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mpharm year 3 sem 2 > week 2 > Flashcards

week 2 Flashcards

1
Q

define atheroma

A

the accumulation of intracellular and extracellular lipids in the intima of large and medium sized arteries

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2
Q

name the 3 macroscopic features of an atherosclerotic plaque

A

fatty streak
simple (fibrous) plaque
complicated plaque

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3
Q

what is a fatty streak and what causes it

A

a slightly elevated zone on the arterial wall caused by accumulation of (a small number of) lipid cells

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4
Q

what is a simple (fibrous) plaque

A

accumulation of lipids both free and in cells
smooth muscle cells migrate from the media
fibrosis develops around the lipid and forms a cap over the lesion

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5
Q

what is a complicated plaque and what can it lead to

A

ulcers and fissures of the fibrous can expose plaque contents
can result in thrombosis

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6
Q

what is atherosclerosis

A

thickening and hardening of arterial walls as a consequence of atheroma
results from accumulation of lipid, connective tissue, inflammatory cells and smooth muscle cells in the intima

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7
Q

which layer of the artery has the most mechanical strength

A

medial (middle) layer

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8
Q

how does plaque develop

A

not fully understood thought to be a response to injury- initiated by endothelial dysfunction

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9
Q

name the 3 main components of plaques

A

lipid containing macrophages
extracellular matrix
cells, proliferating smooth muscle

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10
Q

describe how LDL is removed from circulation

A
  • removed by LDL receptors and scavenger cells (macrophages)
  • 70% is removed via LDL receptor pathway
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11
Q

where are most LDL receptor located- why is this significant

A

hepatocytes
hence liver is very important in LDL metabolism

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12
Q

what do scavenger cells do to LDL
when do they do this?

A

oxidise it
this happens when the patients diet contains a high level of trans fats, they smoke or have poorly controlled diabetes

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13
Q

how is hyperlipidaemia related to plaque formation

A
  • when LDL becomes oxidised it enters the endothelium and may alter endothelium permeability
  • this promotes accumulation of lymphocytes, dendritic cells and macrophages
  • platelets can stick to areas of inflammation and cause hardened areas- called plaques
  • oxidised cholesterol loaded macrophages forms a ‘foam cell’ and the plaque gets thicker
  • macrophages release growth factors which recruit smooth muscle- these may form a cap around the plaque
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14
Q

non drug prevention of plaque formation

A
  • smoking cessation
  • reduce fat intake
  • high intake fruit+veg
  • alcohol in moderation
  • regular exercise and weight management
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15
Q

MOA of aspirin

A

thromboxane A2 - platelet agonist produced by platelets
- aspirin bocks production of thromboxane A2 by inhibiting the platelet enzyme responsible for its synthesis- COX1
- action of aspirin on COX1 is permanent- lasting the lifetime of platelet (7-10 days)

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16
Q

clopidogrel mode of action

A

clopidogrel is an irreversible inhibitor of ADP (a platelet agonist produced and released by platelets) receptor on platelets (P2Y12 receptors) and so prevents ADP from activating platelets

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17
Q

statin MOA

A

HMG-coA reductase inhibitors- HMG-coA is involved in the synthesis of cholesterol
so statins reduce cholesterol synthesis in the liver and increase LDL-cholesterol clearance from the blood

(- given at bedtime because cholesterol synthesis is cyclical with greatest production during fasting states)

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18
Q

antiplatelet antithrombotic functions (3)

A

adenosine diphosphatase (degrades ADP from platelets)
prostacyclin (produced by the enzyme cyclooxygenase)
nitric oxide

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19
Q

anticoagulant antithrombotic functions (3)

A

heparin-like molecules (activate antithrombin 3)
thrombomodulin (activates protein C)
protein S

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20
Q

fibrinolytic antithrombin functions

A

prevents blood clots from growing
t-PA

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21
Q

procoagulant functions (3)

A
  • production of vWF
  • production of tissue factor
  • binding of factors IXa and Xa
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22
Q

platelet adhesion and activation

A
  • adherent platelets release ADP and thromboxane A2
  • ADP and thromboxane A2 are platelet agonists, activate more platelets and recruit them to site of vascular injury
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23
Q

how long can a prescriber take to give a physical Rx after an emergency supply done over the phone, email or fax

A

72h

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24
Q

what is the maximum quantity a prescriber can give via an emergency supply

A

any quantity

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25
Q

which CD schedules can be given via emergency supply- prescriber request

A

schedule 4 (ie zopiclone) and 5 (ie co-codamol)

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26
Q

what is the max quantity that can be given via a emergency supply- patient request

A

30 days treatment

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27
Q

POM register requirements

A
  • entry to be made day of supply or next day
  • prescription date
  • medicine details
  • prescriber details
  • patient details inc why supply was needed (if patient request)
  • must be kept for 2 years from last entry
  • if CD - only needs to go in CD register
  • don’t need to put oral contraceptives in it
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28
Q

CPUS - patient eligibility (4)

A
  • registered with Scottish GP practice - even if temp
  • item has previously been prescribed
  • if second supply in a row- shouldn’t really do it
  • can give up to 1 repeat cycle so if patient normally gets 2 months - we can give this
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29
Q

define ischaemia

A

insufficiency in blood supply- coronary arteries are the only source of blood for heart muscle- if these are blocked the blood supply to the heart will reduce- resulting in chest pain called angina

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30
Q

what is the cause of angina

A

angina is the result of ischema caused by an imbalance between myocardial blood supply and oxygen demand

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31
Q

when does stable angina occur

A

occurs when coronary perfusion is impaired by fixed or stable atheroma or coronary arteries

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32
Q

name the 6 different stable anginas

A
  • exertional angina
  • anginal equivalent syndrome
  • syndrome x
  • silent ischemia
  • decubitus angina
  • nocturnal angina
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33
Q

exertional angina

A

*Arises from an increase in myocardial oxygen demand during exertion or emotion. Relief occurs by rest and nitroglycerine.
*Coronary artery obstructions are not sufficient to result in resting myocardial ischemia.

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34
Q

anginal equivalent syndrome

A
  • Caused by myocardial ischemia
  • Symptoms= shortness of breath or pain at a site- other than the chest (eg arm/ jaw)
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35
Q

syndrome x

A
  • Typical, exertional angina with positive exercise stress test
  • Anatomically normal coronary arteries
  • Reduced capacity of vasodilation in microvasculature
  • Long term prognosis is very good
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36
Q

silent ischemia

A
  • very common
  • More episodes of silent than painful ischemia in the same patient
  • Difficult to diagnose
  • Holter monitor (records heart rate and rhythm over a 24-hour period )
  • Exercise testing
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37
Q

decubitus angina

A
  • chest pain only occurs while lying down
  • Usually associated with impaired left ventricular function
  • Patient usually has severe coronary artery disease
  • Occurs because gravity redistributes fluid in the body- which makes the heart work harder
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38
Q

nocturnal angina

A
  • Awakes patient from sleep
  • May be provoked by vivid dreams
  • It may occur due to coronary artery spasm
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39
Q

unstable angina

A
  • Is characterised by rapidly worsening chest pain on minimal exertion or rest
  • Is associated with an ulcerated atheroma and thrombus formation- this produces a greater reduction of coronary blood flow to produce angina at rest
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40
Q

Prinzmetals

A
  • Coronary artery spasm- sudden involuntary contraction of smooth muscle tissue of coronary artery
  • Spasm temporarily narrows the coronary artery
  • Causes transient impairment of coronary blood supply
  • Not due to atherosclerosis or platelet aggregation
  • Usually occurs at rest
  • Majority of patients have an atherosclerotic plaque but is it often minor when compared to extent of pain
  • Long term prognosis is very good
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41
Q

what are the 3 common causes of angina

A
  • atherosclerosis with blood clot
  • atherosclerosis
  • spasm
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42
Q

cause of prinzmetal’s angina

A

coronary spasm

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43
Q

cause of syndrome X- microvascular angina

A

abnormal contraction or deficient endothelial- dependent relaxation of resistant vessels associated with diffuse vascular disease

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44
Q

define class one angina

A

angina only during strenuous or prolonged physical activity

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45
Q

define class two angina

A

light limitation with angina only during vigorous physical activity

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46
Q

define class three angina

A

moderate limitation - symptoms with everyday living activities

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47
Q

define class four angina

A

severe limitation
inability to perform any activity without angina or angina at rest

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48
Q

define exercise testing of angina

A

goal- is to induce a controlled, temporary ischemia state during clinical ECG observation (ST segment depression occurs with ischemia and reverses after ischemia disappears

normally treadmill/ bicycle - incline+ speed increase every 3 min

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49
Q

unstable angina characteristics

A
  • angina at rest, not responding to therapy
  • recent onset, less than 1 month
  • increased frequency and duration of episode
  • may be a serious indicator of an impending heart attack
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50
Q

why do plaques rupture

A

interplay between plaque vulnerability and external stresses
depends on plaque composition rather than plaque size
plaques rich in soft extracellular lipids are vulnerable to rupture- presence of smooth cells may provide resistance to rupturing

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51
Q

SIGN guidlines- first line for angina

A

beta blocker - bisoprolol 5mg once daily

can also give GTN spray too - to be used for immediate relief or before activities known to trigger

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52
Q

SIGN guidelines- second line for angina

A

if B blocker maxed out or in-tolerated - add or swap to calcium channel blocker ie nicorandil- 5mg 2x daily

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53
Q

how do beta blockers work

A

decrease oxygen demand of myocardium by lowering both rate and force of contractility of the heart

54
Q

how do calcium channel blockers work?

A

stop calcium entering the cell
calcium influx is increased in ischemia because of the membrane depolarisation that hypoxia produces
calcium is essential for muscle contraction

55
Q

how do nitrates work (GTN)?

A

nitrates relax coronary arteries by decreasing coronary vasoconstriction or spasm and increase perfusion of the myocardium
they also relax veins, decreasing preload and myocardial oxygen consumption
nitrates donate nitric oxide which stimulates cyclic guanosine monophosphate cGMP cyclase that can release calcium in muscle

56
Q

how do potassium channel activators work?

A

(nicorandil)
activation of K+ATP channels on smooth muscle cells hyperpolarises the membrane and decreases calcium entry
K+ATP channels in the mitochondria in the myocardium may be involved in response to nicorandil

57
Q

what is the definition of an myocardial infarction (MI)?

A

heart attack- the interruption of blood supply to part of the heart - causing some heart cells to die

58
Q

where does most thrombus formation occur (relating to an MI)?

A

site of an atherosclerotic lesion - this obstructs the blood flow to the myocardial tissues

59
Q

what is thought to be the triggering mechanism for the development of thrombus in patients with an MI?

A

plaque rupture

60
Q

how does plaque rupture cause an MI ?

A

when a plaque ruptures, a thrombus is formed at the site- this can occlude blood flow- thus resulting in an MI

61
Q

what causes a plaque to rupture?

A
  • what they are made of (plaques rich in soft extracellular lipids are vulnerable to rupture)
  • extracellular lipid accumulation (lipid core formulation) and cap weakening predispose the plaque to rupture
62
Q

what is NSTEMI?

A

non ST segment elevation myocardial infarction
- occurs by developing a complete occlusion of a minor artery previously by atherosclerosis
- this causes a partial thickness damage of the heart muscle

63
Q

what is STEMI?

A

ST segment elevation myocardial infarction
- occurs by development of a complete occlusion of a major coronary artery previously affected by atherosclerosis- this causes a thickness damage of heart muscle

64
Q

is a shorter time between coronary occlusion and coronary perfusion better? why?

A

yes- less damage and greater amount of myocardial tissue that may be saved

65
Q

how early can irreversible damage occur after blood flow is interrupted

A

20-40 mins

66
Q

where may cellular death occur after an MI

A

subendocardial layer- it can then spread through the thickness of the wall of the heart

67
Q

how long do we have to restore blood flow in order to save a substantial amount of myocardial tissue

A

6 hours from the onset of coronary occlusion

68
Q

name 3 cellular changes associated with the initial MI

A
  • development of infarct extension (new myocardial necrosis)
  • infarct expansion (a disproportionate thinning and dilation of the infarct zone)
  • ventricular remodelling (a disproportionate thinning and dilation of ventricle) resulting in an enlarged heart
69
Q

name 5 symptoms of an MI

A
  • chest pain (may radiate to neck, left arm or jaw)
  • sweating
  • nausea/ vomiting (may arise from severity of pain and resulting vagal stimulation)
  • breathing difficulty (squeezing, choking or smothering sensations)
  • heavy feeling in the chest- like someone is sitting on them
70
Q

name 4 biochemical markers of an MI

A
  • development of pathologic Q waves on ECG
  • development of ST segment elevation or depression on ECG
  • a rise and gradual fall in troponin
  • rapid rise and fall of creatine kinase MB
71
Q

what is troponin ?

A
  • troponin T and troponin I- components of the myofilamet troponin complex- released from damaged muscle- release prolonged with actin and myosin damage
72
Q

when do troponin I levels rise, how long are the elevated for, when do they peak?

A

rise in about 3 hours, peak at 14 to 18 hours, and remain elevated for 5 to 7 days

73
Q

when do troponin T levels rise, how long are the elevated for ?

A

3 to 5 hours and remain elevated for 10 to 14 days

74
Q

what is high sensitivity troponin used for

A

to detect OR rule out an MI

75
Q

what does an elecsys look for?

A

troponin T

76
Q

what does an architect stat look for?

A

troponin I

77
Q

what is myoglobin?

A

an oxygen- binding protein found in skeletal muscle and cardiac muscle
its release from ischemic muscle occurs earlier than release of CK (creatine kinase)

78
Q

when do myoglobin levels rise and when do they peak?

A

can elevate within 1 to 2 hours of acute MI and peaks within 3 to 15 hours

79
Q

why is elevated myoglobin not specific to an MI?

A

because it is also found in skeletal muscle - therefore its use in diagnosing an MI is limited

80
Q

what does creatine kinase do (CK)?

A

catalyses the conversion of creatine and utilises ATP to create phosphocreatine and ADP
the CK enzyme reaction is reversible and thus ATP can be generated from PCr and ADP

81
Q

what is LDH?

A
  • lactate dehydrogenase
  • a tertraeric protein and made up of 2 types of subunit- H=heart and M=muscle
  • exists as 5 different isoenzymes
82
Q

what is LDH elevated in? (2)

A

MI
blood disorders

83
Q

what are the cells that make up the stratum corneum? (3)

A
  • keratinocytes
  • melanocytes
  • langerhans
84
Q

what are the 3 routes drugs use to penetrate the stratum corneum ?

A
  • shunt route
  • transcellular route
  • intracellular route
85
Q

name 5 physiochemical properties that affect transdermal drug delivery

A
  • ability to cross lipid bilayers (especially corneocytes)
  • diffusion through aqueous environments (viable epidermis)
  • Mw- under 500 Da
  • log P between 1-4
  • max daily dose 10mg
86
Q

how does alcohol help with transdermal drug delivery?

A

partitions into skin
sets up a transient reservoir for drug to partition into
drives maximum thermodynamic activity

87
Q

how does occlusion increase transdermal drug delivery ?

A
  • hydrates skin by blocking transdermal water loss
  • hydration increases permeability of the skin
  • EMLA cream applied under occlusive dressing
88
Q

what does Franz diffusion measure?

A

skin permeation

89
Q

name 4 advantages of transdermal drug patches

A
  • avoids harsh GIT environment
  • avoids first pass metabolism
  • patches can be easily applied and removed
  • high patient compliance
90
Q

why can we not cut patches?

A

cutting the patch damages the membrane that controls drug release

91
Q

name 2 limitations of transdermal drug delivery

A
  • low dose of drug only
  • drug needs to meet specific physiochemical property criteria
92
Q

what is first generation transdermal delivery?

A

transdermal patches

93
Q

name one limitation of first generation transdermal delivery

A

barrier function of stratum corneum

94
Q

what is second generation transdermal drug delivery ?

A

uses skin permeability enhancers - improves delivery for small Mw drugs

95
Q

what are the requirements for second generation TDD?

A
  • Increase skin permeability
  • Reversibly disrupting stratum corneum structure
  • Provide an added driving force for transport into the skin
  • Avoid injury to deeper, living tissues
  • Non-toxic
  • Non-irritant
  • Compatibility with drugs and excipients
  • Patient acceptability
96
Q

how does oelic acid enhance drug delivery?

A

causes fluidisation

97
Q

how does dimethylsulfoxide enhance drug delivery?

A

interacts with polar head groups of lipids- causes fluidisation

98
Q

how does azone enhance drug delivery?

A
  • Polarity alteration
  • Phase separation
  • Makes more fluid
  • Rearranges lipids
99
Q

what’s third generation transdermal drug delivery?

A

disruption of the stratum corneum

100
Q

what is micro needle assisted drug delivery?

A

3rd generation
- small needles that make holes in stratum corneum to improve drug delivery
- long enough to reach epidermis but short enough to avoid pain receptors in the dermis

101
Q

what is electrically assisted drug delivery?

A

3rd generation
- example- radio frequency electrical cell ablation- makes small holes in the stratum corneum due to thermal ablation- helps drug get through

102
Q

which 2 groups of patients are less likely to have severe chest pain with an MI?

A
  • diabetic patients
  • women
103
Q

what is the cause of pain associated with an MI?

A

lack of oxygen

104
Q

what should we give to a patient experiencing an MI? why?

A

300mg aspirin
reduces mortality by 21%- due to anti platelet effects

105
Q

in a patent with an MI- we should give GTN- what preparation should we use?

A

undiluted infusion
1mg/ hour
dose is dependent on pain and BP (can make BP too low)

106
Q

in a patent with an MI- we should give morphine- what preparation should we use? why?

A
  • severe pain- needs to be strong
  • also morphine reduces acute anxiety so helps the patient relax
  • 5-10mg IV (quick)
107
Q

what is a common side effect of morphine and how to we combat it (MI management)?

A

nausea/ vomiting
- give metoclopramide - antiemetic 10mg IV

108
Q

when should we use oxygen treatment in MI management?

A

when patients oxygen saturation is less than 94%

109
Q

why do we give fondaparinux in MI management, what is the dose?

A

helps blood flow again (reperfussion)
2.5mg subcutaneous

110
Q

what tests do we need to do on an MI patient right away? why? (5)

A

full blood count- looking to measure haemoglobin- ensure patient is not anaemic – this can cause chest pain because it transports oxygen, need to know platelets are in normal range

kidney function- meds can affect kidney function

liver function - need to check before starting statin

cardiac enzymes - troponin, CK, LDH, NSTEMI, STEMI

cholesterol - important to do asap as can get a false low reading after starting meds

111
Q

why do we want to do a chest Xray on an MI patient?

A
  • to see if fluid in the lungs
  • enlarged heart?? (long term hypertension)
  • can rule out other things such as pneumonia
112
Q

can we diagnose an MI from an Xray?

A

nope- we use it to rule out other things

113
Q

what is the problem with using CK-MB?

A

not specific to having an MI
- elevated when doing other things - ie running a marathon

114
Q

what is the ejection fraction?

A

a percentage of how much blood the LV pumps out with each contraction

normal - 50-70%
moderate- 41-49%
poor <40%

115
Q

what trigger the release of angiotensin 1?

A

renin

116
Q

why are beta blockers not first line in hypertension?

A

no evidence to say they reduce risk of stroke

117
Q

state one example of an alpha adrenoreceptor blocker

A

doxazosin

118
Q

why is doxazosin used in Benign prostatic hyperplasia?

A

doxazosin is an alpha receptor blocker- High no of alpha receptors in prostate – adrenaline stimulates these to cause prostate enlargement and affect urinary output

119
Q

how long do we wait after starting an ACEi to increase dose?

A

need to wait 4 weeks then check BP again - then can increase dose if no/ not enough improvement
also need to check renal function 1-2 weeks after starting a new dose

120
Q

statin MOA

A

Reduce risk by- pleiotropic effect
* Makes plaque more flexible- reduced plaque fracture which reduces risk of blood clot and therefore reduces stroke+ MI risk

ESR (inflammatory marker)
* When started stain- this reduces- reduction in inflammation- lining of arterial blood vessels- reduces plaque fracture

(hydroxymethyl glutamate) HMG coA inhibitors = statins
* HMG coA- catalyses final step in cholesterol production
* Only reduce cholesterol by 10-20%- this is fine
* Cholesterol is essential in many processes

121
Q

why are NSAIDs not recommend in hypertensive patients

A

can exacerbate his high BP- increases sodium reabsorption, and therefore water reabsorption

Propryonic acid – base of NSAIDs- excreted by kidney- body gets confused between this and sodium- it prefers to excrete propryonic acid of sodium- therefore sodium retention

122
Q

why are soluble tablets not the best choice in a hypertensive patient?

A

they contain lots of sodium

123
Q

63-year-old white male, BP 160/95. No PMH (past med history) or DH (drug history)

what do we do? why?

A

start on a calcium channel blocker - over 55 so likely to be over stimulation of sympathetic drive

amlodipine 5mg once daily

124
Q

56-year-old south Asian female, BP 162/90. PMH: HBP; DH: enalapril 40mg daily

what do we do? why?

A

start calcium channel blocker- over 55 and south asian- so likely to be over stimulation of sympathetic drive

amlodipine 5mg once daily
40mg of enalapril is max dose

125
Q

what is the maximum dose of enalapril?

A

40mg daily

126
Q

52-year-old white female, BP 170/96. No PMH: Mean ABPH mean 130/66

what do we do? why?

A

nothing - no drug treatment required as this is whitecoat hypertension

127
Q

50-year-old white male, BP 146/88. no PMH or DH

what do we do? why?

A

lifestyle advice- see how that goes
if no improvement start on an ACEi - under 55 so likely to be angiotensin, aldosterone system defect
ramipril 2.5mg daily to start

128
Q

what are the functional groups of aspirin?

A

carboxylic acid
aromatic ester group

129
Q

describe aspirin degradation

A

Ester gets hydrolysed when water is present
gives salicylic acid and acetic acid (smells like vinegar)

130
Q

why is aspirin not recommended for children under 16 years old?

A

it can cause Reye’s syndrome

mpharm year 3 sem 2 (11 decks)

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