ILA Flashcards
Describe the normal arterial vessel wall
Tunica intima (innermost layer):
Endothelial cells and basement membrane
Elastic laminae
Tunica media (middle layer):
Smooth muscle cells
Collagen and elastic membranes
Tunica adventitia (outermost layer):
Thin layer of connective tissue
Internal (between tunica intima and media) and external (between tunica media and adventitia) elastic laminae allows stretch and narrowing of vessels
What are the main coronary arteries?
Right Coronary Artery
Right Marginal
Posterior Intraventricular Artery
Left Coronary Artery
Left Anterior Descending
Left Marginal
Circumflex
Describe the formation of an atherosclerotic plaque
- Endothelial cells are damaged from hyperlipidaemia, shearing forces, free radicals or glycosylation products
- Low-density lipoproteins enter the endothelium and get oxidised
- Macrophages engulf lipoproteins, forming a foam cell
- Foam cells form a fatty streak
- There is continued damage, macrophage recruitment and lipid accumulation
- This forms a lipid core –> it is now an atheroma
- Fibrotic tissue forms on the lesion and calcifies –> it is now a fibroatheroma
(It becomes a complex lesion when there is a visible defect in the vessel)
What are the risk factors for atherosclerosis?
Cigarette smoking
Hypertension
Hyperlipidaemia
Poorly controlled Type 2 Diabetes Mellitus
Obesity
Sedentary lifestyle
Stress
Age (older)
Family history
Male sex or menopause
Afro-Caribbean or South Asian ethnicity
What preventative measure can reduce the risk of atherosclerosis complications?
1 & 2. Smoking cessation
Regular exercise
Eating a balanced diet with reduced saturated fats
2. Taking regular statins
3. Surgery - stenting, bypass
Define anaphylaxis
Anaphylaxis is a severe, life-threatening systemic hypersensitivity reaction (type 1). It is characterised by rapidly developing airway and/or breathing and/or circulatory problems and is usually associated with skin or mucosal changes
Describe the pathophysiology of anaphylaxis
IgE mediated hypersensitivity reaction (type 1)
- Exposure to allergen and priming/sensitisation –> memory b cells for that antigen are made
- Re-exposure to allergen –> plasma cells produce IgE which binds to mast cells and causes degranulation, releasing histamines, tryptase and cytokines
- Histamines increase blood vessel permeability causing symptoms
How does histamine cause symptoms in anaphylaxis?
Increases blood vessel permeability
1. Blood leaks into surrounding tissues causing reduced BP and increase HR
2. Blood and inflammatory fluids leak into dermis of skin causing urticaria (hives)
- Bronchoconstriction and increased mucus secretion and oedema in the airway reduced airflow in respiratory tract
- Airway constriction causes hypoxia which causes cyanosis
What are the rapid developing, life-threatening signs and symptoms of anaphylaxis?
Oedema in pharynx and larynx
Increased respiratory rate
Bronchospasm - wheezing, coughing or noisy breathing
Hypotension
Tachycardia
What other symptoms of anaphylaxis are there?
Itchy skin
Raised/red skin rash
Swelling of tongue or throat
Difficulty breathing
Feeling tired or confused
Feeling faint or dizzy
Skin that is cold to touch
What test is diagnostic for anaphylaxis?
Blood test for serum Mast Cell Tryptase
–> released during anaphylaxis and can be measured up to 4 hours after reaction
What is the treatment for anaphylaxis?
DR ABCDE
Diagnose anaphylaxis or suspected anaphylaxis
Call for help or call 999
Remove the trigger if possible
Lie or sit the patient down
Give intramuscular adrenaline
Give high flow oxygen
Give adrenaline again in 5 minutes if there has been no response
In a hospital, you can give IV adrenaline and also give fluids
How would you administer an autoinjector?
In the anterolateral thigh
Check expiry date and it is adrenaline
Blue to sky, orang to thigh
Remove cap
From close by, press it hard into leg
Hold it in for 10-30s
What does adrenaline do in anaphylaxis?
- stimulates alpha 1 receptors causing vasoconstriction –> increasing peripheral vascular resistance, BP, CO and reducing oedema
- stimulates beta 1 receptors –>increases contractility of heart, HR and renin release, increasing BP
- stimulates beta 2 receptors –> causes bronchodilation, reduces oedema
- stimulates alpha 2 receptors –> self-inhibition of catecholamine production
What risk factors increase risk of anaphylaxis/allergies?
Atopy
Hygiene hypothesis
Changes in diet as a population - more processed and less natural/whole food
Changing environment - increased air pollution, changes in pollen cycles, changes in distribution of stinging insects
Increased frequency of c-sections
What is pharmacokinetics?
the fate of a chemical substance administered to a living organism
What is pharmacodynamics?
the biochemical, physiological and molecular effects of a drug on the body
Which pharmacokinetic and pharmacodynamics properties increase drug action?
Lipid solubility/unionised
Small molecule size
Free/unbound molecules
IV and IA administration
An agonist that has high affinity for the receptor
No antagonists
High bioavailability
No or reduced first pass metabolism
Metabolism of pro-drugs to their active form
Slow excretion
Which pharmacokinetic and pharmacodynamics properties decrease drug action?
Water solubility/ionised
Large molecule size
Protein binding
Administration routes with less bioavailability
Low affinity of agonist for receptor
Antagonists
Low bioavailability
First pass metabolism
Pro-drugs (the need to be metabolised to be effective)
Excretion of the drug
What pharmacokinetic and pharmacodynamic principles would ideal anaesthetic induction agent have?
Low protein binding - increased plasma conc
Lipid solubility - can cross blood-brain barrier to reach site of action
Rapid clearing/metabolism
Few side effects
Few drug interactions
High maximum safe concentration to reduce toxicity risk
