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mpharm year 3 sem 2 > week 3 > Flashcards

week 3 Flashcards

1
Q

what is erythropoiesis?

A

red blood cell production

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2
Q

what stimulates erythropoiesis?

A

hypoxia

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3
Q

what hormone controls erythropoiesis and where is that synthesised?

A

erythropoietin
kidneys

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4
Q

what is hemolysis?

A

destruction of red blood cells

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5
Q

name 8 symptoms of anaemia

A
  • pallor (colour- pale)
  • fatigue
  • shortness of breath
  • headache
  • palpitations/ tachycardia
  • slowing of thought
  • weakness
  • parenthesis (pins and needles)
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6
Q

name 6 symptoms of iron deficiency anaemia

A
  • pallor (colour)- most common
  • glossitis
  • fissures of lips
  • sensitivity to cold
  • weakness
  • fatigue
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7
Q

name 6 symptoms of cobalamin deficiency

A
  • sore tongue
  • anorexia
  • weakness
  • pins and needles
  • altered thought process
  • confusion
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8
Q

are myocytes fast or slow depolarising cells?

A

fast

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9
Q

are pacemaker cells fast or slow depolarising cells?

A

slow

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10
Q

in the absolute refractory period, can cells be re-excited?

A

no, they cannot respond to further stimuli at this stage- this is a good situation for cells- safe

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11
Q

in the relative refractory period, can cells be re-excited?

A

yes

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12
Q

is vagal stimulation parasympathetic or sympathetic

A

parasympathetic

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13
Q

how does vagal stimulation affect resting potential an pacemaker cells?

A

makes resting potential more negative
makes pacemaker current slower

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14
Q

are catecholamines sympathetic or parasympathetic

A

sympathetic

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15
Q

name 4 causes of arrhythmias

A
  • abnormal conduction
  • abnormal automaticity (normally SA node fires first, in this case an AV node is firing at the wrong time)
  • re-entry (cells just keep re-entering and re-firing
  • a combination of both 2 and 3
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16
Q

what are class I anti arrhythmic drugs?

A

class I= sodium channel blockers

Ia= quinidine, procainamide- increase AP
Ib= lignocaine- decrease AP
Ic= flecaidide <-> AP

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17
Q

what are class II anti arrhythmic drugs?

A

ß-adrenoceptor antagonists (atenolol, sotalol)- rate control

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18
Q

what are class III anti arrhythmic drugs?

A

prolong action potential and prolong refractory period (suppress re-entrant rhythms) (amiodarone, sotalol)

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19
Q

what are class IV anti arrhythmic drugs?

A

Calcium channel antagonists. Impair impulse propagation in nodal and damaged areas (verapamil)

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20
Q

describe how class I (sodium channel blockers) work in arrhythmias

A
  • Reduce rate and magnitude of depolarization by blocking sodium channels is a decrease in conduction velocity
  • The faster a cell depolarizes the more rapidly adjacent cells will become depolarized
  • Therefore blocking sodium channels reduces velocity of action potential transmission
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21
Q

describe how class II (beta blockers) work in arrhythmias

A
  • Inhibit sympathetic driven electrical activity
  • Sympathetic drive increases conduction velocity
  • Increases aberrant pacemaker activity (ectopic beats).
  • Decrease sinus rate
  • Decrease conduction velocity
  • Increase APD and the ERP
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22
Q

describe how class III (potassium channel blockers) work in arrhythmias

A
  • The primary role of potassium channels in cardiac action potentials is cell repolarization
  • Block the potassium channels that are responsible for phase 3 repolarization
  • Since these agents do not affect the sodium channel, conduction velocity is not decreased
  • Prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias
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23
Q

describe how class IV (calcium channel blockers) work in arrhythmias (8)

A
  • Decrease conduction via the AV node
  • Shorten the plateau phase of the AP
  • Prolong APD (action potential duration)
  • Prolong ERP (effective refractory period)
  • Reduce contraction force
  • Use in SVT and Atrial
  • Not used in Ventricular arrhythmias
  • Class IV agents include verapamil and diltiazem
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24
Q

in what circumstance would we withhold digoxin from an arrhythmia patient?

A

when heart rate is less than 40 bpm

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25
Q

what is acute coronary syndrome? (3)

A
  • unstable angina
  • NSTEMI
  • STEMI
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26
Q

define unstable angina

A

an unprovoked (at rest) or prolonged (not helped by GTN) episode of chest pain- raising suspicion of acute MI

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27
Q

management of ACS (4)

A

think MONA
- morphine 5-10mg slow IV + metoclopramide 10mg IV
- oxygen (if required <94%)
- nitrates (GTN- IV infusion)
- aspirin 300mg

  • fonduparinux 2.5mg SC
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28
Q

what is a GRACE score?

A

a score calculated for patients who have suffered an MI of have unstable angina- the score calculates how like the patient is to die in 6 days, 6 months and 1 year- this allows us to prioritise patients who need treatment faster than others

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29
Q

name the 7 early (<72h) complications of ACS

A
  • death
  • cardiogenic shock
  • heart failure
  • ventricular arrhythmia
  • myocardia rupture
  • thromboembolism
  • pericarditis (extremely painful inflammation)
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30
Q

name the 6 later complications of ACS

A
  • ventricular wall rupture
  • valvular regurgitation
  • ventricular aneurisms
  • cardiac tamponade
  • dresslers syndrome
  • thromboembolism
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31
Q

what is epleronones indication and dose ?

A

Left ventricular systolic dysfunction EF<40%
start on 25mg- can go up to 50mg

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32
Q

side effects of ACE inhibitors

A

think captopril

Cough
Angioedema (emergency)
Potassium excess
Taste changes (metallic taste)
Orthostatic hypotension (dizzy)
Pregnancy contraindication/ Pressure drop (BP)
Renal failure/ Rash
Indomethacin inhibition
Leukopenia (rare)

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33
Q

name a contraindication of beta blockers

A

asthmatics

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34
Q

first line for managing stable angina

A

beta blocker ie bisoprolol 5mg daily

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35
Q

name one contraindication of calcium channel blockers in management of stable angina

A

beta blocker + rate limiting calcium channel blocker- makes heart too slow- patient dies (diltiazem or verapamil)

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36
Q

name 2 rate limiting calcium channel blockers

A

diltiazem or verapamil

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37
Q

when should isosorbide mononitrate doses be taken? why is this?

A

morning and afternoon- this is because there must be a 12h gap between pm and am doses- this is to ensure the patient doesn’t become tolerant to the drug and it no longer works

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38
Q

how do potassium channel activators work in stable angina?

A

they have arterial and venous vasodilation properties
3rd/ 4th line

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39
Q

name 3 side effects of potassium channel activators

A
  • ulcers- almost whole GIT can be affected
  • headache
  • palpitations
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40
Q

how does ivabradine work in stable angina management?

A

it lowers the heart rate by affecting the SA node

however not effective in patients with atrial fibrillation

41
Q

compliance vs concordance vs adherence

A

compliance- patient just being told what to do - not very patient centred

concordance- an agreement which is reached after a discussion between prescriber/ pharmacist and patient- taking into account both the wishes of the patient and their clinical needs

adherence- the degree to which the patient takes medication as directed

42
Q

what are the GTN rules?

A
  • Chest pain- tab under tongue- straight to heart
  • if not worked after 5mins- take a second tab, wait another 5 mins, - still not working
  • take 3rd one, then if not worked -phone 999

-If taking it more than twice a week- needs investigation- suggests uncontrolled

43
Q

what are the 5 questions to ask when determining if we can give a CPUS?

A
  • verify the patient details
  • eligible? (registered with Scottish GP)
  • establish a need- why do we have to give
  • supply quantity- verify the dose
  • clinical assessment of patient- on anything else?
44
Q

how long should we give on CPUS of antidepressants??

A
  • probs only 7 days as they need a review at dr
  • would give more if for example going on holiday
45
Q

what is the definition of heart failure?

A

characterized by impaired cardiac pumping such that heart is unable to pump adequate amount of blood to meet metabolic needs

46
Q

what kind of heart failure is associated with
- Blood backing up through left atrium into pulmonary veins
- Pulmonary congestion and oedema

A

left sided congestive heart failure

47
Q

what kind of heart failure is associated with pulmonary hypertension?

A

right sided congestive heart failure

48
Q

what kind of heart failure is the most common?

A

left sided congestive heart failure

49
Q

what kind of heart failure is likely to occur after heart injury such as MI?

A

acute heart failure- emergency situation

50
Q

does preload increase or decrease with increased blood volume and vasoconstriction?

A

pre load increases

51
Q

does preload increase or decrease with decreased blood volume and vasodilation?

A

decreases

52
Q

which law describes the relationship between preload and cardiac output?

A

starlings law

53
Q

what does stretching muscle fibres in the heart do to the force of contraction?

A

increases it up to a point before the fibres become overstretched and the force of contraction is reduced

54
Q

define after load

A

the resistance against which is the ventricle must pump

55
Q

define pre load

A

the amount of fibre stretch in the ventricles at the end of diastole- before the next contraction

56
Q

does contractility increase or decrease with infarcted tissue and ischemic tissue?

A

decreases

infarcted= no contractile strength
ischemic= reduced contractile strength

57
Q

does contractility increase or decrease with positive inotropes ?

A

increases

58
Q

does cardiac output increase of decrease with vasoconstriction? why?

A

decreases CO- as it increases resistance against which the heart has to pump (increases afterlaod)

59
Q

does cardiac output increase or decrease with sodium and water retention? why?

A

decreases cardiac output
Increase fluid volume- which increases preload – if too much stretch (too much fluid) will be a decreased strength of contraction

60
Q

does cardiac output increase of decrease with tachycardia? why?

A

decreases CO

decreases diastolic filling time- decreasing ventricular filling- decreasing stroke volume and cardiac output

61
Q

name 5 drug groups used in treatment of heart failure

A
  • ACE inhibitor
  • beta blocker
  • aldosterone antagonist (spironolactone)
  • diuretics
  • vasodilators
62
Q

how do clots form when a plaque ruptures?

A

when plaque ruptures it exposes the fatty plaque- this is not recognised by the body and it thinks it is a hole- this triggers the clotting cascade and so a blood clot forms in the artery- depending on the size of the clot - can cause STEMI and NSTEMI

63
Q

when is troponin released?

A

in response to cellular death - ie when heart tissue is starved of oxygen too long so it dies

64
Q

why do we check troponin levels after 2 hours and also a few hours later (after first check) ?

A

troponin is raised 2 hours after chest pain begins- we check to see if cellular death- ie MI has occured- we check again just incase we checked too quickly the first time- some patients may not give an accurate time for the beginning of chest pain

65
Q

what is the second anti-platelet given in MI patients? what is its dose?

A

ticagrelor- loading dose of 180mg then 90mg BD

66
Q

how long should double anti-platelet therapy be given?

A

6 months to 1 year post MI
then ticagrelor can be stoped

67
Q

why is double anti-platelet therapy stopped after 6 months to 1 year?

A

increased risk of GI bleeding/ ulceration with no added cardiac benefit

68
Q

what drug group dissolves blood clots?

A

thrombolytics

69
Q

why are beta blockers contraindicated in asthmatic patients?

A

there are beta 2 receptors in the lungs- salbutamol is a beta agonist-
beta blockers cause bronco-constriction- making asthma worse

70
Q

name one side effect of ticagrelor

A

breathlessness

71
Q

name one side effect of ramipril

A

cough (all ACE I’s)

72
Q

name one side effect of statins

A

muscle pain

73
Q

name two side effects of GTN spray

A

headache, facial flushes

74
Q

name two side effects of beta blockers

A

tiredness
cold hands etc

75
Q

councelling point for both aspirin and ticagrelor

A

take with food to avoid GI upset

76
Q

when giving a beta blocker as treatment for angina- what do we want to patient’s heart rate to be?

A

60 bpm ±5 beats

77
Q

describe the interaction between doxycycline and milk, iron, antacids or zinc

A

ions bind irreversibly to doxycycline- causes chelation (a big un-dissolvable blob) meaning there is no absorption

78
Q

what effect does an enzyme inhibitor have on metabolism of a drug ?

A

if the enzyme responsible for metabolism of a rug is inhibited then the effects of the drug will be prolonged

79
Q

what is the maximum simvastatin dose when given with amlodipine?

A

20mg daily

80
Q

what effect does an enzyme inducer have on metabolism of a drug ?

A

drug is over metabolised and levels are too low to exert a clinical effect

81
Q

what drugs cannot be given with lithium- why?

A

any anti-inflammatory such as ibuprofen
this is due to preferential excretion- the body excretes the anti-inflammatory first and so lithium levels remain too high - toxic effects

82
Q

what kind of drug interaction causes drug level changes?

A

pharmacokinetic

83
Q

what kind of drug interaction causes drug effect changes?

A

pharmacodynamic- no change in drug level

84
Q

what antibiotic group interact with statins?

A

macrolides

85
Q

how long can echinacea be used for?

A

no more than 10 days

86
Q

how does grapefruit interact with statins?

A

grapefruit inhibits CYP450 enzymes -which are required for metabolisation of statins

87
Q

how does glucosamine interact with warfarin?

A

it enhances the anticoagulant effect of warfarin so these should be avoided together

88
Q

which statins interact with grapefruit?

A

simva and atorva

89
Q

Immature RBCs (reticulocytes) are continually released; what is the expected reticulocyte count in a FBC?

A

0.5-1.5%

90
Q

what is the most common anaemia caused by?

A

iron deficiency

91
Q

Symptoms of anaemia in men arise when compensatory responses to tissue hypoxia fail and usually develop when Hb falls below what?

A

10g/ dL

92
Q

Melena is associated with anaemia due to what?

A

occult blood loss (meaning we can’t see it ie internal bleeding like GI)

93
Q

b12 and folate are required for synthesis of what?

A

DNA

94
Q

Serum bilirubin and LDH can help differentiate between haemolysis and blood loss BECAUSE what?

A

both are elevated in haemolysis and normal in acute/ chronic blood loss

95
Q

Blood lose, haemolysis and red blood cell production deficiency can all attribute to what?

A

anaemia

96
Q

Increased serum bilirubin and LDH concentrations can help differentiate between which causes of anaemia ?

A

haemolysis and blood loss

97
Q

what could Peripheral neuropathy in a patient with anaemia indicate

A

vitamin b12 deficiency

98
Q

About 50% of patients with Deep Vein Thrombosis also have what?

A

occult pulmonary emboli

99
Q

what test is used to diagnose DVT?

A

D-Dimer test

mpharm year 3 sem 2 (11 decks)

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