ILA

Question 1

RF Atherosclerosis

Answer 1

HYPERCHOLESTERAEMIA !!!!

Smoking
HTN
DM
Male
↑ Age

Question 2

Prevention Atherosclerosis

Answer 2

Stop smoking
Control BP
↓Weight
Statins - ↓cholesterol
Low dose aspirin - inhibits platelet aggregation (for Pxs with clinical evidence of atherosclerosis)

Question 3

Name the layers in normal arterial structure

Answer 3

Outside to Inside

1. Adventitia/Serosa
2. Tunica externa
3. External elastic membrane
4. Tunica media
5. Internal elastic membrane
6. Tunica intima
7. Endothelium
   LUMEN

Question 4

Progression of atherosclerosis from birth

Answer 4

1. FATTY STREAKS - no clinical signif
   In all ages, starts in childhood esp if ↑fatty diet
   Fatty streaks - comprised of lipid-laden macrophages
2. Turns into plaques
   Happens by injury to endothelium, then tissue responds and repairs
   This process happens repeatedly over years, then forms plaques

Question 5

Quick! How is an atherosclerotic plaque formed?

Answer 5

endothelium injury
∴ inflam response (lots of macro and T-cells enter + lipids enter bc endo is damaged)

Macrophages phagocytose LDLs (form foam cells) and apoptose !
v silly bc releases lipids into core

THEN tissue repair!
Lots of smooth muscle cells ! but also v silly bc just encases core with a fibrous cap !

then lipid core grows, cap remains which increases pressure
then BAM explores and haemorrhage

Question 6

What are the 3 big functional changes that occur when endothelial cells are injured?
In relation to atherosclerotic plaque

Answer 6

1. ↑ expression of cell adhesion molecules for monocytes
2. permeability for macromolecules e.g. LDL
3. ↑ thrombogenicity

Question 7

How does endothelial cell injury start plaque formation?

Answer 7

Bc allows inflammatory cells + lipids to enter intimal layer of arterial wall

If allowed to advance, macrophages and T-cells will also be allowed to accumulate in plaque tissue

Question 8

What are foam cells?

Answer 8

Lipid-laden macrophages

Question 9

How do foam cells propagate the formation of atherosclerotic plaques?

Answer 9

Foam cells phagocytose LDL and apoptose
But this just releases the contents into the lipid core

Question 10

Describe the stages of atherosclerotic plaque formation

Answer 10

Endothelial cell injury
Inflammatory response
Tissue repair - fibrous cap formation
Haemorrhage

Question 11

How is the fibrous cap formed in atherosclerotic plaque formation?

Answer 11

Growth factors cause intimal smooth muscle cells to proliferate !!

∴ ↑ synthesis of collagen and elastin
(by SMCs)

∴ Fibrous cap formed
which encases the lipid core
–
& then More Growth factor secreted by platelets, injured endothelial cells, macrophages, SMCs etc

Question 12

What causes a haemorrhage of an atherosclerotic plaque?

Answer 12

Rupture/leakage of micro vessels within plaque (MC if full developed plaques)

Question 13

Consequences of large haemorrhage of atherosclerotic plaque

Answer 13

Rapid expansion of plaque
May produce clinical symptoms

Question 14

Define anaphylaxis

Answer 14

Severe, life-threatening, systemic type 1 hypersensitivity reaction

Question 15

Pathophysiology anaphylaxis

Answer 15

Allergen reacts w specific IgE antibodies on mast cells and basophils
Triggers rapid release of HISTAMINE & rapid synthesis of newly formed mediators

CAUSES capillary leakage, mucosal oedema and shock/asphyxia

Will get a reaction on the 2nd exposure

Question 16

Mechanisms of some signs/symptoms of Anaphylaxis

Answer 16

↑ Vascular permeability = ↓BP, ↑HR

Mucosal oedema = wheezing, bronchoconstriction

Vasodilation of blood vessels = rash, hives, more tissue fluid (bc ↑permeability)

Question 17

What causes vasodilation of blood vessels?

Answer 17

beta-2 adrenoceptors

Question 18

Triggers for anaphylaxis

Answer 18

Food - peanuts, cow’s milk, tree nuts
Medications - ABx (esp penicillin)

Insect sting
Latex
Exercise (v rare)
Idiopathic

Question 19

RF Anaphylaxis

Answer 19

Previous eps of anaphylaxis
Known allergies
Concurrent allergic conditions (asthma, allergic rhinitis, eczema)
Regular exposure to allergens

Females
EBV, HIV
Uncontrolled asthma
Some HLA groups
Acetylator status

Question 20

Factors that might cause an anaphylactic shock to be more severe

Answer 20

Advancing age
Asthma & other chronic lung disease
CVD
Mast cell disease
Prev biphasic anaphylaxis
If on BBs or ACEi

Question 21

Signs / Symptoms Anaphylaxis

Answer 21

3 Main Factors!
1. Sudden onset, rapidly progressive
2. Life-threatening airway +/- breathing +/- circulation problems
3. Skin +/- mucosal changes

–
Airway problems - dyspnoea, dysphagia, hoarse voice, stridor, swollen tongue/lips, saliva drooling

Breathing problems - dyspnoea, tachypnoea, wheeze, cyanosis

Circulation problems - Tachycardia (rapid, weak thready periph pulse), hypotension, cold clammy skin, prolonged capillary refill time

Skin +/- Muscosal changes - Widespread erythematous rash, generalised pruritus, angioedema, flushing

Question 22

How might the onset and presentation of anaphylaxis vary between causes?

Answer 22

e.g.
Food as cause = less rapid onset, breathing problems predominate
vs
Medication as cause = rapid onset, circulation problems predominate

Question 23

Ix Anaphylaxis

Answer 23

ABCDE

SERUM MAST CELL TRYPTASE LEVEL !!! - diagnostic, confirms anaphylaxis
Should be done within 2 hours BUT NEVER DELAY TREATMENT
(neg result doesn’t rule it out tho)

• If diagnosis still uncertain -
  ECG - to exclude cardiac causes
  Heart rate, BP, pulse oximetry
  Bloods - FBC, U&E, LFTs
  ABG - if hypoxic

Question 24

Tx Anaphylaxis

Answer 24

Basic life support - ABC

Stop drugs if infusion!!!

IM Adrenaline 500micrograms
If no response after 5 mins, repeat
(300micrograms if epi-pen)

High flow O2
IV fluids
Might need IV adrenaline if anaphylactic shock - but IM is always preferred

Corticosteroids are not recommended anymore

Question 25

What is adrenaline?

Answer 25

Non-selective alpha and beta adrenergic receptor agonist

Question 26

What do alpha receptor agonists do?

Answer 26

Mediates peripheral vasoconstriction
Reduces tissue oedema

Question 27

What do beta receptor agonists do?

Answer 27

Mediates bronchodilation
Positive inotropic effects
Suppresses inflam mediator release

Question 28

Describe ABCDE

Answer 28

Airway
Breathing
Circulation
Disability
Exposure

Question 29

Someone is lying on the floor, you suspect anaphylaxis but not sure.
What do you do?
Step by step please

Answer 29

ABCDE

Diagnosis - look for sudden onset of airway/breathing/circulation problems and skin changes

CALL FOR HELP

Remove triggers? (i.e. stop infusion)
Lie patient flat (legs can be elevated) or even sitting might help. If pregnant, lie on left side

GIVE IM ADRENALINE 500MCG
Anterolateral aspect, middle third of thigh

High flow O2
Monitor - ECG, BP etc

If no response - Repeat IM adrenaline, IV fluid bolus (crystalloid)

Question 30

Explain why a second dose of adrenaline might be required

Answer 30

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

Question 31

Why do we give adrenaline IM and not IV?

Answer 31

Well i read that it’s bc it’s easy to mix up doses etc and the risk isn’t worth it

but also bc will close the vessel it enters and not act as an opening ?