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Semester 2 Case Studies > Case 4 > Flashcards

Case 4 Flashcards

1
Q

what is clinical heart failure

A

a state in which the cardiac output fails to meet the body’s demands. extracellular fluid composition and movement off fluid between compartments

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2
Q

what is the extracellular fluid divided into

A

plasma and interstitial

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3
Q

how much of the body is made up of fluid

A

60%

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4
Q

what are the two phases of fluid movement

A
  1. the blood and associated plasma

2. movement from capillaries into interstitial fluid or space

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5
Q

what is the composition of ECF

A
  • na+
  • cl-
  • HCO3-
  • glucose
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6
Q

how much of the ECF is plasma

A

1/5

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7
Q

how far away are cells in the body from capillaries

A

50um

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8
Q

How do water molecules pass through the capillary

A

pores and will include ions like sodium and chloride

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9
Q

how does water move

A

area of high concentration to an area of low concentration

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10
Q

what does the capillary pressure do

A

tends to drive fluid out from the capillary

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11
Q

what is capillary pressure opposed by

A

interstitial fluid pressure which Is usually lower and in fact is sub atmospheric

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12
Q

what does capillary pressure push out

A

water

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13
Q

what does colloid pressure do

A

pulls water into the capillary

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14
Q

what pulls water into the capillary

A

plasma proteins, largely albumin pulling water towards them

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15
Q

what is colloid pressure opposed by

A

interstitial fluid colloid pressure

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16
Q

how big is the interstitium

A

1/6 of the body’s volume,e

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17
Q

what has the interstitium got in it

A

loosely packed proteins, things like collagen fibre bundles and proteoglycan filaments

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18
Q

what consistency is the interstitium

A

gel like consistency

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19
Q

components of intracellular fluid compartment

A
  • K+
  • Mg++
  • Phosphates
  • Proteins
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20
Q

why do proteins draw on ions such as sodium and potassium

A

because proteins are negatively charged and sodium and potassium are positively charged and water follows them into the cell

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21
Q

what is required for active transport

A

kinetic energy

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22
Q

what molecules can cross the lipid bilayer freely

A

fat soluble molecules

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23
Q

what channel proteins transport water into the cell

A

aquaporines, they have a pore inside them which allows water molecules to traverse the cell membrane in single file. red blood cell has aquaporins in it

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24
Q

what are the factors impacting diffusion

A
  1. concentration
  2. charge - ions are negatively charged and inside membrane is positively charged.
  3. pressure affects movement of substances (capillaries and interstitial space)
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25
Q

what is the protein involved in facilitated diffusion

A

carrier proteins that are specific to substances and bind, allowing them to diffuse form one side of the membrane to another after going through a conformational change.

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26
Q

what is the rate limiting factor in facilitated diffusion

A

the carrier protein needs to change shape twice

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27
Q

what is the max rate of transportation denoted as

A

Vmax

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28
Q

how many potassiums does the Na-K-ATPase pump bind to

A

2 potassiums

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29
Q

how man sodiums does the Na-K-ATPase pump bind to inside the cell

A

3 sodiums

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30
Q

what activates the ATP pump

A

binding of potassium and sodium

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31
Q

what is the ATP pump function

A

breaks down adenosine triphosphate which is a high energy phosphate substance

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32
Q

what does the ATP pump break adenosine triphosphate into

A

adenosine diphosphate and a phosphate ion

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33
Q

what does the ATP pump release

A

energy

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34
Q

does the ATP channel go under a conformation change by using energy

A

yes

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35
Q

what does the conformational change do in the ATP pump

A

makes 3 sodium leave the cell and 4 potassium enter the cell

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36
Q

why does the inside of the cell membrane become negatively charged in ATP channel

A

there is a net loss of one positive ion every time

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37
Q

what does losing one sodium ion result in in the ATP pump channel

A

allows some water to follow it from the inside to outside of the cell. partly responsible for it not bursting

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38
Q

what 3 things regulate the cardiac output

A

Frank Sterling, Autonomic nervous system, endocrine system also

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39
Q

cascade of events if patient has a heart attack and develops important amounts of damage to left ventricle

A

Left ventricle pumps blood to the systemic circulation normally, so if there is significant amount of damage to it, this will reduce the amount blood it pumps and reduce the cardiac output
Output of the heart will not be sufficient to reach body’s needs (stroke volume)
Causes a reduction in systemic blood pressure which the body will sense
Because forward force is reduced, the heart is not getting rid of the blood that is inside the left ventricle
The blood is stagnating there and makes it difficult for blood to enter the left ventricle because forward flow is poor
This cause the pressure in the left atrium to increase, which normally of loads its blood into the left ventricle
Blood that wants to return into the left atrium from the lungs also struggles to enter as pressure is increased
Creates a back flow of pressure
The right ventricle is pumping against an increased pressure, and the right atrium is also increased in pressure
Difficult for blood to return into the heart from inferior and superior vena cava because of pressure in right ventricle

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40
Q

what is the neurohormonal response to a reduced cardiac output

A
  • sympathetic nervous system
  • RAAS
  • ADH
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41
Q

What receptors detect low blood pressure

A

baroreceptors

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42
Q

where are the baroreceptors found

A

aortic arch and carotid Sinus

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43
Q

which nerves do the baroreceptors send signals via

A

the vagus and glossopharyngeal nerves

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44
Q

when the vasomotor sends signals to the heart to increase heart rate how many times is the cardiac output increased

A

2-3 fold

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45
Q

what else does sympathetic activation cause

A

innervates the vasculature and causes vasoconstriction in the arteries and veins and also increases the blood pressure

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46
Q

RAAS mechanism

A
  • renin is released by the kidneys in response to decreasing blood pressure
  • vasoconstriction
  • salt and water retention increases circulating volume in the body
  • chronic activation results in progressive water retention
  • increasing circulating volume should increase stretch of the heart muscle
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47
Q

what does angiotensinogen form

A

angiotensin 1

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48
Q

what does angiotensin II lead to

A
  • renal retention of salt and water
  • vasoconstriction
  • angiotensinase
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49
Q

what enzyme converts angiotensin I to angiotensin II

A

ACE

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50
Q

where is ADH released from

A

posterior pituitary

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51
Q

what does ADH result in

A

fluid retention, thirst and dilution of the blood

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52
Q

what does activation of SNS in heart attack lead to

A

increased heart rate and increased myocardial contractility

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53
Q

what do SNS and RAAS lead to

A

vasoconstriction

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54
Q

what do AHD and RAAS lead to

A

ECF expansion

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55
Q

what causes natriuretic peptides

A

increased myocardial stretch

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56
Q

example of a natriuretic peptide

A

BNP

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57
Q

function of BNP

A

passes sodium into urine which causes loss of salt and water which counteracts fluid expansion

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58
Q

what does BNP cause

A

vasodilation - counteracts vasoconstriction which is damaging to heart in long run

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59
Q

what is maladaptive process

A

chronic fluid retention

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60
Q

what does chronic fluid retention lead to

A
  1. no further improvement in the cardiac output
  2. increased workload on already damaged heart
  3. pulmonary and peripheral oedema
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61
Q

mechanism of oedema

A
  • back flow of pressure and venous pressures eventually increase causing an increase in the capillary pressure which will tend to cause more fluid to filtrate out of the capillaries
  • also more circulating volume, salt and water retention, which will again cause more fluid to cross capillary membrane
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62
Q

why is oedema common in lower limbs

A
  • elevated venous pressure in legs due to gravity
  • pressure also elevated in the capillaries leading to leakage of fluid into the tissue spaces (oedema)
  • lowest limbs have highest capillary pressure
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63
Q

what does chronic sympathetic activation cause

A
  1. increased energy demand
  2. vasoconstriction: increased after load
  3. worsening schema
  4. apoptosis/necorisis of heart cells
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64
Q

what does chronic RAAS activation lead to

A
  1. hypertrophy of heart muscle
  2. fibrosis
  3. apoptosis
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65
Q

what gets rid of the fluid overload

A

diuretics

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66
Q

which layer is the heart formed in

A

the mesoderm

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67
Q

what does the ectoderm give rise to

A

skin and neural tissues

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68
Q

what does the mesoderm give rise to

A

most of the muscles

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69
Q

what does the endoderm give rise to

A

internal organs like GI tract

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70
Q

where is heart development visible

A

ventral surface

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71
Q

cardiac development summary

A

cardiac development begins with the initiation of structures called heart fields
These heart fields then converge at the midline of the embryo to form something called the cardiac crescent which assort of an ’n’ shaped structure in the embryo
Those cardiac crescent cells come together to form a linear heart tube
That tube goes under a series of morphological changes called looping so that it takes on the correct position within the embryo
It then further subdivides into the different chambers and we can see structures such as the cardiac cushions, form the valves, begin to develop within that tube
We also get grooves forming on the surface of the tube which will represent the premature or primitive formation of the chambers
Following these events we get the formation of the great vessels and the heart acquires the anatomy it needs for the adult

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72
Q

development of cardiac stages

A
  • cardiac cell fate acquired

- angiogenic cells located in cariogenic plate - cranial and lateral to neural plates

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73
Q

when is cardiac crescent developed

A

at 15 days post fertilisation

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74
Q

what are the two heart fields

A

primary and secondary

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75
Q

what is different about the secondary heart fields

A

they move into the heart and contribute to outflow tract and right ventricle cardiac structures

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76
Q

cardiac crescent fusion

A
  • cardiac crescent fuses at the mid-line to form the cardiac tube
  • elongate at the midline of the embryo
  • forms primary heart tube
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77
Q

when does linear heart tube form

A

21 days

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78
Q

where are ventricles and atria located in heart tube

A

developing ventricles are situated more cranial. atria is at the bottom of the tube and ventricle is in the mid region

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79
Q

what are the heart tube structures in order from top to bottom

A 
1 dorsal aorta 
2 aortic sac 
3 bulbus cordis 
4 primitive ventricle 
5 atrioventricular sulcus 
6 primitive atria 
7 sinus venous
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80
Q

when does cardiac looping occur

A

23-24 days

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81
Q

what does cardiac looping do

A

brings atria more upwards and behind the presumptive ventricle.

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82
Q

what shape is cardiac looping

A

dextral C-shape loop

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83
Q

what is heterotaxy

A

reversed orientation. if it happens to all organs - situs inversus then not necessarily pathological

84
Q

when does septation occur

A

weeks 4-9

85
Q

when does atrial septation occur

A

between 6th and 8th week post fertilisation

86
Q

are atrial septal defects asymptomatic

A

yes

87
Q

what does the foramen ovale do

A

allows transmission of blood between the right and left atrium. blood bypass the lungs

88
Q

what does the foremen ovale turn into

A

fossa ovalis

89
Q

how many people have a patent foremen ovale

A

10-20% of adults

90
Q

when does ventricular septation occur

A

7th to mid 9th wee

91
Q

AV valve formation

A
  • endocardial cushions precursors of the valves
  • important to prevent back flow
  • protrude into the heart tubes
  • mid 7th to 8th week post fertilisation
92
Q

what is the failure of separation of the aorta and pulmonary artery called

A

persistent truncus arterioisus

93
Q

what is a PTA

A

single artery arising from both ventricles

94
Q

what are the semilunar valves

A

the division between left ventricle and aorta and the division between the right ventricle and the pulmonary artery. prevent backflow

95
Q

what layer of the heart is the epicardium

A

outer epithelial layer of the heart

96
Q

what does the epicardium form from

A

precursor called proepicardium located below heart

97
Q

what to epicardial cells differentiate into

A

coronary smooth muscle, myocardial fibroblasts

98
Q

when are heart chambers and major vessels formed by

A

the 8th week

99
Q

what does ductus arterioisus do

A

connects pulmonary artery to aortic arch

100
Q

what does the ductus arteriosus form after birth

A

ligamentum arteriosum

101
Q

what promotes the closure of the ductus aeteriosus

A

increase in neonatal blood oxygen content and withdrawal of maternal prostaglandins promote closure

102
Q

how popular is patent ductus arterioles

A

occurs in 8/1000 premature births. 2/1000 full term births

103
Q

ratio of live births affected by congenital heart defects

A

1:125

104
Q

what is deletion syndrome

A

22q11.2 deletion syndrome

105
Q

how common is 22q11.2 syndrome

A

1 in 4000 births

106
Q

what happens in 22q11.2 syndrome

A

TBX1 loss contributes to cardiac defect phenotypes
TBX1 expressed in secondary heart field which gives rise to outflow tract
loss of TBX1 causes shortening of the outflow tract lacking septation

107
Q

how many CHD patients survive into adulthood

A

90%

108
Q

what does P wave show

A

depolarisation of the atria

109
Q

what does QRS complex show

A

depolarisation of the ventricles

110
Q

what does the T wave show

A

repolarisaion of the ventricles

111
Q

where are V1 and 2 placed

A

right ventricle

112
Q

where are V3 and 4 placed

A

ventricular septum

113
Q

where are V5 and 6 placed

A

anterior and lateral wall left ventricle

114
Q

what lead is overall direction

A

lead one

115
Q

overall direction of electricity is which lead

A

lead 3

116
Q

overall activity electric is which lead

A

lead 2

117
Q

what does atrial fibrillation look like on an ECG

A

no P waves

118
Q

how often does the heart beat per day

A

70bpm

119
Q

what are the contractile working cells of the heart

A

the cardiac myocytes

120
Q

what is the role of the cardiomyocyte

A

to contract in unison in order to provide effective pump action to ensure adequate blood perfusion of the organs and tissues

121
Q

size of cardiomyoctres

A

approx 100mmx20mm

122
Q

how much of Total cell number are cardiomyoctes

A

30-40%

123
Q

what transmit ionic currents from one cell to another

A

gap junctions

124
Q

what are gap junctions made uo of

A

six connexin sub-units which form a hollow tube known as a connexon

125
Q

what glues the cells together

A

desmosomes

126
Q

what spans the gap between the cell membranes

A

glycoproteins called cadherins and design form the intermediate filaments

127
Q

sarcolemma

A

membrane surrounding the cardiomyocyte

128
Q

what are the contractile proteins

A

actin and myosin

129
Q

what is the contractile unit of the cardiomyocye

A

sarcomere

130
Q

what are attached to the actin filaments

A

Z-lines

131
Q

what are the thick filaments

A

myosin

132
Q

what colour do alpha actinic Z lines turn

A

green

133
Q

what colour do connexin 43 gap junctions tuen

A

blue

134
Q

what do the T-tubules do

A

transmit electrical stimulus rapidly into the interior of the cell to promote the synchronous activation of the whole depth of the cell despite the fact that the signal to contract is relayed across the external membrane

135
Q

why does systolic Ca2+ have to be high

A

to activate the contractile machinery in order to pump blood from the heart

136
Q

what triggers contraction

A

a rise in intracellular ca2+ in the cardiomyocte

137
Q

what is an action potential

A

transient depolarisation of a cell as a result of an ion channel activity

138
Q

relationship between action potential and contraction

A

1 voltage gated sodium channels open
2 Na+ inflow depolarises the membrane and triggers the opening of still more Na+ channels creating a positive feedback cycle and a rapidly rising membrane voltage.
3 Na+ channels close when the cell depolarises and the voltage peaks at nearly +30mV
4 Ca2+ entering through slow calcium channels prolongs the depolarisation of the membrane causing a plateau. plateau falls slightly because of some K+ leakage
5 Ca2+ channels close and Ca2+ is transported out of the cell. K+ channels open and rapid K+ outflow returns membrane to its resting potential

139
Q

how is the intracellular calcium concentration regular;ared

A

excitation-contraction coupling

140
Q

contractile mechanism

A
  • when calcium binds to cTnC it induces a rearrangement in the troponin-tropomyosin complex
  • movement of tropomyosin exposes a myosin binding site on actin resulting in cross bridge formation and shortening of the sacromere
141
Q

what is the cardiac cycle

A

the relationship between ventricular pressure and volume

142
Q

what is a murmur

A

abnormal blood flow across the heart valve or across a structure within the heart

143
Q

how is heart murmur diagnosed

A

auscultate and also can pick up with an echocardiogram

144
Q

aortic stenosis

A

aortic valve becomes heavily calcified with reduced opening so you can see the valve becomes thickened
Left ventricle has to become hypertrophy so has to push harder and harder
You get a muscley left ventricle, it doesn’t become bigger so you don’t get apical displacement
Thrusting apex
Abnormal blood flow is during systole because its when the heart is pumping
When blood is becoming turbulent and churned up by that thickened aortic valve
Systolic murmur and that is what we call a crescendo decrescendo

also would expect a low pulse pressure in severe cases
Second intercostal space mid clavicular line

145
Q

what are reasons for aortic stenosis

A
  • most commonly because of degenerative aortic valve disease

- secondly because being born with a bicuspid aortic valve

146
Q

aortic regurgitation

A

blood falls back into left ventricle during diastole
Diastolic murmur and difficult to hear

lub-dub-ahhh
Volume loading of the ventricle
Causes a dilatation of the left ventricle and displaced apex
Loudest on left sternal edge with evidence of apical displacement towards the axillary
Rapid downslope of the pulse, and when you feel it at the pulse its called a collapse pulse
Visible pulsation of the neck vessels

147
Q

what is corrigans sign

A

neck pulsation

148
Q

what is Beckers sign

A

retinal vessel pulsation

149
Q

what is de mussets sign

A

head bobbing in time with cardiac cycle

150
Q

what is duroziezs sign

A

diastolic murmur heard over femoral pulses when partly occluded below stethoscope

151
Q

what is muellers sign

A

uvula pulsation

152
Q

what is quinces sign

A

capillary pulsation in nail bed

153
Q

what is traubes sign

A

pistol shot systolic sound in femoral arteries

154
Q

what is endocarditis

A

infection of the heart valve

155
Q

mitral regurgitation

A

valve that sits between left aorta and ventricle
Instead of all blood going out of atrium during systole, blood flows back into the left atrium

systolic murmor
Hollow sytolic murmur; lub-wind-dub
Loudest in mitral area and radiate towards the axilla
Ventricle becomes volume loaded and apex becomes displaced

156
Q

functional mitral regurgitation

A

stretch left ventricle - the valve leaflets are pulled apart ams there’s a whole during systole in the valve

ischameic MR also, flopping of the valve
Heart attack of artery that supplied papillary muscle

hypertrophic obstructive cardiomyopathy
Genetic thickening of the heart muscle and when heart is in systole, the mitral leaflet is dragged towards the septum causing a leak in the. Mitral valve

157
Q

mitral stenosis

A

thickening of the mitral valve
Only cause really is rheumatic heart disease

mitral valve doesn’t open well and difficult to get blood into left ventricle
No problem with left ventricle - just not getting enough blood
Happening in diastole

158
Q

why is potassium such an important electrolyte

A

98% of K+ is inside cell

159
Q

what is normal range of potassium

A

3.5-5mM

160
Q

what happens when potassium gradient is disrupted

A

hyperkalemia

161
Q

what is hypokalaemia

A

low plasma K+ ( usually due to diuretics and excessive loss in urine)

162
Q

how does K+ alter cellular excitability

A

membrane potential of the cell determines cellular excitability. membrane potential is largely set by the gradient of K+ across the cell membrane

163
Q

what equation is used to find potassium gradient

A

Nernst equation

164
Q

what is the inactivation gate

A

h gate

165
Q

what is the activation gate

A

m gate

166
Q

is closure of h gate slow or fast

A

very slow

167
Q

what happens when h gate is closed

A

it is inactivated

168
Q

what are ion channels to stimulation

A

refractory

169
Q

basic Na+, Ca2+ channel structure

A
  • made of four subunits
  • each submit has 6 transmembrane spanning domains (S1-S6)
  • connected by a series of intra and extracellular loops
  • S4 is the end gate
  • link between S5 and S6 is the pore forming loop
170
Q

how are 4 domains linked

A

convalelty

171
Q

are potassium channels covalently linked

A

no so therefore can come from different potassium channel families. this is why they are so diverse in their function. they have a H gate but more like ball and chain

172
Q

structure of inward rectifier K+ channels

A
  • two transmembrane domains and pore forming loop
173
Q

what is Kir function

A

conduct ions out of the cell. allow K+ to move from inside to outside the cell and that is what sets the membrane resting potential

174
Q

what contributes to resting membrane potential

A

amount of negative charge needed to balance the concentration of K+ ion gradient is the equilibrium potential

175
Q

what happens to electrodes when there is an impermeable membrane

A

they will read 0

176
Q

what does Nernst equation predict K+ value of

A

-86mV

177
Q

why is resting membrane potential around 80mV

A

Ik1 is open as this is letting potassium out of the cell so membrane at rest is permeable to potassium,

178
Q

what is equilibrium potential of Na+

A

around 70mV

179
Q

what is the rate of depolarisation - phase 0 determined by

A

rate which Na enters the cell.

180
Q

what are phases 1 and 3 of action potential brought about by

A

potassium channels

181
Q

what happens in phase 2 of action potential

A
  • potassium going out but opening of calcium channels
  • this allows systolic ejection and refractoriness to re-stimulation to allow time for ventricles to refill with blood before onset of next contraction. long action potential in the heart.
182
Q

what is phase 2 brought about by

A

L-type calcium channels

183
Q

what does phase 3 include

A

delayed rectifier potassium channels.

184
Q

what day does foetus first heartbeat occur

A

day 22

185
Q

where is the ostium secondum located

A

in the septum primum

186
Q

what are the two proteins involved in atrial fibrillation

A

Matrix metaloproteinases and Disintegrin

187
Q

Phospholambn regulates what in the process of cardiocytes relaxation?

A

SERCA pump

188
Q

The 2nd

heart sound represents

A

Aortic and pulmonary valve closure

189
Q

The pressure in the left ventricle after ventricular diastole is the:

A

preload

190
Q

Furosemide acts primarily on what structure of the body

A

Ascending loop of Henlé in the kidney

191
Q

What is ‘Cor Pulmonale’

A

right sided heart failure

192
Q

Brain natriureti

c peptide is released in response to what

A

cardiac muscle stretch

193
Q

what is the syncytium

A

fusion of the nuclei

194
Q

how much additional filling does atrial contraction cause

A

20%

195
Q

What is the after load

A

pressure in the artery leading from the ventricle against which the ventricle must collapse

196
Q

does the SA node have contractile muscle filaments

A

no

197
Q

what factors that affect venous return

A
  • right atrial pressure
  • systemic filling pressure
  • resistance to venous return
198
Q

what does the Frank Starling Mechanism state

A

that the stroke volume increases in response to an increase in the volume of blood filling the heart when all other factors reman constant

198
Q

what does the Frank Starling Mechanism state

A

that the stroke volume increases in response to an increase in the volume of blood filling the heart when all other factors reman constant

199
Q

most common reason for right sided heart failure

A

left sided heart failure

200
Q

BNP make up

A

32 amino acid polypeptide

201
Q

what is rheumatic fever

A

group A streptococcal pharyngitis

202
Q

what layers of the heart does RF affect

A

all three

203
Q

what is the characteristic lesion of rheumatic carditis

A

the Aschoff nodule which is a granulomatous lesion with a central nectroic area occurring in the myocardium. they are macrophages

204
Q

what do translators do

A

written

205
Q

what to interpreters do

A

spoken

206
Q

what is disease of valvular degeneration

A

myxomatous disease

Semester 2 Case Studies (11 decks)

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