2. Ischeamia Infarction And Shock Flashcards

(50 cards)

1
Q

What is hypoxia

A

O2 supply to tissues is impaired

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2
Q

What is Ischemai

A

Interruption/ disturbance of blood flow to cells and tissues
- reduces o2 and metabolites

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3
Q

Why does ischemia injure tissue faster than just hypoxia

A

Lack of glucose in hypoxia means that gylcolytic anaerobic respiration fails

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4
Q

What is cell death

A

Irreversible cell injury (reiuslting from prolonged ischamia)

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5
Q

What is necrosis

A

Individual cell death in ischaemia

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6
Q

Infaraction meaning

A

Tissue necrosis caused by ischaemia

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7
Q

Describe the mechanism of isahcmic cell injury

A

Reduced oxidative phosphorylation = reduced ATP
Switch to anaerobic respiration = more lactate, glycogen stores depleted
Failure of Na pump = accumulation of Na
Membrane damage
Failure of Ca pump = influx of Ca
Less protein synthesis

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8
Q

Give 6 causes of ischaemia

A
Vascular occlusion- atherosclerosis, thrombus etc
Vasospasm 
Vascular damage- vasculitis or rupture 
Extrinsic compression-eg tumour
Mechanical interruption 
Hypoperfusion
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9
Q

Give an example of tissues with a dual vascular supply that are resistant to infarction of a single vessel

A

Lungs - pulmonary and bronical arteries
Liver
Hand - radial n ulnar artery

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10
Q

Why are the kidneys or spleen vulnerable to infarction

A

They have end-arterial circulations so one artery supplies one region

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11
Q

How can ischamia be reversible

A

Short duration - cell injury in ischamia is reversible for limited time

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12
Q

Why are slow developing tissues less likely to infarction tissues

A

It allows time or the development of collateral supply eg in heart

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13
Q

How long does a neurone in the brain take to undergo irreversible cell damage

A

Quick - 3 to 4 mins

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14
Q

How long does a cardiac mycoyte take to undergo irreversible cell damage

A

20 to 30 mins

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15
Q

What is coagulative necrosis

A

Most common
Predominant mode of injury is denaturation
Includes enzymes
Unable to break down cell structure = basic cell outline preserved for ew days = tissue feels firm
Eosinophilic ghost cells

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16
Q

What is the primary mode of cell injury in Liquifactive necrosis

A

Enzyme digestion
Cells completely digested n broken dow
Tissue is liquified
If area heals - forms cyst or cavity in brain

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17
Q

Where does liqufactive necrosis seen

A

Only brain

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18
Q

Difference between red and white infarction

A
White = organs with single blood supply 
Red= organs with dual blood supply
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19
Q

Why are most infarcts wedge shaped

A

Vessels in tissue can branch out in a triangular wedsged shape like a tree- so if a destruction occurs at an upstream point, the entire downstream area will become infarcted

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20
Q

At what stage of an MI does dark mottling occur

A

12 to 24 hrs

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21
Q

At what stage of an MI is there yellow with a haemorrhaging edge

22
Q

Why does dark mottling occur in an MI

A

Ongoing coagualtive necrosis = 12 to 24 hrs

23
Q

At what stage of an Mi does the yellow centre become soft

A

3 to 7 days

Dying neutrophils with macrophage infiltration

24
Q

At how many weeks does an infarcted heart become a red-grey colour

25
After how many weeks of an Mi does a fibrous scar form
2 to 8 weeks
26
What is reperfusion
Re- establishing blood flow to an organ | Good if done in early stages of ischamia
27
How can sudden reperfusion lead to tissue damage
- Generation of reactive o2 species which cant be combatted by ishchamic tissue due to it having membrane damage/ breakdown of proteins etc - cytokines recruit inflammatory cells which can flow into teh tissue during reperfusion - activation of complement pathway
28
What percentage of final infarcts may be due to reperfusion injury
50%
29
What treatment can be used to prevent reperfusion injury
Antioxidants Anti imflammortory treaemtnt
30
Shock meaning
State of reduced SYSTEMIC tissue perfusion (systemic hypoperfusion) due to cardiovascular collapse
31
How does shock affect mean arterial pressure MAP
Reduces it
32
What is MAP
Pressure of blood pumping through body
33
Is shock reversible
Only initially yeS
34
What is stroke volume
How much blood is in the heart
35
What two factors affect MAP
Cardiac output | Total peripheral resistance
36
What do norepinephrine and epinephrine control
(Sympathetic) | How restricted or dilated the blood vessels are
37
A reduction in cardiac output or systemic vascular resistant acne can lead to what
Shock
38
What is hypovalemic shock
Intravascular fluid loss (blood, plasma etc) Less venous return to heart Less stroke volume Less cardiac output
39
How does the body try to compensate in hypovaliemc shock
Tries to increase MAP by: - increases heart rate - constrict vessels to increase teh total peripheral vascular resistance
40
How will a patient with hypovaleimic shock present
Tachycardic Cool, peripherally shut down Normal blood pressure
41
Give two causes of hypovaleimic shock
Haemorrhage | Fluid loss
42
What is cardiogenic shock caused by
Cardiac pump failure - less cardiac output | MAP drops
43
How does the body compensate in cardiogenic shock
Increases total peripheral resistance | Cool, periperhally shut down
44
Give 4 causes of cardiogenic shock
Myopathic (heart muscle failure eg MI) Arrhythmia related Mechanical (eg valvular or ventricular septal defects, atrial myxoma = benign heart tumour) Extra cardiac cardiogenic shock ( something outside heart, eg massive PE)
45
What is distributive shock
Severe vasodilation that decreases MAP
46
How does body compensate in distributive shock
- increase cardiac output | - increase stroke volume
47
How does a patient with distributive shock present
Flushed Warm esp, with septic shock Bounding heart BOIZ
48
What is mixed shock
When diff types of shock co exist in combination
49
Which three types of shock may be present in septic shock
Primary distributive component Hypovaleimic component Cardiogenic component
50
What is heamopericaridum
Blood in the pericardial sac of the heart