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
Q

Give causes of pre renal AKI?

A

Reduced Renal Perfusion:
Reduced CO - HF
Renal artery stenosis
NSAIDs
Shock - Hypovolaemic
Dehydration

26
Q

Give Causes of Renal AKI?

A

Intrinsic Renal Damage:
Glomerulonephritis
Interstitial Nephritis
Nephrotoxic Drugs
Vasculitis
Tubular Acidosis (MC)

27
Q

Give Causes of Post-Renal AKI?

A

BPH
Nephrolithiasis
Malignancy

28
Q

What is the analgesic of choice in Renal Colic?

A

Diclofenac (NSAID)
But CI in AKI or CKD

29
Q

How do NSAIDs cause AKI?

A

Reduce renal perfusion and Reduce GFR (Pre-renal AKI)

Cause glomerulonephritis and interstitial nephritis (intra renal AKI)

30
Q

What is the most concerning thing in AKI?

A

Hyperkalaemia
Do an ECG to see changes

31
Q

What is seen on an ECG in hyperkalaemia?

A

Go, Go Tall, Go Long, Go Wide

Absent P wave
Tall tented T waves
Long PR interval
Wide QRS

32
Q

What is the treatment for Hyperkalaemia if there are cardiac (ECG) changes?

A

IV Calcium Gluconate STAT
To stabilise cardiac membrane

Then Insulin + Dextrose

33
Q

What is the treatment for Hyperkalaemia if there are No cardiac (ECG) changes?

A

Insulin + Dextrose

Insulin - Drives K+ into cells via Na/K/ATPase pump

Dextrose to prevent Hypoglycaemia

34
Q

What are signs of raised ICP?

A

N+V
Seizures
Loss of Consciousness

Cushing Triad (Bradycardia, Hypertension, Irregular Breathing)

35
Q

What is the Treatment for raised ICP?

A

IV Mannitol

Surgical - Burr Holes/Craniotomy

36
Q
A