ILA Flashcards

1
Q

What are the components of a normal artery wall?

A

Tunica Intima
Tunica Media
Tunica Adventitia

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2
Q

Where are the elastic arteries found?

A

Near the Heart

More elastin in media to withstand increased pressures and to elastic recoil

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3
Q

Where are the muscular arteries found?

A

Further from the heart

More muscle in media to vasodilate and vasoconstrict

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4
Q

Where is the site of greatest TPR?

A

Arterioles

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5
Q

Where is the site of greatest TPR?

A

Arterioles

Have < 3 smooth muscle layers in media

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6
Q

What are the basic stages of atherogenesis?

A
  1. Endothelial Injury (often at bifurcations)
  2. Fatty streak: (around 10 years old)
    - Foam cells form in intima
  3. Inflammatory Rxn: Foam cells recruit other inflammatory cells such as neutrophils, macrophages, lymphocytes and fibroblasts/platelets
  4. Fibroblasts produce smooth muscle fibrous cap which covers internal lumen side
  5. plaque rupture to form platelet plug and occlude artery
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7
Q

What is the Primary, Secondary and tertiary prevention of atherogenesis?

A

1’ RF modification

2’ Manage Sx: Statins, Aspirin, ACEi, BB,

3’ PCI stenting or CABG

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8
Q

What are the stages of Anaphylaxis?

A

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

  1. Systemic Effects:
    Bronchodilation - SMS muscle spasm
    Vasodilation - Histamine increase permeability
    CVR Sx - hypotension, tachycardia, shock
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9
Q

What is the Treatment for anaphylactic shock?

A

ABCDE assessment

IM Adrenaline (500mg) - If ineffective then give second IM 500mg Adrenaline Dose

Then
Chlorphenamine - Anti-histamine (H1)
Hydrocortisone - Steroid

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10
Q

Why is a Second dose of Adrenaline given if the first dose is ineffective?

A

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

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11
Q

What is the blood test to confirm anaphylaxis?

A

SERUM MAST CELL TRYPTASE:
Most specific reading for most cell degranulation

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12
Q

Define Prevalence?

A

Number of cases at a given point in time

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13
Q

Define Incidence?

A

Number of new cases in a given time frame

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14
Q

What properties of a drug will help induce anaesthesia quickly?

A

Low protein binding
Means more is free in circulation

Lipid soluble - can cross BBB easily

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15
Q

How is General anaesthesia administered?

A

IV anaesthesia given first to sedate patient

Volatile anaesthesia given to keep the patient Unconscious

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16
Q

Define Bioavailability?

A

Amount of drug reaching circulation unaltered

17
Q

What are the clinical signs of a arterial thrombus?

A

Reduced/absent pulse
Thin cool skin
Intermittent claudication

18
Q

What are the clinical signs of a Venous thrombus?

A

Increased pulse
Rubor and Tumour
Painful and erythematous

19
Q

What are the 6Ps of Acute Critical Limb Ischaemia?

A

Pain
Pallor
Pulselessness
Perishingly Cold
Paraesthesia
Paralysis

20
Q

What is the treatment of DVT?

A

1st Line:
DOACs (apixaban/Rivaroxaban) + LMWH

2nd Line:
Warfarin

21
Q

What do DOACs act on?

A

Directly act on Factor Xa and Factor II (thrombin) inhibiting the intrinsic pathway mainly

22
Q

What does LMWH act on?

A

Acts on Antithrombin to activate it which then reduces thrombin function

23
Q

What does Warfarin Act on?

A

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

24
Q

What cause of AKI is least common?

A

Post-renal causes

25
Give causes of pre renal AKI?
Reduced Renal Perfusion: Reduced CO - HF Renal artery stenosis NSAIDs Shock - Hypovolaemic Dehydration
26
Give Causes of Renal AKI?
Intrinsic Renal Damage: Glomerulonephritis Interstitial Nephritis Nephrotoxic Drugs Vasculitis Tubular Acidosis (MC)
27
Give Causes of Post-Renal AKI?
BPH Nephrolithiasis Malignancy
28
What is the analgesic of choice in Renal Colic?
Diclofenac (NSAID) But CI in AKI or CKD
29
How do NSAIDs cause AKI?
Reduce renal perfusion and Reduce GFR (Pre-renal AKI) Cause glomerulonephritis and interstitial nephritis (intra renal AKI)
30
What is the most concerning thing in AKI?
Hyperkalaemia Do an ECG to see changes
31
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
32
What is the treatment for Hyperkalaemia if there are cardiac (ECG) changes?
IV Calcium Gluconate STAT To stabilise cardiac membrane Then Insulin + Dextrose
33
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
34
What are signs of raised ICP?
N+V Seizures Loss of Consciousness Cushing Triad (Bradycardia, Hypertension, Irregular Breathing)
35
What is the Treatment for raised ICP?
IV Mannitol Surgical - Burr Holes/Craniotomy
36