ILA Flashcards
What are the components of a normal artery wall?
Tunica Intima
Tunica Media
Tunica Adventitia
Where are the elastic arteries found?
Near the Heart
More elastin in media to withstand increased pressures and to elastic recoil
Where are the muscular arteries found?
Further from the heart
More muscle in media to vasodilate and vasoconstrict
Where is the site of greatest TPR?
Arterioles
Where is the site of greatest TPR?
Arterioles
Have < 3 smooth muscle layers in media
What are the basic stages of atherogenesis?
- Endothelial Injury (often at bifurcations)
- Fatty streak: (around 10 years old)
- Foam cells form in intima - Inflammatory Rxn: Foam cells recruit other inflammatory cells such as neutrophils, macrophages, lymphocytes and fibroblasts/platelets
- Fibroblasts produce smooth muscle fibrous cap which covers internal lumen side
- plaque rupture to form platelet plug and occlude artery
What is the Primary, Secondary and tertiary prevention of atherogenesis?
1’ RF modification
2’ Manage Sx: Statins, Aspirin, ACEi, BB,
3’ PCI stenting or CABG
What are the stages of Anaphylaxis?
1: Sensitisation as IgE forms vs antigen and binds to Fc on mast cells
2: Secondary Exposure: Fab of IgE binds to allergen and results in Mast cell degranulation releasing Histamines, Leukotrienes and Tryptases
- Systemic Effects:
Bronchodilation - SMS muscle spasm
Vasodilation - Histamine increase permeability
CVR Sx - hypotension, tachycardia, shock
What is the Treatment for anaphylactic shock?
ABCDE assessment
IM Adrenaline (500mg) - If ineffective then give second IM 500mg Adrenaline Dose
Then
Chlorphenamine - Anti-histamine (H1)
Hydrocortisone - Steroid
Why is a Second dose of Adrenaline given if the first dose is ineffective?
Adrenaline has a very short 1/2 life and therefore if it has not worked first time round this may be due to the concentration of adrenaline dropping too quickly to have a good effect
What is the blood test to confirm anaphylaxis?
SERUM MAST CELL TRYPTASE:
Most specific reading for most cell degranulation
Define Prevalence?
Number of cases at a given point in time
Define Incidence?
Number of new cases in a given time frame
What properties of a drug will help induce anaesthesia quickly?
Low protein binding
Means more is free in circulation
Lipid soluble - can cross BBB easily
How is General anaesthesia administered?
IV anaesthesia given first to sedate patient
Volatile anaesthesia given to keep the patient Unconscious
Define Bioavailability?
Amount of drug reaching circulation unaltered
What are the clinical signs of a arterial thrombus?
Reduced/absent pulse
Thin cool skin
Intermittent claudication
What are the clinical signs of a Venous thrombus?
Increased pulse
Rubor and Tumour
Painful and erythematous
What are the 6Ps of Acute Critical Limb Ischaemia?
Pain
Pallor
Pulselessness
Perishingly Cold
Paraesthesia
Paralysis
What is the treatment of DVT?
1st Line:
DOACs (apixaban/Rivaroxaban) + LMWH
2nd Line:
Warfarin
What do DOACs act on?
Directly act on Factor Xa and Factor II (thrombin) inhibiting the intrinsic pathway mainly
What does LMWH act on?
Acts on Antithrombin to activate it which then reduces thrombin function
What does Warfarin Act on?
Affects extrinsic Clotting pathway as it reduces the synthesis of Vitamin K dependent clotting factors (2, 7, 9, 10)
Warfarin is a Vitamin K antagonist
What cause of AKI is least common?
Post-renal causes
Give causes of pre renal AKI?
Reduced Renal Perfusion:
Reduced CO - HF
Renal artery stenosis
NSAIDs
Shock - Hypovolaemic
Dehydration
Give Causes of Renal AKI?
Intrinsic Renal Damage:
Glomerulonephritis
Interstitial Nephritis
Nephrotoxic Drugs
Vasculitis
Tubular Acidosis (MC)
Give Causes of Post-Renal AKI?
BPH
Nephrolithiasis
Malignancy
What is the analgesic of choice in Renal Colic?
Diclofenac (NSAID)
But CI in AKI or CKD
How do NSAIDs cause AKI?
Reduce renal perfusion and Reduce GFR (Pre-renal AKI)
Cause glomerulonephritis and interstitial nephritis (intra renal AKI)
What is the most concerning thing in AKI?
Hyperkalaemia
Do an ECG to see changes
What is seen on an ECG in hyperkalaemia?
Go, Go Tall, Go Long, Go Wide
Absent P wave
Tall tented T waves
Long PR interval
Wide QRS
What is the treatment for Hyperkalaemia if there are cardiac (ECG) changes?
IV Calcium Gluconate STAT
To stabilise cardiac membrane
Then Insulin + Dextrose
What is the treatment for Hyperkalaemia if there are No cardiac (ECG) changes?
Insulin + Dextrose
Insulin - Drives K+ into cells via Na/K/ATPase pump
Dextrose to prevent Hypoglycaemia
What are signs of raised ICP?
N+V
Seizures
Loss of Consciousness
Cushing Triad (Bradycardia, Hypertension, Irregular Breathing)
What is the Treatment for raised ICP?
IV Mannitol
Surgical - Burr Holes/Craniotomy
