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Phase 2A ICS, Microbiology, Public Health, GP and ILAs > ILAs > Flashcards

ILAs Flashcards

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Biology 101 flashcards
1
Q

What is atherogenesis?

A

The formation of fatty deposits in the arteries

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2
Q

What are the four steps of atherogenesis?

A
  1. Endothelial cell injury
  2. Lipoprotein deposition
  3. Inflammatiory reaction
  4. Smooth muscle cell cap formation
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3
Q

List some factors that can result in endothelial cell injury

A

Tobacco, uncontrolled diabetes, hyperlipidaemia, hypertension

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4
Q

How does lipoprotein deposition cause a fatty streak?

A

The endothelium is injured or disrupted, causing lipoprotein molecules to gain entry, where they are then modified by oxidation of glycation. The LDL is inflammatory and able to be ingested by macrophages, creating foam cells and causing a fatty streak in the arterial wall

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5
Q

How does the fibrous cap of a plaque form?

A

Smooth muscle cells migrate to the surface of the plaque, forming the fibrous cap.

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6
Q

Are thin or thick capped plaques more likely to cause thrombosis?

A

Thin capped plaques are thought to be more prone to rupture or erosion, causing thrombosis

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7
Q

List some modifiable risk factors for atherosclerosis

A

High LDL cholesterol, and low HDL cholesterol, High blood pressure, obestiy, smoking, diabetes

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8
Q

List some non-modifiable risk factors for atherosclerosis

A

Family history, high blood pressure, being a post-menopausal woman, being over 45 for a man, diabetes

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9
Q

How does high LDL cholesterol promote plaque formation?

A

LDLs enter the artery walls and then can be phagocytosed by macrophages to form foam cells that promote inflammation.

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10
Q

How does low HDL cholesterol promote plaque formation?

A

HDLs remove cholesterol from foam cells, inhibit oxidation of LDLs, and limit the inflammatory response underlying atherosclerosis.

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11
Q

How does hypertension promote plaque formation?

A

In hypertension, there is increased dilation and contraction of arteries, damaging the endothelium. This endothelium is then scarred and thus thicker causing a narrower lumen and increased liklihood of atherosclerosis.

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12
Q

How does obesity promote plaque formation?

A

There is generally an increase in blood pressure as a result of higher demands in obesity

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13
Q

How does smoking promote plaque formation?

A

Toxins in tobacco smoke lower HDLs and raise LDLs. The nicotine and carbon monoxide also damage the endothelium. Nicotine is also a vasoconstrictor

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14
Q

How does uncontrolled diabetes promote plaque formation?

A

Diabetes drives inflammation and slows blood flow, dramatically accelerating atherosclerosis. Diabetes is also liked to obesity

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15
Q

How does increasing age promote plaque formation?

A

Arteries stiffen with age

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16
Q

How does being post-menopausal promote plaque formation?

A

A decline in oestrogen may be a risk factor in heart disease. Oestrogen is believed to have a positive effect on the inner layer of the artery wall, keeping vessels flexible

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17
Q

List some preventative measures that could be done to reduce risk of atherosclerosis

A

Reduce BMI, Reduce cholesterol intake, Lower blood pressure through medications, statins, Smoking cessation

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18
Q

What medications can be used to reduce the risk of atherosclerosis

A

Aspirin, statins, beta blockers

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19
Q

What is a co-benefit?

A

Additional benefits that arise from cutting greenhouse gas emissions, specifically health related events

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20
Q

What is anaphylaxis?

A

Anaphylaxis is a type 1 hypersensitibity reaction that causes a severe and potentially life-threatening reaction to a trigger such as an allergy

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21
Q

What are common triggers for anaphylaxis

A

Medication
Food
Insect stings
General anaesthetic
Contrast Agents
Latex

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22
Q

What are some symptoms of anaphylaxis?

A

Feeling lightheaded or faint
Breathing difficulties and wheezing
Low blood pressure due to vasodilation
A fast heartbeat= to combat low bp
High temp= massive vasodilation
Skin changes= Inflammatory process
Low oxygen saturation= Bronchoconstriction
Nausea and vomitting

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23
Q

What is the main chemical released in anaphylaxis?

A

Histamine

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24
Q

How is anaphylaxis treated?

A

Airways, circulation, breathing
Stop trigger
IM adrenaline
IV fluids
Chlorphenamine
Hydrocortisone
Oxygen

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25
Q

What does adrenaline do in anaphylaxis?

A

It targets blood vessels (alpha-1), the heart (beta 1) and bronchus (beta 2), causing vasoconstriction, positive inotropic effects and bronchodilation

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26
Q

Why are IV fluids administered in anaphylaxis?

A

To raise fluid levels to raise blood pressures

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27
Q

Why is chlorphenamine administered in anaphylaxis?

A

It is a histamine receptor blocker, meaning the effects of histamine will be less severe. H1 receptor antagonist

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28
Q

Why is hydrocortisone administered in anaphylaxis?

A

It is an agonist of the glucocorticoid and mineralocorticoid receptors meaning that there will be less inflammation= suppresses prostaglandins and causes vasoconstriction.

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29
Q

Why may adrenaline have to be administered twice after anaphylaxis?

A

It has a short half life

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30
Q

What test can be done to confirm anaphylaxis?

A

Mast cell tryptase
(Tryptase protein is released by basophils)
Also do FBC to rule out anaemia and rule out underlying infection

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31
Q

What factors are linked to an increased risk of anaphylaxis?

A

Certain medications
Alcohol
Exposure to new allergens
Change in season
Predisposition to asthma and eczema

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32
Q

What characteristics should a drug have in terms of protein binding and lipid solubility to work quickly?

A
  • Low protein binding as binding lowers the free conc of a drug
  • High lipid solubility so it can readily cross BBB
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33
Q

During anaesthesia, why must a drug be given throughout the procedure?

A

If not, the initial drug will diffuse into muscle, so plasma conc will lower and the patient will wake up

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34
Q

What is an agonist?

A

A drug that binds to and activates a receptor in the same way that the normal binding chemical would

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35
Q

What are the three types of agonists?

A

Full agonist
Partial agonist
Inverse agonist

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36
Q

Give an example of a full agonist drug

A

Opioids activate opioid receptors in the brain, resulting in the full opioid effect

37
Q

What is an antagonist?

A

A ligand that prevents an agonist from binding to a receptor and thus prevents its effects

38
Q

Give an example of an antagonist drug

A

Propranolol is a beta-adrenoceptor antagonist
This therefore prevents tachycardia

39
Q

What is a competitive antagonist?

A

Binds to the same site as the agonist but does not activate it, thus blocking the agonist’s action.
It is reversible and surmountable

40
Q

What is a non-competitive antagonist?

A

Binds to an allosteric (non-agonist) site on the receptor to prevent activation of the receptor.
It is irreversible and insurmountable

41
Q

Give an example of a competitive antagonist drug

A

Naloxone (Antagonist of opioid receptor= used for opioid overdose)

42
Q

What are the 4 types of drug targets?

A

Receptors
Enzymes
Transporters/ carrier proteins
Ion channels

43
Q

Give an example of a drug that targets a receptor

A

ARB= Angiotensin II receptor blockers
Prevent RAAS system so reduces blood pressure

44
Q

Give an example of a drug that targets an enzyme

A

ACE Inhibitors
Prevents RAAS system, causing vasodilation and reducing blood pressure

45
Q

Give an example of a drug that targets a transporter

A

Proton pump inhibitor (Lansoprazole)
Prevents production of stomach acid by inhibiting proton pump mechanism in parietal cells

46
Q

Give an example of a drug that targets an ion channel

A

Calcium channel blockers (Nifedipine)
Targets calcium channel which leads to arterial vasodilation improving coronary artery blood flow relieving angina

47
Q

What is bioavailability?

A

The amount of drug that reaches the circulation unaltered (IV drugs therefore have 100% bioavailability)

48
Q

What is first pass metabolism?

A

Rapid uptake and metabolism of an agent into inactive compounds by the liver

49
Q

What would the oral dose of morphine be compared to IV?

A

Oral dose is twice the IM/ IV dose
E.G. IV is 5mg, oral is 10mg

50
Q

A patient has just had an invasive surgery. She is 80, and has history of hypertension and renal failure. Her doctor prescribes a lower than normal dose of Morphine, and it is given at longer intervals. Why is this?

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.

51
Q

What are the ideal physical properties for an IV drug?

A

Stable in solution
Long shelf life
No pain on injection
Cheap

52
Q

What are arterial thrombosis normally formed of?

A

Platelets= white thrombus

53
Q

What are venous thrombosis normally formed of?

A

Coagulation factors and RBC= Red thrombus

54
Q

What are some possible complications of arterial thrombus?

A

MI/STROKE

55
Q

What are some possible complications of venous thrombus?

A

DVT/ PE

56
Q

How are arterial thrombosis treated?

A

Anti-platelets e.g. aspirin, clopidogerel

57
Q

How are venous thrombosis treated?

A

Anti-coagulants e.g. warfarin, heparin, NOACs (Rivaroxaban)

58
Q

What are the clinical features of arterial thrombus?

A
  • Diminished or absent pulse
  • Claudication
  • Complications as presentation; MI, Stroke, TIA, critical limb ischaemia
59
Q

What are the clinical features of venous thrombus?

A
  • Usually in the leg
  • Pulse is present
  • Dull aching pain
  • Skin pigmentation
  • Reddish/blue
  • Stiffness and swelling
60
Q

What are the components of Virchow’s triad?

A

Stasis of blood flow
Hypercoagulability
Endothelial injury

61
Q

What are some common risk factors for arterial thrombus?

A
  • Hypertension
  • Diabetes
  • Hypercholesterol
  • Obesity
  • Older age
  • Smoking
  • Family history of MI
  • Thrombophilia
  • Exogenous hormones
62
Q

What are some common risk factors for venous thrombus?

A
  • Immobility
  • Major trauma
  • Surgery
  • Active cancer
  • Pregnancy
  • Long distance travel
  • Older age
  • Obesity
  • Family history of MI
  • Smoking
63
Q

What is plasma D dimer and what does it show?

A

It is a type of fibrinogen degradation product that is released when a clot begins to dissolve. It is not diagnostic, but a normal result can exclude DVT.

64
Q

What is the action of heparin?

A

Activates antithrombin III (a serine protease inhibitor). It Inhibits factor Xa in the common pathway of the clotting cascade. Factor Xa is needed to convert prothrombin to thrombin, therefore LMWHs inhibit coagulation

65
Q

What is the action of Warfarin?

A

It competitively inhibits vitamin K epoxide reductase. It prevents post-translational gamma-carboxylation clotting factors II, VII, IX and X. This results in depletion of active clotting factors II, VII, IX and X; this produces a potent anticoagulant effect.

66
Q

What is the diagnostic criteria of AKI?

A
  • A rise in serum creatinine of 26 mmol/L within 48 hr
  • A 50% rise in serum creatinine in last 7 days
  • A fall in urine output to less than 0.5 mL/Kg/Hour for more than 6 hrs
67
Q

What are the units of urine output?

A

mL/Kg/Hour

68
Q

What are the three major classes of AKI?

A
  • Pre-renal
  • Renal
  • Post-renal
69
Q

What can cause pre-renal AKI?

A

Impaired perfusion of the kidneys= Diarrhoea, vomitting, hypotension, cardiac failure, sepsis

70
Q

What can cause renal AKI?

A

Damage to kidney apparatus= Glomerular disease such as nephritis, NSAIDs, glomerulonephritis

71
Q

What can cause post-renal AKI?

A

Urinary outflow obstruction= A blockage from something such as an enlarged prostate or kidney stones

72
Q

What is the minimum ml/ kg/hr of urine flow in a patient?

A

0.5

73
Q

What is normal urine output (mL/kg/hr)?

A

1-2

74
Q

How do NSAIDs cause kidney injury?

A

Inhibit prostaglandin synthesis (renal vasodilators)= reduced renal flow

75
Q

In AKI, what electrolyte may be raised?

A

Potassium (Hyperkalaemia)

76
Q

What ECG changes are seen in hyperkalaemia?

A
  • Prolonged QRS interval
  • Tall tented T waves
  • Absent P waves
77
Q

In a patient with AKI and resulting hyperkalaemia, how should they be treated?

A
  • Insulin and dextrose
78
Q

How does insulin correct hyperkalaemia?

A

Insulin shifts potassium into cells with glucose

79
Q

Why should dextrose be given at the same time as insulin in hyperkalaemia?

A

Insulin shifts potassium into cells with glucose
This corrects the hyperkalaemia but may cause hypoglycaemia. Dextrose prevents this

80
Q

What is a TIA?

A

A rapid onset of neurological dysfunction due to temporal focal cerebral ischaemia without infarct (Less than 24 hrs)

81
Q

How do you check the risk of stroke after TIA?

A

ABCD2

82
Q

What is amaurosis fugax?

A

Transient visual disturbance during TIA or stroke

83
Q

What causes amaurosis fugax?

A

Insufficient blood flow to one or both the eyes due to a clot

84
Q

What cardiac rhythm is atrial fibrillation?

A

Irregularly irregular

85
Q

What is cushing’s reflex?

A

When there is a raised ICP, there is systemic hypertension to reperfuse the brain

86
Q

What are the symptoms of a posterior circulation stroke?

A

Loss of consciousness
Cerebellar or brainstem syndrome
Isolated homonymous hemianopia

87
Q

What are the symptoms of an anterior circulation stroke?

A

Unilateral weakness and/or sensory deficit of the face and/or arms and/or legs
Homonymous hemianopia

88
Q

What is the most important criteria to consider when initiating a DNACPR?

A

Autonomy

Phase 2A ICS, Microbiology, Public Health, GP and ILAs (5 decks)

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