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PAthology > Cell Injury > Flashcards

Cell Injury Flashcards

1
Q

What is cell injury _

A

Cell injury is defined as functional and morphological effects of variety of stress’s on the cell from various etiological agents which result in changes in its internal and external environment

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2
Q

On what factors cellular response depends

A

① host that is type of cell nutrition it is reaching

@ factors pertaining to injurious agents

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3
Q

What are types of cels

A

Labile cells
Stable cells
Permanent cells

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4
Q

What are labile cells

A

Continuous regeneration from stem cells self renewal
Haematopoitic stem cells
Epithelial cells of surface
Duct epithelial- salivalyglands, pancreas, biliary tract - skin, Oral cavity vagina cervix
Mucous _ git, uterus, fallopian, ubladden

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5
Q

Stable cells

A

. Parenchyma - liver,. pancreas ,renal tubules
Mesenchymal cells - endothelium
regeneration in response to injury

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6
Q

Permanent cells

A

Non proliferative in postnatal life
Neutrons
Cardiomyocytes

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7
Q

What are the different stages of injury

A 
Normalcells
Pathological or physiological stress
Cellular adaptation
If stress persists
Reversible cell injury
Irreversible cell injury or cell death
That is necrosis or apoptosis
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8
Q

What is the definition of adaptation

A

They are reversible
Structural and functional responses to physiological stress or pathological stress
During which a New altered steady state is achieved
Allowing the cell to survive and continue to function

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9
Q

What are different types of adaptations

A 
Hypertrophy
Hyperplasia
Atrophy
Metaplasia
Displasia
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10
Q

Definition of hyperplasia l

A

Increase in No of cells Not size of cells resulting in enlargement of organ or tissue
May or may not be hypertrophy and hyperplasia occurs together
Occurs in labile cells and stable cells

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11
Q

What is the mechanism of hyperplasia

A

Increased production of growth factors and growth factor receptors

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12
Q

How neoplasia differs from hyperplasia

A

In neoplasia hyperplasia occurs without growth regulatory mechanism due to change in genetic composition of cells but in hyperplasia as long as stimulus present the effect will be there

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13
Q

What is physiological hyperplasia

A

Female breast during pubcity, pregnancy, lactation
Uterus in pregnancy
Endometrium after menstrual cycle
These all come under hormonal hyperplasia

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14
Q

What is physiological compensatory hyperplasia

A

Occurs in liver and bone marrow
liver after donation
Bm afterhaemorrageand blood donation -

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15
Q

Examples of pathological hyperplasia

A

Endometrial hyperplasia due to oestrogen excess
Ducal hyperplasia of the Brest
Benign prostatic hyperplasia in old age
Skin warts from human papilloma virus

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16
Q

Definition of hypertrophy

A 
There is increase in size not in number 
see-in permanent cells
May or may not be associated with plasia 
Uterus = both plasia + trophy
Cardiomyo cites - only hypertrophy
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17
Q

What is mechanism of hypertrophy

A

Cellular swells more structural components and proteins

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18
Q

Physiological hypertrophy examples

A

Uterus in pregnancy

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19
Q

Examples of pathological hypertrophy

A

Cardiac muscle
Smooth muscle
Skeletal muscle
Compensatory hype-ropy

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20
Q

In what conditions cardiac hypertrophy occurs -

A

Systemic hypertension
Aortic valve stenosis
Aortic value insufficiency
Mitral value insufficiency

SAAM

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21
Q

In what conditions smooth muscle hypertrophy occurs

A

Cardiac aclasia
Pyloric stenosis
Intestinal strictures
Muscular arteries in hypertension

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22
Q

In what condition skeletal muscle hypertrophy occurs

A

Hylpertropied muscles in athletes and tabours

23
Q

Compensation hypertrophy occurs in?

A

Liver after hepectotomy

Kidney after nephrectomy on one side nephrons increases

24
Q

Morphological features of hypertrophy

A

Organ enlarged

DNA, RNA increase prote synthesis increases and er, and organelle increases myofibrils alto increase

25
Q

Atrophy definition

A

Decrease in size and number of cells without or with shrinkage of the tissue

Atrophied cells are smaller in size but viable there is no guarantee they need to go necrosis or apoptosis

26
Q

What is the mechanism of atrophy

A

Reduction in cell organelles chiefly mitochondria and myofilaments and er

27
Q

Physiological atrophy is seen in

A 
Lymphoid issue with age
Thymus. In adult life
Gonads after menopause
Uterus aft parturition
Brain with aging.
Bony trabuculae in osteoporosis
28
Q

Pathological atrophy seen in

A

Starvation atrophy general weakness,anemia, emaciation known as cache is in cancer patients
Ishemic atrophy kidney in renal atherosclerosis and brain brain in cerebral atherosclerosis
Neuropathic atrophy = poliomyelitis,motor neurone disease

Disuse atrophy wasting of immobilised hand

Endocrine = hypo pituitary secretions may cause atrophy of thyroid

Pressure= erosion of skull in meningioma and erosion of sternum in arch of aorta aneurysm

Idiopathic

29
Q

What are morphology of atrophy

A

Cells smaller in size
Increase in autophagic vacuoles
Shrinkage in cell size due to cell organelles , mito amd myofilamemts

30
Q

Defination of metaplasia

A

A reversible change in which one adult matured cell type is replaced by other adult cell type
It is reversible

31
Q

Mechanism of metaplasia

A

Reprogramming of stem cells occurs not the change in already existing cellls

32
Q

Types of metaplasia

A

Epithelial squamous and columnar

Mesenchymal _ osseous and cartilaginous

33
Q

Epithelial metaplasia

A

Most common type

Replacement of one epithelium by stronger but less well specialised epithelium

Columnar epithelium → squamous epithelium
Bronchus.( pseudostratified columnar ciliated epithelium) in chronic smokers

Uterine endocervix( normally lined by simple columnar epithelium ) in prolapse of uterus

Gallbladder( normally lined simple columnar epithelium)
In cholelithiasis

In prostate(normally lined simple columnar epithelium) in chronic prostatitis

Vita A deficiency, squamous metaplasia in nose, bronchi
Lacrimal and salivary glands

34
Q

Examples of metaplasia

A

Barett’s esophagus → change of normal squamous epithelium to columnar epithelium

Cervical erosion → change of normal squamous epithelium to columnar epithelium

35
Q

Mesenchymal metaplasia

A

Less common

One adult type of mesenchymal tissue to another lie formation of cartilage, bones or adipose tissue

36
Q

Osseus metaplasia

A

Monckebergs medial calorific sclerosis(in arterial
Wall in old age)

Myositis ossificans

Cartilage of larynx and bronchi in eldest ppl

In scar of chronic inflammation of prolonged duration

37
Q

Cartilaginous metaplasia

A

In healing of fractures cartilaginous metaplasia may occur where there in undue mobility

38
Q

Dysplasia definition

A

Disordered cellular development

Characterised by cellular cytologic changes

39
Q

Explain cytological changes

A

No of layers increases
Disorderly arrangement

Loss of basal polarity
Pleomorphism 
Increased n/c ratio
Hyperchromatism
Increased mitotic activity
40
Q

Cell injury

A

Cell injury when cells are stressed so severely or persistently that they are no longer able to adapt or when cells are exposed to damaging genes

41
Q

Types of cell injury

A

Necrosis

Apoptosis

42
Q

What are the causes for cell injury

A 
A) genetic causes 
B)aquired causes
Hypoxia and ischaemia
Physical agents
Chemical agents
Microbial agents
Immunologic agents
Nutritional derangement
Aging
Psychogenic diseases
Iatrogenic factors
Idiopathic diseases
43
Q

What are 5 mechanisms of cell injury

A 
ATP depletion
Mitochondrial damage
Loss of calcium homeostasis
Defects in membrane permeability
Free radical injury
44
Q

Explain ATP depletion mechanism of cell injury os

A

ATP formation decreases

Na+ k+ pump decreases influx of cal and Na+ increases
Efflux of k+ increases

Er swelling, cellular swelling, loss of microvilli, Blebs formation :
. In
Anaerobic glycolysis occurs due to ishecemia lactic acid
Ph v

45
Q

What are effects caused by atp depletion

A

Na and k+ pump stops working

Influx of calcium increases and effulx of k+increases

Er swelling ,cellular swelling loss of microvilli blebs

Anaerobic glycolysis glycogen decreases and lactic acid increases ph decreases

Clumping of nuclear chromatin

Detached ribosomes cause decrease protein synthesis

46
Q

What happens when ishcemia occurs

A

Ischemia

Mitochondria reduces oxidative phosphorylation

Na k pump decreases sodium and water enters and k exists

Endoplasmic reticulum dilates ,the cell swells blebs appears

47
Q

How anaerobic glycolysis affect the cell injury

A

Anaerobic glycolysis

Glycogen decreases

Lactic acid increases ph decreases

Interferes with enzymes and nuclear chromatin

48
Q

Decreased atp

Rer loses ribosomes

Proteins
Synthesis falls

Structural proteins and enzymes depletion

A

Due to atp depletion

49
Q

How the mitochondrial damage effects the cell injury

A

Mitochondrial damage

Mitochondrial permeability transition pore

Loss of mitochondrial membrane

Failure of normal oxidative phosphorylation

Atp decreases

Mitochondrial damage

Abnormal oxidative phosphorylation

Formation of ro

Deleterious effects

As the permeability of mitochondria increases c reactive protein blw outer and inner membranes

Mitochondrial damage c reactive protein come out and promote apoptosis

50
Q

Calcium homeostasis

A

Normally Ca will be less intracellurlly what ever cal present is present on the er and mito

As the mitochondrial damage occurs and permeability increases the ca in the cells increases

Several enzymes like phospholipids
Atpase
Proteases
Endonucleases

51
Q

Consequencesof membrane damage

A

Mitochondrial membrane damage
Plasma damage
Lysososomal membrane damage

52
Q

Explain plasma membrane damage

A

Loss of osmotic balance.

Effluent of fluids and ions

Loss of cellular contents
Atp decreases

53
Q

What is Fenton reaction

A

H202 +fe+2 =fe+3 +oH+oh-

54
Q

Haber Weiss reaction

A

H202 +02= 20H-+ 02

PAthology (10 decks)

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