ILA Flashcards

1
Q

Atherosclerosis formation

A

Endothelial cell injury → caused by smoking, shearing forces at arterial divisions, hyperlipidemia (fatty deposits can injure endothelial lining)

Endothelial cell injury allows for the accumulation of lipid laden foam cells (macrophages that have phagocytosed LDLs) resulting in the formation of a fatty streak.

Platelets aggregate to the site of the injury, forming a thrombus.

Smooth muscle cells migrate to the surface of the plaque forming a fibrous cap. (Thick cap - stable atheroma. Thin cap - unstable atheroma).

In unstable atheroma - bits of plaque can break off causing an embolism in a distal blood vessel or it can rupture and cause a thrombus.

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2
Q

Risk factors of atherosclerosis

A

High cholesterol
High blood pressure
Smoking
Type 1 diabetes mellitus (high glucose can damage the endothelial wall)
Obesity
Physical inactivity
Age
Family history

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3
Q

Ace inhibitor

Drug names/examples
Mechanism of action
Main effect on BP

Side effect

A

Enalapril
Ramipril

Inhibits Angiotensin converting enzyme

Decreases systemic vascular resistance and decreases stroke volume

Side effect: Dry cough, hyperkalemia, headache, fatigue and dizziness (from BP going too low)

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4
Q

Angiotensin receptor blockers

Drug names/examples
Mechanism of action
Main effect on BP

Side effect

A

Losartan
Candesartan

Blocks angiotensin 2 receptors

Decreases systemic vascular resistance and decreases stroke volume

Side effect: headache, fatigue and dizziness

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5
Q

Beta blockers

Drug names/examples
Mechanism of action
Main effect on BP

A

Labetolol
Atenolol

Blocks beta receptors

Decreases heart rate and stroke volume

Side effect: headache, fatigue, dizziness, sexual dysfunction

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6
Q

Calcium channel blockers

Drug names/examples
Mechanism of action
Main effect on BP

A

Amlodipine
Verapamil

Blocks calcium channels (with less calcium, heart and arteries squeeze less strongly and relax more)

Decrease systemic vascular resistance

Side effects: constipation, bradycardia, peripheral oedema, headaches

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7
Q

Diuretics

Drug names/examples
Mechanism of action
Main effect on BP

A

Furosemide

Decrease stroke volume

Side effects: Hypokalemia, vomiting, diarrhoea, hyponatremia, headache, dizziness

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8
Q

Definition of anaphylaxis

A

A severe life threatening type 1 hypersensitivity reaction towards an allergen that threatens airway, breathing or circulation.

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9
Q

Symptoms and treatment of anaphylaxis

A

Sx: Urticaria (hives/rashes), itching, swelling around lips and eyes, tachycardia, cold extremities, central cyanosis, syncope, light headedness

Tx:
Immediate 500mcg IM Adrenaline (if no improvement, repeat IM adrenaline every 5 mins)
ABCDE
- Secure airway with intubation
- Provide oxygen if required
- IV bolus for fluid rehydration
- Assess patients level of consciousness and get them into a position where they are comfortable/able to breathe better
- Remove any triggers

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10
Q

Factors that can increase incidence of allergies/anaphylaxis

A
  • Bee/wasp sting
  • Exposure to latex
  • Family history
  • Exposure to allergens which individuals are sensitive to
  • Previous anaphylactic episodes (increase likelihood of future episodes)
  • Increase in air pollution
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11
Q

Confirmation blood test for anaphylaxis?

A

Tryptase blood test - a marker of mast cell degranulation

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12
Q

Definition of pharmacokinetics
and
Pharmacodynamics

A

The fate of a chemical substance administered to a living organism (ADME)

The effects the drug has on the body when binding to a specific target receptor.

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13
Q

Just take note
- With increased protein binding, there is reduced DISTRIBUTION of drug
- With increased lipid solubility, there is increased ABSORPTION of drug

A

NICE

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14
Q

What is first pass metabolism?

Give examples

A

The metabolism of drugs decreasing the active drug’s concentration upon reaching systemic circulation or its site of action

In older people
- Liver function and enzyme activity may be decreased, resulting in a reduced rate of drug METABOLISM
- Impaired renal function would lead to decreased EXCRETION of the drug (which can lead to accumulation and toxicity)

Not really related but——->
In obese people
- Caution drugs with a low volume of distribution as they may not distribute well into adipose tissue leading to higher concentrations in the plasma and increased risk of toxicity

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15
Q

Characteristics of an ideal intravenous anaesthetic induction agent

A
  • Rapid onset
  • Fast clearance
  • Water soluble - to increase the distribution
  • Minimal cardiovascular and respiratory depression
  • No withdrawal effects
  • Only have an anaesthetic effect and no other side effects
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16
Q

Briefly state the order of coagulation factors in the intrinsic and extrinsic pathway

A

Intrinsic (APTT) - 12-11-9-8-10-5-2-=1/13

Extrinsic (PT) - 3 - 7 - 10 ….

17
Q

Differences between an arterial and venous thrombosis

A

Arterial - Blood clot blocks an artery
Venous - Blood clot blocks a vein

Arterial - mainly caused by atherosclerosis
Venous - Mainly caused by virchow’s triad

Arterial - treated with antiplatelets (platelet rich clots)
Venous - treated with anticoagulants (fibrin rich clots)

Arterial - Can lead to Mi or stroke
Venous - Can lead to PE

Arterial - Usually pulseless and cold (due to lack of blood flow)
Venous - Can feel pulse and usually warm (due to congestion)

18
Q

Causes of venous thrombosis in depth

A

Mostly formed due to components of virchow’s triad
1) Stasis
- Periods of immobility (long flights)
- Pregnancy
- Post surgery

2) Endothelial injury
- Smoking
- Hypertension
- Diabetes
- Surgery

3) Hypercoagulability
(Hypercoagulability - excessively easy clotting of blood) –> alterations in the constitution of blood caused by smoking, sepsis (reaction to an infection), malignancy/cancer – can be due to genetics also - Gene mutations like in essential thrombocythemia (high number of platelets in blood)

19
Q

Preventative measures to reduce risk of DVT

A
  • Being active
  • Exercise legs during long trips
  • Quit smoking
  • Manage other health problems well e.g. diabetes, hypertension
20
Q

Causes of raised intracranial pressure

A
  • Haematomas
  • Neoplasms (gliomas, meningioma)
  • Abscess
  • Hydrocephalus
  • Thrombosis of the venous sinuses - infection, sickle cell anaemia
21
Q
A