ischaemia and infraction Flashcards

1
Q

the cardiovascular system:
* The cardiovascular system comprises all — , — and—
* All roads lead to and from the — (indirectly the — system)
* Vessels are lined by — cells

A

blood vessel , heart , lymphatics
heart
lymphatic system
endothelial cells

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2
Q

isechemia:
Reduced — and/or increased —
requirements but no —
* Characterised by insufficiency of —, lack of — substrates and inadequate— of metabolites(— )
1. Blood not getting—
2. Increase in — by tissue
3. Blood not getting –

A

blood supply
tissue
necrosis
02
nutrients
removal ( perfusion )
in
requirements
out

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3
Q

susceptibility of tissue ischaemia:
1. Poor — e.g. atheromatous arterial supply
2. Presence or absence of — circulation– (latter may compensate for reduced — )
 Good collateral circulation:
- Liver, lung, bowel, brain (arterial anastomoses)
 Poor collateral circulation:
- Kidney, spleen +/- heart
3. — Requirements
 Organs with — metabolic rate and aerobic metabolism — susceptible (heart)
 Supporting tissues (—, —) — susceptible
- suspectibiltiy to schema/infraction:
* Vulnerable tissues
 ‘ —’ areas (esp. during—/—)
- Splenic flexure of the—
- — ant/middle cerebral artery
- Deep —
* ‘One main supplying— ’ - pituitary, renal, exocrine pancreas

A

blood supply
collateral ciruclation
perfusion
tissue metabolism
high
more
fibrous, bone
less
watershed
shock/hypotesnion
colon
brain
deep myocardium
artery

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4
Q

ACUTE/CHRONIC ISCHAEMIA
* Acute ischaemia - thromboembolus to — , intermittent — , — , acute — ischaemia
* Chronic ischaemia - — lower limb — changes, ischaemic —
* Do not let ischaemia turn into –!
* Stercoral ulceration of rectosigmoid colon is a – —-impacted – faeces - local — of — wall by hard faeces —-
-faecal peritonitis - one study only 8% cases diagnosed
preoperatively

A

leg
claudication
angina
mesenteric
chronic
trophic
colitis
infraction
chronic
consotpation
hard
local pressure ishcmeia
bowel wall
perforation

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5
Q

reperfusion injury is due to – of blood supply following – of blood supply
* Restoration of blood flow after ischaemia may cause a — increase in —
* This is due to:
 Formation of — following— of — supplied to cells
 Failure of — pumps - cells unable to control levels of cytosolic – and accumulation in —
 Calcium excess causes loss of cell — and —
 Neutrophils, Reduction NO, cytokines, complement
* Clinically relevant with — into — and —
 Amenable to- – intervention e.g. Tx: calcium channelblockers to slow the re-entry of Ca into cells
 See Robbins for more info

A

restoration
loss
paradoxical
cell injury
free radicals
restoration of 02
Ca2+-ATPase
calcium
mitochondria
cell integrity and cell death
haemorrhage into cerebral and myocardial infracts
therapeutic

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6
Q

infraction : cell/tissue – due to – blood supply
* Area of — caused by — of either the — supply or the — drainage in a particular tissue
* What are the commonest sites for death due to ischaemic necrosis? (Infarction)
* Define necrosis – Cell death in living tissue. A form of
cell death caused by loss of membrane intregrity, intracellular organelle swelling and ATP depletion
leading to an influx of calcium, it is always pathological
- common clinical illnesses due to infraction :
* Myocardial infarction
* Cerebrovascular accident (infarct)
* Pulmonary infarction
* Bowel infarction
* Ischaemic necrosis of the extremities - what does this
mean?

A

death
reduced
ischaemic necrosis
occlusion
arterial
venous drainage

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7
Q

causes of ishcemeia and infraction reduced blood supply:
* —
 Hypotension
 Septic
 Cardiogenic
*— of blood vessel
 ATHEROSCLEROSIS
 THROMBOSIS
 EMBOLUS
* Other
 Vasculitis
 Local vasospasm e.g. cocaine
 Extrinsic compression of vessel
 Extrinsic compression of blood supply by oedema or entrapment
(hernia)
 Torsion of vessel (testis)
 Traumatic rupture of blood supply
* Which is the commonest cause in an artery and which in a vein?

A

shock
obstruction

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8
Q
  • Definition of Thrombosis: — mass in — blood
  • Definition of Embolus:— or — or— mass that moves from one part of the circulation to another
    1- causes of thrombi :
    *— Triad
  • — damage
  • Must be able to give clinical causes of these
  • Causes differ in arteries and veins
    2- types of emboli:
  • Thrombus
  • Tumour
  • Septic
  • Fat
  • Air
  • Cholesterol
  • Foreign Body
  • Nitrogen
  • Amniotic fluid
A

solid
flowing
solid/gaseous/liquid
Virchow’s
endothelial
hyper coagulability
stasis

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9
Q

macroscopic appearances of infract:
* — shaped (occluded vessel at apex)
* Early
 — defined, —
 Narrow rim of — at edge due to inflammation/repair
* Late
 Solid organ ( — )
 Few RBC — –> some haemosiderin pigment
 — and — defined
 Spleen heart kidney
* — Infarction
 this infarctions appear – due to— of — (extravasation). These can be seen in situations where a vessel
becomes twisted such as—. They can be seen in organs that have a loose — (lungs, brain, GIT) where there is a – blood supply.

A

wedged
poorly , iregular
hyperaemia
white
lysed
pale and sharply defined
haemorrhage infraction
red
escape
red blood cells
torsion
parenchyma
dual
( pls check slide 20 and other slides for pics )

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10
Q

microscopic features of infracts:
* May be — in first – to — , only—- (if patient survives)
 — tissue stimulates — response at — (—)
 — of cellular — and – tissue
 — phase with — formation
— exception –> — necrosis

A

little
12 to 18 hrs
haemorrhage
necrotic
inflammatory
edge
1-2 days
phagocytosis
debris and dead tissue
reparative
scar
brain
liquefactive

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11
Q

anticoagulant in brain infraction:
* Why are you very careful of giving anticoagulants in a brain infarct due to a thrombus or embolus?
* An infarct in the brain may become—Why?
* — also ischaemic and ruptures
* Worsen situation by converting an — infarct to an— infarct

A

haemorrhage
vessel wall
ischemic
hameorrhagic

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12
Q

myocardium w polymorphs MI early:
- acute inflammatory cells ( — ) in between necrotic cells within —
- healing: 1-2 weeks replacement by — tissue
- scar: — tissue deposition causing scar formation

A

polymorphs
24 hours
granulation tissue
fibrous

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13
Q

what are the consequences of scar/fibrosis of myocardium following an infract:
* Loss of — function, causing —
failure
summary on microscopical changes in infraction in response to necrosis:
* Cell —
* acute —
* chronic—
*— tissue
*—
* Must be able to define all of these

A

muscle pump
left ventricular
necrosis
inflammation
inflamamtion
granulation
scar

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14
Q
  • types of necrosis - review :
    Definition: Necrosis cell – in – tissue
  • Coagulative - —
  • Liquefactive - —
  • Gangrenous - —
  • Fat necrosis - Trauma to –
  • Caseous - —
A

death
living
MI
stroke
diabetes
fat
TB

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15
Q
  • factors determining degree of ishcmia/infraction summary:
  • Availability of — blood supply
    lungs, liver, vs kidney, spleen
  • — of development of —
    e.g. coronary arteries & atherosclerosis
  • — of tissue
    Neuron( — mins) vs Myocyte (—mins) vs Fibroblast (– )
  • — content of blood –— increases
    likelihood of ischaemia
  • summary ischmaeia vs hypoxia:
     Hypoxia: – deficiency, causes —
     Ischaemia: – of blood supply due to impeded — flow or— drainage
     — is ischaemic necrosis
     Myocardial infarct and stroke are the 2 major vascular killers in Ireland
A

alternative
rate
occlusion
vulnerability
3-4 min
20-30 min
hours
oxygen
anaemia
oxygen
cell injury
loss
artieral
venous
infraction

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