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anatomic pathology > Normal cellular injury > Flashcards

Normal cellular injury Flashcards

1
Q

State the cell theory

A

All living organisms are made up of cells

Cells are the structural and functional unit of life

All cells comes from pre-existing cells

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2
Q

Unicellular eukaryotes includes

A

Yeast and Algae

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3
Q

Centrioles are composed of

A

Microtubules

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4
Q

What are the 4 cellular adaptation and describe

A

Atrophy- Decrease in number and size of

Hypertrophy- Increase in size

Hyperplasia- Increase in number

Metaplasia- Change from one cell phenotype

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5
Q

Liver regeneration is an example of

A

Compensatory hyperplasia

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6
Q

Alzheimer’s disease is a good example of Atrophy. T/F

A

True

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7
Q

What are the ultra structural changes in a reversible cell injury

A

Plasma membrane- Blebbing, blunting, loss of microvilli

Cytosol- presence of “myelin figures” from phospholipids of damaged cell wall

Mitochondria- swelling and presence of amorphous densities

ER- Dilation of ER with detachment of polysomes.

Nucleus- disaggregation of granular and fibrillary elements

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8
Q

Two phenomena consistently characterizes irreversible cell damages. These are?

A
  1. Inability to reverse mitochondria dysfunction .

2. Profound disturbance in plasma membrane function

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9
Q

Hallmark of cell injury

A 
Mitochondria damage
ATP depletion
ROS 
Plasma membrane damage
Entry of calcium 
Misfolding of protein
DNA damage
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10
Q

Read up the differences between necrosis and apoptosis from ur slides as well as

A

Metabolic effect of cell injury- hypoxia

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11
Q

Necroptosis

A

Morphologically like apoptosis but genetically controlled like apoptosis

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12
Q

What triggers necroptosis

A

Ligation of TNFR1 ( TUMUOR necrotic factor receptor)

Proteins found in RNA and DNA viruses

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13
Q

Inflammatory rxns is elicited in

A

Necrosis

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14
Q

Pyroptosis

A

-Occurs in cells infected by microbes

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15
Q

Pathway of pyroptosis

A

Activation of caspases-1 which cleaves a pro IL-1 to active IL-1

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16
Q

Ferroptosis

A

Iron dependent pathway induced by lipid peroxidation

17
Q

Coagulative necrosis occurs in

A

Infarcts/ischaemia

18
Q

Caseation necrosis

A

Having a cheese-look

Has a soft white proteinaceous mass

19
Q

Liquefactive necrosis

A

Liquid viscous appearance

20
Q

Enzymatic and Traumatic fat necrosis

A

Action of digestive enzymes on fats, leading to formation of soaps(white chalky deposits)

21
Q

Fibrinoid necrosis

A

Immune rxn on blood vessels

22
Q

Pathway of apoptosis

A 
Mitochondria(Intrinsic)
Death receptor( extrinsic)
23
Q

Example of accumulation of substances due to slowed down metabolism.

A

Fatty liver acid

24
Q

Example of accumulation of substances due to genetic problem.

A

Alpha-1antitrypsin deficiency leading to accumulation of A-1at in liver causing cirrhosis

25
Q

Example of accumulation of substances due to failure to degrade a metabolite is

A

Storage diseases

26
Q

Causes of fatty liver

A 
Toxins(Alcohol)
Diabetes mellitus
Obesity
Protein malnutrition 
Anoxia
27
Q

What are foam cells

A

Macrophages that phagocytose lipids to form minute membrane bound vacuoles that have a foamy appearance

28
Q

Conditions where foam cells occurs

A

Atherosclerosis
Hyperlipidemic syndromes
Xanthomas

29
Q

What is Nephrotic syndrome

A

Accumulation of plasma protein(albumin) in the nephron after the pinocytic vesicles fuses with lysosome resulting in appearance of pink, hyaline cytoplasmic droplets

30
Q

Aggregation of specific proteins found in some cells like the : Neurons, RBC, Bacteria and virus is

A

Inclusion bodies

31
Q

What is Russell bodies

What is Dutcher bodies

A

Russell- accumulation of newly synthesized immunoglobins found in the RER of some plasma cells. They are eosinophilic

Dutcher-accumulation of newly synthesized immunoglobins found in the Nucleus or overlying them.

32
Q

Mallory body/ Alcoholic hyaline

A

Cytoplasmic Inclusion bodies found in hepatocytes, characteristic of alcoholic liver damage.

33
Q

The most common exogenous pigment is

A

Carbon

34
Q

Anthracosis occurs in

A

Pulmonary lymph node and parenchyma

35
Q

An important marker of past free radical cell injury is

A

Lipofuscin pigmentations

anatomic pathology (4 decks)

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