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002 - Pathology - (01) - Cell Injury > (06) p241 > Flashcards

(06) p241 Flashcards

1
Q

(Necrosis)

  1. what is “hemorrhagic necrosis”?
  2. usually when what to tissue is blocked?
  3. hemorrhagic infarction of what?
A
  1. necrosis + hemorrhage
  2. venous outflow
  3. bowel
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2
Q

(necrosis)

  1. what is it called when vasculature (smooth muscle) is affected?
  2. frequently found in what disease?
  3. histology: what appearance of media of vasculature?
A
  1. fibrinoid necrosis

2 auto-immune disease (also lead toxicosis in eagles for example)

  1. eosinophilia and hyaline appearance
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3
Q

(Consequences of necrosis)

(biochemical changes)

  1. due to leakage of what?
  2. detectable where?

(Inflammation)

  1. beginning at transition of what to what?
A
  1. tissue specific enzymes
  2. in serum
  3. necrotic to healthy tissue
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4
Q

(Outcome of necrosis)

(Restitutio ad integrum - regeneration with restoring of normal function)

  1. if damage is what?
  2. if what of tissue is maintaiend?
  3. if affected tissue has good what?

(…)

  1. What is healing without resitution of normal function called (scarring)?
A
  1. minor
  2. texture (scaffold)
  3. healing capacity
  4. reparation
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5
Q

(Outcome of necrosis)

(Demarcation (including sequester formation/sequestration)

  1. necrotic tissue is surrounded by what?
  2. shedding of damaged tissue in what and what?
  3. sequester - in what and what? with what?
A
  1. area of inflammation (usually reddened)
  2. skin and mucous membranes (–> ulcer)
  3. lung and bone; fistuluous tract
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6
Q

(Apoptosis and “programmed cell death”)

  1. physiologic (suicide signals/noxious stimuli) –> nuclear dissolution with or without loss of membrane integrity?

2-3. cause may be what or what?

A
  1. without loss
  2. physiologic (embryogenesis - invoution of hormone controlled areas after withdrawal of hormone)
  3. pathologic (esp if damage affects cell’s nuclear DNA)
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7
Q

(Apoptosis)

1-5. What are the five causes?

A
  1. embryogenesis
  2. normal turnover (hormone dependent, cell deletion in proliferating population)
  3. immune system
  4. cell death in neoplasms
  5. pathogenic stimuli
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8
Q

(MEchanisms of apoptosis)

  1. genetically determined, energy dependent sequence of molecular events of initial cell signaling - this phase called what?
  2. regulation by what?
  3. executino pahse by what?
  4. dead cell removal by what?
A
  1. “initiation phase”
  2. regulatory molecules
  3. capases
  4. phagocytosis

(then look at diagram on 258)

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9
Q

(mechanisms of apoptosis)

  1. extrinsic pathway is what?
  2. intrinsic is what?
A
  1. receptor initiated
  2. mitochondrial

(not mutually exclusive)

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10
Q

(here are some intrinsic pathways…)

261-262

he talked a decent amount about this…

A
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11
Q

(Apoptosis: execution phase)

  1. proteolytic cascade that utlimately results in the activation of the execuation what and what?

(Caspase)

  1. c stands for what? aspase stands for what?
  2. exist as what? need to be what for activation?
  3. cleave proteins of what three things?
A
  1. caspase 3 or caspase 6
  2. cysteine enzyme (enzyme containing cysteine in active site; its capability to cleave “aspartic acid” residues
  3. proenzymes (zymogens); cleaved
  4. cytoskeleton, transcirption and translation, DNA repair machinery
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12
Q

(Apoptosis)

(morphology)

  1. can considerable apoptosis occur in tissues before it is evident on histology

2-5. what are four things you see?

A
  1. yes
  2. cell shrinkage (packed organelles)
  3. chromatin condensation
  4. formation of cytoplasmic belebs then apoptic bodies
  5. phagocytosis of cells (macrophages with no inflammation)
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13
Q

(Apoptosis: Assays)

1-4. What four techniques are used?

A
  1. nuclear morphology (chromatin condensation and nuclear lobulation/fragmentation)
  2. TUNEL and related assays (in situ detection of ds DNA breaks)
  3. caspase assays (esp caspases 3,2,8, and 9)
  4. cytochorome c release in to cytosol (western blot; immunohistochemistry)
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14
Q

(Adaptatino fot “workload imbalance”)

  1. what occurs when cells are no longer stimulated/needed; what is a congenital defect in which the organ was not or only insufficiently formed?
  2. what when cells are over-stimulated?
  3. What is it when there is replacement of one adult cell type (more specialized) by another cell type of the same germ line (less specialized)? is it reversible?
A
  1. atrophy; apasia/hypoplasia
  2. hypertrophy/hyperplasia
  3. metaplasia; yes

(also dysplasia and anaplasia –> see disturbances of growth lecture)

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15
Q

(Atrophy –> focal or diffuse shrinkage of organ)

  1. reduction of cell size - called what?
  2. reduction of cell number?
  3. what is it called when you have loss of cells but replacement by adipocytes “lipomatous pseudohypertrophy”?)
A
  1. simple atrophy
  2. numeric atrophy
  3. numeric atrophy with lipmatosis
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16
Q

(Atrophy)

(physiologic atrophy)

  1. fetal development
  2. thymus atrophy/atrophy of lymphoid tissue = ?
  3. senile atrophy (heart, nervous system) - “brown atrophy” due to what?
  4. age-independent (cycle-dependent) atrophy = involution of what and what post partum?
A
  1. involution
  2. intracellular lipofuscin accululation
  3. uterus and mammary gland
17
Q

(atrophy)

  1. does pathologic atrophy = involution?

just read this…

A
  1. no
18
Q

(atrophy)

(mechanism: increased protein degradation through what two things?)

A
  1. lysosomal acid hydrolases (eg cathepsin)
  2. ubiquitin-proteasome pathway
19
Q

(Atrophy)

(Ubiquitin-proteasome pathway)

  1. cyotosolic and nuclear proteins conjugated to what?
  2. degradation within what?
  3. atrophy often accompanied by increased numbers of what?
  4. if not digestible - what will remation?
A
  1. ubiquitin
  2. a large cytoplasmic organele (“proteasome”)
  3. autophagic vacuoles
  4. membrane bound residual bodies (eg lipofuscin)
20
Q

Hypertrophy/Hyperplasia (–> focal or diffuse enlargement of organ)

  1. what is response to increased stimulation of post-mitotic cell (quiescent and permanent cells)? what leads to cell enlargement?
  2. What is response to increased stimulation of cells with mitotic capacity?
  3. what often occur together in tissues with mitotic activity?
A
  1. hypertrophy; synthesis of more organelles
  2. hyperplasia
  3. hyperplasia and hypertrophy
21
Q

(Metaplasia: classic examples)

1-3. what are the three examples?

A
  1. chronic irritation/chronic inflammation (squamous metaplasia of respiratory epithelium)
  2. vitamin A deficiency (squamous metaplasia or respiratory epithelium and glandular epithelium in psittacine birds)
  3. hyperestrogenism
    - prostatic squamous metaplasia in ferret with adrenal tumor
    - prostatic squaomus metaplasia in dogs with testicular sertoli cell tumor
22
Q

(intracellular accumulations = evidence of what?)

  1. accumulation of normal cellular component due to what?
  2. accumulation of abnormal cellular component due to what?
  3. accumulation of what?
A

(chronic sublethal cell injury and cellular adapatation)

  1. increased production or decreased disposal
  2. production of abnormal molecules (endogenous) or due to uptake of compounds (exogenous)
  3. pigment
23
Q

(Intracellular accumulations)

  1. increase of what if severe enough?
  2. harmless?
  3. intracytoplasmic or intranucleuar?
  4. reversible or permanent?
A
  1. cell size
  2. usually - but can be toxic
  3. can be either
  4. can be either
24
Q

(Intracellular accumulations)

  1. too much of what?
  2. genetic or acquired defect of metabolism resulting in what?
  3. Inability to degrade what?
A
  1. normal cell component (eg lipid)
  2. producation of abnormal compounds or production of non-functional enzymes (storage diseases)
  3. phagocytized material (eg silica, mycobacteria)
25
Q

(intracellular lipid accumulations - deranged intracellular fat metabolism)

  1. what types?
  2. occurs in what?
A
  1. triglycerides, cholesterol esters, phospholipids
  2. hepatocytes (prototype) and eg cardiomyctes, myocytes, and renal tubular epithelial cels
26
Q

(Hepatocellular degeneration - fatty liver(= hepatic “steatosis” or hepatic “lipidosis”)

(early stages)

  1. fatty acids/triglycerides accumulate in what in the what of what?
  2. liver looks how?
  3. cells?

(severe or long-standing)

  1. globules (contating tgs) fuse –> cause what?
  2. size?
  3. color, texture?
  4. float or sink in water and fixative?
A
  1. small globules in the cytoplasm of hepatocytes
  2. normal size to moderately enlarged, yellowish, soft
  3. sharply delineated round clear cytoplasmic vacuoles
  4. large globule
  5. moderately or greatly enlarged (round edges)
  6. yellow, greasy and friable
  7. floats (normal sinks)
27
Q

(Pathogenesis of hepatocellular lipidosis)

  1. excessive transport of what to liver
  2. abnormal function of what?
  3. decreased sytnehsis of what?
  4. impaired secretion of what from liver?
A
  1. fatty acids and carbs
  2. hepatocyte
  3. apoproteins/lipoproteins
  4. lipoproteins

002 - Pathology - (01) - Cell Injury (8 decks)

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