Pathology basis of disease Flashcards

1
Q

What is the 5 pathological processes?

A
  1. cell injury, necrosis
  2. immunology, inflammation and repair
  3. circulatory disturbance
  4. disorders of growth
  5. pigmentations and deposits
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2
Q

What is the 4 groups of changes in circulatory disturbances?

A
  1. fluid distribution imbalance
    - oedema
  2. disorder of haemostasis
    - haemorrhage
    - inappropriate coagulation (thrombosis/ bleeding disorder)
  3. hyperaemia and congestion
  4. infarction and ischaemia
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3
Q

What is disease?

A
  • it is an abnormality of tissue structure or function (lesion)
  • the outcome of the host-pathogen-environment interactions
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4
Q

What are the factors of H-P-E interactions?

A
  1. agent of disease
  2. effect on host
  3. host response
  4. environment
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5
Q

what is the 4 stages of infectious disease?

A
  1. exposure
  2. colonisation
  3. sub-clinical
  4. clinical
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6
Q

what will free radical do to skin?

A

free radical formation in skin causing cell membrane damage and subsequent cell death, leading to inflammation.

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7
Q

what does cell injury first starts with?

A

cell injury first starts with biochemical alterations. morphological. changes lag behind biochemical changes so a cell showing chnages consistent with moderate cell injury may already be dead.

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8
Q

What is the difference between clinical pathology and anatomical pathology?

A

clinical pathology:
- attempt to detect biochemical changes

Anatomical pathology:
- attempt to detect morphological changes

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9
Q

when will cell injury occur?

A

once the cell’s adaptive capacity is surpassed, it is unable to respond to functional demands for homeostasis: cell injury occurs.

cell injury can be reversible (recovery), but past that point the cell dies (irreversible injury)

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10
Q

cell degeneration and necrosis can lead to:

A
  1. cell injury (cell degeneration)
    - mainly cytoplasmic changes for degeneration (reversible) cloudy swelling, hydropic change, fatty degeneration.
  2. cell death (necrosis and apoptosis)
    - follows mainly detecting nuclear changes e.g. pyknosis, karyorrhexis, karyolysis for cell death
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11
Q

what is the causes of cell injury

A
  1. physical agents
    - heat, radiation, cold
    -the extent of the injuries may be increased by local hypoxia associated with vascular damage
  2. chemical agents
    - toxins, poisons, drugs, metabolites
    - free radicals
  3. genetic factors
    - often operate through deviant biochemical mechanisms that lead to atrophy, dystrophy or even cell death e.g. storage diseases.
  4. infectious agents
    - virus, bacteria, fungi, protozoa, algae, metazoan parasites, prions/infectious proteins
  5. by-products of inflammation/ immunity
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12
Q

2 major causes of cell injury:

A
  1. membrane damage
    - plasma and/or organelle membranes- due to altered biochemical synthesis or structural disruption of molecules
  2. energy (ATP) depletion
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13
Q

how is membrane being damaged?

A
  • many agents damage cell membranes via intermediates known as free radicals.
  • free radicals are highly reactive oxygen species with very short half lives
  • chain reaction such as lipid peroxidation can cause widespread membrane damage and more.
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14
Q

list anti-oxidants in cells.

A
  1. superoxide dismutases
  2. catalases
  3. vitamin E
  4. glutathione
  5. selenium
  6. ascorbate
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15
Q

How will energy (ATP) depletion leads to cell injury?

A
  • Na-K-ATPase ion pump fails if ATP production is disrupted.
  • membrane damage is followed by influx of Na2+, Ca2+ and H2O into the cell and its organelles
  • this leads to cellular and mitochondrial swelling which further disrupts aerobic respiration
  • water influx leads to cellular swelling and mitochondria swelling which will have an on going effect on energy production
  • hypoxia is the most common reason for ATP depletion, as oxygen is vital for energy production.
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16
Q

what may hypoxia develop?

A

hypoxia may develop with a leision anywhere from the nostrils down to mitochondrial enzymes and so may involve:
1. air not reaching the lungs

  1. oxygen not reaching the blood
  2. oxygenated blood not reaching the tissues
    - circulatory disturbance
    - reduced O2 carrying capacity of blood
  3. respiratory poisons acting at specific cellular sites in the respiratory pathway
17
Q

How can ATP be produced in hypoxia?

A
  • in hypoxia, ATP is produced by anaerobic glycolysis which yields much less energy and produces lactic acid which lowers cell pH and inhibits enzymic activity
  • cells with higher metabolic rates (e.g. neurons, myocardial fibres, hepatocytes, renal epithelium) are more susceptible to hypoxia
18
Q

What is the light microscopic changes of cell injury seen in the cytoplasm?

A
  1. membrane failure leads to cytoplasmic swelling (cloudy swelling) - often sublethal and reversible
  2. hydropic degeneration as water accumulates fine vacuoles
  3. small or large lipid droplets (vacuoles) can accumulate (fatty change/ fatty degeneration)
  4. Vacular change (water or lipid) is reversible up to point, but then becomes irreversible leading to cell death.
19
Q

when does reversible cell injury become irreversible?

A
  • become irreversible when it loses the ability to restore mitochondrial function
  • ATP depletion
  • profound disturbances in membrane function
  • ATP is likely yo be the critical substrate determining irreversible cell damage.
20
Q

state the 2 mechanisms in irreversible cell injury (necrosis).

A
  1. oncosis (swelling) = continuum with sublethal cell injury [nuclei can be pyknotic/ karyorrhectic and finally karyolytic]
  2. Apoptosis = programmed cell death
21
Q

what things are with brown pigments?

A
  • haemosiderin
  • bile pigments
  • copper
  • melanin
  • lipofuscin
  • artefact- acid haematin
    etc
22
Q
A