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DDT > trigger 2 - ischaemia > Flashcards

trigger 2 - ischaemia Flashcards

1
Q

central nervous system - CNS

A

brain and spinal cord

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2
Q

peripheral nervous system - PNS

A

all the nerves

split into somatic and autonomic

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3
Q

protection of the brain

A

1 - skull
2 - meninges (3 membranes)
3 - cerebrospinal fluid (CSF)

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4
Q

somatic nervous system

A

voluntary control

relationship with external environment

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5
Q

autonomic

A

involuntary
regulate vital internal functions

split into sympathetic and parasympathetic

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6
Q

grey matter

A

consists of:

  • neurons cells bodies and their dense network of dendrites
  • centre of spinal cord
  • thin outer layer of cereal hemispheres (cerebral cortex)
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7
Q

white matter

A

myelin sheath

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8
Q

brain stem

A

responsible for a variety of automatic functions, such as control of respiration, heart rate, and blood pressure, wakefullness, arousal and attention.

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9
Q

cerebrum structure

A

divided into a right and a left hemisphere
4 lobes:
frontal, parietal, temporal, and occipital

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10
Q

stroke involving cerebellum

A

may result in a lack of coordination, clumsiness, shaking, or other muscular difficulties

important to diagnose early, since swelling may cause brainstem compression or hydrocephalus.

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11
Q

blood supply to the brain

A

right/left common carotid arteries

right/left vertebral arteries.

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12
Q

external carotid arteries

A

supply face and scalp with blood

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13
Q

vertebro-basilar arterial system

A

back of brain

supplies vital brain structures (brain stem, occipital lobes, cerebellum) with blood, oxygen and nutrients

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14
Q

Circle of Willis

A

found central base of brain

a circle of communicating arteries - carotid and verterbrobasilar

other arteries arise from this and travel to all parts of the brain

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15
Q

anterior cerebral artery (ACA)

A

extends upward and forward from the internal carotid artery

supplies the frontal lobes (logic, personality, and voluntary movement, especially of the legs)

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16
Q

what happens if there is stroke in one or both of the ACAs

A

weakness in the leg on the opposite side

if both ACAs are affected - mental symptoms e.g. akinetic mutism

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17
Q

middle cerebral artery (MCA)

A

largest branch of internal carotid artery
supplies parts of frontal/parietal/temporal lobes
often most obstructed artery in strokes

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18
Q

posterior cerebral artery (PCA)

A

stem from basilar artery (mostly)

supply temporal and occipital lobes

visual defects common if infarction occurs

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19
Q

lenticulostriate arteries

A

small, deep penetrating arteries - arise from anterior part of Circle of Willis(by MCA) and affect basal ganglia

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20
Q

lacunar strokes

A

arise when small lenticuloistriate arteries are occluded

v common - high incidence in patients with chronic hypertension

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21
Q

zymogen

A

an inactive substance which is converted into an enzyme when activated by another enzyme

e.g. all enzymes present in plasma of clotting cascade found in this form

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22
Q

final step of clotting cascade

A

thrombin causes fibrinogen to convert to fibrin

fibrin aggregates strengthen the platelet plug

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23
Q

common pathway

clotting cascade

A

thrombin formation

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24
Q

excitotoxicity

A

glutamate becomes toxic and causes damage to neurones due to over excitability

  • intracellular calcium ion overload
  • activation of NDMA receptors
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25
Q

calcium ion sinks

A

mitochondria
endoplasmic reticulum

overloading of sinks reduces ATP synthesis

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26
Q

formation of reactive oxygen species (ROS)

A

danger point reached

positive feedback exaggerates process

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27
Q

problems caused by raised calcium ion conc.

A
  • increased glutamate release from nerve terminals
  • activation of proteases and lipases (membrane damage)
  • activation of nitric oxide synthase
  • arachidonic acid release
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28
Q

activation of reactive oxygen species

A

generate free radicals

- damage membrane lipids, proteins and DNA

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29
Q

oxidative stress

A

over production of ROS which produce free radicals

  • the body’s inability to detoxify them
  • neurons susceptible to excitotoxic damage

e.g. hypoxia

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30
Q

kainic acid

A

glutamate receptor agonist(activator)

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31
Q

arachidonic acid

A

increases free radical production

inhibits glutamate uptake

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32
Q

reducing excitotoxicity

A

glutamate antagonists
calcium channel blocking drugs
free radical scavengers

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33
Q

ischaemia and excitotoxicity

A

ischaemia causes depolarisation of neurones and lots of glutamate release
NMDA receptors activated and Calcium accumulation occurs

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34
Q

alteplase

A

stroke drug

recombinant tissue plasminogen activator

helps restore blood flow by dispersing thrombus

given within 3 hours

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35
Q

2 types of stroke

A

ischaemic - lack of blood flow (atherosclerosis)

hemorrhagic - weakened blood vessel ruptures (less common)

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36
Q

Hypoxia Inducible Factor (HIF)

A

transcription factors that respond to decreases in available oxygen in the cellular environment

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37
Q

stent

A

small mesh tube used to treat narrow/weak arteries

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38
Q

stent surgery procedure

A

percutaneous coronary intervention (PCI)or angioplasty
restores blood flow in blocked arteries
supports inner wall of artery

drug-eluting stents can prevent arteries from becoming blocked again

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39
Q

hypertension

A

high blood pressure

140/90 mmHg

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40
Q

VCAM-1

A

vascular cell adhesion molecule

produced by endothelial cells after damage has occurred

cause monocytes and T-lymphocytes to adhere(using cytokines) to endothelium as part of inflammatory response

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41
Q

oxidation of LDLs

A

occurs due to exposure to nitric oxide, macrophages, and some enzymes e.g. lipoxygenase

macrophages take them up and become foam cells

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42
Q

fatty streaks

A

the first signs of atherosclerosis that are visible without magnification
consist of lipid-containing foam cells in the arterial wall just beneath the endothelium
commonly occur in aorta/coronary arteries of 20/30yr olds
can form atherosclerotic plaques

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43
Q

T-lymphocytes in the intima

A

secrete cytokines
- induce smooth muscle cells to migrate from the media to the intima

smooth muscle cells proliferate due to growth factors and accumulate in intima

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44
Q

ruptured plaques

A

trigger acute thrombosis (activate platelets and clotting cascade)

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45
Q

blood gas test

A

tests oxygen levels in your blood

tests your blood pH - too acidic = acidosis or too alkaline/basic =alkalosis

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46
Q

sample collecting for blood gas test

A

arterial blood used

Allen test checks enough wrist circulation for sample

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47
Q

where is the respiratory centre found

A 
brain stem
(medulla oblongata and pons)
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48
Q

function of respiratory centre

A

control the rate and depth of respiratory movements of the diaphragm and other respiratory muscles

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49
Q

what chemoreceptors are involved with the respiratory centre

A

central chemoreceptors:

- found on the ventrolateral surface of medulla oblongata - detect changes in the pH of spinal fluid

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50
Q

what can desensitise the central chemoreceptors

A

chronic hypoxia (oxygen deficiency) and increased carbon dioxide

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51
Q

oedema

A

excess fluid retention tissues/cavities

can cause swollen ankles

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52
Q

importance of circle of willis

A

provides multiple paths for oxygenated blood to supply the brain
allows brain function to continue if one supplier is constricted

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53
Q

myocardial infarction (MI)

A

heart attack

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54
Q

where are the subunits of HIF-1 found

A

HIF-a in cytoplasm - gets hydroxylated in normoxia
HIF-B in nucleus

dimerisation of HIF-a and HIF- causes transcription

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55
Q

atheroma

A

accumulation of atherosclerotic plaque

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56
Q

4 steps of plaque formation

A

1 - endothelial dysfunction - formation of foam cells
2 - stable plaque formation - fibrous cap formation
3- T-cell activation - pro-inflammatory cytokines produced
4 - thrombus formation - extrinsic clotting cascade

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57
Q

step 1 of plaque formation

endothelial dysfunction

A
  • monocytes attach to endothelium via VCAM-1 receptors
  • monocytes converted to macrophages in intima
  • uptake of modified LDLs
  • macrophages oxidise LDLs and become foam cells
  • foam cells are what cause the fatty streaks
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58
Q

step 2 - stable plaque formation

A
  • foam cells accumulate in intima
  • vascular smooth muscle cells migrate from the intima to epithelium
  • produce collagen and proliferate to form fibrous cap
59
Q

T cell activation in atherosclerotic plaque formation

A

Th1 and Th2 recruited to break down fibrous cap
MMPs produced by foam cells
pro inflammatory cytokines produced

60
Q

4th step of plaque formation

- thrombus formation

A 
fibrous cap broken down 
endothelium becomes exposed
tissue factor released - extrinsic clotting cascade
binds to factor VII 
factor VIIa
61
Q

3 cardiac biomarkers

A

cardiac troponins (Tni and Tnt)
creatine kinase MB
myoglobin

62
Q

cardiac troponins

A 
cardiac biomarker 
i and t 
correlate to severity of infarction 
detected after 12hours of symptoms
long persistence - up to 12 days 
high specificity 
high sensitivity
63
Q

creatine kinase MB

A 
cardiac biomarker
enzyme 
peaks 24 hours after symptoms
lower sensitivty than troponins
only used when troponin not available
64
Q

myoglobin

A

cardiac biomarker
released quickly after onset of symptoms
not specific
high levels seen when any muscle tissue is damaged

65
Q

CRP used to predict thrombotic events

A

found in serum or plasma as a result of inflammatory response

66
Q

ischaemic stroke

A

when a blood blot blocks a blood vessel in the brain
narrowing/stenosis of brain blood vessel

most common type of stroke
causes oxygen deprivation and reduced blood flow

67
Q

2 types of ischaemic stroke

A

thrombotic

embolic

68
Q

embolic stroke

A

type of ischaemic stroke

blood clot develops elsewhere then travels in the blood to the brain

69
Q

important risk factor for ischaemic stroke

A

high blood pressure

70
Q

insoluble protein fibres that cause blood clot

A

fibrin

71
Q

process of primary homeostasis

platelets forming network

A

endothelium of blood vessel damaged
connective tissue exposed
platelets adhere to and form a plug
seal reinforced by fibrin clot

72
Q

clotting factors

A

proteins in the blood that control bleeding

respond in clotting cascade and strengthen platelet plug

73
Q

where do clotting factors come from

A

platelets
damaged cells
plasma

74
Q

tPA

tissue plasminogen activator

A

enzyme catalyses conversion of plasminogen to plasmin

used to treat embolic or thrombic stroke

75
Q

what releases tPA

A

endothelium

76
Q

junctions important in BBB

A

tight junctions

77
Q

excitotoxicity

A

when neurons are damaged or killed by over-stimulation of glutamate receptors

78
Q

why does hypoxia causes increased H+ conc

A

anaerobic respiration

lactic acid production

79
Q

effect of reduced ATP on calcium storage

A

SERCA pump requires ATP

calcium can no longer be stored in ER

80
Q

deleterous Ca2+ effects of excitotoxicity

A

NOS/ROS production - damage cell membrane and DNA

hydroxyl free radicals

81
Q

how does excitotoxcity activate apoptosis

A

glutamate release causes increased intracellular Ca2+ conc
production of ROS/NOS
activation of caspases
apoptosis

82
Q

ischaemic cascade

A

biochemical reactions in aerobic tissue induced by hypoxia following ischaemia

83
Q

can ischaemic cascade continue even when blood flow returns

A

yes

84
Q

effect of decreased blood supply to tissue

A

decreased oxygen
decreased ATP

anaerobic metabolism

85
Q

effects of anaerobic metabolism in ischaemic cascade

A

lactic acidosis
disruption of acid-base balance
failure of neural system - regional brain dysfunction

86
Q

which pumps break in ischaemic cascade

A

Na+ and Ca2+ pumps

87
Q

overview of ischaemic cascade

A

blood supply reduced
anaerobic metabolism
pumps broken - intracelluar Na and Ca conc increased
damage

88
Q

effects of increased intracellular Na+ conc. in ischaemic cascade

A

H2O influx
swelling
cytotoxic oedema
necrotic cell death

89
Q

effects of increased Ca2+ conc in ischaemic cascade

A

production of free radicals and ROS - mitochondrial injury - release of apoptotic factors
excitotoxicity - glutamate accumulation
degrading enzymes - proteases/lipases - necrotic cell death

90
Q

reperfusion injury

A

tissue damage caused when blood flow is restored following ischaemia/hypoxia

91
Q

effects of return of blood supply

A

increased oxygen and ATP
reactivation of dysfunctional Na+ and Ca2+ pumps
production of ROS and free radicals

92
Q

why does mitochondrial permeability increase in reperfusion injury

A

ROS/free radicals cause damage to plasma membrane macromolecules and ER
mitochondrial pore

93
Q

why does intracellular Ca2+ increase in reperfusion injury

A

ROS causes damage to ER membrane

Ca2+ released

94
Q

damage caused by Ca2+ in reperfusion injury

A

activation of degradative enzyme
endothelial injury - clots
pro-inflammtory cytokine release
apoptosis

95
Q

brain stem connects

A

spinal cord and cerebellum

96
Q

order of brain stem from top to bottom

A

thalamus
midbrain
pons
medulla

97
Q

role of midbrain

A

regulates autonomic functions e.g. HR, BR

relays visual and auditory signals

98
Q

where in the brain stem controls eye movements

A

midbrain

99
Q

role of pons

A

transmission of signals from cerebrum to cerebellum
controls balance and posture
regulation of breathing
regulation of deep sleep

100
Q

role of medulla

A

involuntary reflexes e..g sneezing, coughing, vomiting

autonomic centres e..g control of BP

101
Q

how many cranial nerves come from the brainstem

A

10 out of 12

102
Q

where is respiratory centre found

A

pons and medulla oblongata

103
Q

input to respiratory centre

A

neural, chemical and hormonal signals

e..g peripheral chemoreceptors and central chemoreceptors

104
Q

function of respiratory centre

A

control rate and depth of respiratory movements of diaphragm and other respiratory muscles

105
Q

what is known as the pacemaker of the lungs

A

respiratory centre in the pons and medulla

106
Q

3 effects of the respiratory centre

A

1 - altered inspiration-expiration rhythm
2 - altered magnitude of ventilation
3 - modified respiratory activity e.g. coughing/speech

107
Q

increased arterial PCO2 causes

A

decreased blood pH

108
Q

what recognsies blood pH

A

peripheral chemoreceptors

109
Q

effect of ventilation on blood PCO2

A

increased ventilation means more CO2 exhaled

blood pH increases

110
Q

peripheral chemoreceptors

A

sensory extensions of peripheral nervous system into blood vessels
detect changes in chemical concentrattions

111
Q

where are peripheral chemoreceptors found

A

blood
carotid bodies
aortic bodies

112
Q

function of peripheral chemoreceptors

A

detect chemical changes and send info to respiratory centre:

  • decrease in PO2
  • increase in PCO2
  • decrease in arterial blood pH
113
Q

what do peripheral chemoreceptors detect

A
  • decrease in blood PO2
  • increase in blood PCO2
  • decrease in arterial blood pH
114
Q

how do signals detected from peripheral chemoreceptors in aortic arch get to RC

A

via vagus nerve

115
Q

how do signals detected in carotid bodies get to RC

A

via glossopharyngeal nerve

116
Q

where are central chemoreceptors found

A

ventrolateral medullary surfaces near the respiratory centre
in the brainstem
between cranial nerves 9 and 10

117
Q

function of central chemoreceptors

A

detect pH of CSF

decreased pH means too much CO2

118
Q

can H+ diffuse across BBB

A

no

119
Q

when CO2 crosses BBB

A

converted into H+ and HCO3-
decreases pH of csf
detected by medullary chemoreceptor
communicates to inspiratory respiratory centre

120
Q

2 types of respiratory centre

A

dorsal inspiratory

ventral expiratory

121
Q

dorsal expiratory respiratory centre

A

always active

122
Q

ventral expiratory centre

A

active breathing

123
Q

acid-base balance

A

regulation of blood pH to maintain pH between 7.35 and 7.45

124
Q

acidosis

A

when blood pH<7.35

causes depression of CNS, coma

125
Q

alkalosis

A

blood pH<7.45

over-excitability of CNS causes neurons to fire without stimuli

126
Q

how does the kidney regulate acid-base balance

A

addition or secretion of bicarbonate ions (HCO3-)

127
Q

where is HCO3- reabsorbed

A

at the PCT along with H+ at the Na+/H+ pump

128
Q

overview effect of hypoxia

A

activates angiogenic switch to icnrease blood supply by increasing HIF-1a

129
Q

role of HIF-1a in hypoxia

A

activates transcription of genes involved in VEGF

130
Q

HIF-1a mechanism in hypoxia

A

no O2 so no hydroxylation
HIF-1a not degraded so translocates to nucleus
HIF-1a forms a dimer with HIF-beta
binds to HRE to cause transcription

131
Q

HIF-1a mechanism in normoxia

A

prolyl hydroxylase enzymes add -OH group to HIF-1a
attracts E3 ub ligase of polyubiquitin tail
ub targets HIF to proteosome
degraded

132
Q

HRE

A

hypoxia response elements

133
Q

arterial blood gas analysis

A

shows imbalance of O2, CO2 or pH in the blood

O2 saturation can also be calculated

134
Q

blood O2 saturation

A

amount of O2 bound to haemaglobin

135
Q

normal blood pH

A

7.35-7.45

136
Q

normal blood PO2

A

80-100 mmHg

137
Q

normal blood PCO2

A

35-45 mmHg

138
Q

normal blood O2 saturation

A

95-100%

139
Q

normal blood bicarbonate conc

A

22-26

140
Q

where do you take blood samples for arterial blood gas analysis

A

from the radial artery in the wrist

141
Q

why is the wrist radial artery good for sample collection

A

easily accessible

blood flow easily controlled

142
Q

where does 70% of bicarbonate reabsorption take place

A

PCT

143
Q

desribe how bicarbonate is reabsorbed from the PCT into the blood

A

Na+/H+ exchnage pump

DDT (12 decks)

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