week 3 Flashcards
1
Q
what is erythropoiesis?
A
red blood cell production
2
Q
what stimulates erythropoiesis?
A
hypoxia
3
Q
what hormone controls erythropoiesis and where is that synthesised?
A
erythropoietin
kidneys
4
Q
what is hemolysis?
A
destruction of red blood cells
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)
6
Q
name 6 symptoms of iron deficiency anaemia
A
- pallor (colour)- most common
- glossitis
- fissures of lips
- sensitivity to cold
- weakness
- fatigue
7
Q
name 6 symptoms of cobalamin deficiency
A
- sore tongue
- anorexia
- weakness
- pins and needles
- altered thought process
- confusion
8
Q
are myocytes fast or slow depolarising cells?
A
fast
9
Q
are pacemaker cells fast or slow depolarising cells?
A
slow
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
11
Q
in the relative refractory period, can cells be re-excited?
A
yes
12
Q
is vagal stimulation parasympathetic or sympathetic
A
parasympathetic
13
Q
how does vagal stimulation affect resting potential an pacemaker cells?
A
makes resting potential more negative
makes pacemaker current slower
14
Q
are catecholamines sympathetic or parasympathetic
A
sympathetic
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
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
17
Q
what are class II anti arrhythmic drugs?
A
ß-adrenoceptor antagonists (atenolol, sotalol)- rate control
18
Q
what are class III anti arrhythmic drugs?
A
prolong action potential and prolong refractory period (suppress re-entrant rhythms) (amiodarone, sotalol)
19
Q
what are class IV anti arrhythmic drugs?
A
Calcium channel antagonists. Impair impulse propagation in nodal and damaged areas (verapamil)
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
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
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
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
24
Q
in what circumstance would we withhold digoxin from an arrhythmia patient?
A
when heart rate is less than 40 bpm
25
what is acute coronary syndrome? (3)
- unstable angina
- NSTEMI
- STEMI
26
define unstable angina
an unprovoked (at rest) or prolonged (not helped by GTN) episode of chest pain- raising suspicion of acute MI
27
management of ACS (4)
think MONA
- morphine 5-10mg slow IV + metoclopramide 10mg IV
- oxygen (if required <94%)
- nitrates (GTN- IV infusion)
- aspirin 300mg
- fonduparinux 2.5mg SC
28
what is a GRACE score?
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
29
name the 7 early (<72h) complications of ACS
- death
- cardiogenic shock
- heart failure
- ventricular arrhythmia
- myocardia rupture
- thromboembolism
- pericarditis (extremely painful inflammation)
30
name the 6 later complications of ACS
- ventricular wall rupture
- valvular regurgitation
- ventricular aneurisms
- cardiac tamponade
- dresslers syndrome
- thromboembolism
31
what is epleronones indication and dose ?
Left ventricular systolic dysfunction EF<40%
start on 25mg- can go up to 50mg
32
side effects of ACE inhibitors
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)
33
name a contraindication of beta blockers
asthmatics
34
first line for managing stable angina
beta blocker ie bisoprolol 5mg daily
35
name one contraindication of calcium channel blockers in management of stable angina
beta blocker + rate limiting calcium channel blocker- makes heart too slow- patient dies (diltiazem or verapamil)
36
name 2 rate limiting calcium channel blockers
diltiazem or verapamil
37
when should isosorbide mononitrate doses be taken? why is this?
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
38
how do potassium channel activators work in stable angina?
they have arterial and venous vasodilation properties
3rd/ 4th line
39
name 3 side effects of potassium channel activators
- ulcers- almost whole GIT can be affected
- headache
- palpitations
40
how does ivabradine work in stable angina management?
it lowers the heart rate by affecting the SA node
however not effective in patients with atrial fibrillation
41
compliance vs concordance vs adherence
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
what are the GTN rules?
- 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
what are the 5 questions to ask when determining if we can give a CPUS?
- 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
how long should we give on CPUS of antidepressants??
- probs only 7 days as they need a review at dr
- would give more if for example going on holiday
45
what is the definition of heart failure?
characterized by impaired cardiac pumping such that heart is unable to pump adequate amount of blood to meet metabolic needs
46
what kind of heart failure is associated with
- Blood backing up through left atrium into pulmonary veins
- Pulmonary congestion and oedema
left sided congestive heart failure
47
what kind of heart failure is associated with pulmonary hypertension?
right sided congestive heart failure
48
what kind of heart failure is the most common?
left sided congestive heart failure
49
what kind of heart failure is likely to occur after heart injury such as MI?
acute heart failure- emergency situation
50
does preload increase or decrease with increased blood volume and vasoconstriction?
pre load increases
51
does preload increase or decrease with decreased blood volume and vasodilation?
decreases
52
which law describes the relationship between preload and cardiac output?
starlings law
53
what does stretching muscle fibres in the heart do to the force of contraction?
increases it up to a point before the fibres become overstretched and the force of contraction is reduced
54
define after load
the resistance against which is the ventricle must pump
55
define pre load
the amount of fibre stretch in the ventricles at the end of diastole- before the next contraction
56
does contractility increase or decrease with infarcted tissue and ischemic tissue?
decreases
infarcted= no contractile strength
ischemic= reduced contractile strength
57
does contractility increase or decrease with positive inotropes ?
increases
58
does cardiac output increase of decrease with vasoconstriction? why?
decreases CO- as it increases resistance against which the heart has to pump (increases afterlaod)
59
does cardiac output increase or decrease with sodium and water retention? why?
decreases cardiac output
Increase fluid volume- which increases preload – if too much stretch (too much fluid) will be a decreased strength of contraction
60
does cardiac output increase of decrease with tachycardia? why?
decreases CO
decreases diastolic filling time- decreasing ventricular filling- decreasing stroke volume and cardiac output
61
name 5 drug groups used in treatment of heart failure
- ACE inhibitor
- beta blocker
- aldosterone antagonist (spironolactone)
- diuretics
- vasodilators
62
how do clots form when a plaque ruptures?
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
when is troponin released?
in response to cellular death - ie when heart tissue is starved of oxygen too long so it dies
64
why do we check troponin levels after 2 hours and also a few hours later (after first check) ?
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
what is the second anti-platelet given in MI patients? what is its dose?
ticagrelor- loading dose of 180mg then 90mg BD
66
how long should double anti-platelet therapy be given?
6 months to 1 year post MI
then ticagrelor can be stoped
67
why is double anti-platelet therapy stopped after 6 months to 1 year?
increased risk of GI bleeding/ ulceration with no added cardiac benefit
68
what drug group dissolves blood clots?
thrombolytics
69
why are beta blockers contraindicated in asthmatic patients?
there are beta 2 receptors in the lungs- salbutamol is a beta agonist-
beta blockers cause bronco-constriction- making asthma worse
70
name one side effect of ticagrelor
breathlessness
71
name one side effect of ramipril
cough (all ACE I's)
72
name one side effect of statins
muscle pain
73
name two side effects of GTN spray
headache, facial flushes
74
name two side effects of beta blockers
tiredness
cold hands etc
75
councelling point for both aspirin and ticagrelor
take with food to avoid GI upset
76
when giving a beta blocker as treatment for angina- what do we want to patient's heart rate to be?
60 bpm ±5 beats
77
describe the interaction between doxycycline and milk, iron, antacids or zinc
ions bind irreversibly to doxycycline- causes chelation (a big un-dissolvable blob) meaning there is no absorption
78
what effect does an enzyme inhibitor have on metabolism of a drug ?
if the enzyme responsible for metabolism of a rug is inhibited then the effects of the drug will be prolonged
79
what is the maximum simvastatin dose when given with amlodipine?
20mg daily
80
what effect does an enzyme inducer have on metabolism of a drug ?
drug is over metabolised and levels are too low to exert a clinical effect
81
what drugs cannot be given with lithium- why?
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
what kind of drug interaction causes drug level changes?
pharmacokinetic
83
what kind of drug interaction causes drug effect changes?
pharmacodynamic- no change in drug level
84
what antibiotic group interact with statins?
macrolides
85
how long can echinacea be used for?
no more than 10 days
86
how does grapefruit interact with statins?
grapefruit inhibits CYP450 enzymes -which are required for metabolisation of statins
87
how does glucosamine interact with warfarin?
it enhances the anticoagulant effect of warfarin so these should be avoided together
88
which statins interact with grapefruit?
simva and atorva
89
Immature RBCs (reticulocytes) are continually released; what is the expected reticulocyte count in a FBC?
0.5-1.5%
90
what is the most common anaemia caused by?
iron deficiency
91
Symptoms of anaemia in men arise when compensatory responses to tissue hypoxia fail and usually develop when Hb falls below what?
10g/ dL
92
Melena is associated with anaemia due to what?
occult blood loss (meaning we can't see it ie internal bleeding like GI)
93
b12 and folate are required for synthesis of what?
DNA
94
Serum bilirubin and LDH can help differentiate between haemolysis and blood loss BECAUSE what?
both are elevated in haemolysis and normal in acute/ chronic blood loss
95
Blood lose, haemolysis and red blood cell production deficiency can all attribute to what?
anaemia
96
Increased serum bilirubin and LDH concentrations can help differentiate between which causes of anaemia ?
haemolysis and blood loss
97
what could Peripheral neuropathy in a patient with anaemia indicate
vitamin b12 deficiency
98
About 50% of patients with Deep Vein Thrombosis also have what?
occult pulmonary emboli
99
what test is used to diagnose DVT?
D-Dimer test
