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CMOD-Path Block 1 > (02-03) Adaptation, Injury, Death > Flashcards

(02-03) Adaptation, Injury, Death Flashcards

1
Q

Diffentiate ischemic and Hypoxic injury?

A

Ischemic Injury results in a lack of glycolysis substrates as well as lack of oxygen

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2
Q

What is the main mechanism of death for ischemic tissue, necrosis or apoptosis?

A

Necrosis

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3
Q

What are ischemic reperfusion injuries?

A
  • Cells are reversibly injured
  • Resoration of blood flow could help in cell recovery.
  • However it leads to death
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4
Q

What are the causes of reperfusion injuries?

A
  1. Increased generation of ROS
    - O2 introduction leads to more ROS
    - Mitochondrial damage causes incomplete O2 Reduction
    - Antioxidant defenses are compromised by ischemia
  2. Inflammation
    - activated by leukocytes which re-infiltrate
    - complement activation
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5
Q

What are two common pathologies that often lead to reperfusion problems?

A
  1. Myocardial Infarction

2. Brain

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6
Q

What are two basic mechanisms of Chemical (toxic) injury?

A
  1. Direct action - (antineoplastic and chemo drug)

2. Conversion to toxic metabolites (acetaminophen)

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7
Q

What toxic metabolite results from acetomeniophen metabolism?

A

NAPQI

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8
Q

what 4 processes (or disruption thereof) lead to pathologic atrophy?

A
  1. DNA damage
  2. Misfolded proteins
  3. Cell injury in infection
  4. Atrophy from duct obstruction
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9
Q

What 4 processes (or disruption thereof) lead to physiologic atrophy?

A
  1. Embryognesis
  2. Hormone Driven
  3. Proliferating cell populations
  4. Elimination of cells past their due dates
  5. Cytotoxic T lymphocytes
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10
Q

T or F: Atrophy of a virus infected cell as a result of a CD8 T cell binding is an example of pathologic atrophy

A

False, this is physiologic - while the virus is pathologic CD8 T cell killing is an appropriate function

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11
Q

What are apoptotic bodies?

A

Shrunk cells composed of membrane bound vesicles or cytosol and organelles

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12
Q

T or F: inflammation is associated with atrophy.

A

False, the cells are quickly cleared by macrophages

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13
Q

What is the irreversible condensation of chromatin called?

A

Pyknosis

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14
Q

What is the ultimate enzyme the gets activated to result in apoptosis?

A

Caspases

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15
Q

What two pathways causes caspase activation?

A
  • Mitochondrial Pathways

- Death receptor Pathway

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16
Q

What receptors head up the death receptor pathway?

A
  • Fas

- TNF receptor

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17
Q

What type of cell injury results in activation of the mitochondrial apoptotic pathway?

A
  • growth factor withdrawal
  • DNA damage
  • Protein misfoldin
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18
Q

Which apoptotic pathway is associated with Bcl-2 and Bcl-xL regulators?
- what happens when they are antagonized?

A

Mitochodrial pathway
- if Bcl-2 is removed then the Bax and Bak proteins are allowed to combine to drill a hole in the mitochondrial membrane leading to cytochrome c release

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19
Q

What two common cell types die in the absence of growth factor?

A
  • Lymphocytes that are not stimulated by antigens and cytokines
  • Neurons that are deprived of nerve growth factor
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20
Q

How do p53 proteins trigger apoptosis and when do they do this?

A
  • Trigger by activating Bax and Bak and decreasing Bcl-2.

- They do this when DNA is damaged and it accumulates

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21
Q

What are the two possible responses the ER stress?

A

*Note: ER stress is when protein demand exceeds the protein folding capacity

  1. Adaptation
    - decrease protein synthesis
    - increase chaperone production
  2. Apoptosis if adaptation fails
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22
Q

Cystic Fibrosis

  • protein affected
  • pathogenesis
A

Protein:
Cystic Fibrosis transmembrane conductance regulator (CFTR)

Path:
Loss of CFTR leads to defects in chloride transport

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23
Q

Familial Hypercholesterolemia

  • protein affected
  • pathogenesis
A

Protein:
- LDL receptor

Path:
- Can’t take LDL out of the blood so hypercholesterolemia results

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24
Q

Tay-Sachs disease

  • protein affected
  • pathogenesis
A

Protein:
- Hexoaminidase ß-subunit

Path:
- Lack of lysosomal enzyme leads to storage of GM2gangliosides in neurons

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25
Q

Alpha-1-antitrypsin Deficiency

  • protein affected
  • pathogenesis
A

Protein:
- alpha-1 antitrypsin

Path:

  • Storage of nonfunctional protein in heptocytes causing apoptosis
  • absence of enzymatic protein in lungs causes destruction of elastic tissue causing emphysema
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26
Q

Creutzfeld-Jacob disease

  • protein affected
  • pathogenesis
A

Protein:
- Prions

Path:
- Abnormal folding of PrP causes neuronal cell death

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27
Q

Alzheimer disease

  • protein affected
  • pathogenesis
A

Protein:
A-beta peptide

Path:
Abnormal folding of A-beta causes aggregation within neurons and apoptosis

28
Q

What method is used to kill self-reactive T cells when they encounter a self antigen?

A
  • mitochondrial pathway

- Fas death pathway

29
Q

If the apoptotic pathway failed in lymphocytes, what would likely be the result?

A

Autoimmune disease

30
Q

What are two ways that a cytotoxic T cell can CAUSE apoptosis?

A
  1. Granzymes (granule proteases) enter target cell and activate caspases
  2. Fas Ligand (FasL) binds to Fas receptor on the affected cells and triggers death path
31
Q

What happens in autophagy?

A
  • Cell forms a vacuole around its own components then targets them to a lysosome so it can use the nutrients
32
Q

What are 4 pathways that cause intracellular accumulations?

A
  1. Inadequate removal of a normal substance
  2. Accumulation of an abnormal endogenous substance
  3. Failure to degrade a metabolite (storage diseases)
  4. Deposition and accumulation of an abnormal exogenous substance
33
Q

What does Fatty change refer to?

A
  • accumulation of triglycerides within parenchymal cells
34
Q

Steatosis of liver main causes?

A
  • Alcohol abuse

- diabetes

35
Q

What causes atherosclerosis?

A

Phagocytic cells (in vessels) become overloaded with lipid

36
Q

How does atherosclerosis appear on an H and E cross section?

A
  • Occluded vessel lumen

- Jagged WHITE spaces within the lumen indicate areas where cholesterol existed before processing

37
Q

What are Russell bodies?

A

Accumulations of proteins in the RER of some plasma cells

  • These are can be seen when the immune system is ramping up IgG production
38
Q

What are common reasons for glycogen accumulations in tissues?

A

Diabetes Mellitus
- accumates in renal tubular epithelium, cardiac myocytes, ß-cell in islets of langerhans

Glycogenosis (glycogen storage diseases)
- liver

39
Q

When would you expect to see intracellular accumulations of carbon?

A
  • Air pollution: carbon taken up by alveolar macrophages

- smoking

40
Q

When would you expect to see intracellular accumulations of Lipofusion?

A

Wear and Tear Pigment
Intralysosomal
- indication of past radical injury

41
Q

When would you expect to see intracellular accumulations of Hemosiderin?

A

When:
- if there is local or system excess of iron (e.g. people like CF patients that recieve lots of blood transfusions)

  • Hereditary Hemochromatosis
42
Q

What is hemosiderin?

- diffentiate its appearance from that of Lipofusion

A

A pigement derived from hemoglobin

Hemosiderin is more golden yellow to brown in color than lipofusion

43
Q

Where are SMALL amounts of hemosiderin usually found?

- are findings other than this typically pathologic or physiologic?

A
  • Usually Hemosiderin is a pathologic finding

- small amounts are present in mononuclear phagocytes of bone marrow, spleen, and liver where red cells get degraded.

44
Q

Where are melanocytes located?

A

At the dermal-epidermal junction

45
Q

Dystrophic Calcification

  • where can it be found?
  • pathogenesis?
A
  • Found in areas of necrosis
  • Can be incidental in cause or cause organ dysfunction (heart valves)

Pathogenesis:
- initiation (nucleation) and propagation of the calcium phosphate crystal can occur intracellularly or extracellularly

46
Q

Metastatic Calcification

  • where can it be found?
  • common causes?
A
  • Found in NORMAL tissues whenever there is hypercalcemia

Causes:

  • increase secretion of parathyroid hormone
  • Destruction of bone (fast bone turnover)
  • Vit D disorders (too much of it)
  • Renal Failure
47
Q

What is Renal Medullary nephrocalcinosis?

- how does it appear on H and E?

A
  • Calcium salt accumulation in kidney medulla

- Salts appear ad very dark spots on H and E

48
Q

What factors drive aging?

A
  • Environmental and metabolic insults
  • Telomere Shortening
  • Abnormal Protein homeostatis
49
Q

What factors counteract aging?

A
  • Insulin/IGF signaling

- TOR

50
Q

GO THROUGH GUPTA QUESTION SET AGAIN BEFORE TEST

A

GO THROUGH GUPTA QUESTION SET AGAIN BEFORE TEST

51
Q

Metaplasia

  • Pathologic?
  • Reversible?
A

Metaplasia is ALWAYS pathologic and ALWAYS reversible

52
Q

What is the difference in Metaplasia and dysplasia?

A

Metaplasia is a change in tissue type to another organized type that exists elsewhere in the body.

Dysplasia is unorganized, it doesn’t resemble any type of tissue

53
Q

What are some Key Microscopic features of DYSPLASIA?

A

Nucleus:
Increased Mitotic Activity (with normal mitotic spindles)

INCREASED size of NUCLEAR chromatin

Other:
Disorderly proliferation of cells with loss of cell maturation as cells progress to the surface

54
Q

What does vesicular chromatin indicate?

A

Often an indicator of neoplastic growth

55
Q

What is the general principle behind the things that cause hypoxia and those that cause cause icshemia?

A

Hypoxia:
- caused by something that make it difficult for O2 uptake or delivery (e.g. respiratory insuffiency, pulmonary embolism)

Ischemia:
- caused by something that makes it difficult for blood to physically get there (arteriosclerosis, heart failure, etc.)

56
Q

What are the tissues most susceptable to Hypoxia?

A
  • Subendocardium

- Splenic Flexure of the Colon

57
Q

What is hemochromatosis?

A

Genetic disease with excess absorption and accumulation of iron in hepatocytes, joints, pancreas (causing diabetes), and pituitary (causing increased melanocyte stimulating hormone)

58
Q

Common symptoms of hemochromatosis?

A
  • Darkened skin (iron in pituitary causing increased melanocyte stimulating hormone)
  • High ALT and AST (liver dysfunction)
  • High blood glucose (hemochromatosis induced diabetes)
59
Q

What are some key features to look for in caseous necrosis?

A
  • Central area of necrosis
  • Giant cells (merged macrophages)
  • Lymphocytes surrounding
60
Q

How does radiation cause the most damage to Patients?

- what mechanism is usually in place to fix this?

A

Generation of Free radicals, mostly H2O to hydroxyl radical

*Glutathione Peroxidase usually protects us against that

61
Q

What is elevation of Lactate dehydrogenase often an indicator of?

A

Cell Death

62
Q

How does Bcl2 inhibit Cell apoptosis?

A

Binds to Apaf-1 preventing it from becoming activated

63
Q

Determine which of the following corresponds to Apoptosis or to necrosis:

  • Always Pathologic
  • Involving Caspases
  • Inflammatory Response
A

Necrosis:

  • Inflammatory Response
  • Always Pathologic

Apoptosis:
- Involves Caspases

64
Q

What processes would take place on the tissue of the kidney or pancreas as a result of intraluminal pressure?
- what diseases might cause this in pancreas?

A
  • increased pressure results in atrophy

- CF patient would likely have atrophied panceas

65
Q

Which enzyme is more specific for Liver Necrosis?

- AST or ALT

A

ALT

66
Q

When would you expect to see elevated amylase and lipase in an individual?

  • which enzyme is more specific?
  • why?
A
  • Acute Pancreatitis

- Lipase is more specific, because amylase could also be indicative of salivary gland inflammation?

67
Q

What enzymes are raised in myocardial infarction?

  • which is the standard of testing?
  • when do levels of this enzyme peak, when do they hit baseline again?
A

Enzymes

  • Myoglobin
  • CK-MB
  • TROPONIN

TROPONIN - standard of testing, peaks about 3 hours after MI and doesn’t hit baseline again until about 10 days later.

CMOD-Path Block 1 (10 decks)

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