2. Ischeamia Infarction And Shock Flashcards
What is hypoxia
O2 supply to tissues is impaired
What is Ischemai
Interruption/ disturbance of blood flow to cells and tissues
- reduces o2 and metabolites
Why does ischemia injure tissue faster than just hypoxia
Lack of glucose in hypoxia means that gylcolytic anaerobic respiration fails
What is cell death
Irreversible cell injury (reiuslting from prolonged ischamia)
What is necrosis
Individual cell death in ischaemia
Infaraction meaning
Tissue necrosis caused by ischaemia
Describe the mechanism of isahcmic cell injury
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
Give 6 causes of ischaemia
Vascular occlusion- atherosclerosis, thrombus etc Vasospasm Vascular damage- vasculitis or rupture Extrinsic compression-eg tumour Mechanical interruption Hypoperfusion
Give an example of tissues with a dual vascular supply that are resistant to infarction of a single vessel
Lungs - pulmonary and bronical arteries
Liver
Hand - radial n ulnar artery
Why are the kidneys or spleen vulnerable to infarction
They have end-arterial circulations so one artery supplies one region
How can ischamia be reversible
Short duration - cell injury in ischamia is reversible for limited time
Why are slow developing tissues less likely to infarction tissues
It allows time or the development of collateral supply eg in heart
How long does a neurone in the brain take to undergo irreversible cell damage
Quick - 3 to 4 mins
How long does a cardiac mycoyte take to undergo irreversible cell damage
20 to 30 mins
What is coagulative necrosis
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
What is the primary mode of cell injury in Liquifactive necrosis
Enzyme digestion
Cells completely digested n broken dow
Tissue is liquified
If area heals - forms cyst or cavity in brain
Where does liqufactive necrosis seen
Only brain
Difference between red and white infarction
White = organs with single blood supply Red= organs with dual blood supply
Why are most infarcts wedge shaped
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
At what stage of an MI does dark mottling occur
12 to 24 hrs
At what stage of an MI is there yellow with a haemorrhaging edge
1 to 3 days
Why does dark mottling occur in an MI
Ongoing coagualtive necrosis = 12 to 24 hrs
At what stage of an Mi does the yellow centre become soft
3 to 7 days
Dying neutrophils with macrophage infiltration
At how many weeks does an infarcted heart become a red-grey colour
1 to 2 weeks
After how many weeks of an Mi does a fibrous scar form
2 to 8 weeks
What is reperfusion
Re- establishing blood flow to an organ
Good if done in early stages of ischamia
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
What percentage of final infarcts may be due to reperfusion injury
50%
What treatment can be used to prevent reperfusion injury
Antioxidants
Anti imflammortory treaemtnt
Shock meaning
State of reduced SYSTEMIC tissue perfusion (systemic hypoperfusion) due to cardiovascular collapse
How does shock affect mean arterial pressure MAP
Reduces it
What is MAP
Pressure of blood pumping through body
Is shock reversible
Only initially yeS
What is stroke volume
How much blood is in the heart
What two factors affect MAP
Cardiac output
Total peripheral resistance
What do norepinephrine and epinephrine control
(Sympathetic)
How restricted or dilated the blood vessels are
A reduction in cardiac output or systemic vascular resistant acne can lead to what
Shock
What is hypovalemic shock
Intravascular fluid loss (blood, plasma etc)
Less venous return to heart
Less stroke volume
Less cardiac output
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
How will a patient with hypovaleimic shock present
Tachycardic
Cool, peripherally shut down
Normal blood pressure
Give two causes of hypovaleimic shock
Haemorrhage
Fluid loss
What is cardiogenic shock caused by
Cardiac pump failure - less cardiac output
MAP drops
How does the body compensate in cardiogenic shock
Increases total peripheral resistance
Cool, periperhally shut down
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)
What is distributive shock
Severe vasodilation that decreases MAP
How does body compensate in distributive shock
- increase cardiac output
- increase stroke volume
How does a patient with distributive shock present
Flushed
Warm esp, with septic shock
Bounding heart BOIZ
What is mixed shock
When diff types of shock co exist in combination
Which three types of shock may be present in septic shock
Primary distributive component
Hypovaleimic component
Cardiogenic component
What is heamopericaridum
Blood in the pericardial sac of the heart
