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Pathology > Cell Response to Injury: Exogenous injury 1 > Flashcards

Cell Response to Injury: Exogenous injury 1 Flashcards

1
Q

what are the 4 clinical hypoxic states?

A
  • hypoxaemia
  • anaemia
  • ischaemia
  • histoxia
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2
Q

what characterises hypoxaemia?

A

reduced availability of atmospheric O2

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3
Q

what characterises anaemia?

A

reduced O2 capacity of blood

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4
Q

what characterises ischaemia?

A

stagnant circulation

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5
Q

what characterises histoxia?

A

tissues unable to use available O2

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6
Q

what causes reperfusion injury?

A

burst of reactive oxygen species after reoxygenation

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7
Q

what happens when a blood vessel ruptures?

A

blood leaks into CT

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8
Q

what phagocytoses the red blood cells?

A

macrophages

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9
Q

what is iron converted into after blood leaks into CT?

A

brown haemosiderin

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10
Q

how can haemorrhages lead to comas?

A

if there is a haemorrhage in a confined space such as the skull, it means that there is limited space for swelling this causes the pressure to rise and close capillaries resulting in hypoxia and nerve compression = coma

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11
Q

what layers of skin are damaged in a first degree burn?

A

epidermal

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12
Q

what layers of skin are damaged in a second degree burn?

A

epidermal & upper dermis

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13
Q

which degree burn means you feel no pain?

A

third degree and fourth degree

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14
Q

what layers of the skins are damages in a third degree burn?

A

epidermal, dermal, subcutaneous

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15
Q

what are the characteristics of fourth degree burns?

A

epidermal, dermal, subcutaneous; no pain; hair pulls out; ascia, muscle, bone appear blackened, dry; very poorly healing

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16
Q

what causes blistering?

A

separation of epidermal & dermal layers.

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17
Q

what are some of the systemic changes that occur after burns?

A

release of K+ ions → hypervolaemic (burn) shock.

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18
Q

what are the 2 ways that cold causes damage?

A

indirectly – via ischaemia

directly – via freezing of tissues

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19
Q

how can cold indirectly cause damages?

A
  • Cooling –> vasoconstriction
  • reduction in blood supply –> reduced supply of nutrients to the affected tissues
  • return of blood supply
  • -> oedema prolonged ischaemia produces necrosis (trench foot)
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20
Q

how can cold directly cause damage?

A
  • Freezing of tissues –> frost bite
    (due to ischaemia & direct freezing)
    damage worse, thrombosis occurs in damaged vessels.
  • Tissue blackens - erythrocyte leakage
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21
Q

what can chemical exposure injuries be due to?

A
  • therapeutic drugs
  • industrial chemicals (occupational)
  • ‘recreational’ drugs
  • environmental chemicals
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22
Q

what can harmful effects of chemicals be due to?

A
  • direct action on the cells architecture
  • interference with enzyme action
  • toxigenesis or metabolic activation (production of toxic compounds from non-toxic ones)
  • carcinogenesis
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23
Q

what is an example of the direct action of chemicals on cell structure?

A

lead poisoning

24
Q

how can lead affect cell structure?

A

Can join nearby sulphydryl and carboxyl groups in peptides

& proteins so interfere with enzyme action & protein conformation

25
Q

which enzymes do chemicals interfere with?

A

enzymes for generating essential

products and/or removing toxic substrates

26
Q

what chemicals have direct actions on proteins?

A
  • lead

- corrosive agents that inactivate enzymes by stabilising protein structure eg, formaldehyde, mercury

27
Q

how does carbon monoxide cause injury?

A

Carbon monoxide: competes with O2 for haemoglobin and is bound more firmly than O2 → inhibits O2
blood transport → hypoxia

Also, binds Fe++ in cytochrome oxidase in
cells and so reduces cellular O2 absorption

28
Q

what is competitive inhibition?

A

Toxin competes with substrate.

29
Q

what are examples of toxins that use competitive inhibition?

A
  • fluorocitrate

- Folate antagonists

30
Q

what is fluorocitrate?

A

Structural analogue of citrate

31
Q

what does fluorocitrate inhibit?

A

cis-aconitase. Thus inhibits use of citrate in TCA cycle.

32
Q

what do folate antagonists inhibit?

A

DNA synthesis.

33
Q

how is thymine synthesis blocked?

A

via inhibition of Dihydrofolate reductase.

34
Q

what is an example of Steric exclusion of enzyme from site of action?

A

Actinomycin

High affinity for DNA. Binds guanosine residues by intercalating planar rings between adjacent base-pairs. Thus inhibits RNA polymerase & transcription.

35
Q

where are microsomal oxygenases found?

A

mainly in the endoplasmic reticulum of liver cells but most other types

36
Q

what are microsomal oxygenases dependent of?

A

oxygen, NADDPH & cytochrome P450

37
Q

what are the substrates of microsomal oxygenases?

A

aromatic hydrocarbons, CCl4, aromatic amines

38
Q

what happens to the substrates of microsomal oxygenases?

A

metabolised into reactive species, which react with macromolecules

39
Q

what is an example of a microsomal oxygenase effect?

A

carbon tetrachloride (CCl4) Hepatotoxin –> necrosis & fatty globulation –> cirrhosis in central zone of hepatic lobule. Involves swelling of ER cisternae & mitochondria, degranulation & rER ribosome loss

40
Q

where is the site of cancers for polycyclic hydrocarbons?

A

skin

scrotum

41
Q

where is the site of cancers for aromatic amines?

A

bladder

42
Q

where is the site of cancers for aflatoxins?

A

liver

43
Q

where is the site of cancers for nitrosamines?

A

stomach, oesophagus

44
Q

where is the site of cancers for chemotherapy agents?

A

leukaemias

45
Q

where is the site of cancers for asbestos?

A

lung mesothelioma

46
Q

where is the site of cancers for heavy metals?

A

lung

47
Q

what is the mode of action for many carcinogens?

A

usually DNA damage through:

  • Base alkylation
  • Strand breaks
  • Cross-linkages
  • Cellular DNA repair may → mutation eg, insertion/deletion, base substitution
48
Q

what are the non-genotoxic mechanisms of carcinogens?

A
  • Change growth regulatory proteins
  • Synergy with viruses (depressing anti-oncogene activity)
  • Promoters of other toxins/carcinogens
49
Q

what are the primary causes of nutritional deficiencies?

A

Inadequate food intake (malnutrition) Eg, food shortages, poverty, age, alcoholism

50
Q

what are the secondary causes of nutritional deficiencies?

A

Malnutrition despite sufficient nutrients:

Failure of intestinal absorption → deficiency of specific nutrient (eg, vit B12 in pernicious anaemia)

Increased metabolic demand → increased demand for specific nutrient eg, folic acid in pregnancy

Antagonists eg folic acid antagonists like Methotrexate

51
Q

what are causes of nutritional excess?

A

Obesity – excessive intake of cholesterol, saturated fats can lead to atherosclerosis

52
Q

what is an example of microbes causing nutrient deprivation?

A

Cornebacterium diptheriae infection → membrane over larynx obstructs breathing.

leads to problems with the absorption of oxygen

53
Q

how do microbes cause injury through the production of toxins?

A

Clostridium botulinum: toxin prevents release of acetyl choline which leads to paralysis and death

Vibrio cholerae: toxin acts upon adenyl cyclase –> enterocytes secrete large amounts fluid which leads to dehydration

54
Q

what is an example of microbes causing injury through antigenicity?

A

Mycobacterium tuberculosis

Products produce damaging antigenic response. Eg, lipids of cell walls & cytoplasmic proteins

55
Q

what is an example of microbes causing injury through intercellular growth?

A

Neisseria gonorrhoeae/N. meningitidis attract & survive in phagocytic neutrophils. Cells fill with bacteria –> neutrophil death –> necrosis –> pyrogenic inflammation.

56
Q

how can radiation cause injury through direct action?

A

alters/inactivates cell molecules DNA, RNA etc

57
Q

how can radiation cause injury through indirect action?

A

ionisation of intra-cellular water –> reactive free radicals

Pathology (17 decks)

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