Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Semester 2 Case Studies > Case 5 > Flashcards

Case 5 Flashcards

1
Q

what is atherosclerosis

A

refers to plaque formation which is the build up of fats and cholesterol inner artery walls that can restrict or block the blood flow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what happens when the blood flow is restricted or blocked,

A

tissues or organs can suffer from ischaemia which means lack of oxygen.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what is atherosclerosis described as

A

chronic inflammatory process triggered by the accumulation of cholesterol containing low-density lipoprotein LDL particles in the arterial wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

how common is it for death in males

A

most common cause of death in males

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does cigarette smoke cause in the arteries

A

endothelial dysfunction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

when is pharmacotherapy recommend

A

if BP is over 140/90mmHg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Dyslipidemia mechanism

A

Hydrophobic fat molecules, such as triglycerides, phospholipids and cholesterol are transported to all the cells and tissues of the body in lipoprotein particles
Lipoprotein particles consist of a triglyceride and cholesterol centre, surrounded by a phospholipid outer shell
There is a special kind of protein, called apolipoprotein, embedded in the outer shell, to stabilise the complex and to give it a functional identity
Two main types of lipoproteins: the bad low density one (LDL) and the good high density one (HDL)
Lipoproteins are very low and intermediate densities are also considered bad.
In terms of apolipoproteins, apoliprotein B (ApoB) , is embedded in LDL and ApoA1 is in HDL
LDL in the circulation can be brought into the artery wall across the endothelial cells, for example by scavenger receptors
LDL will then be taken by macrophages to become foam cells, leading to plaque formation
On the other hand, HDLs transport the cholesterol back to the liver through reverse cholesterol transport (RCT)
In the liver, cholesterol will be excreted through the biliary route
For the ease of transporting via RCT, cholesterol is usually converted to cholesteryl ester
While reduction of LDL in the blood has proven to lower CAD risk, scientists had been wondering if increasing HDL, for example by taking Niacin, a form of vitamin B3, will help prevent CAD
When proper studies are conducted, increasing HDL levels don’t really show an effect on CAD

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

when genotyping what do most CAD patients tend to have

A

at the single nucleotide polymorphism they tend to have a C instead of. A T

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

what are the genes associated with CAD

A

PCSK9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

how does PCSK9 affect CAD

A
  • increases plasma LDL-C levels by downregulating LDL receptor (LDLR) expression after transcription.- when the 9p21 region is deleted, only the expression of CDKN2a and CDKN2b genes are reduced. without the 9p21 region, the proliferation and senescence of aortic smooth muscle cells are increased, both characteristics of smooth muscle cells in CAD
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what are the layers of the arterial wall

A
  • blood
  • endothelial cells
  • intima
  • internal elastic lamina
  • media
  • adventitia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

(1) infiltration and uptake modification of LDL

A
  • at the hotspots of bifurcation, turbulent flow can happen and cause local recirculation and increase of the local conc of plasma LDL.
  • LDL transport into the arterial wall radially and can be retained by proteoglycans
  • the disturbed blood flow also causes shear stress on the endothelial cells leading to the activation of the pro inflammatory transcriptional programs I the cells
  • given the injury and pro inflammatory activation, endothelial cells losing the function as the barrier, causing more influx of cholesterol and lipoproteins go into the arterial intimata
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

(2) uptake modification

A
  • the LDL particles are retained in the intima and can be modified
  • it is considered as sterile inflammation without external pathogens and so called danger associated molecular pattern against external pathogens
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

(3) endothelial adhesion molecule expression

A
  • the oxidesed LDL particles can induce endothelial cell surface expression of the leukocyte adhesion molecules.
  • these adhesion molecules bind to the ligands expressed on leukocytes
  • the combinational expression of endothelial adhesion molecules and their ligands such as integrins and selectins lead to inflammatory process
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

(4) leukocyte recruitment

A
  • leukocytes that are recruited to the atherosclerotic lesion produce a number of inflammatory mediators
  • they amplify the inflammatory reaction through continuous activation of both leukocytes and endothelial cells and by recruiting further immune cells
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

(5) monocyte to macrophage differentiation

A

monocytes are the most numerous white blood cells recruited into atherosclerotic sites
They differentiate into macrophages under the influence of monocyte-colony stimulation factor (M-CSF) present in lesions

Two types of macrophages activated:
Classically activated or M1 macrophages. They further enrich the proinflammatory milieu through inflammatory proteins and lipid mediators such as cytokines and leukotrienes, to sustain inflammatory responses causing tissue damage
Alternatively activated or M2 macrophages that secrete anti-inflammatory mediators promoting the resolution of inflammation by means of clearance of apoptotic cells and dampening of immune responses. Therefore this type of macrophage promote tissue repair and healing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

what is the stimulation factor that turns monocytes into macrophages

A

M-CSF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

(6) Event of oxLDL uptake and foam cell production

A
  • now the atherosclerotic lesion is emerging with retained LDL and activated leukocytes
  • the oxidised LDL particles can bind to scavenger receptors on macrophages
  • the macrophage then uptake the lipoprotein particles and become foam cells
  • these lipid laden macrophages is a characteristic of the atherosclerotic lesion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

(7) antigen presentation

A

the immune system is cracking up a level from innate to adaptive immunity
The uptake of oxLDL by macrophages and dendritic cells will lead not only to foam cell formation, but also antigen presentation
Leukocyte adhesion molecules and chemotactic factors, produced as a consequence of innate immune activation, can recruit effector CD4+ T cells
The antigen presentation by macrophages and dendritic cells can then activate or differentiate CD4+ T cells into helper T cells and regulatory T cells
Th1 cells promote macrophage activation and inflammation whilst Treg cells act by inhibiting immune responses and inflammation, therefore are considered atheroprotective
Th17 cell subtype promises fibrosis through action of its cytokine IL-17. Th17 activity can therefore enhance the formation of the fibrous cap and plaque stability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

(8) macrophages apoptosis and necrotic core formation

A

in the atherosclerotic lesion, several factors, such as oxidative stress, induce macrophage death through apoptosis
Apoptotic cells are normally cleared by specific phagocytosis process, efferocytosis derived from the Greek word ‘to bury’.
Efferocytosis is important for the normal steady state of tissue and the resolution of inflammation
However, clearance of lipid-laden apoptotic macrophages in the atherosclerotic lesion can be defective and create a lipid necrotic core

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

(9) tertiary lymphoid organs

A

In addition to the inflammation happening in the intima, complex adaptive immune responses also develop in the adventitia
Inflammatory cells observed in the adventitia, include dendritic cells, macrophages, mast cells and lymphocytes. T and B cell activation is present in the adventitia and in advanced stages of atherosclerosis, large lymphoid structures, referred to as adventitial tertiary lymphoid organs, may develop

These adventitial tertiary lymphoid organs are sites of antibody production, including antibodies to plasma lipoproteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what do malfunctioning endothelial cells release

A

vasoactive hormones such as nitric oxide and prostacyclin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

what is secreted from the endothelial cells in the media

A

platelet derived growth factor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what is in the fibrous cap

A

bundles of muscle cells, macrophages, foam cells, lymphocytes, collagen and elastin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what radioactive drug is used to label inflammatory activities

A

18F flurodeoxyglucose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

what do statins target

A

the HMG-CoA reductase in the mevalonate pathway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

what transcription factor gets released when intercellular cholesterol levels are low

A

SREPB-2

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what does SREP-B regular;ate

A

LDL receptor and PCSK9

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

how does PCSK9 control the amount of LDL receptors

A

by degrading them

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

how does LDL receptors reduce the level of LDL in circulation

A

by uptake of circulatory LDLs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

mechanism of LDL receptors and PCSK9

A
  • LDL receptors are binding and internalising circulatory LDLs on the liver cell surface
  • PCSK9 is secreted and then binds to the LDL receptor to mediate the lysosomal degradation of the complex formed by the PSCK9, LDL receptor and LDL
  • if we can inhibit PCSK9 by using inhibitors, LDL receptors will not be degraded and can be recycled to uptake more circulatory LDLs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

what is the resting membrane potential set by

A

inward rectifying potassium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

how do Sino-atrial node cells beat spontaneously

A
  • resting membrane potential is around -60 and is less negative than ventricle resting potential because these SA node cells have fewer inner rectifying potassium channels
  • it is not stable and spontaneously decays towards the pacemaker potential
  • when it reaches the threshold potential we get the generation of an action potential
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

what ion channels are responsible for the pacemaker potential

A

opening of ‘funny’ currents (Na+ influx) and Ca channels (T and L types)
closing of outward channels - K channels slowly close

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

how does SA node action potential vary to ventricular

A

slow to rise - slow Ca channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

what do cardiac muscle cells form

A

a syncytium - intercalated discs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

gap junction formation

A

six subunits of connexin form an ion channel

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

how does excitation spread through the heart

A
  • positive charge moces through the excitation channels and depolarises the second cell
  • on the outside of the cell, the positive charge moves back and decease negative charge on the first cell
  • now there is an action potential in the second cell
  • depolarises the third cell and the opposite happens back to the second
  • channels only go in one direction - refractory
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

the movement of current through the heart

A

SAN - left and right atria - AVN - bundle of HIS - left and right bundle branches - purkinje system - ventricular myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

conduction velocity of the AP of the atrial myocardium

A

1m/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what is the depolarisation in the atrial myocardium from

A

Na rapid entry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

why does the action potential arise before the threshold is reached in the AVN

A

the action potential is generated before the pacemaker potential reaches the threshold potential - this is because in the heart the pacemaker potential in the AV node is very slow. So this is a shallow slope compared to that on the SA node. So what’s happening, is in the SA node, an action potential has been generated and the action potential in the SA node reaches threshold, the action potentials generated travels through the atrial myocardium and reaches the AV node at this point before the pacemaker potential in the AV node itself reaches threshold. So this pacemaker potential has nothing to do with the action potential I the AV node, the action potential is triggered here because of the SA node has produced an action potential much faster than the AV node because of the pacemaker potential in the SA node decays faster. That action potential pass through the atrial myocardium, its hit the AV node and its produced this action potential and then the pacemaker potential in the AV node is still sub threshold. So therefore the pacemaker potential in the AV node Is actually irrelevant because the SA node produces action potentials much faster

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

how fast is conduction through the AV node

A

0.05m/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

why does the purkinje fibres have a long refraction period

A

to prevent the conduction system from being re excited to prevent against arrhythmias

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

how fast is the action potential in the purkinje fibres

A

4m/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

how fast is the AP in the ventricular myocytte

A

1m/s

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

depolarisation wave travelling toward a positive electrode

A

postive deflection

48
Q

depolarisation wave travelling away from a positive electrode

A

negative deflection

49
Q

repolarisation wave travelling toward a positive electrode

A

negative deflection

50
Q

repolarisation wave travelling away from a positive electrode

A

positive deflection

51
Q

what is the atrial repolarisation masked by in the ECG

A

QRS wave

52
Q

why is the T wave a positive deflection even though it is repolarisation

A
  • because there are two ways to flip it and repolarisation is passing in the opposite direction
53
Q

how does SNS affect the heart

A
  • increase HR
  • increases AVN conduction speed
  • decreases AP duration
54
Q

how does PSNS affect the heart

A
  • decreases HR

- decreases AVN conduction speed

55
Q

SNS effect on SA node

A

noradrenaline - B receptors - increase of cAMP and increasing depolarising current e.g funny current and Ca current

56
Q

what does AV node do to the AVN

A

activates beta receptors

57
Q

PNS activation on the SA node

A
  • ACh acts on the muscarinic receptors

- K+ channels open causing hyperpolarisation and a pacemaker potential of a reduced slop

58
Q

where is atheroma

A

in the intima of large and medium sized arteries

59
Q

what are the three stages of atheroma

A
  • fatty streak
  • simple plaque
  • complicated plaque
60
Q

nature of simple atheromatous plaque

A
  • fat in the intima
  • extracellular
  • within modified smooth muscle cells
  • fibrous cap
  • blood vessel proliferation and inflammatory cells
61
Q

complicated athermatous plaque

A
  • calcification
  • plaque disruption
  • haemorrhage into plaque
  • thrombosis
62
Q

encrustation

A

platelets

63
Q

insudation

A

lipid from blood

64
Q

monoclonal

A

proliferation of smooth muscle cells

65
Q

response to injury

A

endothelial damage

66
Q

infection

A

with Ag-Ab complexes deposition

67
Q

what is infarction

A

reduced delivery of blood to an organ sufficient to lead to its death

68
Q

cardiac arrhythmia

A
  • atrial fibrillation
  • heart block
  • ventricular fibrillation
69
Q

angina pectoris

A
  • chest pain

- induced by exercise and relieved bt rest

70
Q

stable angina

A
  • lowish risk of infarct
71
Q

unstable angina

A
  • pain at rest
  • increasing severity of attack
  • pain lasting over 15 mins
72
Q

acute myocardial infarction

A
  • regional or circumferential
73
Q

most common cause of MI

A
  • rupture of an atherosclerotic plaque in a coronary artery
  • formation of intracoronary thrombus
  • causing infarction downstream of the occluded blood vessel
74
Q

how many people who survive an MI will develop heart failure in next 5 years

A

20%

75
Q

MI to heart failure

A
  • blockage of coronary artery
  • ischaemia and MI
  • necrosis
  • inflammatory response to remove dead cells
  • infarct healing and scar formation
  • hypertrophy, dilation and reduced function
  • heart failure
76
Q

how many cardiomyocytes in adult heart

A

5 billion

77
Q

how many cardionyocytes die in large MI

A

1 billion

78
Q

what do cells dying by necrosis release to initiate an inflammatory response and as a diagnostic tool

A

troponin

79
Q

inflammatory response

A
  • neutrophils infiltrate the infarct
  • secrete MMPs and phagocytose debris
  • pro inflammatory cytosine levels rise
  • leads to recruitment of other inflammatory cells
  • pro-reparative phase
80
Q

infarct healing and scar formation

A
  • cardiac fibroblasts -> myofibroblasts
  • main function: secrete new ECM proteins
  • clearance of myofibroblasts by apoptosis
81
Q

glucose metabolism

A

glucose is a major fuel for cells
Once in cells its metabolised
Metabolised by a series of enzymes called glycolysis
Metabolise glucose from six carbon glucose to three carbon units
The end point of this glycolytic metabolism of this series of glycolytic enzymes is a three carbon acid called pyruvate
Pyruvate and lactate are closely related chemical substances because they’re connected by an equilibrium reaction which is catalysed by an enzyme

82
Q

what is anaerobic respiration

A

Anaerobic metabolism is when pyruvate is concerted into lactate and doesn’t require any oxygen
Better way of metabolising the pyruvate and that is the mitochondrial oxidative metabolism
Only problem is you can’t do this without oxygen

83
Q

back up glucose

A

can also get glucose from inside cell stores called glycogen.
It’s a back up storage version of glucose
If hypoxic the pathway is limited
Another problem; if ischaemic, you lose the ability to dump waste products outside the cell, like lactate
If there’s a build up of lactate then that in turn prevents metabolism

84
Q

what are the metabolic changes in first minutes of cardiac victim.

A

No 02 - no oxidative (mitochondrial) metabolism
Cell consumes ‘high energy phosphate’ back-up
Phosphocreatine (PCr) to help maintain ATP level
Anaerobic metabolism switches on to maintain ATP - produces lactate + hydrogen ions
Lactic acid accumulates in extracellular space and cytosol
Contractility is impaired by metabolic changes

85
Q

anaerobic glycolysis equation.

A

glycogen + lactate + H+

86
Q

what does first degree heart block reflect

A
  • a problem in conduction through the AV node and the bundle of HIS
  • slowing in conduction that leads to an increased temporal separation between depolarisation in and contraction of the ratio and the depolarisation and contraction in the ventricles
87
Q

what is complete heart block

A

no conduction through the AV node and the bundle of HIS down into the ventricles
Effectively two separate rhythms being established, one by a pacemaker in the atria and the second by a pacemaker in the ventricles
Each of the atrial depolarisation is associated then with the P wave - normal in ECG
there is a regular QRS but the rhythm is very slow and its come about because some portion of the ventricles have now become the pacemaker region for the ventricles
Its an abnormal shape as the depolarisation has started off in an abnormal position and will therefore be spreading throughout the ventricles in an abnormal way and finally
There is no relationship between the P waves from the QRS complexes

ventricles will be contracting much more slowly
Get about 15 beats per minute and also because the ventricle is contracting abnormally, it won’t be acting as efficiently as it would normally so won’t be a normal cardiac output

88
Q

what is the sinus arrhythmia

A

completely normal and associated with breathing

89
Q

ventricular extrasystole

A
  • beat that has originated from the ventricles outside of the normal systolic heart beat and rhythm
90
Q

atrial fibrillation

A

multiple depolarisation happening across the atria
Creating a series of P like waves in the recording
Relatively small effect on the ventricular filling and therefore ventricular function
Can also produce stagnant areas of blood as atria doesn’t empty completely and can therefore be associated with blood clotting

91
Q

ventricular fibrillation

A

if contracting in an uncoordinated way, you won’t have the rhythmic or the contraction of the muscle and so therefore the stroke that the heart chambers will be contracting unevenly, generating uneven pressure unable to produce the normal cardiac output

92
Q

what does myocardial ischaemia look like on an ECG

A

ST segment elevation/delressuin

- specifically interfere with ion channels mediating repolarisation of the ventricles

93
Q

what are main components in plaque

A

foam cells

94
Q

what is the role of the Lecithin Cholesterol Acyl Transferase enzyme

A

Esterifies free cholesterol in LDLs and HDLs

95
Q

What is the type of angina caused by vasospasms

A

Prinzmetal

variant

96
Q

What is not a role of NO (nitrous oxide)

A

Increases vascular permeability

97
Q

Which of the following causes a side effect of coughing

A

Ramipril

98
Q

CoA inhibitor

A

Atorvastatin

99
Q

Which cholesterol transporter is the body’s main source of energy during prolonged
fasting
?

A

VLDL’s

100
Q

Smoking one cigarette per day puts you at a ____ higher chance of developing
coronary heart disease

A

30%

101
Q

What is Prinzmetal’s (variant) angina characterised by

A

Angina that occurs without provocation

102
Q

What causes ST elevation in myocardial infarctions

A

Opening of K
+
channels

103
Q

the main mechanism by which Nitric Oxide relieves an attack of angina

A

Dilating peripheral capacitance vessels

104
Q

What is the fibrous cap of an atheroma mostly made up of

A

Smooth muscle cells and collagen

105
Q

how does nitric oxide cause vasodilation

A

relaxes vascular smooth muscle by binding to the heme moiety of cytosolic guanylate cyclase, activating guanylate cyclase and increasing intracellular levels of cyclic-guanosine 3’,5’-monophosphate, which then leads to vasodilation.

106
Q

first degree heart block on an ECG

A
107
Q

complete heart block on an ECG

A
108
Q

sinus arythmie on ECG

A
109
Q

ventricular extrasystole on an ECG

A
110
Q

atrial fibrillation on an ECG

A
111
Q

ventricular fibrillation on an ECG

A
112
Q

myocardial ischeamia and the ECG

A
113
Q

ECG limb leads and what plane of the heart do they look at

A

each lead gives out two readings.

114
Q

lead direction on limb leads diagram

A
115
Q

12 lead ECG and where leads are placed diagram

A

Semester 2 Case Studies (11 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions