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Disease, Diagnostics and Therapeutics > Ischaemia > Flashcards

Ischaemia Flashcards

1
Q

What is HIF-1

A

a transcription factor that functions as a master regulator of oxygen homeostasis

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2
Q

What are the key steps of reperfusion injury

A
  • O2 returns and ATP SERCA returns
  • ROS are generated
  • Calcium overload of mitochondria
  • Mitochondrial permeability transition pores open
  • Na/Cl exchanger reverses
  • endothelial dysfunction
  • haemostasis/prothrombosis
  • proinflammatory cytokines released
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3
Q

What adheres to the edges of e.g. a cut

A

platelets

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4
Q

What is t-PA

A

Tissue plasminogen activator an enzyme which dissolves blood clots

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5
Q

What is the precursor of plasmin

A

Plasminogen

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6
Q

What are the 3 tunica layers of blood vessels

A

Tunica Intima
Tunica Media
Tunica Adventita

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7
Q

Under hypoxic conditions, what do the target genes of HIF-1 encode

A

encode proteins which increase O2 delivery and mediate adaptive responses to O2 deprivation

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8
Q

Calculation for specificity

A

TN/(TN + FP)

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9
Q

Define clotting cascade

A

A cascade of proteolytic enzymes and co-factors

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10
Q

What do both the Intrinsic and Extrinsic clotting cascade pathways lead too

A

Factor X –> Xa

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11
Q

What do the brain stem and respiratory centres control

A

the rate and depth of respiratory muscles after receiving neural, chemical, and hormonal signals.

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12
Q

Why is the circle of willis important

A

keep circulation flowing in the event of a blockage to prevent ischemia.

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13
Q

Define arterial blood gas analysis

A

This is a blood sample taken normally from the radial artery of the wrist which is then analysed.

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14
Q

Define bifurcation

A

splitting of blood vessels

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15
Q

Define gas exchange

A

the delivery of oxygen from the lungs to the bloodstream, and the elimination of carbon dioxide from the bloodstream to the lungs.

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16
Q

Calculation for sensitivity

A

TP/(TP +FN)

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17
Q

Give the steps of the common pathway of the clotting cascade

A

factor X activation –> with V –> prothrombin –> thrombin –> fibrinogen –> fibrin –> cross linked fibrin clot

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18
Q

What are the three main cerebral arteries

A
  • Anterior cerebral artery(ACA)
  • Middle cerebral artery (MCA)
  • Posterior cerebral artery (PCA)
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19
Q

Respiratory alkalosis:
A) increased Ph, Increased H, decreased HCO3 and increased pCO2
B) increased Ph, decreased H, decreased HCO3 and decreased pCO2
C) increased Ph, Increased H, increased HCO3 and decreased pCO2
D) increased Ph, increased H, decreased HCO3 and increased pCO2

A

B) increased Ph, decreased H, decreased HCO3 and decreased pCO2

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20
Q

How do cells respond to hypoxia

A

by HIF-1 alpha -mediated upregulation of glucose transporters (Glut-1 and Glut-3) and enzymes of glycolysis

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21
Q

Why is a larger lumen preferential for blood vessels

A

If the blood vessels have a larger lumen for blood flow, blood pressure is not as high, and the likelihood of a MI is reduced

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22
Q

Where are the peripheral chemoreceptors found

A

near the ventral surface of the medulla

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23
Q

What two sets of vessels supply blood to the brain, face, and scalp

A

the right and left common carotid arteries and the right and left vertebral arteries

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24
Q

Where does the majority of bicarbonate reabsorption occur

A

Proximal tubule (90%)

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25
Q

What is the circle of WIllis

A

This circles the pituitary gland and provides communications (anastomosis) between the bloody supply of the forebrain and hindbrain.

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26
Q

In an ABG, what should HCO3 be

A

22-45 mmhg

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27
Q

Metabolic acidosis:
A) decreased Ph, Increased H, decreased HCO3 and increased pCO2
B) increased Ph, Increased H, decreased HCO3 and decreased pCO2
C) decreased Ph, Increased H, decreased HCO3 and decreased pCO2
D) decreased Ph, decreased H, decreased HCO3 and decreased pCO2

A

C) decreased Ph, Increased H, decreased HCO3 and decreased pCO2

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28
Q

What does increased Ca as a result of excitotoxicity activate

A
  • nNos which increase nitric oxides and ROS.
  • Proteases (calpains) and lipases
  • Increased vesicle transport
  • Ryanodine Receptors (RyR)
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29
Q

Give the steps of the intrinsic clotting cascade up to Factor X

A

Damaged surface –> activates XII –> activates XI –> activated IX –> with VIII –> activation of X

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30
Q

Define negative predicted value

A

The proportion of positive tests that come from those free from the disease

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31
Q

Define stent

A

A short, wire mesh tube which acts like a scaffold to help keep your artery open.

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32
Q

Where are the respiratory centres found

A

The respiratory centres are in the medulla oblongata and the pons, in the brainstem

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33
Q

Define biomarker

A

A characteristic that is objectively measured and evaluated as an indicator of normal biological processes, pathogenic processes, or pharmacologic responses to a therapeutic intervention

34
Q

Give 2 other types of receptors (respiratory)

A

stretch
irritant
nociceptive

35
Q

Describe the angioplasty procedure

A

A stent is inserted after using a balloon to stretch open a narrowed/blocked artery. The stents remain in place permanently to allow blood to flow more freely.

36
Q

Calculation for NPV

A

TN/(TN+FN)

37
Q

Give the steps of the extrinsic clotting cascade up to Factor X

A

Trauma –> activates VII –> with tissue factor –> activation of X

38
Q

Describe the Ulceration and thrombus formation stage of atheromatous plaque formation

A

a. Fibrous cap broken by MMPs and cytokines
b. Tissue factor released from the endothelium
c. Start of extrinsic coagulation cascade
d. TF binds to factor VIIa and activates it
e. These catalyses the conversion of factor X to factor Xa
f. Initiates common pathway of blood clotting
i. Prothrombin –> thrombin and fibrinogen –> fibrin
g. Blood vessel stenosis, occlusion or thrombi released

39
Q

What are the functions of plasmin

A
  • digests fibrinogen
  • digests fibrin
  • digests factors II, V and VIII
40
Q

Describe the endothelial dysfunction stage of atheromatous plaque formation

A

a. Monocytes adhere to the endothelium via VCAM-1 and infiltrate
b. Monocytes become macrophages in intima
c. They take up modified LDL
d. Macrophages become foam cells

41
Q

Explain the steps of bicarbonate dissociation

A
  1. H+ reacts with HC03 producing H2CO3
  2. H2CO3 splits into H2O and CO2 and passes into the tubular cells
  3. They recombine to form H2CO3
  4. H2CO3 dissociates into H+ and HC03
  5. HCO3 then enters capillary through the Na/HCO3 transporter or an anion exchanger
42
Q

Calculation for PPV

A

TP/(TP +FP)

43
Q

Define Ischaemia

A

Loss of blood flow to an organ

44
Q

What do the central chemoreceptors respond to

A

changes in H+ in the brain CSF, caused by the diffusion of CO¬2 across the blood brain barrier

45
Q

How do the kidneys contribute to the acid base balance

A

These excrete excess acids or bases via the urine, e.g. uric acid. However, this can take several days to make the adjustments.

46
Q

What are the 5 components of an ABG

A 
Ph
PaO2
PCO2
HCO3
Base excess
47
Q

Describe the steps of t-PA action

A
  1. T-PA binds to fibrin on the surface of the clot
  2. Activates fibrin-bound plasminogen
  3. Plasmin is cleaved from the plasminogen associated with the fibrin
  4. Fibrin molecules are broken apart by the plasmin and the clot dissolves
48
Q

Respiratory acidosis:
A) increased Ph, Increased H, decreased HCO3 and increased pCO2
B) increased Ph, decreased H, increased HCO3 and increased pCO2
C) decreased Ph, Increased H, increased HCO3 and decreased pCO2
D) decreased Ph, increased H, decreased HCO3 and increased pCO2

A

D) decreased Ph, increased H, decreased HCO3 and increased pCO2

49
Q

Which transporter transports H into the lumen on the PCT

A

Na/H antiport

50
Q

What do the peripheral chemoreceptors respond to

A

changes in pO2, pCO2 and pH

51
Q

What are the 4 steps of atheromatous plaque formation

A
  • endothelial dysfunction
  • stable plaque formation
  • T-cell activation
  • Ulceration and thrombus formation
52
Q

What is an ischaemic cascade

A

A series of biochemical reactions which are initiated in the brain and other aerobic tissues after seconds/minutes of ischemia

53
Q

Define specificity

A

percentage of healthy people who will have a negative test (true negative rate). Few false positives

54
Q

How do the lungs contribute to the acid base balance

A

CO2 is acidic and a waste product of cell metabolism. The blood carries it to the lungs where it is exhaled. The brain regulates the expiration of CO2 by increasing/decreasing ventilation as necessary.

55
Q

Define positive predicted value

A

The proportion of positive tests that come from those with the disease

56
Q

What are the two pathways of the clotting cascade called

A

Intrinsic and Extrinsic

57
Q

In an ABG, what should pH be

58
Q

If there are low 02 levels, what isn’t generated

59
Q

When do blood clots form

A

After damage to a blood vessel

60
Q

Whe local H rises, what do the central chemoreceptors do

A

stimulate the respiratory centres to increase ventilation

61
Q

State 2 common atheroma sites

A 
particularly prevalent where there is a bifurcation
	Abdominal aorta
	Coronary Arteries
	Carotid Arteries
	Cerebral Arteries
	Leg arteries
62
Q

How do the buffer systems contribute to the acid base balance

A

These are a combination of the body’s own weak acids and bases e.g. carbonic acid and bicarbonate ions

63
Q

In an ABG, what should Base Excess be

A

-2 –> +2

64
Q

Why does PDK-1 prevent the entry of pyruvate into the TCA cycle

A

(PDK-1) inhibits the conversion of pyruvate into acetyl-CoA by pyruvate dehydrogenase (PDH)

65
Q

In an ABG, what should PCO2 be

A

35-45 mmhg

66
Q

What can occlusion of one of the vertebral arteries cause

A

serious consequences, ranging from blindness to paralysis.

67
Q

In an ABG, what should PaO2 be

A

80-100mmhg

68
Q

Describe the cell activation stage of atheromatous plaque formation

A

a. Th1 and Th2 recruited and activated
b. Matrix metalloproteinases produced by foam cells
c. Proinflammatory cytokines released
d. MMPs break down the fibrous cap

69
Q

How long does it take for CK-MB
CK-BB
CK-MM
to appear

A

Appears 4-6 hours
Peaks 24 hours
Returns to normal 48-72 hours

70
Q

What causes strands of fibrins to stick together and seal the inside of a wound

A

clotting factors

71
Q

What are the main 5 components of the circle of willis

A

the anterior cerebral artery, the anterior communicating artery, the internal carotid arteries, the posterior cerebral artery, and the posterior communicating artery.

72
Q

What is the function of cerebral arteries

A

perfuse the cerebrum of the brain.

73
Q

What cells detect changes in oxygen concentration

A

glomus cells

74
Q

Describe the stable plaque formation stage of atheromatous plaque formation

A

a. Many foam cells in the intima
b. Vascular smooth muscle cells migrate from tunica media, proliferate, and act like myofibroblasts to produce collagen
c. Fibrous cap containing collagen fibres forms

75
Q

What could happen if there is a decrease in blood flow through one of the internal carotid arteries

A

impairment in the function of the frontal lobes. This impairment may result in numbness, weakness, or paralysis on the side of the body opposite to the obstruction of the artery

76
Q

Explain the steps of an ischaemic cascade

A
  1. Lack of oxygen causes the neuron’s normal ATP production system to fail
  2. It begins producing lactate via anaerobic glycolysis
  3. ATP reliant ion transport pumps fail too, and the cells become depolarised allowing calcium to flow into the cell
  4. Intracellular calcium levels get too high (excitotoxic effect)
  5. Glutamate is released by the presence of calcium
  6. Glutamate stimulates AMPA receptors and Ca permeable NMDA receptors, allowing more calcium into the cell
  7. Excess Ca overexcites the cell and causes the generation of free radicals, reactive oxygen species and calcium-dependent enzymes e.g. calpain
  8. The cell membrane is broken down by phospholipases and becomes more permeable
  9. Mitochondria breakdown, releasing toxins and apoptic factors into the cell
  10. The caspase-dependent apoptosis cascade is initiated
  11. The dead cells release glutamate and toxins which poison nearby neurons
  12. The brain can be perfused and undergo reperfusion injury
  13. Phagocytic cells engulf damaged, still viable tissue
  14. Cerebral oedema occurs due to the leakage of the blood brain barrier
77
Q

Define sensitivity

A

percentage of patients with the disease that correctly test positive for disease (true positive rate). Few false negatives

78
Q

Metabolic alkalosis:
A) increased Ph, Increased H, decreased HCO3 and increased pCO2
B) increased Ph, decreased H, increased HCO3 and increased pCO2
C) Increased Ph, Increased H, decreased HCO3 and decreased pCO2
D) decreased Ph, decreased H, decreased HCO3 and decreased pCO2

A

B) increased Ph, decreased H, increased HCO3 and increased pCO2

79
Q

Define reperfusion

A

Return of blood supply, so O2 levels rapidly increase

80
Q

Give 3 specific cardiac biomarkers

A 
CK-MB
CK-BB
CK-MM
cTnI
cTnT
81
Q

Describe atherosclerosis

A

fatty plaques (atheroma’s) builds up on the lining of your arteries, narrowing them. Over time, this builds up and can block them completely.

Disease, Diagnostics and Therapeutics (14 decks)

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