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Path > Cellular stress/toxic injuries: Adaptation, injury, and death > Flashcards

Cellular stress/toxic injuries: Adaptation, injury, and death Flashcards

1
Q

What are the 4 adaptation responses?

A

Hypertrophy (increase size)
Hyperplasia (increase #)
Atrophy (shrinkage of cell/decreased metabolic activity)
Metaplasia (change in phenotype)

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2
Q

What is the response to a patient with chronic hypertension or faulty valves?

A

The heart will go through hypertrophy (left ventricle), if too severe it will cause damage to the heart.

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3
Q

What are the GF required for hypertrophy of the heart?

A 
ANF
GATA 4 (transcription factor)
IGF-1
MEF2 (myocardial enhancing factor)
NFAT (nuclear factor activating T-Cells)
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4
Q

What are some vasoactive elements that will cause hypertrophy of cardiac muscle?

A

alpha adrenergic agonist
Endothelin-1
AT-2 (angiotensin 2)

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5
Q

What causes hypertrophy and hyperplasia of the uterus?

A

Large concentrations of estrogen.

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6
Q

What is the response to liver damage?

A

Hyperplasia

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7
Q

What undergoes rapid cell division when erythropoietin is present?

A

The bone marrow, to be more specific progenitor cells.

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8
Q

What is the characteristic response to viral infections? Give an example and why.

A

Hyperplasia is a characteristic response

HPV is an example of this, it causes skin warts and several mucosal lesions composed of hyper plastic epithelium.

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9
Q

Two organs that undergo atrophy during development are…

A

Notochord

Thyroglossal duct

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10
Q

Prolonged disuse of cells such as skeletal muscle fibers will cause..

A

Atrophy: Decrease in the size of the cells and it might cause apoptosis of certain cells.

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11
Q

What are some common causes of atrophy

A 
Loss of innervation to tissue
Ischemia
Inadequate nutrition (cachexia) 
Loss of endocrine stimulation (loss of GF)
Pressure on tissue
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12
Q

The brain and heart goes through what process as we get older?

A

Atrophy due to atherosclerosis (senile atrophy), this also happens to the heart.

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13
Q

Mechanism for atrophy

A

Degradation of proteins (ubiquitin-proteasome pathway)

Autophagy of organelles to match blood supply

Discoloration because of lipofuscin granules (brown)

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14
Q

What happens to the respiratory epithelium for cigaret smokers?

A

Metaplasia of respiratory epithelium

ciliated columnar epithelium to stratified squamous epithelium.

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15
Q

What are some common causes of metaplasia?

A

Vitamin A deficiency: squamous metaplasia in respiratory system

Stone formation in excretory ducts: pancreas, salivary gland, or bile duct. Columnar to squamous

Smoking: Ciliated columnar to stratified squamous

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16
Q

What causes Barrett Esophagus?

A

The patient has GERD and the esophageal squamous epithelium changes to intestinal like columnar epithelium.

This can develop into adenocarcinoma (glandular carcinoma)

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17
Q

What is myositis ossificans? (it is from a result of injury)

A

Occurs in intramuscular hemorrhage, which results in the formation of cartilage, bone, or adipose tissue.

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18
Q

What are key features of necrosis (6)

A

Irreversible injury
Cell size: swelling

Nucleus: pyknosis->karyorrhexis->karyolysis

Plasma membrane: disrupted
Cellular contents: leak out of cell

Localized inflammation

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19
Q

What are key features of apoptosis (6)

A

Programed death
Cell size: reduced

Nucleus: Fragmentation

Plasma membranes intact, but altered structure.
Cellular contents: apoptotic bodies, buds of cells

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20
Q

What is pyknosis, karyorrehexis, and karyolysis?

A

Pyknosis: condensation of the nucleus (increased basophillia color)

Karyorrehexis: fragmentation of nucleus and disappears

Karyolysis: break down of DNA, fading basophillia color.

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21
Q

Coagulative necrosis: features and location

A

Location is all organs except the brain

Caused by ischemia to target tissues, localized areas are considered infants.

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22
Q

Liqiefactive Necrosis: features and location

A

Generally happens in the CNS (brain)

Caused by digestion of dead cells by leukocytes, which results in a liquid mass. There is a creamy yellow pus like material.

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23
Q

Gangrenous necrosis: features and location for both dry and wet

A

Location in the lower extremities of the body when they lose blood supply.

Normal necrosis (dry), but if there is an infection superimposed on them it will cause wet gangrene, which is an increased level of liquefactive necrosis.

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24
Q

Caseous necrosis: features and location

A

This is found in infections such as TB infections, where there is a characteristic granuloma formation.

There will be a white appearance of necrosis, with fragmented/lysed cells enclosed by an inflammatory boarder.

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25
Q

Fat necrosis: features and location

A

From the release of pancreatic lipase, which are from acinar cells during acute pancreatitis.

This process includes the break down of fat tissue and replace it with calcium deposits. There will be presence of saponification (white chalky substances).

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26
Q

Fibinoid necrosis: features and location

A

Happens in immune responses involving blood vessels like Vasculitis syndromes.

Antigen-antibody complexes collect on the walls of arteries, which causes fibrin to leak out.

When stained with H and E stains it will be a bright pink and amorphous appearance.

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27
Q

Dystrophic calcification

A

Cellular debris from necrotic tissue will provide a location for calcium and other minerals to calcify. It can also happen in aging or damaged heart valves.

This only happens if necrotic tissue is not removed properly. Happens in coagulative, caseous, or liquefactive.

This also happens with asbestos in the lungs, create dumbbells.

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28
Q

What happens if a cell runs out of ATP?

A

This will cause necrotic death because the cell will experience
Cell swelling because no Na/K pump action
Lactic acid build up=decreased pH
Calcium build up= failure of Ca pumps
ER stress response
Damage to mitochondrial and lysosomal membranes.

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29
Q

What can cause cell death via mitochondria damage?

A

Creation of mitochondrial permeability pore.
ROS (reactive oxygen species; linked to Alzheimers)
Cytochrome C leak= apoptosis via caspasees.

30
Q

How do transition metals lead to ROS and what are used in the body to counter this.

A

Tranition metals like iron and copper have charges on them. they like to donate their electrons making ROS.

The body counters this process by keeping most of the transition metals bound to proteins like ceruloplasmin (copper) and transferrin (iron)

31
Q

Examples of cells that go through apoptosis

A

B/T cells that are self reactive
neutrophils
Infected cells (help of CTL and NK cells)
Uterine epithelium after hormone withdrawal.

32
Q

Key characteristics of apoptosis

A

Cell shrinkage
Chromatin condensation
Cytoplasmic blebs
Phagocytosis of apoptotic bodies.

33
Q

What are zymogens?

A

Proteins like caspases that need to be cleaved to become active.

34
Q

Steps for intrinsic mitochondrial apoptosis

A

It is controlled by BCL2 pathway, which when there is no GF going to the cell the transcription of BCL2 stops and the apoptosis proteins can then make a pore on the mitochondria to cause cytochrome C leakage.
Cytochrome C and APAF-1 bind to make the apoptosome, which activates caspase 9 which activates caspase 3.

Apoptisome inhibition is done by SMAC/Diablo
Anti apoptosis proteins involved are BCL2, BCLXL, and MCL-1
Pro apoptosis proteins are BAX and BAK

35
Q

Extrinsic death receptor pathway (Fas/FasL)

A

Triggered by the TNF-receptor family, in which FasL (TCL) activates the death domain in damaged cell). Incorporation of capsize 8 and 10, which causes activation of caspase 3 or 6.

This process is inhibited by FLIP protein.

36
Q

Executioner caspases

A

3 and 6 because they are the ones that cause DNA damage beyond repair

37
Q

Cystic fibrosis: protein effected and function lost

A

Protein effected is CFTR

Causes defective chloride transport.

38
Q

Familial hypercholesterolemia: protein effected and function lost

A

Protein effected is LDL receptor

Causes hypercholesterolemia.

39
Q

Tay-Sachs disease: protein effected and function lost

A

Protein effected Hexosaminidase B subunit

Causes storage disorder for GM2 in neurons. Leads to cherry red macula and onion skin macrophages

40
Q

Alpha-1 antitrypsin deficiency: protein effected and function lost

A

Protein effected in alpha-1 antitrypsin

Causes destruction of elastic tissue in lungs, which causes emphysema.
This is due to the unregulation of neutrophil elastase when alpha-1 antitrypsin is missing.

41
Q

Creutzfeldt-Jacob disase: protein effected and function lost

A

Proteins effected are prions

Cause neuronal cell death because of abnormal folding of PrPsc.

42
Q

Alzheimers disease: protein effected and function lost

A

Defective A-beta peptide

Causes aggregation of neurons and apoptosis.

43
Q

Necropoptosis

A

Programed necrosis that does not activate caspases.
TNF family is used here (RIP 1/3), which causes leaky lysosome, ROS, and decreased ATP formation.
It is a backup for viruses that inhibit caspase 8 activation.

Used for Seatohepatitis, acute pancreatitis, reperfusion injury, and neurodegenerative diseases (Parkinson’s)

44
Q

Pyroptosis

A

This is caused bu activation of the inflammasome, which can activate caspase 1. Caspase 1 causes formation of IL-1, which causes fever symptoms and recruitment of leukocytes.
Apoptosome also activates caspase 11, which is used to cause apoptosis.

45
Q

What features are for reversible injuries?

A

Generalized swelling of cell and organelles, blabbing of plasma membrane, detachment of ribosomes from ER, and clumping of nuclear chromatin.

46
Q

Types of damages to cells that can occur due to ischemic-reprofusion injury.

A

Damage from ROS, intercellular Ca overload, inflammation, and complement system.

47
Q

Types of Direct Toxicity

A

Injure cells by combining with important cellular compounds (mercury [binds to membrane proteins], and cyanide [binds to cytochrome oxidase]
Conversion of toxic elements from non-toxic compounds happens in the liver via cytochrome p450.

48
Q

Steatosis

A

Abnormal accumulation of triglycerides within parenchymal cells

49
Q

Atherosclerosis

A

smooth muscle and macrophages are filled with cholesterol in the intimal layer of the aorta

There will be presence of foamy looking cells

50
Q

Xanthomas

A

intracellular accumulation of cholesterol within macrophages.
Foamy cells will be found at sub-endothelial connective tissue site and tendons.

51
Q

Cholestoerolosis

A

Accumulation of cholesterol-laden macrophages in lamina proper of gal bladder.

52
Q

Neumann-Pick disease type C

A

Lysosomal disorder in which there is cholesterol accumulation at several organs.

53
Q

Classic symptoms seen in proteinuria

A

Reabsorption droplets in proximal tubule.
Protein molecules are reabsorbed by pinocytosis in the proximal tubule.

Appearance is pink hyaline droplets.

54
Q

Russell bodies

A

Eosinophilic inclusions found when plasma cells are engaged in producing a lot of antibodies.

55
Q

Von Gierke disease: enzyme, organ, glycogen status and clinical features

A

Enzyme: Glucose 6 phosphatase
Organ: liver/kidney
Glycogen: increased amounts, normal structure
Clinical Features: enlargement of liver, severe hypoglycemia, ketosis, and failure to thrive.

56
Q

Pompe disease: enzyme, organ, glycogen status and clinical features

A

Enzyme: alpha 1-4 glycosidase (lysosomal)
Organ: all organs
Glycogen: massive increase, normal structure
Clinical fatures: cardiorespiratory failure, causes death before the age of 2

57
Q

Cori disease: enzyme, organ, glycogen status and clinical features

A

Enzyme: Amylo-1,6-glucosidase (debranching enzyme)
Organ: muscle and liver
Glycogen: increased amount, short in length
Clinical features: Similar to von gierke but less severe.

58
Q

Andersen disease: enzyme, organ, glycogen status and clinical features

A

Enzyme: Branching enzyme
Organ: liver/spleen
Glycogen: normal amount, long chains, few branches.

59
Q

Macrocell disease: enzyme, organ, glycogen status and clinical features

A

Enzyme: phosphorylase
Organ: muscle
Glycogen: increased amounts, normal structure
Clinical features: muscle cramps, limited exercise due to this. Patient is fine other then that.

60
Q

Hers disease: enzyme, organ, glycogen status and clinical features

A

Enzyme: phosphorylase
Organ: liver
Glycogen: increased amounts
Clinical features: similar to von gierke but milder

61
Q

What happens in coal worker’s pneumoconiosis

A

Blackening of tissue in the lungs (anthracosis) and causes emphysema.
This happens due to Carbon (coal dust) being eaten by macrophages within alveoli and they travel to the tracheobronchial region of the lung via lymph nodes.

62
Q

How are lipofuscin granules formed

A

They are formed by ROS species causing damage. It is considered the wear and tear pigment. It is often considered a yellow-brown peri-nuclear pigment seen in the liver and heart of aging patients.

63
Q

How is melanin formed

A

Formed with the oxidation of tyrosine to dihydroxyphenylalanine via the enzyme tyrosinase, in melanocytes.

64
Q

Alkapeonuria

A

Build of homogentisic acid, which are pigments deposited in skin, connective tissue, and cartilage.
The pigment is called ochronosis.

65
Q

Hemosiderosis

A

Systemic overload of iron, which can be caused by hemochromatosis (increased absorption o iron), hemolytic anemia, and repeated blood transfusions.
Hemosiderin is found, which is a golden yellow to brown pigment that is found, which stores iron. It is often seen in bruises.

66
Q

Break down of heme into 2 molecules and their color

A

Heme broken into biliverdin (green bile) then into bilirubin (red bile)

67
Q

Metastatic calcification

A

This occurs when Ca is deposited in normal tissue due to secondary Hypercalcaemia.
Increased PTH, multiple myeloma leukemia, skeletal metastasis (breast cancer), accelerated bone turnover (Paget disease), vitamin d intoxication, sarcoidosis (Williams disease), renal failure, secondary hyperparathyroidism, aluminum intoxication, chronic renal dialysis, and milk alkali syndrome (excessive milk/CaCO3 consumption).
This generally happens in the gastric mucosa, kidneys, lungs, systemic arteries, and pulmonary veins.
It appears as hydroxyapatite crystals.

68
Q

Werner Syndrome

A

Premature aging because of defective DNA helicase

69
Q

Bloom syndrome and ataxia telangiectasia

A

Cause rapid aging because go mutations of repair enzymes for dsDNA.

70
Q

What is Telomere attrition

A

This is where telomeres shorten after every progressive generation. Responsible for aging process.

71
Q

Deficency in telomerase

A

Leads to pulmonary fibrosis and aplastic anemia.

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