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Phase 2a > ILA > Flashcards

ILA Flashcards

1
Q

Describe the main stages involved in the formation of an atherosclerotic plaque?

A
  1. Fatty streaks form from young ages
  2. Endothelial damage
  3. Release of inflammatory chemokines that attracts inflammation cells and increased expressoin of adhesion cells
  4. Inflammation
  5. Macrophages start coming into the intima and become FOAM CELLS
  6. Plaque progression: intermediate lesions (smooth muscle cells, platelets, foam cells, T lymphocytes, pools of extracellular lipid)
  7. Fibrous cap forms: smooth muscle cells produce collagen and elastin making it fibrous and forming the cap, necrotic core forms, impeding blood flow (ischaemia)
  8. Plaque rupture, exposing collagen, necrotic tissue and basement membrane, small vessels haemorrage = blood coagulation = clotting = occlusion = infarction = myocardial or cerebral
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2
Q

Describe the structure of an atherosclerotic plaque?

A
  • Tends to be found at bifurcation points
  • Lipid necrotic core, connective tissue, fibrous cap
  • Dangers are angina, myocardial or cerebral infection via blockage
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3
Q

What are some modifiable risk factors of atherosclerosis?

A

Smoking > free radicals in cigarette smoke

Sedentary lifestyle > increase risk of diabetes and hyperlipidaemia (endothelial damage) and hypertension

Hypertension > shearing forces damage endothelium and also increased permeablilty to LDLs

High chloesterol > more LDL deposits = more modified macrophages (foam cells)

Diabetes > more bloody sugar = more LDLs attracting more inflammatory properties also causes more lipids

BMI

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4
Q

What are some non modifiable risk factors of atherosclerosis?

A

Family history > genetic component of hyperlipidaemia, hypertension and diabetes

Gender
Age
Ethnicity

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5
Q

How does smoking increase the risk of atherosclerosis?

A

Free radicals in cigarette smoke damage endothelium

CO and nicotine - ROS - oxidises LDL

Increases LDL levels

Makes blood thicker (thrombogenicity) so more tendency to clot

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6
Q

What primary prevention measures can be taken for atherosclerosis?

A

-Take low-dose aspirin to reduce platelet aggregation
-Exercise regularly
-Stop smoking
-Take blood pressure medication (ACE inhibitors, angiotensin II receptor
blockers, beta-blockers, etc.)
-Healthy diet, less salt
-lose weight

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7
Q

What secondary prevention measures can be taken for atherosclerosis?

A
  • prescribe aspirin and anti-hypertensive medication
  • prescribe exercise
  • diet program/ referral?
  • regular check-ups
  • procedure to widen/bypass affected arteries
  • take statins to reduce cholesterol level
  • if diabetes then metformin
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8
Q

Define anaphylaxis?

A

Anaphylaxis is a severe, life-threatening, generalised or systemic hypersensitivity reaction.

Characterised by rapidly developing life-threatening airway and/or breathing and/or circulation problems usually associated with skin and mucosal changes.

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9
Q

Describe the beta adrenergic receptor activity of adrenaline?

A
  • Stimulation of Beta1-adrenoceptors positive ionotropic and chronotropic effects on the heart
  • Reduces oedema and bronchodilates via beta2-adrenoceptors

• Attenuates further release of mediators from mast cells and basophils by increasing
intracellular c-AMP and so reducing the release of inflammatory mediators

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10
Q

Describe the alpha adrenergic activity of adrenaline?

A
  • Peripheral vasoconstriction increase in peripheral vascular resistance, increased BP and coronary perfusion via alpha1-adrenoceptors
  • Reduction of oedema
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11
Q

Why might a second does of adrenaline be required if symptoms do not initially respond or get worse?

A

Because adrenaline has a short half life and therefore a second dose may be required if the symptoms do not initially respond or get worse

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12
Q

What is the recommended treatment for anaphylaxis? (full)

A

REMOVE THE PRECIPITATING CAUSE e.g. IV antibiotics

Lie flat and raise legs

  1. 500 micrograms of adrnaline intramuscularly unless experiences with IV adrenaline > repeat after 5 mins if no better
  2. High flow oxygen > increases the alveolar oxygen concentration to over come hypoxia due to bronchospasm, reduced ventilatory effort and interstitial oedema
  3. Fluids > help restore circulating volume therefore stroke volume increasing cardiac output
  4. Chlorphenamine > antihistamine blocking histamine-1 receptor thus blocking the action of histamine released during anaphylaxis
  5. Hydrocortisone > surpresses prostaglandin and leukotrine mediators, inflammatory cell recruitment and migration are inhibited and vasoconstriction reduces leakage from blood vessels
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13
Q

What confirmatory blood test will you need to take after an anaphylactic reaction? How will this confirm or refute a diagnosis of anaphyalxis?

A

Blood test is Mast Cell Tryptase.

Anaphylaxis causes an elevated serum mast cell tryptase.

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14
Q

What would the large histamine release in anaphylaxis cause?

A

Histamine causes vasodilation and increased vascular permeability

This causes anigo-oedema and erythema (redness) to local tissues and therefore swelling

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15
Q

Why might someone have a raised heart rate, low bp, and slow capillary refill time?

A

Vasodilation and increased vascular permeability (therefore oedema) means that there is less fluid in the vessels therefore lower bp (hypotension) and the heart pumps faster to compensate

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16
Q

Why might someone what a raised respiratory rate, low oxygen saturation and expiratory wheeze?

A

Contraction of respiratory smooth muscle surrounding trachea therefore airway constriction would cause all three

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17
Q

What cells are involved with anaphylaxis?

A

Mast cells

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18
Q

What antibody is involved in anaphylaxis?

A

IgE

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19
Q

What is the mediator of decreased blood pressure?

A

Histamine

20
Q

What would be immediate treatment for anaphylaxis be?

A

ABCDE, adrenaline, oxygen

21
Q

What is the treatment drug for anaphylaxis and describe its mechanism?

A

= Adrenaline, non-selective agonist of

adrenergic receptors, increases vasoconstriction and bronchodilation

22
Q

What treatments other than adrenaline are given?

A

Hydrocortisol, oxygen, fluids, antihistamine

23
Q

What are normal values for?
O2
BP
HR

A

O2 = 95% <
Heart rate = 60-100
BP = 120/80

24
Q

What does ABCDE stand for in relation to anaphylaxis?

A 
Airway 
Breathing 
Circulation 
Disability 
Exposure
25
Q

What would you look for when diagnosing anaphylaxis?

A
  1. Acute onset of illness
  2. Life-threatening airway and/or breathing and/or circulation problems
  3. Usually skin changes
26
Q

In order to induce anaesthesia quickly what characteristics should a drug have in terms of its protein binding?

A

Protein binding lowers the free concentration of a drug, ideally the induction drug should have LOW protein binding to enable a high initial plasma concentration

If strongly protein bound then plasma concentration of the free drug will be lower

27
Q

In order to induce anaesthesia quickly what characteristics should a drug have in terms of its lipid solubility?

A

In order to put the patient to sleep quicky the drug should have a high lipid soluablilty in order for it to readily cross the blood brain barrier and reach its site of action

28
Q

Explain in terms of the drug distribution of the intravenous drug why an additional volatile
drug needs to be given as soon as the patient is asleep?

A

With IV drug injection there is a high initial plasma concentration and the drug may rapidly
enter well perfused tissue such as brain, liver & lungs…

  • The drug will continue to enter less well perfused tissues lowering the plasma concentration…
  • The concentrations in the highly perfused tissues then decrease.
  • This action is important in terminating some drugs given as a bolus e.g thiopentone produces rapid anaesthesia because of initial high brain concentrations, but is short lived as continued muscle uptake lowers the blood concentration & indirectly the brain concentration
29
Q

What would happen if a second anaesthetic agent was not given?

A

As the plasma concentratoin of thiopentone decreases the patient will start to wake up

30
Q

In addition to ‘receptors’ what three other drug targets are there?

A

Enzymes
Transporters
Ion channels

31
Q

Give an example of a drug that acts on receptors and how it produces its desired effect?

A

Receptors - muscle relaxants are completive antagonists of acetylcholine at the post
synaptic nicotinic receptor. They block the receptor preventing ACh from binding and
causing muscle contraction.

32
Q

Give an example of a drug that acts on enzymes and how it produces its desired effect?

A

Enzymes – Angiotension-converting enzyme (ACE) inhibitors block the conversion of
angiotensin I to angiotensin II (a vasoconstrictor) this causes vasodilation which reduces blood pressure.

33
Q

Give an example of a drug that acts on transporters and how it produces its desired effect?

A

Transporters / carrier proteins – Proton pump inhibitors (lansoprazole) prevent the
production of stomach acid (H+) by inhibiting the proton pump mechanism in the
parietal cells.

34
Q

Give an example of a drug that acts on transporters and how it produces its desired effect?

A

Ion channels Calcium channel blockers (nifedipine, verapamil) target the calcium ion
channels which leads to arterial vasodilation e.g. coronary arteries and improve
coronary artery blood flow helping to relieve angina.

35
Q

Define: bioavailability?

A

Bioavailability – the amount of drug that reaches the circulation unaltered. Intravenous drugs therefore have high bioavailability (100%) as do intramuscular drugs which are absorbed into the blood stream unaltered.

Oral drugs have a bioavailability of less than 100%.

36
Q

Explain this difference in terms of Morphine’s bioavailability and first pass metabolism, and how much more morphine is needed orally?

A

Morphine when given orally undergoes first pass metabolism where a proportion of the drug is which results in a bioavailability of about 50%.

It is metabolised / extracted by the intestine and metabolised by the liver before entering the systemic circulation.

This means that the oral dose of morphine is twice the intramuscular morphine e.g. IM dose is 5mg and oral dose is 10mg

37
Q

If a patient has renal failure, a lower than normal dose of morphine is given at longer intervals, why?

A

Morphine is metabolised in the liver to morphine 6 glucuronide which is more potent than morphine.

It is excreted by the kidneys therefore if a patient has renal failure it will not be as readily excreted.

This requires the dose and frequency of administration to be reduced.

38
Q

What are the physical properties of the ideal anaesthetic drug?

A
  • Stable in solution
  • Long shelf life
  • No pain on intravenous injection
  • Cheap
39
Q

What are the pharmacokinetic properties of the ideal anaesthetic drug?

A

Rapid onset – low protein binding and crosses blood brain barrier easily
• Rapid clearance and metabolism
• No active metabolites

40
Q

What are the pharmacodynamic properties of the ideal anaesthetic drug?

A
  • Minimal cardiovascular and respiratory effects
  • No histamine release/hypersensitivity/ allergy reactions
  • Does not make patients feel sick
  • No hang over effect so patients have a quick recovery.
41
Q

Explain the difference in presentation (signs and symptoms) between an arterial thrombosis and a venous thrombosis?

A

An AVT would present with a lack of pulse, pale skin, coldness to touch which is completely the opposite to DVT which would present as a hot red limb that would still have a pulse

42
Q

Describe virchows triad?

A
  1. Hypercoaguability of blood
  2. Vessel wall injury
  3. Stasis of blood
43
Q

Describe the pathophysiology of thrombus development?

A
  1. Protein adsorption onto vessel e.g. fibrinogen, vWF
  2. Platelet adhesion/activation
  3. Cell deposition and fibrin formation
  4. Thrombus formation
44
Q

What blood test would you do to help confirm a diagnosis of DVT and why?

A

D Dimer

D dimer measure the amount of a protein called fibrin d dimer which is produced whenever fibrin is being actively degraded somewhere within the vascular system - therefore levels generally increase after DVT or PE

Positive does NOT confirm diagnosis

45
Q

Heparin and warfarin are used in the treatment of DVT. In relation to the cogulation cascade, explain the action of each?

A

Heparin: binds to antithrombin, increases its activity, indirect thrombin inhibitor, acts on the extrinsic pathway

Warfarin: antagonist of vitamin K, preventing synthesis of active factors II, VII, IX, X, acts on the intrinsic pathway

46
Q

What potentially fatal complication of a DVT should a patient be made aware of and what signs and symptoms should he look out for?

A

Symptoms: breathlessness, pleuritic chest pain, may have S+S of DVT

Signs: Tachycardia, tachypnoea, pleural rub, those of precipitating cause

47
Q

Advice for long haul flights to reduce risk of DVT?

A

move around as often as possible by walking in the aisles when allowed
• avoid crossing your legs
• avoid wearing tight clothes that can restrict blood flow
• stay hydrated, and avoid alcohol before and during travel
• stretch legs and feet while sitting
• If you are young, non-smoker, not overweight

Phase 2a (13 decks)

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