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DDT > trigger 3 - hypertrophic cardiomyopathy > Flashcards

trigger 3 - hypertrophic cardiomyopathy Flashcards

1
Q

bundles of what make up cardiac myocytes

A

myofibrils

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2
Q

sarcomeres

A

repeating units making up myofilaments
region between two Z-lines
composed of thick and thin filaments

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3
Q

myosin ATPase

A

enzyme that hydrolyses ATP required for actin and myosin cross-bridge formation

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4
Q

3 proteins that make up thin filaments

A

actin
tropomyosin
troponin

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5
Q

troponin complex

A

attached to tropomyosin

contains troponin C - binding site for calcium

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6
Q

when calcium binds to troponin C…

A

conformational change in troponin complex

myosin head exposed

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7
Q

length-dependent activation

A

stretching the sarcomere increases the affinity of Troponin-C (TNC) for Ca2+

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8
Q

types of cardiac action potential

A

non-pacemaker A.P. - fast response

pacemaker A.P. - slow response

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9
Q

where are pacemaker action potentials found

A

sinoatrial node

atrioventricuar node

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10
Q

compare length of duration of between neural/skeletal APs and cardiac APs

A 
neural = 1 ms
skeletal = 2-5 ms

cardiac = 200-400 ms

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11
Q

compare role of Calcium in depolarization of neural/skeletal APs to cardiac APs

A

depolarisation of:

neural/skeletal: - caused by opening of Na+ channels

non-pacemaker cardiac: - caused by opening of Na channels, Ca influx prolongs duration of AP causing plateau phase

pacemaker cardiac: - Ca2+ involved in initial depolarisation

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12
Q

3 examples of non-pacemaker action potentials in the heart

A

purkinje cells
atrial myocytes
ventricular myocytes

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13
Q

phase 4

non-pacemaker AP

A

resting membrane potential = -90mV
K+ channels are open - K+ leaves cell making it more negative inside
both fast Na channels and slow L-type Na channels are closed

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14
Q

phase 0

non-pacemaker AP

A 
rapid depolarisation (by AP in adjacent cell)
-70mV
Na+ influx through fast Na+ channels
K+ channels close
membrane potential gets more positive
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15
Q

phase 1

non-pacemaker AP

A

(small rapid dip after peak on graph)

initial re-polarisation
opening of special/transient K+ channels
short-lived outward K+ hyperpolarisation

however, Ca influx through slow channels delays this repolarisation

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16
Q

phase 2

non-pacemaker

A

plateau phase

Ca2+ influx through long-lasting L-type channels
open when membrane depolarises to -40mV

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17
Q

phase 3

non-pacemaker

A

repolarisation

K+ efflux
Ca2+ channels inactivation

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18
Q

maintenance of resting membrane potential in cardiac

A

K+ channels open - K+ leaves cell making it more -ve

Na+ and Ca2+ channels closed, cannot enter cell

-90mV

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19
Q

antiarrythmic drugs

A

alter fast-response action potentials
alter (ERP) - effective refractory period
block specific ion channels

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20
Q

effective refractory period (ERP)

A

stimulation of cell cannot initiate action potential
during phases 0, 1, 2, 3, and early 4

fast Na channels close and stay inactivated after phase 1

protects the heart by preventing multiple APs
at a high HR, the rate would be unable to properly fill and ventricular ejection would reduce

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21
Q

non-pacemaker cells to pacemaker cells

A

they can transform under certain conditions

e.g. hypoxia, membrane depolarisation, fast Na channels close
Ca2+ still influxing - same as pacemaker

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22
Q

no true resting membrane potential

A

pacemaker action potentials

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23
Q

why is depolarisation slow in pacemaker cells

A

no fast Na+ channels

depolarisation current carried by slow Ca2+ influx

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24
Q

3 phases of SA node action potentials

A

0, 3, 4

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25
Q

phase 4

pacemaker

A

spontaneous depolarisation

triggers action potential once threshold potential is reached (-30/-40mV)

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26
Q

phase 0

pacemaker

A

depolarisation phase

incline on graph

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27
Q

phase 3

pacemaker

A

repolarisation
(decline on graph)

complete repolarisation = around -60mV

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28
Q

phase 3 to phase 4

pacemaker

A

when -60mV (repolarisation) has been reached

slow Na+ channels open creating ‘funny current’ and Na+ influx

cause membrane to spontaneously depolarise and initiate phase 4

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29
Q

T-type (transient) Ca2+ channel

pacemaker

A

opens when membrane potential reaches -50mV during depolariation

influx of Ca2+ causes more depolarisation of membrane to -40mV

causes L-Type Ca2+ channels to open

more Ca2+ influx causes membrane to reach threshold potential (-30/-40mV)

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30
Q

what kind of state is necessary for pacemaker cells to become activated

A

hyperpolarised

-ve voltage needed at end of phase 3

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31
Q

cause of phase 0 depolarisation

pacemaker

A

mainly by increased conductance of Ca2+ through L-type Ca2+ channels that open near the end of phase 4

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32
Q

what happens to ‘funny’ and T-type Ca2+ channels near the end of phase 4 (initial depolarisation of pacemaker)

A

funny currents decline - Na channels close

Ca2+ currents through T-type channels decline - channels close

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33
Q

penetrance

A

probability that a person carrying a disease-associated genotype will develop the disease within a given time period

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34
Q

penetrance calculation

A

number of individuals displaying symptoms, divided by the number of individuals with a disease causing mutation x 100

35
Q

incomplete penetrance

A

when thenumber of individuals who display clinical features of the condition is less than those who carry the mutation.

36
Q

complete penetrance

A

if a person carrying a disease-associated genotype always develops the conditon

37
Q

expressivity

A

measures the extent to which a given genotype is expressed at the phenotypic level

38
Q

physical symptoms of cardiomyopathy

A 
fatigue 
dizzyness - reduced O2 to the brain
breathlessness - fluid build up around lungs
chest pains - reduced O2 to the heart
unusual heart beat - palpatations
39
Q

hypertrophic cardiomyopathy

A

ventricle walls become thicker (mainly left and septum)
muscle cells are in disarray - disorganised

stiffness make it harder to relax and fill with blood and contract and pump blood out

40
Q

HOCM

A

hypertrophic obstructive cardiomyopathy

if the thickening of the heart muscle obstructs blood flow out of the heart

41
Q

causes of HCM

A

single genetic mutation

42
Q

inheritance pattern of HCM

A

autosomal dominant

mutated gene is found on a non-sex chromosome

43
Q

beta-blockers and HCM

A

can prevent arrhythmias

reduce symptoms of obstruction

44
Q

ICD

A

Implantable Cardioverter Defibrillator

detect and correct any dangerous arrhythmias
- could cause cardiac arrest

45
Q

ARVC - Arrhythmogenic Right Ventricular Cardiomyopathy

A

disorder of the myocardium (heart muscle wall)
parts of myocardium break down over time - increase risk of abnormal heart beat

proteins that make up desmosomes affected

46
Q

autosomal dominant with variable penetrance

A

the child of an affected parent will have 50% chance of inheriting the abnormal gene, but will not then necessarily go on to have the condition

47
Q

MRI

A

magnetic resonance imaging

48
Q

why may MRI need to be used instead of ECG for diagnosis of ARVC

A

signs on an echocardiogram can be very subtle in the early stages of the condition

49
Q

ablation

A

if medication doesnt seem to work, the part of the heart causing palpations is targeted and cauterised using wires passing through the heart

50
Q

mechanism to prevent sudden cardiac death

A

implantable cardiac defribrillator (ICD)

51
Q

describe the contractions of vascular smooth muscle (VSM)

A

slow, sustained and tonic (maintained for a few mins)

52
Q

describe cardiac muscle contractions

A

rapid and short duration

53
Q

MLCK

A

myosin light chain kinase

enzyme that phosphorylates myosin light chains in the presence of ATP (leads to cross-bridge formation between myosin heads and actin)

54
Q

noradrenaline from sympathetic nerve binds to which receptors in the heart?

A

beta-1 and beta-2

55
Q

acetylcholine from parasympathetic nerve binds to which receptor type in the hearT?

A

M2

56
Q

P wave on ECG (first small hump)

A

atrial depolarisation

trigger for heart contraction

57
Q

QRS complex

A

ventricle depolarisation

58
Q

bradychardia

A

slow HR

59
Q

why is efficiency so important in economic evaluation (why are health heed and effectiveness not enough?)

A

scarcity of resources

60
Q

3 main types of economic evaluation

A
  1. cost-effective analysis (CEA)
  2. Cost-utiltiy analysis (CUA)
  3. Cost-benefit analysis (CBA)
61
Q

cost-effective analysis

A

effectiveness measured in natural units

e.g. £ per case detected

62
Q

cost-utility analysis

A

effectiveness measured in preference-based units

£ per Quality-Adjusted Life-Year (QALY)

63
Q

cost benefit analysis

A

effectiveness also measured and valued in £

net benefit in £

64
Q

QALY

A

quality adjusted life year

measure of diseased burden on quality and quantity of life

65
Q

morbidity

A

quality of life

66
Q

what should you state to make a good economic evaluation

A

the perspective of the analysis
e.g. patient, patient’s family, primary care, health system,
society

67
Q

sensitivity analysis

A

to see if the results are sensitive to different assumptions

vary input variables or assumptions

68
Q

why might false-positives occur?

A

sample contamination

69
Q

advantage of direct detection methods

A

good for multicoloured labelling
- less prone to non-specific background labelling

fewer steps

70
Q

limitation of direct detection

A

lower sensitivity

requires primary antibody to be specifically labelled

71
Q

advantage of indirect detection

A

higher sensitivity

more versatile

72
Q

immunoglobulin

A

antibody e.g. IgG

73
Q

antigens

A

proteins or polysacchardies within or on the surface of cells

74
Q

what makes immunnohistochemistry so precise

A

antibodies bind specifically to the antigen that triggered the antibody’s pr

75
Q

direct detection method

A

antibody attached directly to indicator molecule e.g. fluorescent molecules or HRP enzyme

excess added washed away

substrate added to localise reaction

76
Q

indirect method

A

primary antibody added first e.g. IgG - binds to and recognises antigen of interest

excess antibody washes away

a linking antibody added to mixture - recognises the primary antibody - retains one antigen binding site

substrate added to localise reaction

77
Q

why is PCR important in diagnosis

A

early stages of processing DNA for sequencing

do detecting the presence or absence of a gene to help identify pathogens during infection

78
Q

3 steps of PCR

A
  1. denaturing - break H-bonds in double-helix
  2. annealing - lower the temp to enable primers to attach by H-bonds to template DNA
  3. extension - raise temp and new DNA is made- taq DNA polymerase enzyme
79
Q

why is electrophoresis used after PCR

A

to check the quantity and size of DNA fragments produced

80
Q

Taq DNA polymerase enzyme

A

adds DNA bases to the template strand in 5’ to 3’ direction

taken from thermophilic bacteria - thermus aquaticus

stable at high tempertures

optimum temp = 72

81
Q

5 steps of traditional cloning methods

A
  1. vector preparation
  2. insert preparation
  3. ligation
  4. transformation
  5. colony screening
82
Q

vector preparation

A

restriction enzymes digested by vector (plasmid)

dephosphorylation of vector prevents self-ligation

‘sticky ends’ - more compatible

purification of desired fragments recommended for successful ligation

83
Q

insert preparation

A

restriction digestion

blunt end creation

purification

DDT (12 decks)

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