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SEM2 BIOSCIENCE > Case 5 > Flashcards

Case 5 Flashcards

1
Q

What is shear stress? How does it cause damage to endothelium?

A

Shear stress is the force of flowing blow against the endothelium

Turbulent blood flow causes low shear stress. This promotes apoptosis of endothelium and secretion of mediators of vasoconstriction and coagulation

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2
Q

What is the initial trigger in the formation of an atherosclerotic plaque?

A

Endothelial dysfunction

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3
Q

Outline the three main causes of endothelial dysfunction

A

Low shear stress due to turbulent blood flow
ROS (smoking)
Elevated LDL

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4
Q

In which part of the blood vessel wall is vascular smooth muscle found?

A

Tunica media

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5
Q

In which part of the blood vessel wall does the initial fatty streak formation take place?

A

Tunica intima

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6
Q

What receptor do macrophages use to phagocytose oxidised LDL?

A

Scavenger receptors

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7
Q

What cytokines are relased by endothelial cells and smooth muscle cells in response to vascular damage that results in the migration of smooth muscle cells to the tunica intima?

A

IL1 and TNFa

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8
Q

What is the name given to macrophages that have phagocytosed oxidised LDL?

A

Foam cells

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9
Q

The next stage on from fatty streak development is the formation of a fibro-fatty lesion. What is this?

A

Calcified and fibrosed fatty streak

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10
Q

What is the fibrous cap of the plaque made from?

A

SMC that have undergone apoptosis

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11
Q

What protease is responsible for the eventual rupture of the plaque? From what cells is it secreted?

A

Matrix metaloprotease (MMP)

Foam cells secrete in response to oxidised LDL

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12
Q

What are the consequences of fibrous cap rupture

A

Subendothelial layer exposure

Platelet adhesion

Thrombosis

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13
Q

Summarise the main events in the formation and rupture of an atherosclerotic plaque (7 stages)

A 
Endothelial dysfunction
LDL migration, oxidisation and entrapment
Foam cell formation
Leukocyte adhesion
Fibro-fatty lesion formed
Cap formation
Rupture
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14
Q

What molecule is responsible for the oxidation of LDL in the tunica intima?

Where is the molecule produced?

A

ROS

Produced by endothelium, macrophages and smoking

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15
Q

What protein binds LDL in the tunica intima to cause entrapment?

A

Proteoglycans

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16
Q

In normoxic conditions, what process facilitates the majority of ATP production?

A

Mitochondrial TCA cycle

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17
Q

What is the metabolic building block produced by glycolysis that can produce lactate anaerobically?

A

Pyruvate

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18
Q

ATP is essential for cardiac muscle function. Specifically what are the two main functions of ATP within the cardiomyocyte?

A

SERCA pump function to remove Ca2+ from cytosol

Myosin ATPase to induce muscle contraction

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19
Q

How is ATP produced in the absence of oxygen?

A

Anaerobic glycolysis

Phosphocreatine

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20
Q

How is ischaemia different to hypoxia in terms of myocardial metabolic responses?

A

In a hypoxic environment anaerobic glycolysis can continue indefinitely as lactate can be removed from the cardiomyocytes

Ischaemia is lack of flow and O2 delivery meaning lactate builds up and damages tissue

21
Q

What are the eventual consequences of myocardial ischaemia?

A

Phosphocreatine and glycogen store depletion
Rise in lactate and intracellular pH
Fall in ATP

22
Q

What are the two main consequences of depleted ATP stores on cardiomyocytes?

A

Myosin ATPase dysfunction (hence no contraction)

Ion pump dysfunction (meaning membrane potential disturbance)

23
Q

In addition to membrane potential disturbance, what is the additional effect of elevated Ca2+ levels within cardiomyocytes?

A

Apoptosis induction

24
Q

What is reperfusion injury?

A

When the reinstatement of blood supply following ischaemia results in inflammation and oxidative damage

25
Q

What is the determinating factor for cardiomyocyte viability post-MI?

A

[ATP] during ischaemic episode

26
Q

What are the 5 stages of cardiac remodelling post-MI?

A 
Necrosis
Inflammatory response
Healing and scar formation
Hypertrophy and dilation
Heart failure
27
Q

What is a transmural infarct?

A

Infarct that spans the entirety of the ventricular wall

28
Q

What molecule is used as a diagnostic biomarker for MI?

A

Cardiac troponin T

29
Q

How does cardiac troponin T levels indicate MI status?

A

Elevated from 4-8 hours post MI, stays elevates for 4-7 days

Level of troponin correlates with size of infarct

30
Q

Arrhythmias within hours of MI are most likely to be caused by…

A

Distruption of gap junctions

31
Q

Arrhythmias within months of MI are most likely caused by…

A

Excessive collagen deposition which slows cardiac conduction impulses

32
Q

What is concentric hypertrophy?

A

Hypertrophic growth of a hollow organ without overall organ growth

33
Q

What happens in the proreparative phase of cardiac remodelling?

A

IL10 and TGFb secreted to inhibit pro-inflammatory actions of IL1 and TNFa

Allows tissue to progress onto repair/healing phase

34
Q

What are visceral afferent nerves?

A

Sensory nerves that conduct impulses from internal organs to CNS

35
Q

Ischaemic in cardiac muscle is sensed by which nerves?

A

Sympathetic visceral afferent nerves

36
Q

Why is pain from the heart misinterpreted at pain in the chest, axilla and arm?

A

Sympathetic visceral afferent nerves intersynpase with somatic sensory nerves from T1-4 dermatome in CNS

Brain unable to distinguish original location of pain once signals are in CNS

37
Q

Neck and jaw pain is also associated with MI. This pain can be associated with which nerves?

A

C7-8 somatic sensory afferent nerves

38
Q

What is ‘acute coronary syndrome’?

A

A group of serious conditions ranging from unstable angina to myocardial infarction

39
Q

What is angina?

A

Myocardial ischaemia due to coronary artery narrowing (atherosclerosis) which results from differences between O2 supply and demand in cardiac muscle

40
Q

What is stable angina?

A

Chronic, transient, predictable

Induced by emotional or physical stress

Reversed using GTN

41
Q

What is unstable angina?

A

Worsening of stable angina, often a precursor to MI

42
Q

What are the symptoms of stable angina?

A

Chest pain
Pain radiation to axilla, left arm, jaw and neck
SOB

43
Q

What are the symptoms of unstable angina?

A 
Chest pain
Nausea
Dyspnoea
Sweating
Dizziness
Fatigue

SYMPTOMS INDENTICAL TO MI

44
Q

Angina is almost always caused by what irreversible pathological process?

A

Atherosclerosis

45
Q

Differentiation of MI and unstable angina by ECG is difficult, why is this?

A

Unstable angina can produce ST changes on ECG

46
Q

What investigation is used for the differential diagnosis of angina/MI?

A

Cardiac troponin T levels

Elevated = MI (always)
Normal = angina
47
Q

A patient presents with symptoms of acute coronary syndrome. ECG shows no significant findings. How can you differentiate between a NSTEMI and unstable angina?

A

You cannot

Cardiac troponin T levels will only rise after 8-12 hours in case of NSTEMI

Treatment regimes the same

48
Q

Dyspnoea is a symptom of ACS. Why is this?

A

Ischaemia impairs ventricular relaxation

Blood backs up from LA to pulmonary vasculature causing pulmonary oedema

SEM2 BIOSCIENCE (13 decks)

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