do beta-blockers work in treating hypertension?

A

Block effects of sympathetic activity on kidney + heart (b1 adrenoceptors) kidney - decreased renin release -> decreased downstream effects of AngII/aldosteronne heart - decrease CO (rate; contractility)

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16
Q

How do PDE inhibitors work to relieve symptoms in acute heart failure?

A

reduce phosphorylation of b1-adrenoceptors -> less reduced sensitivity to b1-adrenoceptor agonists

PDE = phosphodiesterase - phosphorylates receptors to reduce their sensitivity

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17
Q

How do venodilators work in heart failure? Example

A

Eg. nitrates - more used in angina

venodilation -> reduces preload in heart failure

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18
Q

How do you diagnose MI

A

ECG

  • STEMI - reflects transmural MI; loss of amplitude of R and small Q
  • NSTEMI - usually reflects smaller infarction - generally subendocardial

Biomarkers

  • troponins - cardiac specific; but don’t elevate till 6 hrs or so - peak at 36hrs
  • CK-MB - somewhat cardiac specific - released from damaged muscle - peak 24hrs
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19
Q

How does aldosterone act to retain Na+ and water in kidneys?

What blocks this process

A

aldosterone

  • activates Na+ channels - increase reabsorption of Na+ from lumen
  • stimulates synthesis of Na/K pumps - actively pump Na+ from cells to interstitium -> drive Na+ reuptake from lumen

Blocked by aldosterone receptor antagonists - eg spironolactone

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20
Q

how does concentric hypertrophy compensate for high afterload? what are the consequences?

A

thicker wall - reduce wall stress and maintain pumping ability
- maintain systolic function

  • diastolic dysfunction - thick wall; doesnt fill as well.

need increast EDP to get the same EDV (causing back pressure)

  • contraction from left atrium becomes important to fill LV - can lead to atrial fibrillation
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21
Q

How does ivabradine work to control symptoms in ischaemic heart disease

A

“purely” reduces HR

  • inhibits inward Na/K I-funny current in SA node
  • decreases the slope of the I-f - decreases velocity of diastolic depolarisation

This decreases O2 demand by the heart (pumping less); and also increases O2 supply to cardiac muscle (allows muscle to perfuse)

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22
Q

How does niacin work in lowering cholesterol levels?

Is it widely used?

A

End up with a better lipid profile (lower LDL; higher HDL etc)

  • but mechanism is unclear
  • reduce secretion of VLDL from liver
  • reduce plasma LDL and triglycerides
  • increase HDL

Not widely used - except in combo after others haven’t worked

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23
Q

hypoxia - definition - causes (3)

A

Deficiency of oxygen in tissues

Causes include:
– Reduction of blood supply (ischaemia)
– Impaired respiratory function
– Decrease in oxygen carrying capacity of the blood - eg decrease Hb

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24
Q

Infarcts of the circumflex artery typically involve..

A

lateral LV wall

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25
Infarcts of the RCA (30-40% of cases) typically involve..
inferior/posterior wall of LV posterior part of IV septum (if right dominant) inf/posterior RV free wall in some cases
26
Mechanism of action of statins What do they result in (change in blood levels)
competitive inhibitors of HMG-CoA reductase also there is a compensatory increase in hepatic LDL receptors -> increase clearance of LDL from blood result in - reduced plasma total cholesterol and LDL - increased plasma HDL
27
Nitrates -mechanism
nitrates cause vasodilation -> decrease preload on heart -> less to pump; so needs less O2 mechanism - NO is released - NO stimulates guanylate cyclase in vascular smooth muscle -> GTP converted to cGMP - cGMP -> dephosphorylation of myosin light chain -> can't interact with actin -> relaxation
28
Potassium sparing diuretics - what are the 2 different groups
Spironolactone triamterene + amiloride
29
structure of HDL
has a circular ApoAI protein - makes a hydrophobic ring rounds up cholesterol + phospholipids in plasma
30
Sudden cardiac death - definition - mechanism - other causes
unexpected fatal event occuring within 1hr of the beginning of symptoms; or asymptomatic in an apparently healthy subject mechanism - most often: lethal arrhythmia - usually related to coronary atherosclerosis - unstable plaque - acute ischaemia in myocytes -> these are electrically unstable; initiate an abnormal rhythm eg. VF; asystole; Ventricular tachycardia other causes - tamponade -> haemopericardium
31
The most commonly occluded coronary artery is the LAD. Its infarcts usually involve..
Anterior wall of LV near apex Anterior portion of IV septum Apex circumferentially
32
Typical sequence of events in an MI
- initial event: sudden change in morphology of atheromatous plaque (disruption: intraplaque haemorrhage; erosion; ulceration; rupture; fissuring) - platelets are exposed to subendothelial collagen and necrotic plaque contents - platelets undergo adhesion; aggregation; activation; release of aggregators - vasospasm is stimulated by platelet aggregation and release of mediators - coagulation extrinsic pathway is triggered by other mediators - thrombus evolves to completely occlude lumen Consequeces - decreased ATP - generation of ROS - irreversible cell injury after 20-40 mins of severe ischaemia
33
Unstable angina - mechanism - signs/symptoms - consequences
mechanism - usually induced by disruption of atherosclerotic plaque with superimposed partial thrombosis and possible embolism or vasospasm signs - pain - increasingly frequent; less exertion required - crushing pain often prodrome for MI
34
Upper limit of recommended cholesterol levels in australia
5.5 mmol/L
35
Ventricular tachyarrhythmias - pathophysiology
- diseased myocardium has automaticity | - diseased muscle disturbs propagation of the ventricular impuse -> and develop intraventricular re-entry
36
What are 3 mechanisms through which cardiac failure occurs
- Loss of myocardial muscle (therefore loss of contractility) -> most common eg. Ischaemic heart disease; cardiomyopathy - Pressure overload eg. valve stenosis; aortic stenosis; hypertension - Volume overload eg. aortic regurgitation; shunts
37
What are bile acid sequestrants/resins? Examples Mechanism Precaution
Used in hypercholesterolaemia - eg cholestyramine Mechanism - bind bile acid (cholesterol metabolites - prevent their reabsorption by the gut - increase their excretion - increases demand for cholesterol to synthesise more -> upregulation of hepatic LDL receptors Precaution: relatively nonspecific -> decreases absorption of other drugs
38
What are contraindications for beta-blocker use?
asthma diabetes AV block take care with - heart failure - metabolic syndrome
39
what are fibrates - give example mechanism of action results precaution
fibrates - used as adjunct to dietary changes for hypertriglyceridaemia agonist at nuclear receptors - regulate gene expression - increase synthesis of lipoprotein lipase results - moderate decrease in plasma TAG - moderate increase in HDL - variable effects on LDL precaution: potential for liver toxicity - monitor serum aminotransferase
40
What are macroscopic pathological changes seen after MI - hours - 1-2 days - 1-2 weeks - 6-8 weeks
hours - nothing 1-2 days - pale yellow area 1-2 weeks - more pale area; patchy surrounding haemorrhage 6-8 weeks - scar tissue formed; thinned out wall
41
What are possible mechanisms behind nitrate tolerance? (4)
- "classic" - depletion of thiols required for NO production from GTN - increase release/sensitivity to constrictors - increased endothelial free radical production - reduce NO bioavailability - decrease activity of muscle mitochondrial ALDH2; decreased NO production; increased free radicals
42
What are some adverse effects of ivabradine
- brightness in visual field (also have I-funny current in retinas) - conduction abnormalities
43
What are some adverse effects of nitrates
- postural hypotension - headache; flushin - excessive arterial dilation in head/neck - reflex tachycardia - with large drop in BP - react with viagra -> viagra decreases phosphodiesterase (breaks down cGMP) + NO increases production of cGMP -> heaps of cGMP and fatal drop in BP
44
What are some serious adverse effects of statins When must you withhold statins?
reduce Q10 production -> can stop mitochondria functioning properly - cause skeletal and cardiac muscle complications -> heart failure withhold - pregnancy - infection - pre-surgeery - post-trauma
45
What are the 3 fates of cholesterol in the body?
1. ester formation for storage in liver (then export as VLDL) - ester - replaces the OH group at C3 with a fatty acid chain - without OH group - will not insert into membrane 2. bile acid formation in liver - liver synthesises bile salts - which is then stored in gall bladder; then released to emulsify fatty meals - bile: 3OH groups - detergent 3. membranes - C3 OH group lines up with polar heads of phospholipids - cholesterol ensures that membranes are not too fluid - rigid ring system - fine tunes membrane for 37C
46
What are the common sites of atherosclerosis in the coronary arteries?
Prinarily in the first few cm of LAD and LCX; along entire RCA
47
What are the consequences of increase Na+ and water retention by the kidneys in heart failure?
Increased pulmonary vein pressure -> pulmonary congesion Increased blood pressure -> oedema
48
What are the differences between stable and unstable angina
stable - occlusion >70%; symptoms with increased demand unstable - occlusion >90%; symptoms even at rest
49
What are the long run consequences of increases SNS activation in heart failure?
Deleterious - vasoconstrction - icreases afterload on the heart - ventricular arrhythmias - direct toxic effect on myocardium of NA
50
What are the main sites of action for beta-blockers?
heart -> reduce heart rate; contractility kidney - reduce renin release
51
What are the two forms of true aneurysm?
Saccular - berry aneurysm = only on one side = focal dilation fusiform - entire circumference (most atherosclerotic aneurysms)
52
What are thrombi in the heart chamgers/aortic lumen called? Why are they formed?
mural thrombi form due to abnormal myocardial contraction
53
what changes in ventricular volumes are seen in cardiac decompensation? why does decompensation occur?
decompensates because LV dilates to extent that it can no longer maintain SV - so have fall in systolic function and SV See- decreased ejection fraction increased LVEDV increased LVESV
54
What combination of drugs used for ischaemic heart disease must you never combine
beta-blocker + cardio-selective calcium channel blocker (verapamil) -> both cardiodepressive (can combine beta-blocker and vascular-selective - because this may cause tachycardia as well - can have atenolol + nifedipine)
55
what conditions cause increased preload on the heart?
mitral regurgitation | aortic regurgitarion
56
what conditions increase afterload in the heart?
hypertension | aortic stenosis
57
What do thrombi look like in aneurysms?
Have lines of Zahn - grossly apparent laminations - alternating pale layers of platelets mixed with some fibrin; and dark with more RBC
58
What do you often have to combine GTN with?
- combine with beta-blocker - > GTN causes reflex tachycardia - combine with N-acetyl cystein (because of tolerance)
59
What drugs are used in ishaemic heart disease (4)
nitrates calcium channel blockers beta blockers ivabradine
60
What effect do ACE inhibitors have in heart failure?
ACE - blocks coversion of AngI to AngII - reduce vasoconstriction - reduce aldosterone production -> reduce salt; water retention - reduce cardiac hypertrophy ACE = kininase II - reduce bradykinin breakdown -> increase bradykinin -> vasodilation
61
What effects does angiotensin II have? (5)
- increases sympathetic activity - increases tubular Na+; Cl- reabsorption; H2O retention; K+ excretion - increases aldosterone secretion (further stimulating Na+; H2O retetion) - increases vasoconstriction -> inc BP - increases ADH secretion by pituitary -> increases H2O absorption in collecting duct
62
What is a short acting nitrate? Long acting nitrate?
GTN - short acting (glyceryl trinitrate) isosorbide dinitrate - longer acting
63
what is activated protein C
a natural anti-coagulant -> neutralises factor V
64
What is arteriosclerosis? What does it include
General term for thickening and hardening of walls of arteries Includes - atherosclerosis - age related changes (may be exacerbated by high BP)
65
What is claudication in the legs?
Periods of ischaemia due to atherosclerosis + exertion
66
what is coronary steal? how do you avoid it?
if you vasodilate a coronary artery: - blood will move away from poorly perfused area to well perfused -> takes blood away from ischaemic area NO avoids this - because is a venodilator
67
what is dyslipidaemia?
abnormal lipid profile includes - hypercholesterolaemia - hypertriglyceridaemia - mixed hyperlipidaemia
68
What is familial hypercholesterolaemia? Clinical manifestation
Inherited dominant disorder - mutations in LDL receptor gene -> elevate circulating LDL -> infiltrate arteries -> stops inhibition of cellular synthesis of cholesterol -> liver isn't getting any LDL in so keeps making it (HMG-CoA reductase is not inhibited) - atherosclerosis before puberty - early heart attacks - xanthomas: thick; waxy plaques of skin over elbows; knees; buttocks
69
what is lipoprotein lipase?
enzyme found on outside of muscle/adipose tissue which use fats as energy source - take up fats from lipoproteins
70
What is Smith-Lemli-Opitz syndrome?
Defective enzyme that is used in the last step of cholesterol synthesis (squalene -> cholesterol) - multiple malformations + behavioural problems -> illustrates importance of cholesterol in development
71
What is the aim of pharmacological treatment of ischaemic heart diseases?
relieves symptoms Want to either: Increase O2 supply - dilate coronary arteries - reduce heart rate Decrease O2 demand - reduce preload on heart (dilate veins; reduce venous return) - reduce afterload on heart (dilate arterioles; decrease resistance)
72
What is the main risk factor for aortic dissection?
high BP also: Marfan's
73
what is the mechanism of action of ezetimibe?
- binds specific sterol transporter -> specifically inhibits cholesterol absorption in the intestine -> lowers LDL - doesn't affect absorption of anything else
74
What is the primary role of chylomicrons and VLDL
deliver triacylglycerols to tissues
75
what is the primary role of HDL
scavenge cholesterol
76
what is the primary role of LDL
donate cholesterol
77
What is the significance of ApoA-I (apolipoprotein)
marks HDL activates LCAT - converts phospholipids from cell membranes -> adds cholesterol to phospholipid to make an ester -> fills middle of HDL
78
What is the significance of ApoB-100
found on VLDL; LDL - binds to LDL receptor on liver
79
what is the significance of ApoC-II
found on chylomicrons; VLDL; HDL activates lipoprotein lipase
80
What is the two types of infarction in cardiac muscle? How long do they take to develop; and which direction What is their usual cause?
Transmural - involves full/nearly full thickness of the wall - Develop over 6-8hrs - begin in subendocardium and move outwards - Usual cause: thrombosis following acute plaque event in atheromatous artery Subendocardial - damage limited to subendocardium (inner 1/3 of wall) Two types: 1. regional (occurs with early intervention of local atherosclerotic narrowing) 2. circumferential (occurs with >1 territory) -> only if all 3 vessels are occluded; or if there is prolonged reduction in systemic BP (shock)
81
What leads to an MI or sudden death?
Acute plaque event - atherosclerosis with a unstable plaque - rupture/fissure of the plaque -> blood exposed to subendothelial tissues -> thrombus formation -> platelets activated by exposed collagen -> adhesion; secretion; segregation -> tissue factor activates coagulation cascade -> fibrin is formed from fibrinogen
82
Which cells are most vulnerable to ischaemia?
Neurons | cardiac muscle cells (20mins)
83
Which classes of drugs are used symptomatic relief in heart failure?
Ionotropes - beta-adrenoceptor agonists; PDE inhibitors; glycosides Diuretics Venodilators
84
Which drug modifies risk of MI?
Only ivabradine
85
Which drugs improve mortality in heart failure?
beta blockers ACE inhibitors aldosterone antagonists
86
Which drugs increase O2 supply to the heart in ischaemic heart disease?
Drugs that reduce heart rate - ivabradine - betablockers - calcium channel blockers
87
Which part of the cardiac muscle is most susceptible to ischaemia?
Subendocardial muscle - endocardium: perfused through wall - cardiac vessels run in epicardium; then myocardium; - subendocardium is furthest away - also subject to greatest pressure; impairing flow
88
Whihc ionotropes are used in acute heart failure?
beta-adrenoceptor agonists | PDE inhibitors
89
Why do people vary in their probability of atherosclerosis?
Variation in activity of HMG-CoA reductase pathway -> we all regulate feedback inhibition of HMG-CoA differently
90
Why does cardiac failure lead to oedema?
kidneys can take care of increases of end diastolic pressure of 20-30mmHg; but above this; pressure in the capillaries is too great and fluid leaks into interstitium in cardiac failure; body wants to increase EDP to maintain CO kidneys can take care of this to a certain point; but not beyond that also exacerbated by Na+ ad water retention by kidneys
91
Why does pain occur in stable angina?
Hypoxia on exertion -> lactic acid + adenosine are formed -> act on nerve endings to cause pain

Cardio block (6 decks)

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