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Medicine Sem 2 > Case 5 > Flashcards

Case 5 Flashcards

1
Q

what is an atheroma?

A

accumulation of intracellular and extracellular lipid in the intima of large and medium sized arteries

  • consists of a raised lesion with a soft, yellow, grumous core of lipid (mainly cholesterol and cholesterol esters) covered by a white fibrous cap
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2
Q

what are the three types of plaques?

A
  1. Fatty streak
  2. Simple plaque
    - Fat in the intima:
     - Extracellular lipids
     - Within modified smooth muscle cells and in macrophages.
    • Fibrous cap
      - Blood vessels (cause proliferation)
      - Inflammatory cells
  3. Complicated plaque
    - Calcification (cholesterol crystals)
    - Plaque disruption
    - Hemorrhage into plaque
    - Thrombosis
    - Aneurysm formation
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3
Q

how can plaques lead to aneurysm formation?

A

by weakening the underlying media

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4
Q

what is arteriosclerosis?

A

thickening of the walls of arteries and arterioles usually as a result of hypertension or diabetes mellitus

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5
Q

what’s a genetic disease that could lead to atherosclerosis?

A

familial hypercholesterolemia

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6
Q

what can high dose oral contraceptive pills lead to?

A

atherosclerosis

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7
Q

which personality type is more likely to lead to atherosclerosis?

A

type A

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8
Q

how is inflammation linked to atherosclerosis? and what’s C-reactive protein?

A

It is intimately linked with atherosclerotic plaque formation and rupture.
 - C-reactive protein (CRP) is the most effective marker of inflammation to test for.
 - When CRP is secreted from cells within the atherosclerotic intima, it can activate local endothelial cells and induce a prothrombotic state and also increase the adhesiveness of endothelium for leukocytes.
 - It strongly and independently predicts the risk of myocardial infarction, stroke, peripheral arterial disease, and sudden cardiac death, even among apparently healthy individuals.
 - Smoking cessation, weight loss, exercise and statins all reduce CRP.

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9
Q

what are pathogenic steps of atherosclerosis

A
  1. endothelial injury
  2. accumulation of lipoproteins
  3. platelet adhesion
  4. monocyte adhesion and foam cell creation
  5. factor release
  6. smooth muscle cell and fibrous tissue proliferation and ECM production
  7. lipid accumulation/occlusion
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10
Q

describe the pathogenic steps of atherosclerosis in detail

A
  1. Endothelial injury:
     - This increases the adhesion of leukocytes to the endothelial cells in two ways:
    1. The expression of adhesion molecules on endothelial cells that encourage leukocyte adhesion are increased. Vascular cell adhesion molecule (VCAM-1) binds monocytes and T cells.
    2. There is a decreased ability of the endothelial cells to secrete substances, such as nitric oxide, that prevent the adhesion of platelets and monocytes to the endothelial cells.
    o This leads to thrombosis and leukocyte adhesion.
     Endothelial injury also causes increased vascular permeability which allows leukocytes to leak into the intima.
  2. Accumulation of lipoproteins:
     - Lipids (mostly LDLs) begin to accumulate at the site of endothelial injury.
  3. Platelet adhesion:
     - Circulating platelets accumulate at the site of injury.
  4. Monocyte adhesion and Foam Cell creation:
     - Circulating monocytes begin to accumulate at the site of injury as a result of adhesion molecules.
     - The monocytes cross the endothelium, enter the tunica intima of the vessel wall.
     - Here they differentiate to become macrophages.
     - The macrophages ingest (via CD36 or SR-A receptors) and oxidise the accumulated lipoproteins, giving the macrophages a foam-like appearance.
     - The macrophage foam cells then aggregate on the blood vessel and form a visible fatty streak.
     - With time the fatty streaks grow larger and merge together.
     - The surrounding fibrous and smooth muscle tissues proliferate to form larger plaques.
  5. Factor release:
     - Macrophages release chemical mediators of inflammation and secrete substances that cause further proliferation of smooth muscle and fibrous tissue on the inside surfaces of the arterial wall.
     - Cells within the atherosclerotic intima secrete CRP which activates local endothelial cells and induces a prothrombotic state (by activating platelets) and also increases leukocyte adhesion (by increasing number of adhesion molecules on the endothelium).
     - Activated platelets produce thromboxane A2 which leads to platelet aggregation.
     - Cytokines are secreted which increase monocyte recruitment.
  6. Smooth muscle cell and fibrous tissue proliferation and ECM production.
  7. Lipid accumulation/ Occlusion:
     - The lipid deposits plus the cell proliferation can become so large that the plaque bulges into the lumen of the artery.
     - This greatly reduces blood flow, sometimes completely occluding the vessel.
     - Even without occlusion, the fibroblasts of the plaque eventually deposit extensive amounts of dense connective tissue – sclerosis (fibrosis) causes arteries to become stiff.
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11
Q

where are common sites for atheromas?

A
  • Aorta
  • Coronary arteries
  • Carotid arteries
  • Cerebral arteries
  • Leg arteries
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12
Q

how are lipids (cholesterol) transported in the bloodstream?

A

bound to apoproteins (forming lipoproteins)

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13
Q

what can dyslipoproteinaemias result from?

A

mutations that alter the apoproteins or the lipoprotein receptors on cells or from other disorders that affect the circulating levels of ipids

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14
Q

what can hyperlipidaemia do?

A
  • it can directly impair endothelial cell function by increasing local oxygen free radical production
  • oxygen free radicals can injure tissues and accelerate nitric oxide decay, reducing its vasodilator activity
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15
Q

what happens with chronic hyperlipidaemia?

A

lipoproteins accumulate within the intima:
- These lipids are oxidized through the action of oxygen free radicals locally generated by macrophages or endothelial cells.
- Oxidized LDL is ingested by macrophages through a scavenger receptor, and accumulates in phagocytes, which are then called foam cells.
- In addition, oxidized LDL stimulates the release of growth factors (cytokines) and by endothelial cells and macrophages that increase monocyte recruitment into lesions and cause smooth muscle cell proliferation.
- Finally, oxidized LDL is cytotoxic to endothelial cells and smooth muscle cells and can induce endothelial cell dysfunction.

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16
Q

why is inflammation caused at the site of injury? what happens?

A
  • Caused as a result of monocyte and T cell accumulation at the site of injury.
  • The monocytes differentiate to form macrophages and enter the intima.
  • Here, they ingest oxidized LDL and become foam cells.
  • Foam cells produce reactive oxygen species that aggregate LDL oxidation and elaborate growth factors that drive smooth muscle cell proliferation.
  • T cells recruited to the intima interact with the macrophages and can generate a chronic inflammatory state.
  • Activated T cells in the growing intimal lesions elaborate inflammatory cytokines, which can stimulate macrophages as well as endothelial cells and smooth muscle cells (cell proliferation).
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17
Q

describe what happens during smooth muscle proliferation

A
  • Intimal smooth muscle cell proliferation and ECM deposition convert a fatty streak, into a mature atheroma.
  • The recruited smooth muscle cells synthesize ECM (notably collagen) that stabilizes atherosclerotic plaques.
  • However, activated inflammatory cells in atheromas can cause intimal smooth muscle cell apoptosis, and also increase ECM catabolism resulting in unstable plaques.
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18
Q

what are the three principal components of atherosclerotic plaques?

A
  1. Cells: smooth muscle cells, macrophages, and T cells
  2. ECM: including collagen, elastic fibres, and proteoglycans
  3. Lipid: intracellular and extracellular
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19
Q

what happens to plaques over time?

A

Plaques generally continue to change and progressively enlarge due to cell death and degeneration, synthesis and degradation (remodeling) of ECM, and organization of thrombus. Moreover, atheromas often undergo calcification, forming cholesterol crystals.

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20
Q

what’s the clinical significance of rupture, ulceration or erosion?

A

- Rupture, ulceration, or erosion of the luminal surface of atheromatous plaques exposes the bloodstream to highly thrombogenic substances and induces thrombus formation.
- Such thrombi can partially or completely occlude the lumen and lead to downstream ischemia.

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21
Q

what’s the clinical significance of haemorrhage into a plaque?

A

- Rupture of the overlying fibrous cap or of the thin-walled vessels in the areas of neovascularization can cause intra-plaque haemorrhage.
- A contained hematoma may expand the plaque or induce plaque rupture.

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22
Q

what’s the clinical significance of an atheroembolism?

A

Plaque rupture can discharge debris into the bloodstream, producing microemboli composed of plaque contents.

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23
Q

what’s the clinical significance of aneurysm formation?

A

Atherosclerosis-induced pressure or ischemic atrophy of the underlying media, with loss of elastic tissue, causes weakness of the vessel wall and development of aneurysms that may rupture.

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24
Q

what are three general categories that plaque changes fall into?

A
  1. Rupture/fissuring, exposing highly thrombogenic plaque constituents.
  2. Erosion/ulceration, exposing the thrombogenic subendothelial basement membrane to blood.
  3. Hemorrhage into the atheroma, expanding its volume.
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25
Q

what are ‘vulnerable plaques’ and what does this mean?

A

plaques that contain large areas of foam cells and extracellular lipid, and those in which the fibrous caps are thin or contain few smooth muscle cells or have clusters of inflammatory cells, are more likely to rupture

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26
Q

what triggers abrupt changes in plaque configuration and superimposed thrombosis?

A
  • intrinsic factors - e.g. plaque structure and composition

- extrinsic factors - e.g. blood pressure

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27
Q

what is collagen in atherosclerotic plaques primarily produced by?

A

smooth muscle cells

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28
Q

what is collagen degraded by?

A

matrix metalloproteinases (MPs), enzymes elaboratd largely by macrophages within the atheromatous plaque

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29
Q

what modulates MP activity

A

tissue inhibitors of metalloproteinases (TIMPs), produced by endothelial cells, smooth muscle cells and macrophages

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30
Q

The balance of collagen synthesis versus degradation affects cap stability and so affects the atheroma’s susceptibility to acute plaque changes. explain how this happens.

A

- Collagen in atherosclerotic plaque is produced primarily by smooth muscle cells, so that loss of these cellular elements results in a weaker cap.
- Collagen is degraded by matrix metalloproteinases (MPs), enzymes elaborated largely by macrophages within the atheromatous plaque.
- Tissue inhibitors of metalloproteinases (TIMPs), produced by endothelial cells, smooth muscle cells, and macrophages, modulate MP activity.

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31
Q

what does plaque inflammation do to the fibrous cap and how?

A

Plaque inflammation results in a net increase in collagen degradation and reduces collagen synthesis, thereby destabilizing the integrity of the fibrous cap.

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32
Q

what is a thrombus formed of?

A

A thrombus (pathogenic blood clot) is composed of the same components as a normal haemostatic blood clot, namely a meshwork made from the protein fibrin.

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33
Q

what becomes imbedded in the clot?

A

platelets and blood cells

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34
Q

where does a thrombus normally begin?

A

attached to the vessel wall - embolus when no longer attached

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35
Q

describe the process of thrombus formation

A
  1. Damage to vessel.
  2. This exposes connective tissue.
  3. Platelet aggregation begins with damage to the wall of a blood vessel.
  4. Proteins within the connective tissue (e.g. collagen) then bind to glycoprotein receptors on the surface of platelets.
  5. The platelet then undergoes a shape change and becomes activated.
  6. The activated platelet:
     Releases factors that will activate surrounding platelets such as Thromboxane A2 (TXA2) and ADP.
     Begins to express a different type of glycoprotein receptor on its surface.
    o The receptor is able to bind fibrinogen.
  7. Other platelets are activated and a chain reaction begins.
  8. The platelets become cross-linked by fibrinogen.
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36
Q

vasoconstriction at sites of atheromas is stimulated by what?

A
  1. Circulating adrenergic agonists.
  2. Locally released platelet contents (CRP).
  3. Impaired secretion of endothelial cell relaxing factors (nitric oxide) relative to contracting factors (endothelin) as a result of endothelial cell dysfunction.
  4. Mediators released from perivascular inflammatory cells.
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37
Q

what is ischaemic heart disease?

A

This is a disease of the heart whereby there is reduced blood delivery to it, leading to a compromise in its function. It is also known as coronary artery disease.

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38
Q

what are the clinical consequences of ischaemic heart disease?

A 
•	Nothing
•	Cardiac arrhythmia: atrial fibrillation; heart block; ventricular fibrillation
•	Angina pectoris
•	Acute myocardial infarction
	Distribution:
	- Regional/ circumferential
	- Subendocardial/ transmural
	Causes:
	- Coronary artery thrombosis
	- Increased demand
•	Acute left ventricular failure
	- Coronary artery thrombosis
	     - Regional  or Transmural (across the entire ventricular wall) compromise in function.
	- Increased demand
	- Leads to pulmonary oedema
•	Chronic heart failure
	- Gradual onset
	- Pump failure of both ventricles
	- Inadequate systemic blood supply
	- Symptoms: tiredness; ankle swelling; minor liver dysfunction
•	Sudden unexpected death
	- IHD is the commonest cause of sudden unexpected death.
	- A few are acute myocardial infarction.
	- More are acute left ventricular failure.
	- Most are cardiac arrhythmia.
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39
Q

what is ischaemic heart disease caused by?

A

oxygen deficiency and accumulation of metabolites, which stimulate the sensory nerve endings of the myocardium
- this leads to chest pain that can be referred to other parts of the body, such as the arm and the jaw

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40
Q

what is angina pectoris characterised by? and caused by?

A
  • characterised by sudden and usually recurrent attacks of chest discomfort
  • it’s caused by transient (15 seconds to 15 minutes) myocardial ischaemia that falls short of inducing myocyte necrosis
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41
Q

what are the different types of angina?

A
  1. classical/exertional angina pectoris/stable angina
  2. unstable angina/pre-infarction angina
  3. Varlant angina
  4. Decubitus angina
  5. nocturnal angina
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42
Q

what’s stable angina?

A
  • This is provoked by physical exertion, especially after meals and in cold, windy weather (vasoconstriction).
    - Commonly aggravated by anger or excitement.
    - The pain fades quickly (usually within minutes) with rest.
    - The pain disappears with continued exertion (‘walking through the pain’).
     - Whilst in some patients the pain occurs predictably at a certain level of exertion, in most patients the threshold for developing pain is variable.
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43
Q

what’s unstable angina?

A

- This refers to increasingly frequent pain, often of prolonged duration, that is brought on suddenly by progressively lower levels of physical activity or even at rest.
- In most patients, it is caused by disruption of an atherosclerotic plaque with superimposed partial (mural) thrombosis and possibly embolization or vasospasm (or both).
- Unstable angina serves as a warning that an acute MI is imminent.

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44
Q

what’s Varlant angina?

A

- This refers to angina that occurs without provocation.
- Usually occurs at rest, as a result of coronary artery spasm.
- It occurs more frequently in women.
- Characteristically, there is ST elevation on the ECG during the pain.
- Prinzmetal angina responds quickly to vasodilators.

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45
Q

what’s Decubitus angina?

A

- This is angina that occurs on lying down.

- It usually occurs in association with impaired left ventricular function, as a result of coronary artery disease.

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46
Q

what’s nocturnal angina?

A

- This occurs a night and may wake the patient from sleep.
- It can be provoked by vivid dreams.
- Tends to occur on patients with critical coronary artery disease and may be the result of vasospasm.

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47
Q

what investigations are used to diagnose angina?

A

Resting ECG
- This is usually normal between attacks.
- Evidence of old myocardial infarction may be present.
- During an attack, transient ST depression, T wave inversion or other changes of the shape on the T wave may appear.

Exercise ECG
- Helps confirm the diagnosis of angina (exertional).
- Useful in giving an indication as to the severity of the CAD.
- A normal test doesn’t exclude CAD, although these patients, as a group, have a better prognosis.

Echocardiography
- Used to assess ventricular wall involvement and ventricular function.
- Regional wall motion abnormalities at rest reflect previous ventricular damage.

Coronary Angiography
- Used to diagnose CAD and exclude other factors, such as pulmonary embolism.
- The test is performed to highlight the exact coronary anatomy in patients being considered for revascularization (i.e. coronary artery bypass grafting or coronary angioplasty).

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48
Q

what is primary prevention? what are the two types of primary prevention?

A
  1. Population:
    - Aims to modify the risk factors of the whole population through diet and lifestyle advice, on the basis that even a small reduction in smoking or average cholesterol, or modification of exercise and diet will produce worthwhile benefits
  2. Targeted strategies:
    - Aims to identify and treat high-risk individuals who usually have a combination of risk factors and can be identified by using composite scoring systems.
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49
Q

what are patients advised to take before undertaking exertion that may induce angina?

A

sublingual glyceryl nitrate

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50
Q

the treatment of angina is aimed to do what?

A
  1. Reduce the oxygen demand (reduce workload)
    - Vasodilation of peripheral blood vessels:
    o Heart does not have to push so hard.
    o Less blood returned to heart: lower force of contraction.
    - Increase venous return
    o Frank-Starling Mechanism
  2. Increase oxygen supply (improve blood flow)
    - Vasodilation of coronary arteries
    o Both the normal coronary arteries and collateral coronary vessels.
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51
Q

what are the five groups of drugs that are used to help relieve or prevent the symptoms of angina?

A
  1. nitrates - glyceryl trinitrate
  2. beta-blockers - bisoprolol
  3. calcium channel antagonists
  4. potassium channel agonists
  5. If channel antagonist
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52
Q

glyceryl trinitrate

  • what does it do
  • how
  • taken when
A

- Cause vasodilation.
- Help increase myocardial oxygen supply.
- Should be taken as prophylactic medication before taking exercise that is liable to provoke symptoms.

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53
Q

beta-blockers

  • how work
  • what do they do
  • side-effects
A

- Lower myocardial oxygen demand by lowering the heart rate, BP and myocardial contractility.
- Coronary flow improved as a consequence of prolongation of diastole.
- They may provoke bronchospasm in patients with asthma.

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54
Q

calcium channel antagonists

- what do they do

A

- Inhibit the slow inward current (ICa) caused by the entry of extracellular calcium through the cell membrane of excitable cells, particularly cardiac and arteriolar smooth muscle.
- Lower myocardial oxygen demand by reducing BP and myocardial contractility.

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55
Q

potassium channel agonists

  • what do they do
  • how effective
A

- Cause vasodilation.

- Not as effective as nitrates.

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56
Q

If (pacemaker current, funny current) channel antagonist

  • example
  • how work
  • positive
A

- Ivabradine is a selective and specific inhibitor of the cardiac pacemaker If current.
- If controls the spontaneous diastolic depolarization in the sinus node and regulates heart rate.
- In contrast to β-blockers and rate-limiting calcium antagonists, it does not have other cardiovascular effects.
- It appears to be safe to use in patients with heart failure.

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57
Q

what do eluting stents do?

A

these are coated with anti-proliferative drugs that limit smooth muscle cell hyperplasia, resulting in markedly diminished intimal thickening

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58
Q

what vessels are mainly used in coronary artery bypass? how successful is procedure?

A

• The vessels that are mainly used in this procedure include:
- Internal mammary arteries
- Radial arteries (Allen’s Test)
- Reversed segments of the patient’s own saphenous vein (leg)
• Approximately 90% of the patients that undergo this procedure are free of angina.

59
Q

how are sensory nerve endings of the myocardium stimulated? what happens once they’re stimulated?

A

Once the sensory nerve endings of the myocardium have been stimulated by ischaemia and accumulation of metabolites:
- The afferent (visceral) nerve fibres ascend to the central nervous system through the cardiac branches of the sympathetic trunk and enter the spinal cord through the posterior roots of T1-T4 nerves.

60
Q

why visceral pain felt as though it originates from the skin?

A
  • In the figure, branches of visceral pain fibres are shown to synapse in the spinal cord on the same second-order neurons (1 and 2) that receive pain signals from the skin.
  • When the visceral pain fibres are stimulated, pain signals from the viscera are conducted through at least some of the same neurons that conduct pain signals from the skin, and the person has the feeling that the sensations originate in the skin itself.
61
Q

why is visceral pain felt in skin not necessarily where the dermatomal segment from where visceral organ lies?

A

When visceral pain is referred to the surface of the body, the person generally localizes it in the dermatomal segment from which the visceral organ originated in the embryo, not necessarily where the visceral organ now lies.

62
Q

explain how heart pain is referred

- where and why

A

• The heart originated in the neck and upper thorax, so the heart’s visceral pain fibres pass upward along the sympathetic sensory nerves and enter the spinal cord between segments C-3 and T-5.
 - Therefore, pain from the heart is referred to the side of the neck and jaw, over the shoulder, over the pectoral muscles, down the arm, and into the substernal area of the upper chest.
 - These are the areas of the body surface that send their own somatosensory nerve fibers into the C-3 to T-5 cord segments.
 - Most frequently, the pain is on the left side rather than on the right because the left side of the heart is much more frequently involved in coronary disease than the right.
• The skin areas supplied by the upper four intercostal nerve fibres and by the inercostobrachial (T2) nerve are therefore affected.
• The intercostobrachial (T2) nerve communicates with the medical cutaneous nerve of the arm and is distributed to skin on the medial side of the upper part of the am.
• A certain amount of spread of nervous information must occur, for the pain is felt in the neck and jaw.

63
Q

what is myocardial infarction?

A

when cardiac myocytes die due to prolonged myocardial ischaemia

64
Q

what are the two types of myocardial infarction?

A
  1. ST (fragment) Elevation Myocardial Infarction (STEMI)

2. Non-ST (fragment) Elevation Myocardial Infarction (NSTEMI)

65
Q

STEMI

  • what is it
  • what does ST-segment elevation indicate
  • which more serious
A
  • It is defined as the development of heart muscle necrosis results from an acute interruption of blood supply to a part of the heart.
  • Presence of ST-segment elevation in ECG indicates full thickness damage of heart muscle occur in this type of myocardial infarction.
  • For this reason, STEMI is more severe heart attack in compare to NSTEMI where partial thickness damage of heart muscle occurs.
66
Q

what is the pathophysiology of STEMI?

A

- STEMI usually develops by formation of an occlusive thrombus in a coronary artery previously affected by atherosclerosis.
- The most common cause is rupture or erosion of an atherosclerotic plaque that triggers platelet aggregation and fibrin deposition, which lead to formation of an occlusive thrombus in a coronary artery at the site of the atherosclerotic plaque.
- This arterial occlusion causes interruption of blood supply to part of the myocardium (heart muscle), profound changes take place in the myocardium (heart muscle) that lead to irreversible changes and death of myocardial cells, and as a result STEMI develops.

67
Q

NSTEMI

  • what is it
  • what does absence of ST-segment elevation indicate
  • which mores serious
A
  • It is defined as the development of heart muscle necrosis results from an acute interruption of blood supply to a part of the heart.
  • Absence of ST-segment elevation in NSTEMI indicates partial thickness damage of heart muscle occurs.
  • Therefore, NSTEMI is less severe type of heart attack compared to STEMI in which full thickness damage of heart muscle occurs.
68
Q

what is the pathophysiology of NSTEMI?

A

- NSTEMI usually occurs by developing a partial occlusion of a major coronary artery or a complete occlusion of a minor coronary artery previously affected by atherosclerosis.
- The most common cause is rupture or erosion of an atherosclerotic plaque that triggers platelet aggregation, which lead to formation of a thrombus in a coronary artery at the site of the atherosclerotic plaque.
- This arterial thrombus causes interruption of blood supply to part of the myocardium, profound changes take place in the myocardium that lead to irreversible changes and death of myocardial cells, and as a result NSTEMI develops.

69
Q

how is a heart attack diagnosed?

A

• Made with an appropriate clinical history + findings from repeated 12-lead ECGs (ST elevation) + elevated biochemical markers (troponin T and I).
 - 12 lead ECG is an ECG which contains 10 electrodes (V1-V6, aVR, aVL, aVF, earth electrode).
 - It is called a 12 lead ECG as we are presented with 12 traces (V1-V6, aVR, aVL, aVF, Leads I, II and III)
• Signs and Symptoms:
o Heavy, crushing chest pain. This would be diagnosed as angina and may be referred.

- Autonomic Symptoms:
o Pale, clammy and sweating
- Irregular heart rate (bradycardia/tachycardia).
- Light headed

Venous Blood Samples:
- Cardiac Troponin T and I levels
- Glucose levels
- Lipid Profile:
      o	LDL, HDL and Triglycerides
70
Q

what is the treatment/management for a myocardial infarction?

A 
A&E:
- Aspirin
- Sublingual GTN
- Oxygen 
- Beta-blocker (Bisoprolol)

Other:
- Percutaneous Coronary Intervention (PCI)
o Angioplasty
- Coronary Artery Bypass Surgery

Post-MI drug therapy:
- Aspirin
    - Beta-blocker (Bisoprolol)
- ACE inhibitor
    - Statins (Atrovastatin)
71
Q

what are complications of myocardial infarction?

A
  • cardiac arrhythmia
  • cardiac failure
  • cardiac rupture
  • sudden unexpected death
72
Q

what’s LDL?

  • what does it do
  • what do they increase the risk of
A
  • LDL and VLDL are known as ‘bad cholesterol’
  • they inhibit fibrinolysis
  • they activate platelets, thus increasing aggregation
  • they increase the risk of atherosclerosis
73
Q

what’s HDL?

- what does it do

A
  • increase fibrinolysis
  • increase prostacyclin formation, thus decreasing aggregation
  • a high HDL/LDL ratio = lower risk of atherosclerosis
74
Q

what’s the treatment for hyperlipidaemia?

A

statins

75
Q

how soluble is cholesterol in water? how is it transported?

A
  • Cholesterol is minimally soluble in water; it can dissolve and travel in the water-based bloodstream only at exceedingly small concentrations.
  • In order to carry large quantities of cholesterol, it is transported in the bloodstream by binding to apoliproteins (forming lipoproteins).
76
Q

what do lipoproteins carry?

A
  • cholesterol
  • triglycerides
  • phospholipids
  • cholesterol esters
77
Q

where is cholesterol transported form and by what?

A

cholesterol is transported from the liver towards peripheral tissues by the lipoproteins:

  • chylomicrons
  • VLDL
  • LDL
78
Q

where is cholesterol transported back to and by what?

A

cholesterol is transported back to the liver from peripheral tissues by:
- HDL - known as reverse cholesterol transport (RCT)

79
Q

where is cholesterol produced?

A

in the liver

80
Q

why does reduced blood flow lead to faulty nerve impulses?

A
  • reduced oxygen
  • reduced oxidative metabolism
  • reduced ATP production
  • impaired function of ATPase pump
81
Q

what does reduced blood flow lead to stimulation of?

A
  • stimulation of ‘back-up’ system: the cell consumes ‘high energy phosphate’ back-up called phosphocreatine (PCr) to maintain high ATP levels
  • anaerobic metabolism:
    - conversion of pyruvate (end of glycolysis) into lactate and H+ ions (lactic acid)
    - lactic acid accumulates in extracellular space and cytosol
82
Q

what’s the equation for phosphocreatine?

A

PCr + ADP ATP + Creatine

83
Q

what is converted into lactic acid? and what happens to the lactic acid?

A
  • pyruvate is converted into lactic acid
  • this is excreted from inside the cell and into the blood
  • this excretion is carried out via transporter proteins found in the cell membrane of the muscle cells
  • as the transporter proteins pump the lactate acid out of the cell, the concentration of lactic acid increases extracellularly, thus reaching a concentration equilibrium (this happens in ischaemic tissue)
84
Q

in ischaemic necrotic tissue (infarcted zone of myocardium), what happens to different parts of the tissue?

A
  • the core of the tissue is dead

- the peripheries don’t die dut to collateral circulation (perfusion from other vessels)

85
Q

aspirin

  • what is it used for
  • what’s the active ingredient
  • what used for treatment of
  • side effects
A
  • An analgesic (pain killer) drug that also works as an anti-inflammatory and an antipyretic.
  • It is also taken in low doses as an antiplatelet drug.
  • Active agent in aspirin is salicylic acid.
  • It is used in the treatment for pain, headaches, fever, heart attacks and strokes.
  • Side effects: Irritation of the stomach lining; nausea; vomiting; abdominal pain; bleeding; Reye’s syndrome.
86
Q

what’s the mechanism of action of aspirin?

A

- Suppresses the production of prostaglandins and thromboxane.
- This is carried out by irreversible inactivation of the cyclooxygenase (COX) enzyme.
- COX is responsible for the formation of prostaglandins and thromboxane.
- Prostaglandins:
 - Inhibition of prostaglandin production has anti-inflammatory effects.
- Thromboxane:
 - Thromboxane A2 is produced by activated platelets.
 - It stimulates the activation of new platelets.
 - It also increases platelet aggregation.
 - This leads to the formation of blood clots.
 - Irreversibly blocking the formation of thromboxane A2 in platelets, produces inhibitory effects on platelet aggregation.

87
Q

bisoprolol

  • what is it
  • what does it treat
  • mechanism of action
  • side effects
A

• A β1-adrenergic receptor antagonist.
• It is used to treat angina pectoris, hypertension and heart failure.
• Mechanism of Action:
 - Blocks the β1-adrenergic receptors.
 - This decreases the adrenergic stimulation of the heart muscle and pacemaker cells.
• Side effects:
 - Breathing difficulties; fatigue; cold extremities; sleep disturbances; hypotension; bradycardia.

88
Q

ticagrelor

  • what is it
  • what used fro
  • what usually given with
  • mechanism of action
  • side effects
A

• An antiplatelet drug.
• It is used in the prevention of thrombosis in patients with myocardial infarction with ST elevation.
• It is usually given in combination with aspirin.
• Mechanism of Action:
 - It is a platelet aggregation inhibitor.
 - It works by blocking adenosine disphosphate (ADP) receptors of platelets. ADP is used in the activation and aggregation of platelets.
• Side effects:
 - Dyspnea; various types of bleeding.

89
Q

atorvastatin

  • what is it
  • what used for
  • what does it do
  • mechanism of action
  • side effects
A

• A statin.
• It is used for lower blood cholesterol levels.
• It stabilises plaque and prevents stroke through anti-inflammation.
• Mechanism of Action:
 - Competitive inhibitor of HMG-CoA reductase enzyme.
 - This enzyme is found in the liver and is involved in the catalysis of hepatic cholesterol biosynthesis.
 - Inhibition of this enzyme decreases cholesterol synthesis, increasing the expression of LDL receptors on hepatocytes.
 - This increases LDL uptake by the hepatocytes, decreasing the amount of LDL-cholesterol in the blood.
• Side effects:
 Weakness; dizziness; headache; raised concentration of hepatic enzymes.

90
Q

what’s the leading cause of death in the UK?

A

CHD

91
Q

what are the seven core components of cardiac rehabilitation?

A
  1. health behaviour change and education
  2. lifestyle risk factor management
    - physical activity and exercise
    - diet
    - smoking cessation
  3. psychosocial health
  4. medical risk factor management
  5. cardioprotective therapies
  6. long-term management
  7. audit and evaluation
92
Q

what physiological effects does anxiety/fear lead to?

A
  • increased SNS activity
  • hyper-vigilance
  • increased platelet activity
  • increased blood viscosity
  • increased vasomotor motility
93
Q

what is hostility, anger and aggression? what are the physiological effects?

A
  • Hostility = negative pattern of thoughts
  • Anger = emotional response to perceived threat
  • Aggression = behavioural expression of anger
  • Probably the same effects as fear.
94
Q

what physiological effects does depression lead to?

A
  • Less clear mechanism related to cortisol production - hypercortisolism
  • Increased heart rate variability
  • Decreased vagal tone
  • Insulin sensitivity decreased
  • Strong predictor of second MI and death
95
Q

what is Leventhal’s Self-regulatory model for? what is it?

A

adherence

  • interpretation - representation of health threat (identity, cause, consequences, time line, cure/control), emotion response to health threat (fear, anxiety, depression)
  • coping - approach or avoidance
  • appraisal - was my coping strategy effective?
96
Q

what are the three types of troponin proteins? and what do they do?

A

troponin C, T and I

  • troponin C initiates contracting by binding calcium and moves troponin I so that the two actin and myosin can interact
  • troponin T anchors the troponin complex to the fibre structure
97
Q

what are the metabolic changes that happen in the first minutes of a heart attack and what does this cause?

A
  • No O2 – no oxidative (mitochondrial) metabolism (any O2 that is there used up in seconds)
  • Cell consumes ‘high energy phosphate’ back-up Phosphocreatine (PCr) to maintain [ATP]i
  • Anaerobic metabolism switches on to maintain [ATP]i – produces lactate + H+ ions
  • Lactic acid accumulates in EC (extracellular) space & cytosol (intracellular fluid) – accumulates inside and outside cell as no blood flow to remove it
  • Contractility impaired by metabolic changes (incr’d Pi – inorganic phosphate - & reduced pHi) (more phosphate means less phosphocreatine)
98
Q

what’s anoxia?

A

no oxygen at all

99
Q

what happens over time to the infarcted myocardium?

- what triggers cell damage in particular

A
  • Glycolysis now beginning to struggle
  • Glycogen reserves depleted
  • Cell full of lactic acid (can’t get out)
  • Intracellular pH now very, very acid
  • Glycolysis becoming inhibited (as pH is too low for enzymes to work)
  • [ATP]i falling
  • What are effects of sub-mM/microM [ATP]i?
  • No normal contraction – rigor? (rigor = stiffness)
    (also, ion gradients in trouble if no ATP)
  • ‘core’ [Na+]i: 10 mM -> 20-30-40s mM
  • ‘outer’ [Ca2+]: 0.1-1 uM -> 10s uM (very bad for heart cells – triggers cell damage)
  • [ATP]i now low microM at best
  • Ion pumps have no fuel
  • [Na+] and [Ca2+] in cells rise
  • Ca2+ rise in particular triggers cell damage
  • Compromised mitochondria release ‘cell death trigger factors’ (due to increase in calcium)
  • Some cells lose membrane integrity – even more Ca2+ rise, leak cellular contents = necrosis
100
Q

in SAN cells, what is the rise of action potential brought about by? what’s its rate?

A

an influx of calcium - the rate of this is slower

101
Q

why do the SAN cells never reach a membrane potential that is as negative as that in ventricular cells?

A

because the membranes of these SAN cells have very few inward rectifying potassium channels that make the ventricular cell membranes very permeable to potassium

102
Q

how do the membrane potentials in ventricular cells and SAN cells compare with each other?

A
  • in ventricular cells they have a very stable resting membrane potential - it’s flat between beats
  • but in SAN cells the resting membrane potential isn’t stable - it spontaneously decays towards the threshold potential = pacemaker potential
103
Q

what’s important in setting the heart rate?

A

the rate of decay of the pacemaker potential

104
Q

which ion channels are responsible for the pacemaker potential?

A

Decay of the pacemaker potential (becoming more positive):
- Opening of inward currents
-If – ‘funny’ current (activated by hyperpolarisation rather than depolarisation) – small Na+ influx (slow)
-Causes opening of Ca2+ channels (T-type (not important in the ventricles but important here), and L-type secondly)
- Closing of outward currents
-K+ channels slowly close
(like in the ventricle, repolarisation is brought about by potassium efflux)

105
Q

what are the properties of the SAN action potential?

A

In comparison to the ventricular action potential:

  • Slow to rise
  • fast Na channels (only a few of these), slower Ca channels
  • Small amplitude
  • Slow conduction (through the SAN)
106
Q

what causes the refractory period with sodium channels?

A

the h gate has to reopen when the membrane returns to resting level

107
Q

the speed of conduction is fastest when what?

A
  • Cells are wider – lower axial electrical resistance (Purkinje fibres (very wide cells) vs. SAN (very narrow cells))
  • Action potentials are large and rapid to rise – generate large propagating currents (rate of ion influx – e.g. sodium in ventricles vs. calcium in SAN) – so travel quickly through myocardium
108
Q

describe the action potential of the atrial myocardium

A
  • True resting membrane potential (like in ventricles)
  • Depolarisation by rapid Na+ entry (like in ventricles)
  • Brief plateau (phase 2) – but merges into phase 3 of repolarisation
  • The APD (duration) in the atria is shorter than the ventricle – one reason is that the atria have delayed rectifying potassium channels, Ikur (ultra-rapid potassium channel)
  • Cells are relatively large
  • Conduction velocity 1 m/s – relatively fast
109
Q

describe the action potential in the AVN

A
  • Depolarised by calcium influx
  • No true resting potential – pacemaker potential, similar to that of the SAN
  • The rate of decay of pacemaker potential is slower than that of the SAN
  • action potential arises before the threshold is reached

Only conducting path between the atria and ventricles – slow (delay), because:
- Small diameter cells
- Action potential slow to rise – due to calcium
- Complex pathway – convoluted pathway for the excitation to travel through
Conduction velocity = 0.05 m/s = slow

110
Q

in the AVN, why does the action potential arise before the threshold is reached? and why does this make the pacemaker potential of the AVN cells irrelevant?

A

Why does the action potential arise before threshold is reached?
- Because the pacemaker potential in the SAN decays more quickly, in the SAN the pacemaker potential has already reached the threshold and fired and action potential
- That action potential spread through the myocardium and reached the AVN before the pacemaker potential actually reached the threshold itself
- So, the action potential in the AVN is triggered no by the pacemaker potential in the AVN but by an action potential that’s arisen from the SAN
So actually, the fact that these AVN cells have a pacemaker potential is irrelevant, because they will be stimulated by the action potential that arises from the SAN

111
Q

describe the action potential of the Purkinje fibres

A
  • Rapid to rise – depolarised by sodium
  • Large amplitude
  • Long duration – long plateau due to calcium influx
  • Pacemaker potential – but extremely weak – like in AVN cells this is irrelevant under normal conditions
  • Largest cells in the heart
  • Rapid depolarisation
  • Refractory
  • Conduction velocity = 4 m/s = extremely fast
112
Q

describe the action potential of the ventricular myocyte

A
  • True resting membrane potential – set by high permeability to potassium
  • Rapid and large influx – depolarisation
  • Plateau – calcium influx
  • Repolarisation – potassium efflux
  • Cells relatively large
  • Conduction velocity = 1 m/s = relatively fast
113
Q

when do ECGs pick up current?

A

if voltage difference points towards them

114
Q

what’s the effect of the sympathetic nervous system on different aspects of the heart? and how does it have this effect?

A

Sinoatrial node:
Stimulation of sympathetic nerve supply -> tachycardia
Why?
Noradrenaline -> activates B-receptors -> increase cAMP -> affect in SAN cells:
- Increase depolarising currents e.g. Funny & Ca current (so pacemaker potential decays more quickly towards the threshold)
- More quickly deactivating repolarising (K) currents

Atrioventricular node:
Activates B-receptors in the AVN -> increased conduction speed

Atria and ventricle:
Atrial and ventricular action potential is shortened due to increased repolarising (K) current

115
Q

how does the parasympathetic nervous system work on different aspects of the heart? and what does it do this?

A

Sinoatrial node:
Stimulation of vagus nerve -> slowing of pacemaker potential so takes it longer to reach threshold -> bradycardia
Why?
- ACh acts on muscarinic receptors (?)
- K+ -> channel opening -> causes hyperpolarisation (so it’s got further to go to reach threshold potential)
- And a pacemaker potential of reduced slope – due to opening of K+ channels

Atrioventricular node:
Reduces conduction through the AVN -> if strong enough can get heart block (condition where the heart beats more slowly or with an abnormal rhythm)

116
Q

which part of ANS predominates at rest?

A

Nerve fibres are always active -> pacemaker firing continuously modified by ANS
Parasympathetic predominates at rest
- Atropine + propranolol (inhibits ANS) = intrinsic rate (about 105 beats per minute) = rate generated by the SAN

117
Q

what’s the inflammatory response from a myocardial infarct?

A

INFLAMMATORY RESPONSE (starts a few hours of occlusion and lasts just under a week)
Clear dead cells – provide a stable base for a collagen scar
1. Neutrophils infiltrate the infarct
2. Secrete MMPs (matrix metalloproteinases) and phagocytose debris
3. Pro-inflammatory cytokine levels increase
4. Leads to recruitment of other inflammatory cells
5. Pro-reparative phase: neutrophils undergo apoptosis – further recruitment of inflammatory cells – initiation of the healing process

118
Q

describe the process of infarct healing and scar formation

A

Collagen-rich scar replaces cardiomyocytes in infarct zone

  • Cardiac fibroblasts (activated by inflammatory markers and mechanical stresses to differentiate) -> myofibroblasts
  • Main function: secrete new ECM proteins – form a strong ECM -> strong scar
  • Clearance of myofibroblasts by apoptosis – otherwise they’ll keep laying down more collagen
  • if too much collagen, you’ll get a very stiff ventricular wall and function will be reduced
  • if not enough collagen, you’ll get a thin scar forming which will make the heart more prone to aneurysm or cardiac rupture

After 2-3 months the infarct has healed – leaving a non-contracting region of the LV wall

119
Q

what happens to the non-infarcted tissue?

A

REMODELLING ALSO OCCURS IN THE NON-INFARCTED TISSUE
- The scarred part of heart is not no longer pumping, so the rest of the heart has to make changes so that the function of the heart remains normal – rest of the heart has to take on pump function for that dead part
LV hypertrophy:
- Muscle wall thickens
- Concentric hypertrophy – each cardiomyocyte gets a lot thicker – more and more sarcomeres are lay down
- This can go on from a few weeks, months to a few years – it maintains the normal functioning of the heart
But eventually, the heart can’t cope with the good part of the heart having to pump for the rest of the heart, so the heart starts to remodel again:
- Dilatation of left ventricle

120
Q

what are common ECG abnormalities?

A
  • First degree heart block (electrical signals are slowed as they move from the atria to the ventricles – longer, flatter line between the P and R waves)
  • Second degree heart block (electrical signals between the atria and ventricles are slowed to a large degree, some signals don’t reach the ventricles – the pattern of QRS waves don’t follow each P wave as it normally would)
  • Complete heart block (none of the electrical signals reach the ventricles – the P waves occur at a faster rate, and it isn’t coordinated with the QRS waves)
  • Sinus arrhythmia – the P-P interval may vary by > 0.16 seconds
  • Ventricular asystole
  • Atrial fibrillation
  • Ventricular fibrillation
  • S-T segment changes
121
Q

which ECG recording is the typical looking one?

A

limb lead 2 (right arm to right leg)

122
Q

complete heart block

  • what seen on ECG
  • what happens in the heart
A
  • Regular P waves (normal atrial depolarisation)
  • P waves rate 145 per minute
  • Regular QRS, but complexes highly abnormal because of abnormal conduction through ventricular muscle
  • QRS (ventricular escape) rate 15 per minute
  • No relation between P waves and QRS complexes

There’s a complete block from the atria to ventricles, but somewhere in the ventricles becomes a locus that will depolarise and become the trigger to cause contraction of the ventricles

Abnormal conduction through ventricles, so abnormal contraction, and abnormal stroke volume

123
Q

sinus arrhythmia

  • what seen on ECG
  • consequences
  • when seen
A
  • One P wave per QRS complex
  • Constant PR interval
  • Progressive beat-to-beat change in R-R interval
  • Entirely normal arrhythmia
  • Associated with breathing – ANS
  • At rest – parasympathetic tone will be slowly heart rate during expiration, and heart accelerates during inspiration as less parasympathetic drive to the heart
  • Much more common in children and tends to decrease with age
124
Q

what is heart block due to?

A

conduction problems in the AV node and bundle of his

125
Q

what’s the base line of atrial fibrillation like?

A

wobbly

126
Q

what causes a ST segment elevation/depression during myocardial ischaemia?

A

ST segment elevation/depression: an effect of myocardial hypoxia on repolarisation

  • When you have hypoxic cardiac muscle, it won’t repolarise normally
  • Therefore, you either get an elevation or depression in the ST segment
  • Sign of hypoxic cardiac muscle
127
Q

describe the structure of arteries and veins

A

tunica interna:

  • endothelium ‘
  • basement membrane
  • internal elastic lamina

tunica media:

  • smooth muscle
  • external elastic lamina

Tunica externa:
- advential layer

128
Q

what is the function of the endothelium?

A
  • A single intact layer of specialised cells lining the blood vessel wall
  • Responsible for preventing adhesion of platelets and monocytes
  • Exquisitely sensitive to alterations in blood pressure and flow
  • Release various vasoactive agents involved in maintenance of vascular tone e.g. NO (EDRF), endothelin, cyclooxygenase-dependent vasoconstrictors, EDHF, etc.
129
Q

what are foam cells?

A
  • a variety of macrophages that try to cope with excessive cholesterol
  • the lipid material inside a foam cell is typically LDL
130
Q

what are the stages of atheroma formation?

A
  • initial lesion
  • fatty streak
  • intermediate lesion
  • atheroma
  • fibroatheroma
  • complicated lesion
131
Q

fatty streaks

  • what stage of atherosclerosis
  • when appear
  • what consist of
A
  • Earliest lesion of atherosclerosis
  • Appear at a very early age (<10 years)
  • Consist of aggregations of lipid – laden macrophages and T lymphocytes within the intimal layer of the vessel wall
132
Q

describe the stages of fatty streak formation

A
  • Smooth-muscle migration
  • Foam-cell formation
  • T-cell activation
  • Adherence and aggregation of platelets
  • Adherence and entry of leukocytes
133
Q

what are intermediate lesions composed of?

A

Composed of layers of:

  • Lipid laden macrophages (foam cells)
  • Vascular smooth muscle cells
  • Isolated pools of extracellular lipid
134
Q

fibrous plaques or advanced lesions

  • what do they do
  • what covers them
  • what may happen to them
  • what do they contain
A
  • Advanced lesion
  • Impedes blood flow
  • Prone to ruptures
  • Covered by dense fibrous cap that overlies lipid core and necrotic debris
  • May be calcified
  • Contains: smooth muscle cells, macrophages & T lymphocytes
135
Q

what is self-efficacy?

A

believing you have the skills, energy and ability to make changes in your life

136
Q

what does the self-regulatory model compose of?

A
  • health threat
  • cognitions
  • emotions
  • coping
  • appraisal
137
Q

what is added to the SRM under the core cognitions?

A
  • coherence
  • emotions

these can drive behaviour

138
Q

what stops the chain reaction of increase platelet activation?

A

prostacyclin

139
Q

what are the 4 targets in antiplatelet drugs?

A
  1. Indirect prevention of platelet activation (thrombin inhibitors) (thrombin acts as a serine protease that converts soluble fibrinogen into insoluble strands of fibrin, as well as catalysing many other coagulation-related reactions)
  2. Inhibition of the synthesis of biologically active agents (e.g. thromboxane A2) within the platelets
  3. Inhibition of the expression or blocking of glycoprotein IIb/IIIa receptors on the surface or platelets
  4. Raising cAMP levels in platelets (dipyridamole)
140
Q

what is the most widely used antiplatelet drug?

A

aspirin

141
Q

which drug acts via glycoprotein IIb/IIIa receptors?

A
  • Ticagrelor allosterically inhibits the ADP receptor
  • Clopidogrel inhibits glycoprotein IIb/IIIa receptor expression on platelets by blocking the ADP receptor irreversibly (ADP is another signal released by activating platelets to trigger neighbouring platelets)
  • Differences: reversibility & clopidogrel is a prodrug
142
Q

what’s arteriosclerosis?

A
  • The thickening of walls of arteries and arterioles usually as a result of hypertension or diabetes mellitus
  • Some would include atheroma as a form of arteriosclerosis
143
Q

describe features and consequences of a complicated atheromatous plaque

A
  • Calcification – when fat broken down by WBCs, fatty acids released from triglycerides, which will react with calcium in the extracellular fluid and cause calcification
  • Plaque disruption – bleeding into plaque, or cap falling apart
  • Haemorrhage into plaque – blood vessel proliferation
  • Thrombosis
  • Aneurysm formation – inflammation near the elastic wall (in the aorta in particular) causes damage to the elastic tissue, which means reduced elastic recoil in the aorta, which can lead to an aneurysm – which can rupture, and there can be a lot of blood clotting
144
Q

what are causes of sudden unexpected death?

A
  • IHD is commonest cause of sudden unexpected death
  • A few are acute myocardial infarction
  • More are acute left ventricular failure
  • Most are (probably) cardiac arrhythmia – not visible on heart after someone’s died from it

Medicine Sem 2 (10 decks)

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