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Block 1: Physiology > CTB > Flashcards

CTB Flashcards

1
Q

What are the phases of the cell cycle?

A

Interphase:

G0 (resting)
Gap 1
S phase (DNA replication/ synthesis)
Gap 2

Divison:

M phase (mitosis)

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2
Q

In which phase of the cell cycle is DNA polymerase most active?

A

S phase (DNA replication and synthesis)

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3
Q

How do cells respond to stress?

A

Adaptation - reversible changes in response to changes in environment as an attempt to preserve cell vitality but when stress exceeds adaptability this can result in cell injury

Adaptation can include changes in cell number, size or type

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4
Q

What does severe and progressive injurious stimuli do to cells?

A

Initially cell injury (which can be reversible if stimulus is minor or removed) eventually resulting in cell death (apoptosis or necrosis)

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5
Q

What are the 2 types of cell death?

A

Apoptosis (generally physiological and internally programmed)
Necrosis (pathological and caused by external factors)

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6
Q

What causes hypertrophy and hyperplasia of cells?

A

Increased functional demand (metabolic), excess endocrine stimulation or persisting tissue injury

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7
Q

What is metaplasia?

A

Reversible change in cell type from one adult cell type to another as an adaptive response to a stimulus - can be physiological or pathological and generally involves epithelium

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8
Q

What is dysplasia?

A

The presence of abnormal cell type within a tissue - a premalignant condition involving increased cell growth, altered cellular differentiation and cellular atypia

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9
Q

What is neoplasia?

A

Abnormal cellular proliferation that persists after initiating stimulus is removed - can be benign or malignant (tumours)
Involves both increased cell number and change in cell type

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10
Q

What are some common causes of cellular injury and death?

A 
Oxygen deprivation (hypoxia)
Physical agents
Chemicals/ drugs 
Infectious agents
Immune reactions 
Genetic derangements 
Nutritional imbalance
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11
Q

What are the pathophysiological features of necrosis?

A

Cell death caused by external factors (e.g. hypoxia or chemical toxins)
Damage to cell physiology and degradation of cell
Uncontrolled influx of water and ions causing organelles to swell and rupture (and released into ECF)
No regulated signals to phagocytes to remove necrotic cells and avoid immune surveillance

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12
Q

What factors can cause necrosis?

A 
Injury
Infection 
Cancer
Infarction 
Toxins 
Inflammation
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13
Q

What are the morphological features of necrosis?

A

Loss of cell membrane integrity
Lysosomal hydrolases resulting in small, condensed and deeply stained nuclei, nuclei fragmented into particles, deeply stained cytoplasm
Typically affects large groups of cells

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14
Q

What are the morphological features of apoptosis?

A

Organelles remain intact
Nucleus and cytoplasm condense to form apoptotic bodies with intact membrane surrounding
Apoptotic bodies phagocytosed by macrophages
No inflammatory response
Typically affects isolated cells

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15
Q

What are the 6 types of necrosis?

A 
Coagulative 
Liquefactive 
Fat necrosis
Caseous 
Gangrenous (less common)
Fibrinoid (less common)
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16
Q

What is coagulative necrosis?

A

Typically occurs in hypoxic conditions (except in brain) with minimal digestion by lysosomal enzymes - common (e.g. in myocardial infarction) - gives gelatinous appearance

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17
Q

What is liquefactive necrosis?

A

Liquefied tissue caused by cell death and lysosomal enzyme activity - typically occurs in the brain after ischaemia or post inflammation

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18
Q

What is fat necrosis?

A

Digestion of fat tissue by lipase leakage into the abdomen (e.g. post pancreatitis)

[Not true necrosis]

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19
Q

What is caseous necrosis?

A

Cottage cheese appearance - can be seen in infection with tuberculosis

20
Q

What are the 3 types of proliferative capacity a cell can have?

A

Labile - continuously divide throughout adult life
Stable - infrequent divisions but can rapidly divide if necessary (e.g. bone)
Permanent - no division (at least not to a clinically significant level) e.g. brain

21
Q

What is cell hyperplasia?

A

Increase in number of cells within a tissue (cannot happen in permanent cells)

22
Q

What is cell hypertrophy?

A

Increase in cell size - can occur in any cells but common in permanent cells experiencing an increased demand - involves increase in cellular structural proteins not just swelling

23
Q

Give an example of physiological hormonal hyperplasia and compensatory hyperplasia

A

Hormonal: endometrium
Compensatory: following partial hepatectomy

24
Q

Give 2 causes of pathological hyperplasia

A

Excessive hormone or growth factor stimulation
Chronic irritation

[Some increased risk of tumour development]

25
Q

Give 2 examples of physiological hypertrophy

A

Mechanical and skeletal muscle in response to increased functional demand
Uterine muscle during pregnancy (combination with hyperplasia as a result of exposure to hormonal stimuli)

26
Q

Give an example of pathological hypertrophy

A

Left ventricular hypertrophy in response to increased functional demand (e.g. due to hypertension or aortic stenosis)

27
Q

What is atrophy?

A

Shrinkage in cell size due to loss of cell substance - self digestion of organelles (autophagy)

28
Q

What can cause atrophy?

A 
Reduced workload
Loss of nerve supply
Reduced blood supply
Inadequate nutrition
Loss of endocrine stimulation 
Ageing
29
Q

Give an example of physiological metaplasia

A

Normal physiological development involves change from glandular to squamous epithelium in the pubertal cervix

30
Q

Give an example of pathological metaplasia

A

Squamous to glandular epithelium in reflux oesophagitis (Barrett’s)

31
Q

Where does dysplasia commonly occur?

A

Bladder
Stomach/ oesophagus
Cervix

32
Q

How does oxygen deprivation cause cell injury?

A

Impairs aerobic metabolism

Can be due to solitary problems (e.g. altitude or anaemia) or ischaemia

33
Q

Which is worse, hypoxia or ischaemia?

A

Ischaemia due to inability to supply cell with other elements (e.g. nutrients) and loss of ability to clear toxins causing quicker and more severe cell injury

34
Q

How can chemicals cause cell injury?

A

Damage osmotic environment, biochemical cell reactions (e.g. loss of ATP) and damage to integrity of the cell membrane

35
Q

What is an example of chemical cell injury?

A

Retinopathy of prematurity (where increased oxygen levels in newborns causes scarring and retinal detachment)

36
Q

What is an example of a physical cause of cell injury?

A

Frostbite

37
Q

How can immune responses cause cell injury?

A 
Inappropriate targeting (autoimmune)
Immunodeficiency 
Excessive immune response (e.g. anaphylaxis)
38
Q

Give an example of inadequate nutrition causing cell injury

A

Marasmus (body begins to metabolise vital structures due to insufficient diet)

39
Q

What impact does depletion of ATP have on a cell?

A

Dependent on glycolytic activity of cell but lack of oxygen will cause anaerobic respiration and a subsequent build up of lactic acid rather than ATP synthesis resulting in significant cell dysfunction

40
Q

What impact does mitochondrial damage have on a cell?

A

Site of ATP production so depleted ATP, generation of ROS, loss of organelle function and apoptosis through release of mitochondrial membrane proteins

41
Q

What impact does loss of calcium homeostasis have on a cell?

A

Cell injury causes influx of calcium ions resulting in activation of enzymes that cause breakdown of cell membranes, DNA damage and ATP depletion

42
Q

What impact does oxidative stress have on a cell?

A

Release of free radicals (e.g. ROS) - imbalance in generation and removal results in cell injury

43
Q

What causes increased free radicals in a cell?

A

Absorption of radiant energy
Metabolism of exogenous chemicals
Inflammation

44
Q

What normally removes free radicals?

A

Spontaneous decay
Anti-oxidants (e.g. Vitamin E, A)
Storage proteins (e.g. Transferrin, Ferritin)
Enzymes (e.g. Catalase)

45
Q

How do free radicals injure cells?

A

Membrane lipid peroxidation
Interaction with proteins (fragmentation and protein-protein cross-linkage)
DNA damage

46
Q

What is an infarction?

A

Area of ischaemic necrosis due to reduced or absent blood supply (white indicates arterial occlusion and red indicates venous occlusion)

Block 1: Physiology (15 decks)

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