ILA

Question 1

Structure of an atherosclerotic plaque

Answer 1

Lipid, Necrotic core, Connective tissue, Fibrous “cap”

Question 2

Stimulus for an atherosclerotic plaque

Answer 2

Adhesion- Chemoattractants released from leukocytes

Question 3

Examples of non-modifiable risk factors for atherosclerosis

Answer 3

Age, gender, race, family history, Type 1 diabetes

Question 4

Examples of modifiable risk factors for atherosclerosis

Answer 4

smoker, lack of exercise, weight, (borderline) type 2 diabetes, hypertension, high cholesterol

Question 5

Risk factor for atherosclerosis- smoking

Answer 5

Releases free radicals, nicotine + CO into the body/blood
-These damage endothelial cells

Question 6

Risk factor for atherosclerosis- hypertension

Answer 6

Increased pressure 🡪 increased damage of the wall

Question 7

Risk factor for atherosclerosis- diabetes

Answer 7

-High glucose levels in the blood
-Increased Free radicals
-Increased oxidation of LDLs 🡪 means they get stuck
-Loss of nitric oxide (NO)
-Which normally allows relaxation of vessel + increased flow
-Promotes platelet aggregation

Question 8

Risk factor for atherosclerosis- cholesterol

Answer 8

High LDLs
-Can pass in and out of the arterial wall in excess, accumulates in arterial wall, undergoes oxidation and glycation

Question 9

Risk factor for atherosclerosis- Obesity

Answer 9

Increases proinflmmatory cytokines

Question 10

Risk factor for atherosclerosis- Exercise

Answer 10

-Helps rebalance of low- and high-density lipoproteins
-Reduces blood pressure

Question 11

Pathophysiology of atherosclerosis

Answer 11

1. Endothelial cell dysfunction
2. High levels of LDL in the blood
3. Inflame (activate) endothelial cells (leukocytes)
4. Macrophages take up lipid to form foam cells
5. Foam cells
6. Formation of a fatty streak in intimal layer
7. The activated macrophages (release products - cytokines and growth factors)
8. Smooth muscle proliferation (to intima) around the lipid core 🡪 formation of a fibrous cap (collagen)
9. Plaque either: -Occludes lumen 🡪 angina
   -Ruptures
   -Result of inflammatory conditions
   -When the plaque ruptures
   -Platelets adhere and clotting process begins

Question 12

Role of macrophages in atherosclerosis

Answer 12

take up lipid (oxidised LDLs) to form foam cells (inflammatory response)

Question 13

Main 3 coronary arteries to be occluded

Answer 13

-LAD (left anterior descending)
-Right coronary A
-Left circumflex

Question 14

Role of foam cell in atherosclerosis

Answer 14

-Promote migration of SMCs from tunica media 🡪 tunica intima
-When foam cells die 🡪 Lipid content released 🡪 plaque growth

Question 15

Secondary preventative measures- atherosclerosis

Answer 15

Statin, antihypertensive, diabetes control (meds, carbs intake), social prescribing

Question 16

Primary preventative measures-atherosclerosis

Answer 16

Exercise more, eat more healthily, stop smoking

Question 17

Define anaphylaxis

Answer 17

Anaphylaxis a severe, life-threatening, generalised or systemic hypersensitivity reaction which is likely when both of the following criteria are met:
-Sudden onset and rapid progression of symptoms.
-Life-threatening airway and/or breathing and/or circulation problems usually associated with skin and mucosal changes

Question 18

Symptoms of anaphylaxis

Answer 18

Occurs within minutes and lasts 1-2 hours
Vasodilation
Increased vascular permeability
Bronchoconstriction
Urticaria (hives)
Angio-oedema (rapid, oedema, or swelling, of the area beneath the skin or mucosa)

Question 19

Common triggers of anaphylaxis

Answer 19

Foods, venom (bee/wasp stings), drugs, contast agents

Question 20

Common triggers of anaphylaxis- Foods

Answer 20

peanuts, pulses, tree nuts (brazil nuts, almond, hazlenuts), fish and shellfish, eggs, milk, sesame

Question 21

Common triggers of anaphylaxis- Drugs

Answer 21

antibiotics, opoids, NSAIDs, muscle relaxants (Baclofen, Diazepam), contrast agents (used in x-rays)

Question 22

Pathophysiology of anaphylaxis- Sensitization phase

Answer 22

• Exposure to allergen results in IgE for the allergen binding to mast cells and basophils, they are primed to react for the next time the cells come into close proximity with the allergen

Question 23

Ig that mediates type 1 hypersensitivity reactions

Answer 23

IgE mediated

Question 24

IgE antibodies

Answer 24

formed to an antigen (or allergen), with an individual’s tendency towards making IgE being determined by factors including: genetics, T cell responsiveness and antigenic burden

Question 25

Pathophysiology of anaphylaxis- re-exposure phase phase

Answer 25

-Re-exposure to allergen causes cross-linking of IgE on the cell surfaces causes rapid (mast cell) cellular degranulation and liberation of a number of chemical mediators (most importantly histamine) - Reaction of antigen with IgE on mast cells also stimulates synthesis and release of platelet activating factor (PAF), leukotrienes and prostaglandins

Question 26

Mediators released from mast cell degranulation

Answer 26

preformed molecules histamine, protease enzymes, proteoglycans and chemotactic factors

Question 27

Physiologic responses to the release of anaphylaxis mediators

Answer 27

Smooth muscle spasm in the respiratory and GI tracts Vasodilation- makes you feel hot and itchy Increased vascular permeability Stimulation of sensory nerve endings Increased mucous secretion and increased bronchial smooth muscle tone, as well as airway oedema Cardiovascular effects result from decreased vascular tone and capillary leakage

Question 28

Physiologic responses to the release of anaphylaxis mediators- CV effects

Answer 28

Cardiovascular effects result from decreased vascular tone and capillary leakage. Hypotension, cardiac arrhythmias, syncope and shock can result from intravascular volume loss, vasodilation and myocardial dysfunction, increased vascular permeability can produce a shift of 35% of vascular volume to the extravascular space within 10 minutes

Question 29

H1 receptors action

Answer 29

-Vasodilation, hypotension, and flushing are mediated by H1 receptors -H1 receptors alone mediate coronary artery vasoconstriction, tachycardia, vascular permeability, pruritus (itchy skin), bronchospasm, and rhinorrhoea (runny nose)

Question 30

H2 receptors action

Answer 30

H2 receptors increase atrial and ventricular contractility, atrial chronotrophy, and coronary artery vasodilation

Question 31

Rapid assessment for anaphylaxis- ABCDE

Answer 31

Airway: look for and relieve airway obstruction. Remove any traces of allergen Breathing: look for a treat bronchospasm and signs of respiratory distress Circulation: colour, pulse, BP Disability: assess whether responding or unconscious (AVPU) Exposure: assess skin with adequate exposure, but avoid excess heat loss

Question 32

When to consider anaphylaxis

Answer 32

when there is compatible history of raid-onset severe allergic-type reaction with respiratory difficulty and/or hypotension, especially if there are skin changes present

Question 33

1st line treatment for anaphylaxis

Answer 33

IM Adrenaline (epinephrine)

Question 34

Adrenaline (epinephrine) action for treatment of anaphylaxis

Answer 34

Stimulation of beta1-adrenoceptors: positive ionotropic (force of heart contraction) and chronotropic (heart rate) effects on the heart Stimulation of beta2-adrenoceptors: reduces oedema and brocnhodilates Attenuates further release of mediators from mast cells and basophils by increasing c-AMP(cellular signal induction) and so reducing the release of inflammatory mediators

Question 35

Why give IV fluids after an anaphylactic shock

Answer 35

To help restore the circulating volume and therefore the stroke volume thus increasing the cardiac output

Question 36

Action of Chlorphenamine after initial resus for anaphylaxis

Answer 36

Chlorphenamine is an antihistamine which blocks the Histamine 1 receptor thus blocking the action of the histamine released during anaphylaxis

Question 37

Action of Hydrocortisone after initial resus for anaphylaxis

Answer 37

Suppresses prostaglandin and leukotriene mediators, inflammatory cell recruitment and migration are inhibited and vasoconstriction reduces leakage from the blood vessels

Question 38

Explain why a second dose of adrenaline might be required for treatment of anaphylaxis

Answer 38

Adrenaline has a short half life therefore a second dose may be required if the symptoms of not initially respond or get worse

Question 39

What blood test will you need to take to confirm an anaphylactic shock

Answer 39

Serum mast-cell tryptase can be measured in cases of anaphylaxis. Tryptase is the preferred marker for demonstrating mast-cell degranulation

Question 40

Risk factors for anaphylaxis

Answer 40

Middle to older age Previous anaphylaxis. Allergies or asthma. Certain other conditions- These include CVD and an irregular accumulation of a certain type of white blood cell (mastocytosis)