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

(02-03) Adaptation, Injury, Death Flashcards

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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
Alpha-1-antitrypsin Deficiency - protein affected - pathogenesis
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
26
Creutzfeld-Jacob disease - protein affected - pathogenesis
Protein: - Prions Path: - Abnormal folding of PrP causes neuronal cell death
27
Alzheimer disease - protein affected - pathogenesis
Protein: A-beta peptide Path: Abnormal folding of A-beta causes aggregation within neurons and apoptosis
28
What method is used to kill self-reactive T cells when they encounter a self antigen?
- mitochondrial pathway | - Fas death pathway
29
If the apoptotic pathway failed in lymphocytes, what would likely be the result?
Autoimmune disease
30
What are two ways that a cytotoxic T cell can CAUSE apoptosis?
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
What happens in autophagy?
- Cell forms a vacuole around its own components then targets them to a lysosome so it can use the nutrients
32
What are 4 pathways that cause intracellular accumulations?
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
What does Fatty change refer to?
- accumulation of triglycerides within parenchymal cells
34
Steatosis of liver main causes?
- Alcohol abuse | - diabetes
35
What causes atherosclerosis?
Phagocytic cells (in vessels) become overloaded with lipid
36
How does atherosclerosis appear on an H and E cross section?
- Occluded vessel lumen | - Jagged WHITE spaces within the lumen indicate areas where cholesterol existed before processing
37
What are Russell bodies?
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
What are common reasons for glycogen accumulations in tissues?
Diabetes Mellitus - accumates in renal tubular epithelium, cardiac myocytes, ß-cell in islets of langerhans Glycogenosis (glycogen storage diseases) - liver
39
When would you expect to see intracellular accumulations of carbon?
- Air pollution: carbon taken up by alveolar macrophages | - smoking
40
When would you expect to see intracellular accumulations of Lipofusion?
Wear and Tear Pigment Intralysosomal - indication of past radical injury
41
When would you expect to see intracellular accumulations of Hemosiderin?
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
What is hemosiderin? | - diffentiate its appearance from that of Lipofusion
A pigement derived from hemoglobin Hemosiderin is more golden yellow to brown in color than lipofusion
43
Where are SMALL amounts of hemosiderin usually found? | - are findings other than this typically pathologic or physiologic?
- 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
Where are melanocytes located?
At the dermal-epidermal junction
45
Dystrophic Calcification - where can it be found? - pathogenesis?
- 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
Metastatic Calcification - where can it be found? - common causes?
- 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
What is Renal Medullary nephrocalcinosis? | - how does it appear on H and E?
- Calcium salt accumulation in kidney medulla | - Salts appear ad very dark spots on H and E
48
What factors drive aging?
- Environmental and metabolic insults - Telomere Shortening - Abnormal Protein homeostatis
49
What factors counteract aging?
- Insulin/IGF signaling | - TOR
50
GO THROUGH GUPTA QUESTION SET AGAIN BEFORE TEST
GO THROUGH GUPTA QUESTION SET AGAIN BEFORE TEST
51
Metaplasia - Pathologic? - Reversible?
Metaplasia is ALWAYS pathologic and ALWAYS reversible
52
What is the difference in Metaplasia and dysplasia?
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
What are some Key Microscopic features of DYSPLASIA?
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
What does vesicular chromatin indicate?
Often an indicator of neoplastic growth
55
What is the general principle behind the things that cause hypoxia and those that cause cause icshemia?
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
What are the tissues most susceptable to Hypoxia?
- Subendocardium | - Splenic Flexure of the Colon
57
What is hemochromatosis?
Genetic disease with excess absorption and accumulation of iron in hepatocytes, joints, pancreas (causing diabetes), and pituitary (causing increased melanocyte stimulating hormone)
58
Common symptoms of hemochromatosis?
- Darkened skin (iron in pituitary causing increased melanocyte stimulating hormone) - High ALT and AST (liver dysfunction) - High blood glucose (hemochromatosis induced diabetes)
59
What are some key features to look for in caseous necrosis?
- Central area of necrosis - Giant cells (merged macrophages) - Lymphocytes surrounding
60
How does radiation cause the most damage to Patients? | - what mechanism is usually in place to fix this?
Generation of Free radicals, mostly H2O to hydroxyl radical *Glutathione Peroxidase usually protects us against that
61
What is elevation of Lactate dehydrogenase often an indicator of?
Cell Death
62
How does Bcl2 inhibit Cell apoptosis?
Binds to Apaf-1 preventing it from becoming activated
63
Determine which of the following corresponds to Apoptosis or to necrosis: - Always Pathologic - Involving Caspases - Inflammatory Response
Necrosis: - Inflammatory Response - Always Pathologic Apoptosis: - Involves Caspases
64
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?
* increased pressure results in atrophy | - CF patient would likely have atrophied panceas
65
Which enzyme is more specific for Liver Necrosis? | - AST or ALT
ALT
66
When would you expect to see elevated amylase and lipase in an individual? - which enzyme is more specific? - why?
- Acute Pancreatitis | - Lipase is more specific, because amylase could also be indicative of salivary gland inflammation?
67
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?
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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