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PATH2220 > W8 > Flashcards

W8 Flashcards

1
Q

what are the causative agents of cellular injury

A
  • Trauma
  • Thermal injury HOT or COLD
  • Poisons
  • Drugs
  • Infectious organisms
  • Ionising radiation
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2
Q

what is ischaemia and infarction

A

Ischaemia is brought on by reduced blood flow
• No transfer of oxygen to cells
• No transfer of fuel/glycolytic substrates Accumulation of metabolites
Mechanisms include occlusion of the blood flowvia end arteries to the organs
The injury is amenable to repair up to a certain point of no return and ultimate cell damage and death

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3
Q

what is shock

A

Shock is a pathological process characterised by profound circulatory failure resulting in life threatening hypo perfusion of the bodies vital organs. Compensatory mechanisms maintain blood pressure until they fail leading to hypotension

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4
Q

what is the classification of shock

A

Cardiogenic - commonly due to myocardial infarction - failure of the heart’s pumping mechanism
• Hypovolemic - due to reduction in the effective circulation blood volume - loss of blood, loss of fluid, shift of fluid into the cellular component and body cavities and away from the circulation; examples include:
o anaphylactic reaction - change in permeability
o extensive burns - loss of fluid through exposed skin surface o bacterial toxaemia

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5
Q

what are the consequences of shock

A

irreversible neural damage
• renal failure
• cerebral infarction
• infarction distal to any area of pathological narrowing within feeding blood vessels

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6
Q

how does trauma lead to cell death

A
  • Disrupting cells (example shearing force)
  • Denaturing proteins (breaking its structure)
  • Causing vascular thrombosis/blocking of blood flow - which in turn leads to ischaemia and infarction
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7
Q

what are the ways that tumour can cause damage

A
  • direct pressure effect on adjacent tissues and organs can lead to pressure effect and loss of blood flow to adjacent organs leading to ischaemia and cell death
  • tumours can compress and even infiltrate blood vessels leading to decreased blood flow downstream and causing ischaemic damage and cell death
  • Some tumours release hormones and active components that can cause systemic effects and subsequent damage as seen in the paraneoplastic syndromes
  • Destructive effect with metastasis and direct invasion - for example destruction of bony vertebrae by prostatic adenocarcinoma
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8
Q

what are tumours

A

Tumours result from genetic alteration in cells with subsequent loss of cell growth regulators resulting in abnormal ‘neoplastic’ growth.

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9
Q

what are the two phases of inflammation

A

Initial reaction of tissue to injury

  1. Vascular phase - dilation and increased permeability
  2. Exudative phase - fluid and cells escape from the permeable venules
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10
Q

what are the outcomes of inflammation

A
  • Resolution
  • suppuration/puss/abscess
  • Organisation
  • progression to chronic inflammation
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11
Q

what are the consequences of acute inflammation

A
  • Inflammatory cell infiltrate
  • Increased vascularity and blood flow
  • Increased permeability
  • Cell build up and attraction via chemotaxis
  • Cytokines, enzymes, factors and other inflammatory mediators
  • Resolution
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12
Q

what are the complications of healing

A
  • Dehiscence
  • Hypertrophic scar
  • Keloid
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13
Q

how can cellar injury affect the cell

A 
On a cellular level
• Blockage of protein synthesis - glucose deprivation
• Prevention of oxygen utilisation – deprivation
• Failure of membrane integrity
o complement mediated cytolysis - end product of
complement cascade
o Perforin mediated cytolysis
o Blockage of ion channels
o Failure of membrane ion pumps
o alteration of membrane lipids
o cross linking of membrane proteins
• Build up of free radicals - toxic
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14
Q

how can cellar injury affect the nucleus and nucleolus

A
  • Damages both transcription and translation
  • If the cell goes into mitosis before the damage is repaired it leads to cell death
  • Damaged DNA can lead to mutations
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15
Q

how can ceulluar injury affect the mitochondria

A
  • Damage to mitochondria leads to impairment of the metabolic pathways
  • This results in energy deficiency, particularly of ATP within the cell
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16
Q

how can cellular injury affect the lyosome

A

Injury of lysosome leads to cell degeneration - the liberation and activation of the enzymes leads to autophagy/ self digestion

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17
Q

what are the 4 different adaptation methods to cellar injury

A

hypertrophy, hyperplasia, atrophy, metaplasia

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18
Q

what is hypertrophy

A
  • Increase in the size of individual cells resulting in overall increase in organ size.
  • Example: increased workload on a muscle
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19
Q

what is hyperplasia

A
  • Increase in the number of cells in an organ, also resulting in an increase in organ size.
  • Example: Thickened keratinising squamous epithelium of skin in area of rubbing or chronic irritation
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20
Q

what is the atrophy

A

Decrease in cell size and number of cells.

• Example: Disuse limb immobilised following fracture or loss of innervation

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21
Q

what is metaplasia

A

Reversible change from one differentiated cell type to another.
• Example:Intestinal metaplasia in the oesophagus in the setting of reflux disease

22
Q

what does the effect of the injury depend on

A

Duration of injury
• Nature of the injurious agent
• the amount of tissue/cells involved and the type of cells
• ability of the tissue involved to regenerate

23
Q

what are the different outcomes to cellular injury

A
  • Necrosis - cell death any cause
  • Apoptosis - programmed cell death and energy dependent process to get rid of unwanted cells - without eliciting a inflammatory reaction
  • Inflammation - defend against foreign agents, mop up dead and damaged cells, immobilise injured area (swelling)
  • Cell renewal - regeneration by replacement from stem cell pool - complete restoration
  • Organisation/scarring
24
Q

how can blunt trauma cause problems

A

• Bruising/contusion- blunt impact tears the capillaries and larger blood vessels deep to the skin surface, leading to bleeding into the extravascular space
or
• laceration- when the blunt object injury exceeds the elastic capacity of the skin and underlying tissues forceful tearing of the skin occurs
or
• avulsion- tearing away of tissue from its attachments for instance skin torn from thigh after fall from height

25
Q

what is incision

A

longer in length than it is deep

26
Q

what is a stab wound

A

deeper than it is long

27
Q

what are problems with fracture healing

A 
Movement
• Interposed soft tissue
• Gross misalignment
• Infection
• Pre existing bone disease
28
Q

what is myocardial infarction

A

“irreversible necrosis of myocardium due to inadequate blood flow”

29
Q

what is the path-physiology of myocardial infarction

A

 Inadequate blood supply (O2) for the needs of the myocardium.
 Caused by a narrowing or blockage of blood vessels supplying the heart.

30
Q

what does the site and degrees of damage of myocardial ischaemia and infarction depend on

A

 Which vessel is affected and how far along  How narrow the stenosis
 How great the demands
 How long the imbalance (30 minutes)
 How soon intervention

31
Q

what are the risk factors for atherosclerosis

A 
 Family History
 Cigarette smoke
 Diabetes
 Hyperlipidaemia
 Infections
 Haemodynamic forces (Hypertension)  Immune mechanisms
32
Q

what is angina and what are the symptoms of myocardial infarction

A

cardiac pain that arises from cardiac ischaemia due to inadequate blood flow. causes nausea and vomiting, shortness of breath

33
Q

what are some investigations for myocardial infarct

A

electrocardiogram, blood tests, angiography,

34
Q

what are the supportative treatment for myocardial infarction

A

 Rest, lying flat, O2

 Glyceryl trinitrate GTN (dilates arteries)  Betablockers(slowsheartrate)

35
Q

what are the acute treatments for myocardial infarct

A

 Thrombolysis (dissolves the clot)  Stenting (opens up the stenosis)

36
Q

what is the chronic treatment methods for myocardial infarction

A

 Aspirin (decreases platelet stickiness)  Stenting

 Bypass

37
Q

what is the acute consequences of myocardial infarction

A

 Sudden death (40%)
 (from acute left ventricular failure  from an arrhythmia)
 Other arrythmias
 Mural thrombus and thromboembolism
 Rupture (free wall or septum or papillary muscle)

38
Q

what is the chronic consequences of myocardial infarction

A 
 Heart failure
 Left ventricular or bi-ventricular
 Arrythmias
 Ventricular aneurysm  mural thrombus
 thromboembolism
39
Q

define cerebro-vascular accident

A

A focal neurological deficit that persists for >24hr and is due to a vascular cause

40
Q

what is the pathophysiology of a stroke

A

1.
Narrowing or blockage of blood vessels supplying the brain
 Thrombus (50%)
 Embolus (30%)
2. Rupture of a vessel (hypertension or aneurysm) with haemorrhage (20%)

41
Q

describe brain ischemia

A

 The brain highly dependant on aerobic metabolism and therefore very sensitive to hypoxia.
 Irreversible neuronal damage occurs after a few minutes.
 Critical ischaemia is when the neurone receives 30% of normal O2 supply – then it will shutdown.
 It implies inadequate blood supply (O2) for the needs of the brain.

42
Q

what are the three type of cerebral aneurysm

A

saccular, fusiform and ruptured

43
Q

what doe site site and degrees of damage for a cerebro-vascular accident depend on

A

 Which vessel is affected and where
 How complete the block
 How long the ischaemia (30 minutes)
 How soon intervention

44
Q

what is the macroscopic features of a CVA

A

 Soften, loss of definition, pale or haemorrhagic  Shrunken, yellow, cystic

45
Q

what is the microscopic features of a CVA

A

 Neuronal necrosis, pallor of myelin, oedema, haemorrhage
 Macrophages, gliosis but no fibrosis, cystic change instead of scarring
 haemosiderin

46
Q

what is the clinical prevention for a stroke

A

Pain
Clinical presentation
 A decrease or loss of consciousness, ie coma.
 Symptoms and signs are variable and depend on the site of damage and the function of that area

47
Q

what is the symptoms and signs of a CVA

A

Neurological deficit (depends on region involved)  Sensory
 Motor
 Speech - receptive and expressive dysphasia  Visual
 Memory
 Tremor/ balance/ vertigo (cerebellar)

48
Q

what might a patient die because of a stroke

A

 Critical areas are affected (brain stem)  The damage is too massive
 Increased intracranial pressure can cause coning, ie trying to squeeze the brain out of the skull through the foramen magnum

49
Q

what are the investigations for CVA

A

x-rays, angiography,

50
Q

what is the acute treatment for CVA

A

 Support
 Thrombolysis
 Clipping of an aneurysm  Evacuation of blood clot

51
Q

what is the chronic treatment for CVA

A

Chronic  Aspirin

52
Q

what is the prevention techniques for CVA

A

 Atherosclerosis
 HT, smoking, hypercholesterolaemia, DM
 Stent, bypass, surgery of atherosclerotic stenoses  Aneurysm repair
 Anti-platelet agents

PATH2220 (14 decks)

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