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Molecular Basis Of Disease > Disease and Homeostasis > Flashcards

Disease and Homeostasis Flashcards

1
Q

What are the causes of cell injury?

A
  • oxygen deprivation
  • chemicals
  • enzymes
  • infectious agents
  • immunological reactions
  • genetic defects
  • nutritional imbalances
  • trauma
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2
Q

How does oxygen deprivation cause cell injury?

A

oxygen deprivation = hypoxia

tissues therefore do not get adequate oxygen ad begin to die (ischemia)

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3
Q

How do chemicals cause cell injury?

A

affects osmotic environment either causing or by altering membrane permeability

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4
Q

Immunological reactions which can cause cell injury

A
  • anaphylaxis

- autoimmune disorder

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5
Q

Traumas which can affect cell injury

A
  • extremes of temperature
  • radiation
  • atmospheric pressure
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6
Q

What are the consequences of ischemia to cells

A
  1. No aerobic energy production
    • depletion of ATP
    • if ATP is low then anaerobic glycolysis and AMP become increased leading to
      the accumulation of lactic acid and a drop in intracellular pH (can lead to
      protein degradation and function impairment)
  2. Removal of wastes cannot occur as blood has stopped flowing to the area
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7
Q

What are free radicals

A
  • atoms with a single unpaired electron
  • unstable
  • very reactive
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8
Q

How are free radicals formed in normal respiration

A

molecular oxygen has a single unpaired electron

If two come together with the addition of a floating electron a superoxide radical is formed

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9
Q

How are free radicals formed in the body

A
  • radiation exposure
  • oxygen toxicity
  • ageing
  • inflammation
  • chemicals (smoking, air pollution)
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10
Q

What damage do free radicals cause

A
  1. lipid peroxidation of membranes (double bonds attacked losing structure and function)
  2. DNA oxidation
    • 8-oxoguanine and thymine glycol are common oxidative lesions
    • if not fixed by base excision repair will cause mutations when multiplying
  3. Protein cross linking
    • new covalent or ionic bonds added
    • can change structure and function
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11
Q

How do you remove free radicals

A
  • electron donation

- antioxidants

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12
Q

REMOVING FREE RADICAL PATHWAYS

What factors facilitate O2 becoming superoxide

A
  • enzymes in the ER

- peroxisomes

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13
Q

REMOVING FREE RADICAL PATHWAYS

What enzyme facilitates superoxide becoming H2O2 (hydrogen peroxide)

A

superoxide dismutase (SOD)

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14
Q

REMOVING FREE RADICAL PATHWAYS

Once superoxide has become H2O2 what are the two different end products and which are safe for the body

A
  1. O2 + H2O
    • safe
  2. OH
    • hydroxyl radical (not safe)
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15
Q

REMOVING FREE RADICAL PATHWAYS

What enzymes facilitate hydrogen peroxide becoming O2 and H2O

A
  • glutathione peroxidase

- catalase

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16
Q

REMOVING FREE RADICAL PATHWAYS

Which 2 reactions facilitate H2O2 to hydroxyl radical

A

Fenton reaction
- Fe3+ and H2O2 = Fe2+ and OH-

Haber-Weiss Reaction
- H2O2 and superoxide = OH-

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17
Q

REMOVING FREE RADICAL PATHWAYS

Why can metals (Fenton reaction) factor in to facilitating this pathway

A

transition metals can accept or donate electrons ap can catalyse free radical formation

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18
Q

Which antioxidants are important for removing free radicals

A
  • vitamin C

- coenzyme Q10 (ubiquinone)

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19
Q

What are the cellular adaptations to injury/physiological change

A
  • atrophy
  • hypertrophy
  • hyperplasia
  • metaplasia
  • dysplasia
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20
Q

what is atrophy

A

decrease in size or number of cells

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21
Q

examples of atrophy

A

Muscle atrophy
- decrease in muscle mass due to decrease workload (immobilisation of limb)

atrophy of optic nerve
- decrease in vision due to a loss of hormones (e.g. during menopause)

cerebral atrophy

  • decrease of cerebral cortex
  • alzheimers, ageing, alcohol
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22
Q

What is the role of lysosomes

A
  1. degrade proteins, carbohydrates, lipids and acids

2. storage of. substances which cannot be metabolised completely (creates residual bodies)

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23
Q

Lysosome catabolism can occur in 2 ways. What are these ways

A
  1. Heterophagy
    - environmental substances endocytosed
    - fuses which amphisome
    - fuses with lysosome to create and autolysosome which breaks down substance
  2. Autophagy
    - cytoplasm or damaged organelles enclosed in autophagosome
    - fuses with lysosome to create autolysosome to break down contents
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24
Q

Lysosome Storage disorders

A
  1. Hurler Syndrome
    - defect in glycosaminoglycan breakdown allowing it to accumulate in cytoplasm
  2. Tay-Sachs disease
    - defect in degradation of lipids in nerve cells
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25
Q

Cellular Basis of atrophy

A

two proteolytic systems (breakdown of proteins)

  1. lysosomes
  2. ubiquitin pathway
    • digestion in protostomes
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26
Q

what is hypertrophy

A

increased size of cells

27
Q

What can cause hypertrophy

A
  • exercise
  • hormones (uterus and breast during puberty)
  • toxins (can cause liver enlargement)
  • hypertension (high blood pressure which causes heart muscle to work harder and therefore thicken)
28
Q

What is hyperplasia

A

increase in number of cells

29
Q

Examples and causes of hyperplasia

A

example:
- benign prostatic hyperplasia
- gingival hyperplasia

causes:
physiological: hormonal, growth factors
pathological: excessive hormones (endometriosis)

30
Q

What is metaplasia

A

reversible conversion of normal cells to less specialised cells due to prolonged exposure to stimulus

can withstand stress better but may not retain same functions

31
Q

Example of metaplasia

A

Chronic gastric reflux

- stratified squamous of lower oesophagus becomes intestine like due to chronic gastric acid exposure from reflux

32
Q

What is dysplasia

A

disorderly growth

  • cells become variable in morphology and disorganised
  • may give rise to cancer
33
Q

Examples of dysplasia

A

cervical dysplasia
- precursor for squamous cell carcinoma of cervix

can be detected via cervical screening test

34
Q

Cellular stress causes which 2 types of injury

A
  1. reversible injury

2. irreversible injury

35
Q

What are the consequences of reversible injury to cells

A

cellular adaptations

  • atrophy
  • hypertrophy
  • hyperplasia
  • metaplasia
  • dysplasia
36
Q

What are the consequences of irreversible injury

A
  1. cellular senescence
  2. cancer
  3. necrosis
  4. apoptosis/autophagy
37
Q

What can cause cellular ageing

A
  1. cellular senescence
38
Q

What can cause cellular death

A
  1. cancer
  2. necrosis
  3. apoptosis/autophagy
  4. ageing
39
Q

Lifespan has changed over the years what factors contribute to this?

A

early 19th century to 1900
- improved housing, sanitation and antiseptics

1900-1935
- improved public health, hygiene and immunisation

1935-1960
- antibiotics, improved medical practices, nutrition, health education

1960-1980
- recent biomedical advancements

40
Q

What is cell senescence

A

inbuilt programme to irreversibly arrest cell growth
- prevents damaged cells developing into cancer cells

Happens at a higher frequency with age

41
Q

Cells show what sort of phenotypic changes in senescence

A

increased size and presence of intracellular inclusions

different gene expression pattern

different metabolic programme

secrete pro-inflammatory cytokines, chemokines, protein digesting extracellular matrix proteases
- can cause cells around them to undergo damage and possibly enter senescence

42
Q

How are natural selection and ageing connected

A

natural selection diminishes with age as it only affects organisms during reproducing stages

If diseases develop post reproduction age = the contributing genes will not be selected against
(if you have already reproduced then these genes will already be passed to the next generation)

Examples:

  • cancer
  • heart disease
  • Alzheimer’s
43
Q

Which diseases illustrate the effects of genes expressed before and after reproductive years

A

before reproduction
- Progeria

after reproduction
- Huntingtons disease

44
Q

What is Progeria

A

AKA Hutchinson-Gilford Progeria Syndrome

Rare disease as individuals die before reproducing

Autosomal dominant genetic mutation (not inherited mutations)

45
Q

Progeria symptoms

A

resemble aspects of ageing manifested at an early age

  • wrinkles and slow growth
  • boldness
  • large head compared to body
  • skin ageing
  • joint stiffness
  • cardiovascular problems
  • death at about 12 years from heart attack or stroke
46
Q

Genetic factors involved in Progeria

A 
Lamin A (LMNA) gene 
- needed for structural scaffolding of the nuclear envelope at embryonic stage

this gene is mutated causing disrupted nucleus and limits ability of cells to divide

47
Q

What is Huntington’s Disease

A

autosomal dominant neurodegenerative disorder

- arises in middle age so natural selection is powerless

48
Q

Symptoms of Huntington’s Disease

A
  • involuntary contorting movements
  • dementia
  • slurred speech
  • delusions
  • immobilised contorted positions
49
Q

Normal and disease gene contributing to Huntington’s

A

increased repeated sequence of CAG in huntin protein (HTT) Chromosome 4

normal = 6-34 repeats
HD = 40-55 repeats
early onset HD = 70 + copies

50
Q

Molecular basis of Huntington’s

A
  • HTT is expressed in all somatic tissues and highly expressed in neurons
  • more repeats the more unstable the protein and may cause protein aggregation
  • HTT interacts with many other proteins
51
Q

Molecular effects of mutant HTT proteins

A

not well known but:

  1. formation of inclusion bodies in nucleus of cells
  2. protein aggregation in cytoplasm

leading to:

  • synaptic dysfunction
  • mitochondrial toxicity
  • decrease in rate of axonal transport
52
Q

Huntington’s effect on the brain

A

atrophy and cell death of basal ganglia
- degeneration of cells from putamen and caudate nuclei

basal ganglia involved in:

  • motor control of movement
  • cognition
  • sensory pathways
53
Q

What are common ageing disorders

A
  1. Werner disease (adult progeria)
    - premature with later onset than progeria (usually teens)
    - average lifespan = 46
  2. Progeria (Hutchinson-guildford)
    - premature ageing with early onset
    - average lifespan = 12 years
54
Q

What is werner disease and symptoms

A

autosomal recessive

symptoms:
- atherosclerosis
- diabetes
- cataracts
- osteoporosis
- cancer
- wrinkles
- greying of hair

55
Q

What genetic mutation causes Werner’s Disease and how does this effect the protein?

A

nonsense, frame shift mutation in WRN gene Chromosome 8
- creates a truncated, short protein

WRN is a helicase
- separates strands of DNA for replication

56
Q

Werner Disease molecular basis

A
  • cells sensitive to DNA cross linking and ionizing radiation
  • cells show impaired DNA replication
  • reduced replicative lifespan
  • defects in telomeres causing genomic instability and cancer
57
Q

What are the two processes of death at a cellular level

A
  1. Necrosis

2. Apoptosis

58
Q

What is necrosis and the molecular basis

A

Necrosis is the result of death from cell injury
- death by autolysis

  1. cells swell and burst and spills its contents
  2. causes an inflammatory response
  3. organelles disintegrate and mito dialtes, no change to nucleus

Causes gangrene

59
Q

What causes necrosis

A

toxins

hypoxia

inhibition of major biochemical pathways

 - glycolysis 
 - oxidative phosphorylation 
 - krebs cycle 
 - all leads to no ATP
60
Q

What is gangrene and the types of gangrene

A

lack of blood in an area which causes large area of dead tissue
- often occurs in extremities but sometimes in bowel

types:
- dry
- wet
- gas
- freezing

61
Q

What is dry gangrene

A

symptoms:
- black, dry wrinkled tissue
- black due to black iron sulphide from leftover haemoglobin

where:
- only in extremities

why:
- ischemia

62
Q

What is wet gangrene

A

where:
- internal organs

why:
- bacteria and toxins which invade the blood

63
Q

What is gas gangrene

A

why:
- bubbles of gas from anaerobic bacteria Clostridium

symptoms:
- black blister like sores

64
Q

What is freezing gangrene

A

why:
- formation of water crystals which increase pressure of remaining fluid and cells burt

symptoms:
- blister like

Molecular Basis Of Disease (17 decks)

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