Topic 5 Flashcards

Pathological Changes (35 cards)

1
Q

Aetiology

A

Cause of disease

eg. smoking

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2
Q

Pathogenesis

A

Mechanism causng disease

eg. genetic alteration

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3
Q

Clinical manifestations

A

Functional consequences (signs and symptoms) eg. breathlessness

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4
Q

Epidemiology

A

Incidence, prevalence and distribution

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5
Q

Pathology

A

Molecular and morphologic changes to cells or tissues eg. lung tumor

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6
Q

Hyperplasia

A

Increase in cell number
Increase in organ size
Driven by growth factors

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7
Q

Hypertrophy

A

Increase in cell size
Increase in organ size
Driven by increased work load

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8
Q

Metaplasia

A

Change in cell type

Cells are replaced by others that can better withstand the stress

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9
Q

Atrophy

A

Decrease in cell number/size

Caused by reduced workload, neurovascular supply

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10
Q

Morphological changes of a reversibly injured cell (5)

A
  1. Cell swelling
  2. Organelle swelling
  3. Chromain clumping
  4. Blebbing
  5. Lipid vacuoles
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11
Q

Adaptation

A

A cellular response to an injurous stimuli/stress that doesn’t compromise cell function

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12
Q

Reversible cell injury

A

A cellular response to an injurous stimuli that compromises cellular function that can be reversed whenthe stimuli is removed

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13
Q

Irreversible cell injury

A

A cellular response to an injurous stimuli that compromises cellular function leading to cell death

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14
Q

Morphological changes of an irreversibly injured cell (2)

A
  • Mitochondrial dysfunction is irreversible

- Lysosomal, plasma and mitochondrial membranes lose structural integrity

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15
Q

Morphological changes of necrotic cells

A
  • denatured proteins
  • vacuolation - digested organelles
  • discontinuous membranes
  • myelin figures
  • DNA breakdown
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16
Q

Kayolysis (Necrosis)

A

DNA breakdown

decreased basophilia

17
Q

Pyknosis (Necrosis)

A

Nuclear shrinkage

Increased basophilia

18
Q

Karyorrhexia (Necrosis)

A

Nuclear fragmentation

19
Q

Coagulative (Necrosis)

A

Denaturation > digestion
Nucleus lost but architecture is preserved
Most common type
Due to ischaemia

20
Q

Liquefactive (Necrosis)

A

Digestion > denaturation
Complete enzymatic digestion of dead cells
Inflammatory response contributes to digestion
Associated with infection
Ischaemia in brain

21
Q

Caseous (Necrosis)

A

Digestion and denaturation
Mixture of liquefactive and coagulation
Architecture gone

22
Q

Fat (Necrosis)

A

Enzymes liquefy membranes of fat tissue
Released fat reacts with calcium to cause fat saponification/patchy white lesions
Most common in acute pancreatitis

23
Q

Fibrinoid (Necrosis)

A

Leakage of fibrin and inflammatory cells

Occurs in blood vessels in response to deposition of immune complexes

24
Q

Gangrenous (Necrosis)

A

Coagulative necrosis in a lower limb without blood supply

Liquefactive may accompany bacterial infection -wet gangrene

25
Phosphatidylserine
Protein flips to outer membrane to prevent inflammatory response in apoptosis
26
Necroptosis
Hybrid of necrosis and apoptosis Loss of ATP, swelling, increased ROS, rupture of membrane Caspase independent
27
Calor
Heat | Vasodilation -increased blood flow
28
Rubor
Redness - erythema -vasodilation and stasis
29
Tumour (inflammation)
Swelling - vasodilation and vascular permeability leading to extravasation of fluid
30
Dolor
Pain - compression of tissues, effect of inflammatory mediators
31
Functio laesa
Loss of function - effect of injury, pain, swelling
32
Serous inflammation
Watery protein poor fluid | Found in body cavities and skin blisters
33
Fibrinous Inflammation
High vascular permeability Exudate contains large molecules (fibrinogen) Characteristic of inflammation of meninges, pericardium, pleura
34
Supparative (puralent) Inflammation -PUS
Associated with pyogenic (puss inducing) bacterial infectial Heme of neutrophil gives exudate blue colour Absecesses
35
Ulceration
Necrosis and inflammation near the surface | Mucosa and lower extremities with poor circulation