Brainscape's Knowledge GenomeTM

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


See full index

Y2 EMS- Theme 2- Genetic And Environmental Causes Of Disease > 2. Ischeamia Infarction And Shock > Flashcards

2. Ischeamia Infarction And Shock Flashcards

1
Q

What is hypoxia

A

O2 supply to tissues is impaired

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

What is Ischemai

A

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

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

Why does ischemia injure tissue faster than just hypoxia

A

Lack of glucose in hypoxia means that gylcolytic anaerobic respiration fails

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

What is cell death

A

Irreversible cell injury (reiuslting from prolonged ischamia)

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

What is necrosis

A

Individual cell death in ischaemia

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

Infaraction meaning

A

Tissue necrosis caused by ischaemia

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

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

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

Why are the kidneys or spleen vulnerable to infarction

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

How can ischamia be reversible

A

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

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

A

Quick - 3 to 4 mins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

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

A

20 to 30 mins

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

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

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

Where does liqufactive necrosis seen

A

Only brain

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

Difference between red and white infarction

A 
White = organs with single blood supply 
Red= organs with dual blood supply
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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

At what stage of an MI does dark mottling occur

A

12 to 24 hrs

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

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

A

1 to 3 days

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

A

1 to 2 weeks

25
Q

After how many weeks of an Mi does a fibrous scar form

A

2 to 8 weeks

26
Q

What is reperfusion

A

Re- establishing blood flow to an organ

Good if done in early stages of ischamia

27
Q

How can sudden reperfusion lead to tissue damage

A
  • 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
Q

What percentage of final infarcts may be due to reperfusion injury

A

50%

29
Q

What treatment can be used to prevent reperfusion injury

A

Antioxidants

Anti imflammortory treaemtnt

30
Q

Shock meaning

A

State of reduced SYSTEMIC tissue perfusion (systemic hypoperfusion) due to cardiovascular collapse

31
Q

How does shock affect mean arterial pressure MAP

A

Reduces it

32
Q

What is MAP

A

Pressure of blood pumping through body

33
Q

Is shock reversible

A

Only initially yeS

34
Q

What is stroke volume

A

How much blood is in the heart

35
Q

What two factors affect MAP

A

Cardiac output

Total peripheral resistance

36
Q

What do norepinephrine and epinephrine control

A

(Sympathetic)

How restricted or dilated the blood vessels are

37
Q

A reduction in cardiac output or systemic vascular resistant acne can lead to what

A

Shock

38
Q

What is hypovalemic shock

A

Intravascular fluid loss (blood, plasma etc)
Less venous return to heart
Less stroke volume
Less cardiac output

39
Q

How does the body try to compensate in hypovaliemc shock

A

Tries to increase MAP by:

  • increases heart rate
  • constrict vessels to increase teh total peripheral vascular resistance
40
Q

How will a patient with hypovaleimic shock present

A

Tachycardic
Cool, peripherally shut down
Normal blood pressure

41
Q

Give two causes of hypovaleimic shock

A

Haemorrhage

Fluid loss

42
Q

What is cardiogenic shock caused by

A

Cardiac pump failure - less cardiac output

MAP drops

43
Q

How does the body compensate in cardiogenic shock

A

Increases total peripheral resistance

Cool, periperhally shut down

44
Q

Give 4 causes of cardiogenic shock

A

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
Q

What is distributive shock

A

Severe vasodilation that decreases MAP

46
Q

How does body compensate in distributive shock

A
  • increase cardiac output

- increase stroke volume

47
Q

How does a patient with distributive shock present

A

Flushed
Warm esp, with septic shock
Bounding heart BOIZ

48
Q

What is mixed shock

A

When diff types of shock co exist in combination

49
Q

Which three types of shock may be present in septic shock

A

Primary distributive component
Hypovaleimic component
Cardiogenic component

50
Q

What is heamopericaridum

A

Blood in the pericardial sac of the heart

Y2 EMS- Theme 2- Genetic And Environmental Causes Of Disease (7 decks)

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