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Patho > 2 . Cell > Flashcards

2 . Cell Flashcards

1
Q

Types of cells in relation to miyotic cell division

A

Permanent neurons cardiac and skeletal

Stable - G0 state - Hepatocyte endothelial cells pct

Labile cells - stem cells
Epidermis mucosal lining bone marrow elements

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2
Q

Causes of cellular stress or injury

A

Physical
Chemical
Biological

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3
Q

Ischemic reperfusion injury because of

A

Free oxygen radicals

Ca influx but there is already ca build up in cell because of damage to SR
So state of hyper contraction in myocardium

Inflammation cytokines

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4
Q

Generation of ROS

A

Physiological - partial reduction of O2 during oxidative phosphorylation

Pathological
Ionizing radiation
Inflammation
Fenton reaction

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5
Q

Ratio of Reduced glutathione to oxidized is indicator of

A

Health when it’s high

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6
Q

Unfolded protein response and ER stress

A

When misfolded proteins accumulate in the ER they trigger the UPR
Response is
Increased production of chaperons which control the proper folding of proteins

Enhance proteosomal degradation of misfolded proteins

Slow protein translation

If UPR doesn’t work it cause apoptosis and is called ER stress

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7
Q

Intracellular accumulation of misfolded protein caused by

A

Increased misfolding
Viral infection mutation ph and redox state
Or
Decreased correction
Atp for foldase and aging

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8
Q

Cellular adaptation by

A

Hyperthrophy
Hyperplasia
Metaplasia
Atrophy

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9
Q

Protein degradation by

A

Ubiquitin proteasome system
Autophagy lysosome system

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10
Q

Ubiquitin proteasome system stimulated by and inhibited by

A

Stimulate -
Glucocorticoid
Thyroid
Cytokines

Inhibited -
Insulin

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11
Q

Physiologic hyperplasia 2 types

A

Hormonal hyperplasia uterus and breast

Compensatory hyperplasia regeneration of liver

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12
Q

Pathological hyperplasia
Hyperplasia of

A

Of CT in wound healing

Of epidermis in skin warts due to HPV infection

Of endometrial hyperplasia due to unopposed estrogen

Of prostatic nodes due to androgen

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13
Q

Mechanism of hypertrophy

A

•Due to increased synthesis of structural components
•Through gene activation, protein synthesis, and production of organelles
•Nuclei may have a higher DNA content probably because cell cycle arrest without mitosis

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14
Q

Physiologic hyperthrophy

A

Uterus
breast

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15
Q

Pathological hyperthrophy

A

Cardiac muscle hyperthrophy

Compensatory hyperthrophy hepatomegaly

Bladder trabiculation in BPH

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16
Q

Metaplasia

A

Reversible change in which one adult cell type is replaced by another adult cell type

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17
Q

Pathologic hyperplasia can progress to cancer and dysplasia except

A

BPH

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18
Q

Atrophy by decrease in cell size and cell number

A

Size
UPS and Autophagial lysosome system

Number
Apoptosis

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19
Q

Dysplasia

A

Dysplasia refers to abnormal changes in the size, shape, and organization of mature cells
Is Not a True Adaptive Change

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20
Q

Slowly developing ischemia (e.g., renal artery atherosclerosis) results in……… ; whereas, acute ischemia (e.g., renal artery embolus) results in …… (AKI).

A

atrophy
injury

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21
Q

2 types of cell injury

A
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22
Q

reversible cell injury plus hallmark

A

The structural and functional changes can revert to normal on removal of the an injurious stimulus
The hallmark of reversible injury are cellular swelling and fatty change

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23
Q

irreversible cell injury plus hallmark

A

The structural and functional changes cannot be reversed even after removal of the injurious stimulus
The hallmark of irreversible injury is membrane damage

24
Q

cell death plus hallmark

A

The end result of irreversible injury
The morphologic hallmark of cell death is loss of the nucleus

25
Q

types of cell death

A

necrosis and apoptosis

26
Q

pyknosis
karyorrhexis
karyolysis

A

nuclear condensation (pyknosis), fragmentation (karyorrhexis), and/or dissolution (karyolysis).

27
Q

necrosis

A

is localized death of cells, tissues, organs, or parts of the body in a living organism
Due to some underlying pathologic process; never physiologic

28
Q

Cytoplasmic changes in necrosis

A

loss of RNA and denaturation of proteins(increased eosinophilia)

Glassy homogenous cytoplasm b/c of loss of glycogen

Swelling and vacuolation of the cytoplasm

Cell and organelle membranes rupture

Formation of myelin figures

29
Q

Nuclear changes in necrosis

A

Nuclear shrinkage and increased basophilia (pyknosis)
Nuclear fragmentation (karyorrhexis)
Fading of basophilia due to DNase activity (karyolysis)

30
Q

types of necrosis

A

Coagulative necrosis
Liquefactive necrosis
Caseous necrosis
Fat necrosis
Fibrinoid necrosis

31
Q

coagulative type

A

tissue firm and pale and preserved
most common
because of ischemia or infraction except brain
ischemia leads to protein/enzyme denaturation

32
Q

coagulative in order

A

reduced ph
denatured enzymes
no proteolysis

33
Q

liquefactive necrosis or colliquative

A

Enzymatic breakdown&raquo_space; protein denaturation
Usually associated with bacterial or fungal infections and form abcess or pus

Seen in organs that have a high-fat and low protein content -brain
high-enzymatic content (eg, the pancreas) or lack of a proper collagenous connective tissue framework

34
Q

gangrene types

A

dry
wet
gas

35
Q

dry and wet gangrene difference

A
36
Q

caseous

A

Combination of coagulative and liquefactive necrosis.
Typically found in tuberculous and fungal granuloma.
On gross; it is soft and greasy, resembling cottage cheese.

37
Q

fat necrosis

A

Fat necrosis: This type of necrosis occurs when there is damage to adipose tissue, resulting in the release of fatty acids, which can combine with calcium ions to form chalky white deposits. It is commonly seen in the breast and acute pancreatitis
chalk white deposit is soap so saponification

38
Q
A

limited to small blood vessels.
No distinct macroscopic features.
This type of necrosis is characterized by the deposition of immune complexes and fibrin in the walls of blood vessels, which can lead to vessel damage and inflammation.
Characteristic of malignant hypertension and vasculitis. It may also be seen in rheumatic fever, rheumatoid arthritis, hepatitis B virus (HBV) infection, systemic lupus erythematosus (SLE), etc

39
Q

Sequence of Morphological Changes in Apoptosis

A
40
Q

Examples and causes of apoptosis

A

Physiologic
Involution following hormone withdrawal
Removal of cells during embryogenesis
Negative selection of thymocytes in thymus
Death of cells after fulfilling their function
Pathologic
CD8⁺ T cell-mediated killing of virally infected cells
DNA damage beyond repair
Atrophy of parotid, kidney, pancreas after duct obstruction

41
Q

Sequence of Morphological Changes in Apoptosis

A
  1. Cell shrinkage (increased density of the cytoplasm with tightly packed organelles)
  2. Chromatin condensation under the nuclear membrane followed by nuclear fragmentation (karyorrhexis)
  3. Surface blebbing followed by fragmentation into membrane-bound apoptotic bodies
  4. Phagocytosis of apoptotic bodies (ingestion by macrophages followed by lysosomal degradation)
42
Q

Sequence of Biochemical Events in Apoptosis

A

protein cleavage by proteolytic enzymes/caspases
protein cross link
DNA condensation and breakdown
recognition of dying cells by phagozytes

43
Q

Mechanism of Apoptosis

A
  1. Initiation of apoptosis by activation of signalling pathways:
  2. Control and integration:
  3. Execution phase:
  4. Removal of dead cells:
44
Q

intrinsic mitochondrial activation of apoptosis

A

This pathway is initiated by the release of cytochrome c from the mitochondria into the cytosol. Cytochrome c then binds to Apaf-1 (apoptotic protease activating factor-1), which leads to the activation of caspase-9 and the subsequent activation of downstream caspases.
all because of increase in permeability of mitochondial membrane
Release of these factors is regulated by Bcl family of proteins on mitochondrial membrane

45
Q

extrinsic death receptor pathway

A

This pathway is initiated by the binding of ligands such as tumor necrosis factor (TNF) or Fas ligand (FasL) to death receptors such as TNF receptor-1 or Fas. This binding leads to the activation of caspase-8, which can then activate downstream caspases.

46
Q

p53 pathway

A

This pathway is initiated by the binding of ligands such as tumor necrosis factor (TNF) or Fas ligand (FasL) to death receptors such as TNF receptor-1 or Fas. This binding leads to the activation of caspase-8, which can then activate downstream caspases.

47
Q

other way of activation of apoptosis hint lymphocytes

A

Lymphocytes release perforins that punch a hole in the cell membrane of the target cell
Then, they release granzyme B into target cell that activates the caspases

48
Q

Control and integration:

A

controlled by BCL2 family of proteins which include ‘antiapoptotic proteins’ (BCL2, BCL-XL and MCL1); ‘proapoptotic proteins’ (BAX and BAK); and ‘BCL2 sensor proteins’ (BAD, BIM, Puma, Noxa).

49
Q

Execution phase:

A

Proteolytic cascade involving execution caspases (caspases 3 and 6).

50
Q

Removal of dead cells:

A

by macrophages
Removal is aided by expression of phosphatidylserine, secretion of soluble factors like thrombospondin and coating of apoptotic cells by natural antibodies and of the complement proteins (opsonization)

51
Q

Phosphatidylserine and thrombospondin for removal of death cells

A

Phosphatidylserine is normally located on the inner leaflet of the plasma membrane, but during apoptosis, it becomes exposed on the outer leaflet. This serves as a signal for phagocytic cells, such as macrophages, to recognize and engulf the apoptotic cell.

Soluble factors such as thrombospondin can also contribute to the recognition and removal of apoptotic cells. Thrombospondin can bind to receptors on phagocytic cells and promote the engulfment of apoptotic cells.

52
Q

Disorders associated with decreased apoptosis

A

cancer and autoimmunity

53
Q

Disorders associated with increased apoptosis:

A

Neurodegenerative diseases (Alzheimer, Huntington, Parkinson)
Ischemic injury in stroke and myocardial infarction
Death of virus-infected cells as in AIDS
Graft rejection

54
Q

difference between necrosis and apoptosis

A
55
Q

other types of cell death

A

necroptosis
ferroptosis
pyroptosis

56
Q

necroptosis

A

hybrid

Patho (33 decks)

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