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Pathology Quiz 1 > 02_Cell Injury_Q and A_Jonathan > Flashcards

02_Cell Injury_Q and A_Jonathan Flashcards

1
Q

Distinguish reversible from permanent and lethal cell injury.

A

• Reversible injury leads to altered cell composition such that if and when the offensive stimulus is removed, the cell will restore its original function
• Hallmarks include: reduced oxidative phosphorylation with resultant depletion of energy stores in the form of ATP, cell swelling due to ion concentrations, alterations in cytoskeletal structures, organelles, and mitochondria
o Examples of reversible ischemic injury include
• Mitochondrial swelling
• Membrane blebs
• Increased cell volume
• Cytoskeletal disorganization
• Influx of Ca, Na, H2O
• Efflux of K
• Decrease in protein synthesis and increase in lipid deposition
• Irreversible injury leads to either a permanently altered cell or cell death
o Ex: Mitochondria
• become porous and enter a low energy state.
• Lose enzymatic systems and cannot recover normal function.
• Swell and Ca precipitate forms (pathologic calcification)
• Apoptosis cascade may begin

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2
Q

What are the three causes of cell death?

A
  • apoptosis
  • necrosis
  • (also autophagy during nutrient deprivation)
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3
Q

What is necrosis?

A
  • When damage to membranes is severe, lysosomal enzymes enter the cytoplasm and digest the cell, and cellular contents leak out
  • This is always a pathologic process
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4
Q

What is Apoptosis?

A
  • a form of cell death that is characterized by nuclear dissolution, fragmentation of the cell without complete loss of membrane integrity, and rapid removal of the cellular debris
  • This is sometimes a pathologic process and sometimes a normal cell function
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5
Q

Details: apoptosis and necrosis sometimes have similar causes. Apoptosis can sometimes lead to necrosis. Autophagy can sometimes be similar to apoptosis.

A

Details: apoptosis and necrosis sometimes have similar causes. Apoptosis can sometimes lead to necrosis. Autophagy can sometimes be similar to apoptosis.

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6
Q

What are the causes of cell injury?

A
  • O2 deprivation aka hypoxia
  • Physical agents (temperature, pressure, radiation, electric shoc)
  • Chemical agents
  • Infectious agents (microbiology to large tapeworms)
  • Immune reactions
  • Genetic derangements (ex: decreased life span of RBCs)
  • Nutritional imbalances
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7
Q

What are two features of reversible cell injury that can be recognized under the light microscope?

A
  • cellular swelling

* fatty change

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8
Q

What causes cellular swelling?

A

• lack of ATP causes ion pumps to not function and osmotic imbalance occurs

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9
Q

What causes fatty change?

A
  • found usually in cells that depend on fat metabolism: heart, liver, and others
  • Several mechanism (check back later)
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10
Q

What are the ultracellular changes of reversible cell injury?

A
  • plasma membrane: blebbing, blunting, loss of microvilli
  • mitochondria: swell and have small amorphous densities
  • dilation of the ER and detachment of ribosomes
  • nuclear alterations: desegregation of granular and fibrillar elements
  • may include increased eosinophillic staining
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11
Q

What is the mechanistic cause of necrosis?

A

• denaturation of intracellular proteins and enzymatic digestion of the lethally injured cell

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12
Q

See Table 1-2 page 13 robbins for differences between necrosis and apoptosis.

A

See Table 1-2 page 13 robbins for differences between necrosis and apoptosis.

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13
Q

What digests the contents of necrotic cells?

A
  • lysosomes from the necrotic cells
  • lysosomes from inflammatory leukocyte
  • Note: this takes hours, so may not occur in sudden infarct. Instead, cellular components from the heart are released into the blood stream
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14
Q

What are the ultrastructural changes in general necrosis?

A

• increased esosinophilia due to the loss of cytoplasmic RNA (blue) and increased denatured proteins
• glassy homogenous: loss of glycogen
• dead cells may be replaced by myelin figures (from damaged cell membranes)
• calcification
• discontinuous cell and organelle membranes
• very large mitochondria
• Nuclear changes (3)
o Karyolysis (fade of basophilia)
o Pyknosis (nuclear shrinkage)
o Karyorrhexis (nuclear fragmentation)

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15
Q

What are the six types of necrosis?

A
  • Coagulative necrosis
  • Liquefactive necrosis
  • Gangrenous necrosis
  • Caseous necrosis (cheese-like)
  • Fat necrosis
  • Fibrinoid necrosis
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16
Q

What are the features of Coagulative necrosis?

A
  • denaturation of proteolytic enzymes, so much of the structure of the cells remain intact.
  • Eosinophilic, anucleate cells
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17
Q

Ischemia can lead to coagulative necrosis in all organs except? Why?

A
  • the brain

* Why?

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18
Q

What degrades the coagulative necrosis?

A
  • note: may persist for weeks

* degraded by leukocytes

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19
Q

What are the characteristics of liquefactive necrosis?

A
  • digestion of dead cells, resulting in a viscous mass
  • seen in focal bacterial or fungal infections because microbes stimulate the accumulation of leukocytes, which then digest the necrotic cells
  • Pus
  • Infarction of the brain produces liquifactive necrosis
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20
Q

What are the characteristics of Gangrenous necrosis?

A
  • a type of liquifactive necrosis
  • usually on a limb that lacks circulation
  • bacteria invade and attract leukocytes, which digest the tissue
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21
Q

What are the characteristics of Caseous necrosis?

A
  • classically in tuberculosis infections with granuloma
  • caseous = cheese-like
  • white, appears like it can be broken into pieces like cheese
  • collection of fragmented or lysed cells and amorphous granular debris within a distinctive inflammatory border (granuloma)
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22
Q

What are the characteristics of fat necrosis?

A
  • focal areas of fat destruction from the release of pancreatic lipases in the pancrease or peritoneal cavity
  • occurs during acute pancreatitis
  • lipases split fat esters ==> fat combines with Ca to form chalky white areas of saponification
  • see Robbins page 17, figure 1-14
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23
Q

What is fibrinoid necrosis?

A
  • antigen-antibody complexes deposit in blood vessels
  • Immune complexes leak out of the vessels bound to fibrin
  • Result in bright pink and amorphous H&E stain, called “fibrinoids”
  • Seen in vasculitis
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24
Q

Term: dystrophic calcification come back later

A

Term: dystrophic calcification come back later

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25
Q

What are the basic principles of Cell Injury?

A
  • cellular response depends on the nature of the injury, duration, and severity
  • consequences of cell injury depend on the type, state, and adaptability of the injured cell
  • cell injury results from different biochemical mechanisms action on cell components
26
Q

What are the different biochemical mechanisms action on cell components that cause cell injury?

A
  • ↓ATP
  • Mitochondrial damage
  • ↑ Ca
  • ↑ ROS
  • Membrane damage
  • Protein misfolding and DNA damage
27
Q

What are the causes and effects of ↓ATP?

A

• cause: reduced O2 or nutrients, mitochondrial damage
• effects:
o Na/K pump (ouabain sensitive) effects ion balance
o Cellular energy metabolism altered (glycolysis, etc..)
o Ca pump ==> increased intracellular Ca
o Reduction in protein synthesis and increase in protein misfolding

28
Q

What are the causes and effects of mitochondrial damage?

A

• Causes: ↑ Ca, ↑ ROS, hypoxia
• Effects:
o Mitochondrial membrane ==> loses H gradient
o Cytochrome C release ==> caspase cascade

29
Q

What are the sources of ↑intracellular Ca?

A
  • cell injury lets in extracellular Ca
  • mitochondrial Ca
  • Smooth ER
30
Q

What are the effects of ↑ Ca?

A 
•	↑ mitochondrial permeability
•	May induce apoptosis via direct activation of caspases
•	activation of many cellular processes
o	phospholipase
o	protease
o	endo-nuclease
o	ATPase
31
Q

What causes Free Radicals?

A 
•	normal byproducts of redox reactions
o	O2 superoxide
o	H2O2 peroxide
o	–OH
•	radiation
•	inflammation
•	metabolism of exogenous drugs
•	Transition metals
•	NO
32
Q

What removes free radicals?

A 
•	Antioxidants
•	Lower Fe and Cu levels
•	Radical-Scavenging systems
o	Catalase
o	Superoxide dismutase
o	Glutathione peroxidase
33
Q

What are the effects of free radicals? Pg 22

A
  • Lipid peroxidation in plasma and organelle membranes
  • Oxidative modification of proteins
  • Lesions on DNA
34
Q

Know: apoptosis occurs as part of normal physiology as well as pathology

A

Know: apoptosis occurs as part of normal physiology as well as pathology

35
Q

What are the benefits of Apoptosis in pathological conditions.

A

• eliminates cells without eliciting a host reaction, thus limiting collateral tissue damage.

36
Q

What are some common pathological states that recruit apoptosis?

A

• Growth factor deprivation
• DNA damage
• Protein misfolding
• Cell death in certain infections (esp viral)
o CTL-mediated via FasL and TNF
• Pathological atrophy in parenchymal organs after duct obstruction

37
Q

What are the morphological features of Apoptosis?

A
  • Cell shrinkage
  • Chromatin condensation ==> then nucleus breaks up ==> fragments
  • Cytoplasmic blebs and apoptotic bodies
  • Phagocytosis of apoptotic cells or cell bodies, usu by macrophages
  • Plasma membranes remain intact until last stages
38
Q

What are biochemical features of apoptosis?

A
  • caspase cascade
  • DNA and protein breakdown
  • Membrane alteration and recognition by phagocytes
39
Q

What are the mechanisms of apoptosis? (intrinsic then extrinsic)
Robbins pg 28 and 29

A

• Intrinsic: Cell injury (Growth Factor withdrawal, DNA damage, protein misfolding) ==> Bcl-2 sensors ==> Bcl-2 effectors (Bax and Bak) ==> mitochondrial release of Cytochrome C and other pro-apoptotic proteins ==> initiator caspases ==> exocutioner caspases ==> nuclear and cytoskeleton breakdown
o Note: Bcl-2 and Bcl-x are inhibitors of Bax and Bak
o Bcl-2 and Bcl-x are anti-apoptotic
• Extrinsic: Fas or TNF receptor ==> FADD ==> procaspase-8 ==> exocutioner caspases

40
Q

What is Steatosis?

A
  • abnormal accumulations of triglycerides within parenchymal cells
  • LV, heart, muscle, and KD
41
Q

What are the causes of steatosis?

A
  • usu alcohol abuse and nonalcoholic fatty liver disease
  • excess accumulation of tryglycerides within the liver may result from excessive entry or defective metabolism and export of lipids
  • defects induced by alcohol alter mitochondrial and microsomal functions ==> increased synthesis and reduced breakdown of lipids
  • CCL4 and protein malnutrition cause fatty change by reducing apoprotein synthesis
42
Q

What is the morphology of fatty LV?

A
  • development of lipososomes

* small vacuoles

43
Q

What are the features of Hyaline Change?

A
  • alteration within cells or extracellular space that gives a homogeneous, glassy, pink appearance with H and E
  • does not represent a specific accumulation (its related to many things)
44
Q

What is hemosiderin?

A
  • hemoglobin-derived, golden yellow brown, granular pigment

* storage form of iron

45
Q

How is iron stored in cells?

A

• stored in association with apoferritin to form apoferritin micelles

46
Q

When there is ↑ Fe, ferritin forms hemosiderin granules

A

When there is ↑ Fe, ferritin forms hemosiderin granules

47
Q

Local excess ==> from hemorrhages in tissues ==> RBCs are phagocytosed ==> Fe accumulates

A

Local excess ==> from hemorrhages in tissues ==> RBCs are phagocytosed ==> Fe accumulates

48
Q

Systemic overload of Fe ==> deposited in organs (process called hemosiderosis)

A

Systemic overload of Fe ==> deposited in organs (process called hemosiderosis)

49
Q

What are the main causes of hemosiderosis?

A
  • increased absorption of Fe
  • hemolytic anemias
  • repeated blood transfusions
50
Q

What is hemochromatosis?

A

• excessive accumulation of Fe
o deposited in LV, Pancreas, heart, and joints
• Primary hemochromatosis: homologous recessive disorder ==> excessive iron absorption
• Secondary hemochromatosis/hemosiderosis: acquired disease

51
Q

Why is excessive iron toxic?

A
  • lipid peroxidation via Fe free radicals
  • stimulates collagen formation in hepatic stellate cells
  • interaction with O free radicals which damage DNA
52
Q

What is the morphology of hemochromatosis?

A

• deposition of hemosiderin in LV and pancreas, and others
• cirrhosis
• pancreatic fibrosis
• In the Liver
o Iron ==> golden brown ==> stain blue with Prussian blue stain
o Iron is a direct hepatoxin, therefore inflammation is absent (not necessary for damage)

53
Q

Classic triad of hematochromatosis (often occurs late)

A
  • pigment cirrhosis with hepatomagaly
  • skin pigmentation
  • diabetes
54
Q

Is there treatment for hematochromatosis?

A

Hematochromatosis is a genetic disease that is treatable with bleeding and reduced iron intake.

55
Q

What are the 3 forms of alcoholic liver disease?

A
  • hepatic steatosis
  • alcoholic hepatitis
  • cirrhosis
56
Q

What is the morphology of hepatic steatosis?

A
  • microvesicular or macrovesicular globules displace nucleus
  • organ becomes enlarged, yellow, and greasy
  • chronic alcohol use cause fibrous tissue around veins and sinusoids
57
Q

Is hepatic steatosis reversible?

A

• completely reversible upon abstension

58
Q

What are the morphological features of Cirrhosis?

A
  • final and irreversible form of alcoholic liver
  • usu slow and insidious
  • yellow-tan ==> brown, shrunken, nonfatty organ
  • fibrous septa extend through the sinusoids from central to portal regions
  • parenchymal micronodules ==> mixed micronodule macronodule pattern ==> ischemia ==> obliterates nodules ==> tough pale scar tissue
  • resembles viral hepatitis cirrhosis
59
Q

How does alcohol cause steatosis?

A
  • Alcohol dehydrogenase and acetyladelhyde DH ==>↑ NADH ==> shunt substrates away from catabolism and toward lipid synthesis
  • Impairs assembly and secretion of lipoproteins ==> ↓ lipid export
  • ↑ peripheral catabolism of fatty acids ==> ↑ delivered FA to the liver
60
Q

The effect of EtOH on hepatic lipid metabolism

A
  1. Mobilization of fatty acids from body stores
  2. Decreased fatty acid oxidation
  3. Increased triglyceride synthesis
  4. Decreased lipoprotein synthesis
  5. Decreased transport, glycosylation and secretion of VLDL
61
Q

What are Mallory’s bodies?

A
  • Characteristic, but not specific of, alcoholic liver disease.
  • Accumulations of cytokeratin intermediate filaments eosinophilic

Pathology Quiz 1 (6 decks)

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