Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathophysiology > Cell Injury and Adaption > Flashcards

Cell Injury and Adaption Flashcards

Lecture 2 (77 cards)

Start Studying
1
Q

Name 5 reversible adaptive changes/ mechanisms

Tip* (AHH Mom Dad)

A

i. Atrophy
ii.Hypertrophy
iii. Hyperplasia
iv. Metaplasia
v. Dysplasia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is Atrophy

A

Decrease in cell size, number and function = Reduced size of organ or tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What is the atrophy mechanism

A

Reduction in protein synthesis

Increased degradation of cellular proteins (autophagy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the Physiological component of Atrophy?

A

Part of normal development – involution of thyroglossal duct, involution of gravid uterus after delivery

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is the Pathological component of Atrophy?

A

example - broken bone after 6 weeks in a cast

 Decreased workload or functional
demand (disuse atrophy)
- Prolonged immobilisation, bed-
ridden/wheel-chair bound persons

 Inadequate blood supply (ischaemic
atrophy)

 Inadequate nutrient supply
- Cancer patients, chronic inflammatory diseases, starvation

 Loss of innervation (denervation atrophy) - Trauma, degeneration

 Loss of trophic signals from endocrine organs - Hormone dependent tissues (breast)]

 Pressure on surrounding organs or tissue
by an expanding mass - May compromise blood/nutrient supply

 Ageing process (not a disease) -Shrinkage of brain, decrease size of ovaries, testes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is Hypertrophy

A

Increased in size and functional capacity of cell

Increase in the structural components or tissue mass -Increase in the size of the organ

Influences muscle mostly

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What is the mechanism of Hypetrophy?

A

Increases synthesis of cellular proteins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the physiological reasoning of Hypertrophy?

A

Increased workload
- Increased size of heart and skeletal
muscle mass after workout at gym

Increased hormonal influence
-Increased size of uterus in pregnancy – oestrogen stimulation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the pathological reasoning of Hypertrophy?

A

Excessive / abnormal stress on the
muscles
- Increased size of left ventricle of the heart in hypertensive patients

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Hypertrophy of the heart caused by?

A

High Blood presure - then left ventricle needs to contract more thus get bigger to compensate to get blood to the brain.

( Cardiachypetrophy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is Hyperplasia?

A

Increase in number of cells in a tissue or organ - Increase size of organ or tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the mechanism of Hyperplasia?

A

Growth factor-driven proliferation of mature cells - hormonally influenced tissue

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is the physiological reasoning of Hyperplasia?

A

Hormonal stimulation
- Decreased RBC production in renal failure
- Erythropoietinsecretion bykidneys  - – - — Female breast development during at
puberty

Persistent injury producing calluses on foot due to ill-fitting shoes

Compensatory – following damage (trauma) or partial resection (hepatectomy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is the Pathological cause of Hyperplasia?

A

Excessive hormonal stimulation or growth
factors acting on target cells
-Endometrial hyperplasia (oestrogen) - Prostatic hyperplasia (androgens)

Viral infection (papillomavirus) – skin warts

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is Metaplasia?

A

 Conversion of one differentiated adult cell type to another adult cell type – better able to survive injury

 Reversible change

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is the mechanism of Metaplasia?

A

Reprogramming of stem cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What is the causes of Metaplasia ?

A

As a response to irritation or inflammation
Chronic smoking
- Bronchial columnar ciliated
epithelium to squamous epithelium

Stones or calculi in bile duct, gall bladder, kidneys -Columnar epithelium to squamous epithelium

Barrett’s oesophagus
- Squamous epithelium to to columnar epithelium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What is Dysplasia?

A

Alteration to the size, shape, uniformity, architectural orientation and organization of the cell

Commonly occurs in cells that have already undergone metaplasia or hyperplasia

May be considered as “atypical hyperplasia” or “pre- cancerous”

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the mechanism of Dysplasia?

A

Increased cell division with propagation of ‘bad’ gene

Genetic change gives cell substantial growth advantage

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What causes Dysplasia?

A

Ongoing injury – cigarette smoking or gastric acid reflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

What is the flow of cells to cancer?

A

Normal -> Hyperplasia -> Dysplasia -> Cancer

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

What happens with Irreversible cell injury

A

Necrosis and Apoptosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Necrosis

A

Cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Apoptosis

A

Specialized , purposed cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
What does Irreversible injury results in?
1. Degeneration Deterioration and loss of function in the tissue or organ. 2. Cell necrosis Structural changes which results in biological cell death
26
What is Degeneration?
Deterioration and loss of function in the tissue or organ.
27
What is cell necrosis
Structural changes which results in biological cell death
28
What is Hyaline Degeneration?
 Structure-less glassy appearance  Seen in collagen of old fibrous tissues, smooth muscles of arterioles or uterus or as droplets in parenchymal cells  Seen as pink acellular material
29
What is mucoid degeneration?
Due to Accumulation of mucoproteins and mucopolysacchrides Example: myxoedema of hypothyroidism
30
Examples of mucoid degeneration?
myxoedema of hypothyroidism
31
What is Necrosis?
Structural changes that occur in cells following irreversible cell injury in a living tissue or organism ALWAYS associated with inflammation
32
What does the Manifestation of necrosis depends on?
 Nature, intensity and duration of injurious agent  Type of cell affected
33
What is Pathogenesis due to?
May be due to either:  Denaturation of proteins  Enzymatic digestion of organelles and other cytoplasmic component
34
What are the Types of necrosis?
1. Coagulative necrosis 2. Liquefactive necrosis 3. Caseous necrosis 4. Fat necrosis 5. Fibrinoid necrosis
35
What is Coagulative necrosis?
Characteristic of hypoxic or ischaemic death in all solid organs (heart, kidney, spleen) except the brain
36
Characteristic of hypoxic or ischaemic death in all solid organs (heart, kidney, spleen) except the brain
Coagulative necrosis
37
What is the underlying mechanism of Coagulative necrosis?
Denaturation of proteins with preservation of cellular and tissue framework Genetic material clumps, nuclear membrane shrivels and breaks up Leucocytes digest dead cells by lysosomal enzymes Debris removed by phagocytic cell
38
What happens on a macroscopic level with Coagulative necrosis?
Pale demarcated area surrounding by well vascularised tissue
39
What happens on a microscopic level with Coagulative necrosis?
Lighter staining tissue with absent or ill defined nucleus – “ghost cells”
40
What is Liquefactive (colliquative) necrosis?
Generally seen in the cells of CNS due to hypoxia or infection
41
What is the mechanism of Liquefactive (colliquative) necrosis?
 Enzymatic digestion of tissue (lysosomal enzymes)  Results in liquefaction (liquid mass) composed of necrotic tissue and dead leucocytes  Gets either absorbed or infected and forms an abscess
42
What is Caseous necrosis?
Result of a granulomatous inflammation Example: tuberculous infection
43
What is an example of Caseous necrosis?
tuberculous infection TB
44
What happens on a macroscopic level with regards to Caseous necrosis?
Appears as soft friable cheese-like material
45
What happens on Microscopy leve with regards to Caseous necrosis?l
Chronic inflammation with granuloma formation
46
What is Fat necrosis?
Specific to adipose tissue, it the Release of enzymes – auto-digestion of surrounding fat tissue. and may undergo calcification.
47
What happens on a macroscopic level with regards to Fat necrosis?
Appears as white chalky material Examples: -Retroperitoneal and omental fat in acute pancreatitis -Breast tissue following trauma
48
What is Fibrinoid necrosis?
Specific to injury caused by immune complexes in immune mediated diseases
49
What happens on a macroscopic level with regards to Fibrinoid necrosis?
Results in fibrin-like material deposited in tissue May be seen in blood vessels – malignant hypertension, vasculitis, rheumatic nodules
50
Where may Fibrinoid necrosis be seen?
blood vessels – malignant hypertension, vasculitis, rheumatic nodules
51
What happens on a microscopic level with regards to Fibrinoid necrosis?
Eosinophilic, homogenous appearance
52
What is gangrene?
Not a distinct pattern of cell death but a clinical form of necrosis Morphological changes of cell death in a dead or dying tissue
53
What typres of gangeren can you get?
Wet or Dry
54
What is Wet gangerene associated with?
Liquefactive necrosis
55
What is dry gangeren associated with?
Coagulative necrosis
56
Describe Dry gangrene
Form of coagulative necrosis Part is dry and shrunk Skin wrinkled - dark brown or black in colour Slow spread Symptoms not marked, Frost-bite
57
What is the Line of demarcation, Dry gangrene.
Distinct area between dead and healthy tissue Confined to extremities (+ internal organs) (diabetics)
58
Describe Wet gangrene
A Form of liquefactive necrosis Area cold, swollen and pulseless Skin is moist and tensed; Blebs on surface  Foul smell – bacterial action Rapid spread Severe symptoms Death unless treated
59
IS there a line of demarcation with wet gangrene?
No
60
What is Gas Gangrene?
Due to anaerobic infection of devitalised tissue by spore forming organisms - Clostridium species – C. perfringens
61
Where is Gas Gangrene mostly seen?
Seen in trauma injuries and compound fractures - Exposed to dirt and debris Other Sites - Stomach, gall bladder, intestines etc.
62
How does gas gangrene effect the body?
Toxin produced by bacteria dissolve cell membrane and causes death of muscle cells – results in wide spread oedema Associated with * Haemolysis = haemolytic anaemia, haemoglobinuria * Production of hydrogen sulphide gas between muscle fibres = crepitus Serious and dangerous
63
What is gas gangeren associated with?
Haemolysis = haemolytic anaemia, haemoglobinuria Production of hydrogen sulphide gas between muscle fibres = crepitus
64
What is apoptosis?
Form of programmed cell death - The number of cells in tissues is regulated by balancing cell growth and cell death.
65
Apo - Greek means
Apart
66
ptosis greek meens
fallen
67
Greek translation for Apoptosis
fallen apart
68
Does apoptosis have inflammation?
No
69
Describe apoptosis.
Highly selective process Eliminates injured and aged cells - Controls cell regeneration; Genetically determined, internal self destruct mechanism of cell death Activated under a variety of circumstances or is induced (energy dependent process)
70
What causes apoptosis
 Selective removal of individual cells may be essential in embryological process (morphogenesis) Eg. digital webs, neurones and synapses, conduction system of heart, proper development  Physiological process Hormonal withdrawal and normal involution process – post lactation, menopause, ageing  Pathological stimuli Vast majority of cancer cells when subjected to chemo- or radio therapy  Destruction of cells that are threat to the integrity of the organism eg. Cells infected with viruses, damaged DNA or cancer cells
71
What are the reversible stages of Apoptosis
Initiation
72
Describe intiation of apoptosis
Withdrawal of positive signals required for survival (GF, IL-2) Receipt of negative signals (increased levels of oxidants, damage to DNA) Release of apoptosis inducing factors Hormonal influences
73
What are the irreversible stages of the apoptosis?
Priming - increased enzyme activation Triggering - Sustained rise in cytosolic calcium levels Execution – final proteolytic cascade Phagocytosis Macrophage recognise apoptotic bodies – phagocytosis
74
What happens in apoptosis when there is an increase in enzme activation during priming?
Affected cell shrinks Fragmentation of both nucleus and cytoplasm Detachment from surrounding cells Nuclear chromatin condensation Cell emits signals to attract macrophages
75
What happens in apoptosis when Execution takes place th final proteolytic cascade during the Irreversible stage?
Cross linking protein forming insoluble layer beneath intact cell membrane - Formation of apoptotic bodies Cell contents are contained and not released into extracellular space
76
Compare Necrosis to Apoptosis (5)
Necrosis Groups of cells involved Injurious agent responsible Cells are swollen Haphazard destruction Inflammatory response Apoptosis Single or selected cells Programmed cell death Cell shrinkage Ordered destruction No inflammatory response
77

Pathophysiology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions