ILAs Flashcards

1
Q

Describe the evolution of the atherosclerotic plaque

long so just read through

A
  • Atherosclerosis develops over a long time (around 50 years) usually beginning in the early teenage years – only develops in high-pressure systems such as systemic arteries
  • Endothelial injury has the inciting role in the formation of a plaque, this can be caused by the risk factors described later.
  • Early fatty streak development begins in childhood and adolescence. Fatty streaks are accumulations of lipid-rich foam cells in the intima of the artery.
  • Lipid retention and oxidation is followed by chronic inflammation at susceptible sites in artery walls leading to fatty streaks.
  • During this immune response, macrophages take up oxidised LDLs to form foam cells.
    o These promote the migration of smooth muscle cells into tunica intima from tunica media
    o When foam cells die, their lipid content is released
  • Lipid pools form in the intima with a core of necrosis, these develop an overlying fibrous cap
  • This can develop into a thin-cap atheroma where the fibrous cap has thinned and is more susceptible to rupturing
  • Cyclic healing of these ‘clinically silent’ ruptures leads to multiple layers of healed tissue.
  • These plaques cause stenosis of the arteries and can themselves rupture, throwing out potentially fatal thrombi.
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2
Q

Modifiable risk factors for atherosclerosis

A
Smoking
Sedentary Lifestyle
Overweight
High blood cholesterol
Hypertension
Diabetes type 2
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3
Q

Non-modifiable risk factors of atherosclerosis

A

Old age
Male
Family history
Ethnicity

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4
Q

How does being male affect atherosclerosis?

A

Sex hormones alter immune response (not fully understood)

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5
Q

How does smoking affect atherosclerosis?

A

Releases free radicals, nicotine and CO. All damage epithelial cells

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6
Q

How does hypertension damage epithelial cells?

A

Shearing forces

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7
Q

How does poorly controlled diabetes cause atherosclerosis?

A

Superoxide anions and glycosylation products released

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8
Q

Hyperlipidaemia on atherosclerosis

A

Directly damages epithelial cells

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9
Q

Primary prevention of atherosclerosis

A

Smoking cessation
Increase activity levels
Improve diet

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10
Q

Secondary prevention of atherosclerosis

A

Prescribing gym sessions etc.
Statins to reduce LDL levels
Low-dose aspirin
Antihypertensives

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11
Q

What are co-benefits when it comes to health and climate change?

A

Changes that both improve people’s health and the climate. For example, walking rather than taking the car when possible.

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12
Q

Define anaphylaxis

A

A severe and potentially life-threatening reaction to a trigger such as an allergen

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13
Q

Possible trigger agents for anaphylaxis

A
  • Foods
  • Medicines (penicillin)
  • Insect stings
  • General anaesthetic
  • Contrast agents
  • Latex
  • Plants
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14
Q

Signs and symptoms of anaphylaxis

A
Swelling around throat and mouth
Low oxygen saturation
Raised heart rate
Low blood pressure
Prolonged capillary refill time
Urticaria
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15
Q

Pathogenesis of anaphylaxis

A

The first time an allergy protein runs across an allergen they make IgE antibodies which attach themselves to mast cells.

The second time the person encounters the antigen, causes cross linkage of IgE leading to mast cell degranulation. Histamines and other chemical mediators are released.

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16
Q

What do the chemical mediators cause in anaphylaxis?

A

Smooth muscle spasm in GI and respiratory tracts
Vasodilation and increased vascular permeability
Stimulation of sensory nerve endings
Increased mucous secretion
Increased bronchial smooth muscle tone
Airway oedema
Increased histamine in skin = Urticaria

17
Q

Recommended treatment of anaphylaxis.

A
ABCDE
Adrenaline (2 doses may be required)
Establish airway, high flow oxygen, IV fluid challenge
Chlorphenamine
Hydrocortisone
18
Q

Confirmatory test of anaphylaxis

A

Mast cell tryptase in blood