ILA Flashcards
RF Atherosclerosis
HYPERCHOLESTERAEMIA !!!!
Smoking
HTN
DM
Male
↑ Age
Prevention Atherosclerosis
Stop smoking
Control BP
↓Weight
Statins - ↓cholesterol
Low dose aspirin - inhibits platelet aggregation (for Pxs with clinical evidence of atherosclerosis)
Name the layers in normal arterial structure
Outside to Inside
- Adventitia/Serosa
- Tunica externa
- External elastic membrane
- Tunica media
- Internal elastic membrane
- Tunica intima
- Endothelium
LUMEN
Progression of atherosclerosis from birth
- FATTY STREAKS - no clinical signif
In all ages, starts in childhood esp if ↑fatty diet
Fatty streaks - comprised of lipid-laden macrophages - Turns into plaques
Happens by injury to endothelium, then tissue responds and repairs
This process happens repeatedly over years, then forms plaques
Quick! How is an atherosclerotic plaque formed?
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
What are the 3 big functional changes that occur when endothelial cells are injured?
In relation to atherosclerotic plaque
- ↑ expression of cell adhesion molecules for monocytes
- permeability for macromolecules e.g. LDL
- ↑ thrombogenicity
How does endothelial cell injury start plaque formation?
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
What are foam cells?
Lipid-laden macrophages
How do foam cells propagate the formation of atherosclerotic plaques?
Foam cells phagocytose LDL and apoptose
But this just releases the contents into the lipid core
Describe the stages of atherosclerotic plaque formation
Endothelial cell injury
Inflammatory response
Tissue repair - fibrous cap formation
Haemorrhage
How is the fibrous cap formed in atherosclerotic plaque formation?
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
What causes a haemorrhage of an atherosclerotic plaque?
Rupture/leakage of micro vessels within plaque (MC if full developed plaques)
Consequences of large haemorrhage of atherosclerotic plaque
Rapid expansion of plaque
May produce clinical symptoms
Define anaphylaxis
Severe, life-threatening, systemic type 1 hypersensitivity reaction
Pathophysiology anaphylaxis
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
Mechanisms of some signs/symptoms of Anaphylaxis
↑ Vascular permeability = ↓BP, ↑HR
Mucosal oedema = wheezing, bronchoconstriction
Vasodilation of blood vessels = rash, hives, more tissue fluid (bc ↑permeability)
What causes vasodilation of blood vessels?
beta-2 adrenoceptors
Triggers for anaphylaxis
Food - peanuts, cow’s milk, tree nuts
Medications - ABx (esp penicillin)
Insect sting
Latex
Exercise (v rare)
Idiopathic
RF Anaphylaxis
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
Factors that might cause an anaphylactic shock to be more severe
Advancing age
Asthma & other chronic lung disease
CVD
Mast cell disease
Prev biphasic anaphylaxis
If on BBs or ACEi
Signs / Symptoms Anaphylaxis
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
How might the onset and presentation of anaphylaxis vary between causes?
e.g.
Food as cause = less rapid onset, breathing problems predominate
vs
Medication as cause = rapid onset, circulation problems predominate
Ix Anaphylaxis
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
Tx Anaphylaxis
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
What is adrenaline?
Non-selective alpha and beta adrenergic receptor agonist
What do alpha receptor agonists do?
Mediates peripheral vasoconstriction
Reduces tissue oedema
What do beta receptor agonists do?
Mediates bronchodilation
Positive inotropic effects
Suppresses inflam mediator release
Describe ABCDE
Airway
Breathing
Circulation
Disability
Exposure
Someone is lying on the floor, you suspect anaphylaxis but not sure.
What do you do?
Step by step please
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)
Explain why a second dose of adrenaline might be required
Adrenaline has a short half life
∴ a second dose may be required if the symptoms do not initially respond or get worse
Why do we give adrenaline IM and not IV?
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 ?
