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Phase 2a > ILAs > Flashcards

ILAs Flashcards

1
Q

How does atherosclerotic plaque form?

A
  1. endothelial cell injury
    caused by toxins eg tobacco, diabetes + at areas of great force eg arterial bifurcation
  2. lipoprotein deposition
    increased permeability to lipoprotein due to eci
    gain entry + are modified
    forms LDL = inflammatory
    taken up by macrophages = foam cells
    causes fatty streaks in arterial wall = transitional plaque
  3. inflammatory reaction
    LDL are antigenic
    release of cytokines eg PDGF attracts more macrophages
  4. smooth muscle cell cap formation
    cytokines cause smooth muscle migration + proliferation
    collagen production keeps increasing
    creates fibrous collagen cap = advanced plaque
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2
Q

How does stable atherosclerotic plaque form?

A

grows slowly + reduces lumen size

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3
Q

How does unstable atherosclerotic plaque form?

A

grows rapidly + becomes unstable
undergoes thrombosis + obstructs vessel or ruptures
= complicated plaque

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4
Q

What are the modifiable risk factors for atherosclerosis?

A 
smoking
sedentary lifestyle
obesity
high BP
raised cholesterol
diabetes
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5
Q

What are the non-modifiable risk factors for atherosclerosis?

A

family history of angina (under 55 especially)
age (55+)
gender - male
south asian/afro-caribbean descent

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6
Q

How does smoking cause atherosclerosis?

A

smoke contains free radicals = oxidative stress + endothelial cell injury
components activate neutrophils + cytokine release = increases adhesion of inflam cells, LDL levels + thrombosis

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7
Q

How does a sedentary lifestyle cause atherosclerosis?

A

increases oxidative stress and endothelial dysfunction by increasing vascular ROS

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8
Q

How does obesity cause atherosclerosis?

A

increased cholesterol, risk of diabetes + BP

elevated LDL = higher lipoprotein deposition

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9
Q

How does a high BP cause atherosclerosis?

A

mechanical shear stress on arterial walls = endothelial cell injury
triggers plaque build-up

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10
Q

How does raised cholesterol cause atherosclerosis?

A

elevated LDL = induces inflam reaction + increases plaque
leads to smooth muscle migration + proliferation
increases LDL = increases endothelial cell injury

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11
Q

Does HDL contribute to atherosclerosis?

A

no, HDL is protective

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12
Q

How does diabetes cause atherosclerosis?

A

increases free radicals = increases apoptosis and reduces NO
increases blood flow + inflammation + high blood sugar + = increased damage to endothelial cells + increased plaque
increased deposition of LDL

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13
Q

How does family history put someone at risk of atherosclerosis?

A

genetic alteration may make endothelium more susceptible

history of increased cholesterol

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14
Q

How does the male gender put someone at risk of atherosclerosis?

A

men do more risk-taking behaviour

sex hormones contribute

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15
Q

What are the non-medicinal primary prevention measures of atherosclerosis?

A

healthy diet with reduced fat intake (<30% total energy) + lower cholesterol
lower saturated fats and replace with unsaturated fats
increase physical activity (>150 mod/intense aerobic/week)
reduce BMI below 25
reduce alcohol intake
smoking cessation
manage diabetes + BP effectively

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16
Q

What are the medicinal primary preventions for atherosclerosis?

A

aspirin (or clopidogrel)

statins

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17
Q

How does aspirin work as a primary prevention method for atherosclerosis? Side effects?

A

at low doses = anti-thrombotic, prevents STEMI/NSTEMI

SE: stomach ulcers (give PPI)

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18
Q

What dose of aspirin should be used for atherosclerosis and why?

A

low dose 75mg: anti-thrombotic = prevents STEMI/NSTEMI

high dose 300mg: PROMOTES THROMBOSIS = for pain relief and inflammation only

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19
Q

What medicine is given for primary prevention of atherosclerosis if aspirin is contraindicated?

A

clopidogrel: inhibits platelet aggregation

after an MI give both aspirin and clopidogrel

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20
Q

How do statins work as a primary prevention method for atherosclerosis? Side effects?

A

lowers LDL levels = prevents atheroma forming

SE: rhabdomyolisis (muscle aches and pains)

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21
Q

What are the secondary prevention measures for atherosclerosis?

A 
GTN spray
longer acting nitrates
beta-blockers
ca2+ channel blockers
ACE inhibitors
surgery - stent or bypass
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22
Q

How does GTN spray work as a secondary prevention method for atherosclerosis?

A

nitrate: fast-acting vasodilator
sublingual route
reduces flow, pressure + resistance

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23
Q

What does GTN spray stand for?

A

glyceryl trinitrate

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24
Q

What are the side effects of GTN spray?

A

fainting
dizziness
headaches

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25
Q

How do longer acting nitrates work as a secondary prevention method for atherosclerosis?

A

vasodilator = prevents thrombus forming

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26
Q

How do secondary prevention measures work for preventing atherosclerosis?

A

vasodilation

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27
Q

Give an example of a longer acting nitrate for atherosclerosis?

A

isosorbide dinitrate

come oral, skin plasters etc

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28
Q

When are blood thinners used for thrombi?

A

venous thrombosis only - DVT, pulmonary embolisms

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29
Q

Give 2 examples of beta-blockers?

A

end in -lol
atenolol
bisoprolol

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30
Q

How do beta-blockers work as a secondary prevention method for atherosclerosis?

A

block beta receptors and inhibit sympathetic NS
= vasodilation in heart + bronchoconstriction in lungs
= decrease heart rate and BP

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31
Q

What are the side effects of beta-blockers?

A

bradycardia
can worsen lung diseases eg asthma, COPD - contraindicative
sometimes need cario specific ones to avoid bronchoconstriction

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32
Q

Give an example of a Ca channel blocker?

A

end in -pine

nifedipine

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33
Q

How do ca channel blockers work as a secondary prevention method for atherosclerosis?

A

decrease contractility of heart

decreases force of LV contraction = more fluid backed up

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34
Q

What are the side effects of ca channel blockers?

A 
peripheral + pulmonary oedema
postural hypertension (BP drops from lying to standing)
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35
Q

How do ACE inhibitors work as a secondary prevention method for atherosclerosis?

A

control of hypertension: stop conversion of angiotensin I to II
increase vasodilation = decreases BP
acts as a diuretic
continued until BP has dropped

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36
Q

What are the side effects of ACE inhibitors?

A

fainting
dizziness
chronic dry cough
K+ diuretics cause galactorrhea in men (breasts enlarge and produce milk)

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37
Q

Give 2 examples of ACE inhibitors?

A

ends in -il
ramipril
lisinopril

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38
Q

How does a stent work as a secondary prevention method for atherosclerosis?

A

angioplasty procedure

side effects: death, acute MI, restenosed later on

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39
Q

When are surgical interventions used for atherosclerosis?

A

when angina persists with medication

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40
Q

How does a bypass work as a secondary prevention method for atherosclerosis?

A

coronary artery bypass graft

usually uses mammory artery + connects it to the coronary artery

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41
Q

Is stent or bypass surgery more effective for atherosclerosis?

A

bypass = higher success + less likely to be restenosed

but is higher risk

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42
Q

What are the contents of an atheroma?

A

lipids (LDL), macrophages, smooth muscle

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43
Q

What are the key features of stable angina?

A 
crushing chest pain
comes on AFTER exertion
retro-sternal
lasts a few minutes
no sweating, nausea or vomiting
fibrous cap remains
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44
Q

How does stable angina become unstable?

A

fibrous cap ruptures = thrombosis

either embolises and blocks other arteries or leads to unstable angina

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45
Q

What are they key features of unstable angina?

A

comes on AT REST

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46
Q

Are ischaemia or infarction associated with angina?

A

ischaemia associated

no infarction

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47
Q

What do serum cardiac markers look like for stable and unstable angina?

A 
stable = normal
unstable = abnormal
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48
Q

What are the 3 acute coronary syndromes?

A
  1. unstable angina
  2. NSTEMI angina
  3. STEMI angina
    (worsen in this order)
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49
Q

What are the signs and symptoms of ACS?

A

nausea, vomiting, radiating pain

increased cardiac markers

50
Q

What is an NSTEMI?

A

non-ST elevated MI

partially occluded artery

51
Q

What is a STEMI?

A

ST elevated MI

full occluded artery

52
Q

What is the difference between an NSTEMI and a STEMI?

A

ST elevation in STEMI, otherwise present similarly

NSTEMI may show ST depression

53
Q

What are the cardiac markers tested for?

A

creatine kinase

troponin

54
Q

What ECG changes are there in stable angina?

A

no changes, unless done during an acute attack - rare

sometimes ST depression or T wave inversion

55
Q

Define anaphylaxis

A

severe + potentially life-threatening allergic reaction to a trigger with rapid onset
type 1 hypersensitivity reaction, IgE mediated
involves mast cells and basophils

56
Q

Why does anaphylaxis generally occur on the 2nd exposure and not the first?

A

1st time immune system becomes sensitised to the trigger

triggers small immune response, sometimes unnoticed

57
Q

What are the common triggers for anaphylaxis?

A

food - nuts, shellfish, dairy and egg
idiopathic
venoms - wasps, bess, hornets
medication - antibiotics, antisera (tetanus, diptheria), latex, painkillers, opioids, dextran

58
Q

What is the cause of low oxygen in anaphylaxis?

A

histamine release: vasodilation + increased vascular permeability
more leaky = blood leaks out into interstitium
reduces BP + blood flow = reduces oxygen
anaphylactic shock when multiple organ systems starved of oxygen

59
Q

What is the cause of oedema in anaphylaxis?

A

histamine release: vasodilation + increased vascular permeability
more leaky = blood leaks out into interstitium
= angio-oedema eg in tongue

60
Q

What is the cause of a high resp rate + expiratory wheeze in anaphylaxis?

A

histamine release: smooth muscle contraction in airways = wheeze
= reduced airflow to lungs = high resp rate

61
Q

What is the cause of a high heart rate and low BP in anaphylaxis?

A

histamine release: increases heart rate and vasodilation

= decreases BP

62
Q

What is the cause of prolonged capillary refill in anaphylaxis?

A

> 2 seconds abnormal

due to low BP

63
Q

When does hypertension start?

A

140/90 mm Hg

64
Q

What is the cause of a widespread urticarial rash in anaphylaxis?

A

histamine release: vasodilation

65
Q

What is synosis?

A

symptom of anaphylaxis
severe hypoxia
body goes blue as lungs don’t get enough oxygen
(deoxygenated blood is blue)

66
Q

What is stridor?

A

symptom of anaphylaxis

abnormal high-pitched sound when airflow passes through an obstructed airway

67
Q

What is the term for hypertension combined with tachycardia?

A

haemodynamically unstable

68
Q

What are main chemical mediators in anaphylaxis?

A

histamine
leukotriene
prostaglandins
tryptase

69
Q

What are the main 3 effects of histamine in anaphylaxis?

A

increased vascular permeability
smooth muscle contraction
vasodilation

70
Q

What to do in an emergency anaphylactic reaction?

A

ABCDE Adrenaline
A- airway (swelling, hoarseness, stridor)
B- breathing (rapid, wheeze, fatigue, cyanosis, low sats, confusion)
C- circulation (pale, clammy, low BP, faint, drowsy)
D- disability
E- exposure

diagnosis: look for ABC and skin changes
call for help: lie flat and raise their legs
give adrenaline

71
Q

How is adrenaline given for anaphylaxis?

A

via an EPI pen
or intra-muscularly
IV is only for specialist use

72
Q

What are the contraindications for adrenaline? What is given instead?

A

allergy or if on beta-blockers

salbutamol (IV) given instead - doesn’t affect the heart, only the lungs (B2 receptor selective)

73
Q

What is the action of adrenaline in anaphylaxis?

A

eases breathing difficulty + restores cardiac output
reduces release of chemical mediators
alpha 1 adrenoceptor agonist: vasoconstriction = increases vascular resistance, coronary perfusion + BP + decreases oedema
beta 1 adrenceptor activity: positively ionotropic and chronotropic
beta 2 adrenoceptor activity: reduce oedema + bronchodilation

74
Q

Why is high flow oxygen given in anaphylaxis?

A

to prevent collapse of reservoir on inspiration

to increase O2 sats

75
Q

What is the recommended treatment for anaphylaxis?

A 
adrenaline
high flow oxygen
IV fluids
antihistamines
steroids
76
Q

Why are IV fluids given in anaphylaxis?

A

to increase BP
large volumes will have leaked from circulation
type does not matter

77
Q

Why are antihistamines given as a 2nd line treatment in anaphylaxis?

A

decreases histamine-mediated vasodilation and bronchoconstriction
not life-saving alone

78
Q

Which antihistamine is given in anaphylaxis?

A

chlorphenamine

79
Q

Why are steroids given in anaphylaxis?

A

anti-inflammatory

strop release of chemical mediators

80
Q

What is a biphasic anaphylactic reaction?

A

symptoms occur again a few hours later

81
Q

What is a protracted anaphylactic reaction?

A

symptoms last for hours or days

82
Q

When is a 2nd dose of adrenaline given?

A

repeated 5 minutes after 1st dose if no improvement is seen

according to BP, pulse and resp function

83
Q

What is the conformational blood test for anaphylaxis?

A

mast cell tryptase - shows elevated levels

84
Q

When is the mast cell tryptase done in anaphylaxis?

A

immediately, 1-2 hours after and 24 hours after

24 hrs to see baseline levels

85
Q

When does mast cell tryptase peak during anaphylaxis?

A

1-2 hours after onset

86
Q

What tests are done during anaphylaxis?

A

mast cell tryptase
IgE levels
monitor BP, SATs, pulse
continuous ECG

87
Q

What should be done after an anaphylactic reaction?

A

give patient an EPI-pen and medical information bracelet with details of anaphylaxis
do allergy skin prick test to confirm trigger

88
Q

What type of drug is Ramipril?

A

ACE inhibitor

89
Q

What type of drug if Furosemide?

A

loop diuretic

90
Q

How do drugs travel in the blood?

A
  1. some of the drug binds to plasma proteins (albumin, lipoproteins)
  2. rest if left unbound
91
Q

Why do some drugs need to be bound to plasma proteins?

A

they are a reserve for when all the unbound drug has been metabolised

92
Q

What level of protein binding should an anaesthetic drug have for anaesthesia to be induced quickly?

A

low protein binding

high levels of unbound drug

93
Q

Why should an anaesthetic drug have low protein binding and high levels of unbound drug?

A

unbound can diffuse across cell membranes as they are not bound to proteins
able to cross blood-brain barrier = fast onset
only unbound provide substrate for drug metabolising enzymes

94
Q

The volume of distribution of a drug is inversely proportional to what?

A

protein binding

95
Q

What level of lipid solubility should an anaesthetic drug have for anaesthesia to be induced quickly?

A

high lipid solubility

96
Q

Why should an anaesthetic drug have a high lipid solubility?

A

can freely diffuse across cell membranes due to phospholipid bilayer
can cross blood-brain barrier
= rapid brain uptake = high distribution = fast onset

97
Q

Why does an additional volatile gas drug have to be given after the first anaesthetic IV drug and as soon as as a patient is asleep?

A

otherwise patient would wake up
IV drugs act quickly eg thiopental
distribute very rapidly to highly perfused tissues
have a high lipid solubility = redistribution
drug goes back into blood and into lower perfused tissues eg fat, muscles and away from the brain

98
Q

What happens when the first anaesthetic IV drug in reaches an equilibrium between the blood and tissue?

A

diffusion slows
lots of drug goes to brain so diffusion favours the blood
= need a second drug to maintain anaesthesia

99
Q

What is an agonist drug?

A

chemical that binds to a receptor and activates it

can be full or partial

100
Q

Give 2 examples of agonist drugs?

A

morphine (u-opioid receptor)

clonidine (a2-adrenceptor)

101
Q

What is an antagonist?

A

binds to a receptor in order to decrease the effect of an agonist
doesn’t activate the receptor

102
Q

Give 2 examples of antagonist drugs?

A

naloxone (competitive, opioid receptors)

ketamine (non-competitive, NMDA-glutamate receptor)

103
Q

What are competitive antagonists?

A

competes for and binds to the same site as the agonist to block the agonist binding

104
Q

Give an example of a competitive antagonist?

A

atenolol (b1-adrenergic receptor) for high BP

105
Q

What is a non-competitive antagonist?

A

binds to an allosteric site to prevent an agonist activating the receptor

106
Q

Give an example of a non-competitive antagonist?

A

ketamine (NMDA-glutamate receptor)

107
Q

What are the 4 drug targets?

A
  1. receptors
  2. enzymes
  3. transporters
  4. ion channels
108
Q

Give an example of a drug which targets enzymes and how it works?

A

NSAIDS: ibuprofen
inhibit enzymes cyclooxygenase (COX)
= prevents production of prostaglandin H2 which is involved in inflammation, pain, fever and swelling

109
Q

What is the pathway for how NSAIDS acts on their enzyme target?

A

membrane phospholipid > (PLA2) > arachidonic acid > (COX) > prostaglandin H2
NSAIDS inhibit enzyme COX

110
Q

Give an example of a drug which targets transporters and how it works?

A

proton pump inhibitors eg lansoprazole
inhibits acid secretion by irreversibly inactivating the proton pump
= gastro protection to stop ulceration

111
Q

Give an example of a drug which targets ion channels and how it works?

A

calcium channel blockers eg amlodipine
blocks channel = prevents influx of calcium
less vasoconstriction, stops cardiac action potential = reduces heart rate + BP
treats hypertension

112
Q

What is bioavailability?

A

proportion of drug which enters the circulation so is able to have an active effect

113
Q

What is 1st pass metabolism?

A

goes to liver first before it’s target by which time most of the drug will have been eliminated
= limited uptake of drug via the oral route

114
Q

Which route is fastest for morphine uptake? IM or oral?

A

IM

115
Q

What % of oral morphine is metabolised by 1st pass metabolism? What effect does this have on it’s bioavailability?

A

50%

bioavailability hugely reduced

116
Q

How much more oral morphine is required compared to IM morphine?

A

give double the amount for oral route

same efficacy as IM route

117
Q

Why is lower doses + longer intervals of morphine given to patients with renal failure?

A

patient may not clear drug for up to a week - don’t want it to stay in the body
morphine > morphine-6-glucuronide
m-6-g much more potent + renally excreted
builds up in renal failure = respiratory depression + seizures

118
Q

What is the difference between pharmacodynamics and pharmacokinetics?

A

dynamics: how the drug effects the body eg side effects
kinetics: how the body effects the drug eg how fast it’s taken up

119
Q

What are the ideal pharmacokinetic properties of a anaesthetic drug?

A 
low protein binding
high lipid solubility
= rapid onset, reaches brain fast
no active metabolites (lengthen onset time)
rapid clearance and metabolism
120
Q

What are the ideal physical properties of a anaesthetic drug?

A

cheap
long shelf life
stable in solution (often given with saline)
not painful on injection

121
Q

What are the ideal pharmacodynamic properties of a anaesthetic drug?

A 
no cardio/resp effects
no histamine release (increase risk of anaphylaxis)
no gastro irritation
no sickness
quick recovery
no hypersensitivity reaction

Phase 2a (5 decks)

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