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Block 1 > Cell Adaptations And Damage > Flashcards

Cell Adaptations And Damage Flashcards

1
Q

How do cells function normally and what happens if this goes wrong?

A

For cellular homeostasis, cells must exist in a narrow range of physiological parameters e.g. pH, temperature, oxygenation
If these change the cell will become stressed + try to reach a new steady state by adapting to preserve its vitality
If the cells adaptability is exceeded -> cell injury (can be reversed if stimulus is small or removed) -> if injury is severe/progressive cell with die by apoptosis/necrosis

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2
Q

Will a cell always try to adapt in injury?

A

No, if the stimulus is inherently injurious it will straight up be injured

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3
Q

What is clinically significant about cell death?

A

It is the key event in the evolution of many diseases

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4
Q

What is cell adaptation?

A

Reversible changes in cells in response to change in environment (physiological or pathological), involves changes in: cell number, size or type depending on proliferative capacity of tissue

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5
Q

What are the 3 classes of cells in terms of proliferative capacity?

A
  1. Labile - continuously dividing e.g. gut epithelia
  2. Stable - infrequent dividing but rapid division is needed (‘conditional renewal cells’) e.g. bone
  3. Permanent cells - never divide (at least not a clinically significant level) e.g. brain
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6
Q

Hyperplasia is a type of cell adaptation. What is it?

A

Increase in no. of cells in a tissue so cells must be stabile or labile (not permanent)

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7
Q

What is are 2 examples of physiological hyperplasia?

A
  1. Hormonal for e.g. endometrium as part of the normal menstrual cycle as a response to hormonal signals
  2. Compensatory e.g. in a partial hepatectomy
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8
Q

What are causes of pathological hyperplasia?

A

Excessive hormone/growth factor stimulation
Chronic irritation
-> Some increased risk of tumour development
(may occur alongside hypertrophy)

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9
Q

Hypertrophy is a type of cell adaptation. What is it?

A

Increase in cell size
Can occur in any cells but common when permanent cells experience increased demand as hypertrophy will produce more cellular structural proteins to meet new demands (as cells cannot divide)

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10
Q

When can physiological hypertrophy occur?

A
  • Increased functional demand e.g. mechanical from persistent exercise - skeletal muscle
  • Hormonal/growth factor e.g. uterine muscle in pregnancy hormonal changes - combination with hyperplasia
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11
Q

When can pathological hypertrophy occur?

A

Increased functional demand e.g. cardiac muscle left ventricle primarily in hypertension + aortic stenosis

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12
Q

Atrophy is a type of cell adaptation. What is it?

A

Shrinkage in cell size by loss of cell substance - involves self-digestion of organelles in a process called autophagy

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13
Q

What is the correct term for a reduction in organ size through cell loss?

A

Involution

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14
Q

What are the causes of atrophy?

A 
Reduced workload
Loss of nerve supply
Reduced blood supply
Inadequate nutrition
Loss of endocrine/hormonal stimulation
Ageing
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15
Q

Metaplasia is a type of cell adaptation. What is it?

A

Reversible change from one adult cell type to another adult cell type where the new cell type is better adapted to the stimulus - usually involves epithelium in response to changed environment (fertile ground for later cancer development)

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16
Q

When can physiological metaplasia occur?

A

In normal growth + development e.g. glandular to robust squamous epithelium in pubertal cervix due to exposure to acidic environment of vagina

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17
Q

When can pathological metaplasia occur?

A

When an abnormal environment causes adaptive response e.g. squamous stratified to glandular columnar in reflex oesophagitis i.e. Barrett’s due to squamous cells not coping with acidic environment

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18
Q

Define the 4 different types of developmental abnormalities.

A
  1. Agenesis: organ completely failures to develop
  2. Aplasia: failure of differentiation to organ-specific tissues
  3. Dysgenesis: abnormal structural organization of tissues in organ
  4. Hypoplasia: organ not grown to full size
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19
Q

Dysplasia is a type of abnormal cell growth. What is it?

A

A premalignant condition where there is increased cell growth, cellular atypia (structural abnormality) + altered differentiation
Can range from mild to severe
Occurs in epithelia e.g. cervix, bladder + stomach/oesophagus

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20
Q

Neoplasia is a type of abnormal cell growth. What is it?

A

Abnormal growth of cells which persist after initiating stimulus has been removed (contrast with hyperplasia which is reversible) so cell growth has escaped from normal regulatory mechanisms
Can be benign or malignant (invasion + metastases)

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21
Q

What are some causes of cell injury?

A 
Physical agents
Chemicals/drugs
Infectious agents
Immune reactions
Genetic derangements
Nutritional imbalances
Oxygen deprivation
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22
Q

How are cells injured via oxygen deprivation and what are some of the causes of it?

A

Hypoxia impairs aerobic metabolism
Solitary phenomenon e.g. oxygen problems (altitude) or haemoglobin problems (anaemia)
Can reflect problems with blood supply i.e. ischaemia e.g. locally (embolus in toe for e.g.) or systemic (cardiac failure)
Ischaemia > hypoxia because there is loss of delivery of other elements + toxin build up so cell injury is quicker + more severe

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23
Q

How can chemicals damage cells?

A

Directly or as a result of metabolism/generation of breakdown products
Main modes of damage are: damaged osmotic environment of cell, biochemical cell reactions (e.g. ATP levels dropping) + integrity of cell membrane
Chemicals range from oxygen (e.g. retinopathy of prematurity)/water to poisons

24
Q

What infections can cause cell injury? Give an example of how they do this.

A

Fungi, bacteria (e.g. rickettsiae, TB) + prions

E.G. viruses can take over protein translation machinery and subvert it entirely to the production of new virions

25
Q

How can cells be injured physically?

A

Via direct physical effects such as exposure of tissue to extreme heat or cold - often irreversible resulting in a pattern of coagulative necrosis
E.g. frostbite

26
Q

How can the immune system cause cell injury?

A

When it is excessive, inappropriately targeted e.g. autoimmune or insufficient e.g. immunodeficient states
E.g. anaphylaxis

27
Q

How can nutrition cause cell injury?

A

Dietary insufficiency; leads to injury due to interference in metabolic pathways e.g. glucose
Dietary excess; abnormal concentrations of molecules in normal or abnormal cellular locations affecting metabolic pathways e.g. cholesterol
E.g. marasmus (inadequate calorie intake) + kwashiorkor (inadequate protein intake)

28
Q

How can depletion of ATP occur and what is the impact of this on cells?

A

Reduced synthesis can cause ATP depletion
The impact will depend on glycolytic activity of skills e.g. skeletal muscle would survive longer than cardiac muscle
5-10% reduction causes significant dysfunction

29
Q

What can happen if blood supply to an organ is disrupted due to a thrombus causing ischaemia on a cellular level?

A

Decreased ability for aerobic respiration so oxidative phosphorylation is decreased in the mitochondrion depleting ATP stores;

  • Increases anaerobic respiration increasing lactic acid reducing cell pH damaging nuclear material
  • Systems requiring ATP to function reduced e.g. active transport so Na+ is increased causing swelling due to osmotic pressure
  • Detachment of ribosomes decreasing protein synthesis
30
Q

What are the consequences of mitochondrial damage?

A

Depletion of ATP (they are ATP factories)Generation of ROS
Formation of pores in mitochondrial membrane leading to loss of organelle microenvironment + loss of function
Mitochondrial membrane proteins released into cytosol, triggering apoptosis in cells

31
Q

What happens in a cell if injury causes a loss of calcium homeostasis?

A

Cell injury causes influx of Ca2+ in the cytoplasm from EC + IC compartments -> Ca2+ activates enzymes which cause breakdown of cell membranes, DNA damage + ATP depletion -> can directly activate enzymes e.g. caspases responsible for apoptosos

32
Q

What are free radicals?

A

Free radical are generated in oxidative stress and are chemical species with a single unpaired electron in their outer orbital e.g. ROS. They react with organic + inorganic compounds e.g. nucleic acids, proteins + lipids & generate free radicals from molecules they react with (propagating ROS generation).

33
Q

How are free radicals in oxidative stress produced?

A

Increased free radical generation occurs by;
Absorption of radiant energy e.g. x-ray, UV light
Enzymatic metabolism of exogenous chemicals e.g. carbon tetrachloride
Inflammation by-product

34
Q

How are free radicals removed?

A

Spontaneous decay
Anti-oxidants e.g. Vitamin E + A, ascorbic acid, glutathione
Storage proteins e.g. transferrin, ferritin + ceruloplasmin
Enzymes e.g. catalase, SOD + glutathione peroxidase

35
Q

How can free radicals injure cells?

A
  • > imbalance in generation + removal causes cell injury via:
  • Membrane lipid/fats peroxidation damaging cell membrane via autocatalytic chain reaction
  • Interaction with proteins e.g. protein fragmentation + protein-protein cross-linkage
  • DNA damage e.g. single strand breaks (genomic + mitochondrial)
36
Q

Where are the 3 key membranes that can be damaged?

A
  1. Mitochondrial
  2. Plasma
  3. Lysosomal
37
Q

How can membrane permeability of a cell become defected?

A

Reduced production (with reduced ATP) or increased breakdown (from increased Ca2+ for e.g.) of phospholipids
Damage by ROS
Cytoskeletal damage by enzymatic digestion
Build up of lipid breakdown products act as a detergent on cell membrane

38
Q

What is necrosis?

A

Unprogrammed cell death that is pathological/abnormal + includes enzymatic cell digestion where cellular contents leak out

39
Q

What are the 6 types of necrotic tissue?

A
  1. Coagulative
  2. Liquefactive
  3. Caseous
  4. Gangrenous
  5. Fat
  6. Fibrinoid
40
Q

What is coagulative necrosis?

A

Cells are non-vital i.e. nucleus not identifiable but structure of tissue visible histologically still -> reflects cell death without enzymatic digestion of tissues
Commonly seen in ischaemic injuries (except in brain)

41
Q

What is liquefactive necrosis?

A

Dead tissue replaces by liquefied material where tissue’s structure is lost -> reflects cell death accompanied by enzymatic digestion of tissues e.g. post inflammation (seen post-ischaemia in brain as except due to lack of architecture of tissue)

42
Q

What is caseous necrosis?

A

Looks like cottage cheese e.g. TB infection

43
Q

What is fat necrosis?

A

Not true necrosis rather enzymatic digestion of tissue e.g. post-pancreatitis with leakage of digestive enzymes into the abdomen

44
Q

What is infarction?

A

An area of ischaemic necrosis in a tissue or organ i.e. due to reduced/absent blood supply

45
Q

Explain the 2 different types of necrosis.

A
  1. White - arterial occlusion in most solid tissues
  2. Red/haemorrhagic (when there is plenty of blood around) - in venous occlusion, loose tissues, dual bloody supply or previously congested (i.e. blood in capillary bed but static)
46
Q

What is apoptosis?

A

Programmed cell death that can be pathological or physiological that is internally controlled and involves nuclear dissolution

47
Q

When does physiological apoptosis occur?

A

Embryogenesis
Involution of hormone dependent tissue
Cell loss in proliferating cell populations
Elimination of potentially harmful lymphocytes
Cells no longer required

48
Q

When does pathological apoptosis occur?

A

Cells with DNA damage
Cells with ER stress
Some infections e.g. viruses
Pathological atrophy if a duct is obstructed

49
Q

What are the biochemical features of apoptosis?

A

Imbalance between pro-apoptotic + anti-apoptotic molecules in the cell -> activation of caspases, DNA + protein breakdown (fragments detected) & membrane alterations + recognition by phagocytes

50
Q

What are the 2 different pathways of apoptosis?

A 
Mitochondrial (intrinsic) pathway
Death receptor (extrinsic) pathway
51
Q

What are the disorders associated with dysregulated apoptosis?

A
  • Defective apoptosis + increased survival in neoplastic cells + autoimmune cells
  • Defective apoptosis + decreased survival in ischaemic injury + death of virus infected cells
52
Q

What are the morphological features of necrosis?

A

Enlarged (swelling)
Pyknosis (condense) -> karyorrhexis (fragment) -> karyolysis (dissolve/fade) of nucleus
Disrupted plasma membrane
Enzymatic digestion; may leak out of cell
Frequent adjacent inflammation
Invariably pathologic (culmination of irreversible cell injury)

53
Q

What are the morphological features of apoptosis?

A

Reduced (shrinkage)
Fragmentation into nucleosome-size fragments of nucleus
Intact plasma membrane; altered structure, especially orientation of lipids
Intact cellular contents; may be released in apoptotic bodies
No adjacent inflammation
Often physiologic as a means of eliminating unwanted but may be pathologic after some forms of cell injury e.g. DNA damage

54
Q

All clinical disease arises due to derangements in _________

A

Cellular function

55
Q

Cells can do 3 things in response to a change of environment. What are they?

A
  1. Adapt
  2. Become injured
  3. Die (via necrosis or apoptosis)

Block 1 (54 decks)

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