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Phase 3 > Week 2 - General Pathological Mechanisms > Flashcards

Week 2 - General Pathological Mechanisms Flashcards

1
Q

What are the 4 main levels of magnification?

A
  1. Gross (naked eye)
  2. Light microscopy
  3. Electron microscopy
  4. Molecular cell biology
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2
Q

Define morphology

A

The appearance

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3
Q

What enzyme is required for DNA replication?

A

DNA polymerase

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4
Q

What enzyme is required for gene transcription?

A

RNA polymerase

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5
Q

What organelle is required for gene translation?

A

Ribosome

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6
Q

What are the 3 main cellular processes which can be disrupted in pathology?

A
  1. proliferation
  2. growth & differentiation
  3. cell death
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7
Q

What is involved in the process of cell growth and differentiation?

A
  • protein production
  • energy production
  • signalling with cells/ storm
  • maintenance of structure
  • maintenance of genome/DNA
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8
Q

What is the function of haemtolymphoid tissue?

A

Transportation

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9
Q

What are the 2 main things which, combined, cause disease to occur?

A
  1. Causative agent

2. The body’s response to it

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10
Q

Define homeostasis

A

Where normal cells can adjust to mild environmental changes

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11
Q

Give examples of external environmental stressors to a cell

A

Physical harm
Chemicals
Infection
Nutrition

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12
Q

Give examples of internal environmental stressors to a cell

A

Functional demand
Hormones/metabolic
Immune response

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13
Q

Define atrophy

A

Shrinking/ fewer cells

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14
Q

Define hypertrophy

A

Increase in cell size

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15
Q

Define hyperplasia

A

Increase in cell number

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16
Q

Define metaplasia

A

Change from one mature differentiated cell type to another

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17
Q

Define dysplasia

A

Abnormal genetic changes

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18
Q

Define neoplasia

A

The formation of an abnormal growth of tissue

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19
Q

List the progress of change from a normal cell to cell death

A

Normal -> cell with adaptation -> reversible injury -> irreversible injury -> cell death

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20
Q

What is the VITAMIN CDEF pneumonic for disease classification?

A 
Vascular
Infective/Inflammatory
Traumatic
Autoimmune
Metabolic
Iatrogenic/Idiopathic
Neoplastic
Congenital
Degenerative/ developmental
Endocrine/ Environmental
Functional
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21
Q

List the possible causes/mechanisms of disease

A
  • (Congenital versus acquired)
  • Physical agents
  • Chemicals/drugs
  • Infections
  • Hypoxia/ischaemia
  • Immunological reactions
  • Nutritional
  • Endocrine/ metabolic
  • Genetic disease
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22
Q

Examples of physical agents causing disease

A
  • Mechanical trauma - strictures, adhesions, hernia, violence
  • Temperature extreme
  • Ionising radiation(DNA damage)
  • Electric shock
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23
Q

Examples of chemical agents causing disease

A

Drugs (chemo/ paracetamol)
Poison (cyanide)
Environmental (insecticide)
Occupational hazard (asbestos)

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24
Q

What causes hypoxia?

A
  • Anaemia

- Respiratory failure

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25
Q

What is the difference between ischemia and hypoxia and whys the damage more severe?

A

Ischemia - loss of all blood supply, including oxygen and nutrients
Hypoxia - loss of oxygen only

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26
Q

What causes ischemia?

A

Blockage of arterial supply or venous drainage

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27
Q

Examples of immunological reactions causing disease

A

Anaphylaxis

Autoimmunity - antibodies attacking own antigens on cells OR antigen-antibody complexes and their deposition

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28
Q

What type of hypersensitivity is anaphalaxis?

A

type 1

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29
Q

What type of hypersensitivity is antigen-antibody complexes?

A

type 3

30
Q

What type of hypersensitivity is self antibodies attacking own cells?

A

type 2

31
Q

How do genetic defects lead to disease?

A

Too much/ little protein or an abnormal/different protein is produced , changing cell processes.

32
Q

How does damage to the mitochondria cause disease?

A

Disrupted aerobic respiration/ ATP synthesis

33
Q

How does damage to the cell membrane cause disease?

A

Disrupted ion concentrations, particularly calcium

34
Q

How does damage to the cytoplasm (including ribosomes) cause disease?

A

Disrupted protein synthesis and architecture

35
Q

How does damage to the nucleus cause disease?

A

Disrupted DNA maintenance and damage to DNA

36
Q

What is oxidative stress?

A

Where pathological amounts of oxygen free radicals are formed by radiation, toxic chemicals, hypoxia etc

37
Q

What are free radicals?

A

By-product of respiration

38
Q

Microscopic characteristics of REVERSIBLE cell damage

A
  • Cloudy swelling - osmotic disturbance
  • Cytoplasmic blebs
  • Disrupted microvilli
  • Swollen mitochondria
  • Accumulation of substance within cell (e.g. fat)
39
Q

Why does cloudy swelling occur in reversible cell damage?

A

Loss of energy dependent sodium pump -> osmotic disturbance and sodium influx and build-up of intracellular metabolites

40
Q

Microscopic characteristics of IRREVERSIBLE cell damage

A
  • Disrupted membranes

- Pyknotic nucleus

41
Q

What is a pyknotic nucleus?

A

The irreversible condensation of chromatin inside a cell nucleus undergoing necrosis or apoptosis

42
Q

True/ False? Necrosis is always pathological

A

True

43
Q

Is necrosis controlled or uncontrolled?

A

Uncontrolled

44
Q

Is apoptosis controlled or uncontrolled?

A

Controlled

45
Q

Define infarction (in relation to necrosis)

A

Necrosis caused by loss of blood supply

46
Q

What is the main difference between necrosis and apoptosis?

A

Cell contents leak out in necrosis but not apoptosis

47
Q

True/ False? Apoptosis is always physiological

A

False - usually but not always (can be pathological)

48
Q

Describe the histological changes during necrosis

A
  • Cell swelling
  • Vacuolation
  • Disruption of cell membranes and organelles
  • Release of cell contents (lysis) including enzymes
  • subsequent damage to adjacent cells
  • DNA disruption and hydrolysis
49
Q

Describe the nuclear changes during necrosis

A
  1. Karyolysis - nuclear fading (chromatin dissolution by DNAases and RNAases)
  2. Pyknosis - shrinkage(DNA condenses into shrunken basophilic mass)
  3. Karyorrhexis - membrane rupture and nuclear fragmentation
50
Q

What microscopic morphological changes occur to the following during necrosis?

a) muscle tissue
b) cytoplasm
c) nuclei

A

a) darker pink
b) thicker and cloudier
c) paler and ill-defined

51
Q

Describe coagulative necrosis

A

Firm, tissue outline and architecture maintained

52
Q

Describe colliquitive necrosis

A

Tissue turns to liquid and structure is lost

53
Q

Describe caseous necrosis

A

Combination of coagulative and colliquitive.

Cheese-like appearance.

54
Q

Example of coagulative necrosis

A
  • Haemorrhagic - blockage of venous drainage

- Gangrenous - blood supply inadequate for tissue

55
Q

Example of colliquitive necrosis

A
  • Infective abscess

- Cerebral infarct

56
Q

Example of caseous necrosis

A

Granulomatous inflammation e.g. TB

57
Q

Describe the difference in appearance of a haemorrhage coagulative infarct depending if it is of arterial or venous origin

A

Arterial - affected area becomes yellow due to lack of blood arriving at site

Venous - area becomes bright red as drainage is blocked

58
Q

What morphological change is characteristic of pancreatitis?

A

Fat deposition on pancreas

59
Q

How does necrosis cause inflammation?

A

Release of cell contents activated inflammation by signalling for inflammatory mediators

60
Q

What is apoptosis?

A

Programmed cell death

61
Q

Does apoptosis cause inflammation

A

No

62
Q

True/ False? Apoptosis requires energy

A

True

63
Q

Examples of when normal physiological apoptosis occurs

A

-Embryogenesis - deletion of cell populations
-Hormone dependent shrinking of uterus, breast, ovary
-Cell deletion in proliferating cell types (epithelium)
-Deletion of inflammatory cells after response
Deletion of self-reactive lymphocytes in thymus

64
Q

Examples of when pathological apoptosis occurs

A
  • Viral infection (cytotoxic T lymphocytes)
  • DNA damage
  • Hypoxia/ ischemia
65
Q

Describe the morphology of apoptosis

A
  • Cell shrinks
  • Chromatin condenses in nucleus
  • Membranes remain intact
  • Cytoplasmic blebs formed and break off as apoptotic bodies
66
Q

What happens to apoptotic bodies?

A

Phagocytosed by macrophages

67
Q

What are depositions?

A

Abnormal accumulation of a substance either intracellularly, extracellularly or in connective tissue

68
Q

Examples of endogenous intracellular deposition

A
  • Melanin
  • Haemosiderin
  • Bile
  • Lipids/cholesterol
  • Storage disease (alpha-1-antitrypsin)
  • Degeneration products (lipofuscin)
69
Q

Examples of exogenous intracellular deposition

A
  • Tattoo pigment
  • Carbon (anthracnosis)
  • Asbestos
70
Q

Examples of endogenous extracellular deposition

A
  • Amyloid
  • Fibrosis
  • Calcification
71
Q

PAGE 10/15 CELL INJURY/DEATH

A

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Phase 3 (4 decks)

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