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92 Cards in this Set

  • Front
  • Back
1) List the four (4) general, major types of cellular and tissue responses to stress
a) Physiologic
i) Adaptations
b) Pathologic
i) Injury (morphologic changes and outcomes)
ii) Death
(1) Types
(a) Apoptosis
(b) Necrosis
iii) Accumulations
2) What is the goal of cellular adaptation? What does it reflect the cells ability to do?
a) Adjust to new conditions/demands for optimal functioning
b) Reflects dynamic ability of cells to alter their CELL CYCLE ACTIVITY
i) Aka gene transcription and translation (G1, G2)
ii) Synthesis of new DNA/chromosomes (S)
iii) Proliferation (M)
3) List and describe the four (4) major types of cellular adaptation
a) Hyperplasia: increased NUMBER of cells
b) Hypertrophy: increased SIZE of cells
c) Atrophy: decreased SIZE of cell
d) Metaplasia: change from one mature cell type to another
4) What are the 2 forms of hyperplasia?
a) Physiologic and Pathologic
5) What does hyperplasia require?
a) Remember this is an increase in the NUMBER of cells
i) Thus it requires DNA synthesis and cell division
6) What are the 2 forms of physiologic hyperplasia?
a) Hormonal: stimulation to increase the number of cells due to functional demand (ex: endometrial proliferation, or increased lactation cells)
b) Compensatory: regain functional capacity after loss of cells (ex: increase cell number after removal of liver tumor)
7) Please discuss pathologic hyperplasia
a) Proliferation in response to “damaging” stimulus
b) Think of proliferation for protection
c) Ex: fibroblast proliferation with increase collagen deposition in response to tissue destruction (scar tissue)
what is psoriasis?
a) Psoriasis
i) Epidermal hyperplasia; inflammation
ii) Reaction to chronic inflammation with tissue destruction
iii) Think of the purple spots on people
9) What is Lichen Simplex?
a) Another epithelial hyperplasia
b) Due to rubbing and scratching
c) See hyperkeratosis, thick epithelium
11) How does hypertrophy increase the size of an organ?
a) By increasing the SIZE of CELLS
b) NOT an increase in cell number!!
12) Does hypertrophy increase protein synthesis or cellular swelling? What type of cells are effected (general)
a) Due to increased protein synthesis
b) Generally occurs In cells that would not typically divide (e.g muscle cellscardiac hypertrophy)
13) Can adaptive responses involve both hyperplasia and hypertrophy? Example?
a) Yes
b) Gravid uterus, mammary tissue during lactation
14) Why is cellular substance lost in atrophy? (2)
a) Cellular environment (nutrients, O2, Trophic signals) cannont support current size of cell, so it shrinks
i) Decreased size=decreased function
b) Functionally stimuli are diminished, cell protein content decreases
15) Please list 5 causes for atrophy
a) Decreased workload (disuse; eg: skeletal muscle; bone)
b) Loss of nerve supply (denervation, eg: skeletal muscle)
c) Ischemia (brain atrophy in elderly)
d) Poor nutrition (generalized cachexia)
e) Reduced endocrine stimulation (mammary tissue, uterus in postmenopausal state)
16) What is metaplasia and an example in epithelial tissues
a) Change from one cell type to another
b) Squamous to columnar (Barrett’s esophagus)
17) What is an example of mesenchymal metaplasia?
a) Muscle to bone (myositis ossificans: bone formation within skeletal muscle)
18) How does metaplasia occur?
a) Results from reprogramming the gene expression of stem cells present in tissue
19) Why does metaplasia generally happen?
a) Protective to noxious stimuli
i) Change from susceptible cell type to more resistant/protective type of cell
20) Is metaplasia Typically reversible?
a) You bet your sweet ass it is
21) If an injurious stimulus continues, what may metaplastic changes become? What does this mean?
a) They become dysplastic (pre-neoplastic change)
i) Eg: with chronic gastric acid reflux, prolonged Barrett’s metaplasia of the esophagus can lead to glandular dysplasia, and eventually esophageal adenocarcinoma
22) List and briefly describe the seven (7) major causes of cell injury
a) Hypoxia (diminished O2)
b) Physical agents/mechanical forces (temp extremes, radiation, electricity, pressure, stretch)
c) Chemicals/Drugs
d) Infectious agents
e) Immunologic reactions
f) Genetic mutations/derangements
g) Nutritional imbalances
23) What is the difference between hypoxia and ischemia?
a) Ischemia is IMPAIRED blood flow; involves diminished delivery of nutrients as well as O2
i) More “potent” injury stimulus than hypoxia
24) List and describe four (4) primary mechanisms of cell injury
a) Disruption of oxidative phosphorylation and depletion of ATP
b) Disruption of cell membranes
c) Disruption of calcium homeostasis
d) Oxidative stress: reactive oxygen species (ROS)
25) How does disruption of oxidative phosphorylation cause cell injury?
a) Lowered ATP
i) Decreased Na pump leads to influx of H2O, Na, and Ca
(1) Leads to ER swelling and cellular swelling
ii) Increases anaerobic glycolysis, leading to decreased pH (lactic acid build up)
iii) Leads to decreased protein synthesis, lipid deposition, detachment of ribosomes, etc.
26) Please discuss how membrane disruption occurs (2 mechs)
a) Decreased O2
i) Decreased ATP (due to mitochondrial dysfunction)
(1) Lowered phospholipid synthesis
(a) Phospholipid loss leads to membrane damage
b) Increased Ca2+
i) Leads to phospholipase activation
(1) Increases phospholipid degradation
(a) Leads to phospholipid loss and lipid breakdown products
(i) Both lead to membrane damage
ii) Leads to protease activation
(1) Causes cytoskeletal damage
27) Explain how increased cystosolic Ca2+ can lead to cell injury
a) Leads to membrane damage
b) Increased intracellular calcium can lead to increased enzymatic activity that degrades structural components of cells
28) How do ROS lead to injury?
a) H2O2, OH, etc
b) Lead to membrane lipid peroxidation
c) Lead to protein cross-linking and fragmentation
d) Lead to DNA fragmentation
29) ROS damage is prevented by what?
a) Gluthione, vitamins, etc.
b) Neutralize free radicals
30) Explain how the process of cellular injury is on a continuum and the structural and functional significance of these changes
a) The severity and duration of cause(s) of injury determines the reversibility of cell damage
32) Compare and contrast the primary morphologic changes associated with reversible and irreversible cell injury
a) Reversible
i) cell swelling (hydropic swelling): disruption of fluid homeostasis
(1) ATP-dependent ion pumps
ii) Fatty change
(1) Accumulation of lipid vacuoles
(2) Cells utilizing fatty acid metabolism (liver, heart)
b) Irreversible
i) Ultimately leads to cell death
33) In the nucleus what can be a sign of cell injury (that can be either reversed or lead to eventual cell death)?
a) Clumping of chromatin
34) In cell death, what are some of the morphologic changes? (5 + 1 in nucleus)
a) Swelling of ER and loss of ribosomes
b) Lysosome rupture
c) Membrane blebs
d) Swollen mitochondria
e) Nuclear condensation
35) Please discuss Ischemia-Reperfusion injury
a) While some cells may recover following restoration of blood flow, other cells will proceed to die
i) Necrosis or apoptosis
b) Mechanisms not well understood
c) Reperfusion may cause cell death by
i) Generating ROS
ii) Some inflammatory mechanisms
d) Important in ischemia in CNS, heart
36) Compare and contrast necrosis and apoptosis
a) Necrosis
i) Leakage of cellular proteins and constituents of cells into interstitum or even vasculature
ii) Some of leaked proteins can be used for diagnosis (e.g. CK from dying muscle)
b) Apoptosis
i) Controlled, programmed cell death
ii) No leakage of contents into blood, cell eating by phagocyte
37) When comparing DNA fragments in apoptosis and necrosis what would look different between them as compared to normal (I forget the biological name of this…hmmm…bunch of lanes, proteins travel down based on size…nope can’t think of it) [electrophoresis]
a) Apoptosis shows “laddering” of DNA
b) Necrosis shows “smear” of DNA
38) Discuss what happens to the nuclei in Necrosis vs. Apoptosis
a) Necrosis: nuclei shrink and fragment or “dissolve”
b) Apoptosis: nuclei shrink and fragment
39) What happens to the cell membrane in Necrosis vs. Apoptosis
a) Necrosis: loss of membrane integrity, leads to leakage of cellular material
b) Apoptosis: membrane blebbing with fragmentation of membrane-bound cytoplasm
40) Discuss the generalized region of occurance for Necrosis vs. Apoptosis (many vs. isolated)
a) Necrosis: involves larger area of tissue (many cells)
b) Apoptosis: (involves isolated cells or small groups of cells)
41) Discuss the inflammatory nature of Necrosis vs. Apoptosis
a) Necrosis: inflammatory response
b) Apoptosis: no inflammatory response
MemoryStream methods
GetBuffer - Retrieves the array of unsigned bytes that were used to create the stream. ToArray - Writes the entire stream to an array of bytes.
WriteTo - Writes the memoryStream to another stream
43) Describe the four (4) major patterns of necrosis and provide a clinical example for each type of necrosis
a) Coagulative: Dry Gangrene
b) Liquefactive: Wet gangrene (or any fungal or bacterial)
c) Caseous: TB
d) Fat necrosis: acute pancreatitis
44) Please describe the morphology of coagulative necrosis
a) Preservation of basic cell outline and tissue architecture for at least ~48 hours after death
b) Cytoloplasmic changes: shrunken, with increased eosinophilia (¯ pH causes coagulated proteins)
c) Nuclear changes
i) Pyknosis – nuclear shrinkage and darkening
ii) Karyolysis – nuclear dissolution
iii) Karyorrhexsis – fragmentation of pyknotic nucleus
iv) Nuclei disappear within a few days
d) Process: denaturation of cytosolic proteins
45) What is Pyknosis
a) nuclear shrinkage and darkening
46) what is Karyolysis
a) nuclear dissolution
47) What is Karyorrhexsis
fragmentation of pyknotic nucleus
48) Describe Liquefactive necrosis
a) Complete enzymatic digestion of dead cells
i) Bacterial & fungal infections
ii) CNS necrosis
b) If cell death is associated with dead inflammatory cells --> pus
c) Tissue architecture is lost; cell outlines not present
49) Describe the gross and microscopic appearance in Caseous necrosis
a) Gross (macroscopic): “cheesy” white/yellow, crumbly (friable) material
b) Microscopic: amorphous granular material; no tissue architecture; surrounded by “granulomatous” inflammation (will discuss more in Inflammation lecture)
50) What type of necrosis would be seen in tuberculosis?
a) Caseous
51) Describe Fat Necrosis
a) Destruction (death) of adipocytes within fatty tissue
i) Enzymatic digestion from lipases “leaked” into adipose tissue: acute pancreatitis
ii) Traumatic destruction of fat cells (includes surgical “injury”)
iii) Inflammatory destruction of fat cells
iv) Neoplastic destruction of fat cells
b) Large-scale destruction: can lead to soponification with deposition of calcium salts in tissue
52) What is “Dry” gangrene? What type of necrosis is it
a) Coagulative necrosis of tissues secondary to profound ischemia
i) E.g., extremities (diabetes); intestines
53) What is “Wet” gangrene? What type of necrosis is it
a) Liquefactive necrosis from inflammatory necrosis superimposed on ischemic necrosis
b) Usually secondary to bacterial infections at site of ischemic damage
54) Describe how apoptosis as a physiological process
a) Involution of structures during development
b) Elimination of immune cells
i) E.g., self-reactive lymphocytes
ii) E.g., neutrophils in inflammatory process
c) Involution following hormonal withdrawal
i) E.g., menstruation: shedding of endometrium
d) Cytotoxic T-cell mediated elimination of infected cells or neoplastic cells
55) Describe apoptosis as pathologic process
a) “Insults:” radiation; drugs; DNA damage
b) Viral infections
i) E.g., Councilman (acidophil) body: apoptotic hepatocyte in viral hepatitis
c) Autoimmunity
d) Neoplastic cells
56) Describe the two major pathways of apoptosis, please briefly list examples
a) Intrinsic: injury, radiation, toxins, ROS, withdrawal of growth factors
b) Extrinisc: death receptors, cytotoxic T-cell meditated
57) What is the common execution pathway for apoptosis?
a) Caspase enzyme cascade
58) From the Bcl family, what are 2 pro apoptotic regulators?
a) Bax, Bak
59) From the Bcl family, what are 2 anti-apoptotic regulators?
a) Bcl-2, bcl-x
60) What are the 2 major players in the intrinsic apoptotic pathway?
a) Injury (toxins, radiation, DNA damage)
b) Withdrawal of growth factors
61) Discuss the intrinsic pathway of intrinsic apoptosis
a) increase­ p53 tumor suppressor gene product
i) Arrests cell in G1 to repair DNA
ii) If unsuccessful repair -->apoptosis
iii) increased­ Pro-apoptotic members of Bcl family of proteins: Bax, Bak
62) Discuss what happens with a withdrawal of growth factors (with respect to apoptosis)
a) Alter balance in Bcl family to favor apoptosis
i) increase­ Bax, Bak;
decrease bcl-2, bcl-x
63) Increased activity of Bax/Bak promotes what?
a) Apoptosis
64) Increased activity of bcl-2 and bcl-x promote what?
a) Anti-apoptosis
65) What are the 2 major players in the extrinsic pathway of apoptosis?
a) Death receptors/Ligands
b) Cytotoxic T-cell mediated cell death: granzyme B (I don’t know what this is…yet)
66) What are 4 examples of death receptors/ligands?
a) Fas/FasL
b) TNFR1/TNF
c) E.g. elimination of self-recognizing lymphs
67) Provide clinical examples for both physiologic and pathologic apoptosis
a) Pathologic: insults, radiation, drugs, viral infections (councilman bodies)
b) Physiological: self reactive lymphocytes, involution of structures during development, etc.
68) What can happen when you have too little apoptotic activity (2 examples)
a) Cancers
i) Neoplastic cells proliferate despite DNA damage
b) Autoimmunity
i) Failure to eliminate self-reacting lymphocytes
69) What can happen with too much apoptotic activity (3 examples)
a) Neurodegenerative disorders (e.g., Parkinson disease)
b) Ischemic injury
c) Death of virally infected cells
70) List five (5) major types of intracellular accumulations that occur typically as part of a pathologic process
a) Pigments
b) Glycogen
c) Proteins
d) Lipid
e) Cholesterol
71) What is hepatic steatosis? Commonly due to?
a) Accumulation of lipid in the liver
b) Most commonly due to alcohol (acts a s a hepatotoxin that interferes with mitochondrial and microsomal function in hepatocytes, leading to accumulation of lipid)
72) What is xanthelasma?
a) Hypercholesterolemia
b) Accumulation of lipid-laden macrophages around the eye
73) What are the 2 type of pigment accumulations (general)
a) Exogenous and endogenous
74) What are the exogenous pigment accumulations?
a) Carbon dust (coal, soot, smog): anthracosis
75) What are 3 forms of endogenous pigment accumulations?
a) Melanin
b) Lipofuscin (wear and tear or aging pigment: phospholipids/protein; NOT iron, does not stain with iron stains)
c) Hemosiderin
what is Lipofuscin ?
(wear and tear or aging pigment: phospholipids/protein; NOT iron, does not stain with iron stains)
76) What is hemosiderin?
a) An endogenous pigment accumulation
b) Hemoglobin breakdown product; form of iron stored in cells
77) What is the difference between localized and systemic hemosiderin?
a) Localized: hemorrhage
b) Systemic
i) Hemosiderosis (hemolytic anemia)
ii) Hemochromotosis (genetic disorder)
78) Discuss dystrophic calcification (ca level, diseases associated with [5])
a) Dystropic
i) Normal systemic calcium levels
ii) Associated with dying or degenerating cells
(1) Calcific atherosclerosis and valvular disease
(2) Fat necrosis
(3) Certain neoplasms: psammoma body
(a) Papillary thyroid carcinoma; ovarian carcinoma
(b) Meningiomas
79) Describe metastatic calcification (calicum levels, due to, causes [4])
a) Hypercalcemia (­ serum calcium), due to …
i) ­ PTH: causes bone resorption
(1) Hyperparathyroidism (adenoma)
(2) Ectopic PTH-like protein produced by some tumors
(3) Renal failure: retention of phosphate leads to ­ PTH
b) Destruction of bone
i) Tumors: multiple myeloma, metastases; Paget’s
c) Too much vitamin D
i) Vit D intoxication; sarcoidosis
80) Metastatic vs dystrophic: Calcium levels
a) Metastatic: high Ca
b) Dystrophic: normal
81) Metastatic vs dystrophic: destruction of bone
a) Metastatic, due to PTH causing bone resorption
82) What is the idea of replicative senescence?
a) Cells have limited capacity to replicate
i) Telomeres/telomeric shortening
83) As you age what happens to the function of proteosomes? What does this mean?
a) Declines
b) This is the cellular machinery that eliminates unwanted or abnormal proteins within the cell…so ya that is trouble
What tissue is normally involved in metastatic calcification?
gastric mucosa; kidneys; lungs; blood vessels
which is more localized, dystrophic or metastatic?
Dystrophic (think heart valve)
1. If you see peripancreatic tissue being effected, what kind of necrosis should you immediately think?
a. Fat necrosis
2. If you see hypercalcemia or increased PTH, or parathyroid hyperplasia what should you be thinking?
a. Metastatic calcification
3. If you have a an old woman who dies and her autopsy shows hepatocytes with golden cytoplasmic granules that do not stain with Prussian blue. What is the pigment that she has?
a. Prussian blue automatically kicks out anything with iron
b. So it can’t be anything with hemosiderin
c. Advanced age due to lipofuscin
4. A 22-year-old construction worker sticks himself with a sharp, rusty nail. Within 24 hours, the wound has enlarged to become a 1-cm sore that drains thick, purulent material. This skin wound illustrates which of the following morphologic types of necrosis? Caseous , Coagulative, Fat, Liquefactive
a. Liquefactive
5. If you see acidophil body, what should you be thinking?
a. Apoptosis
6. What are the initiator pathways for apoptosis? Common?
a. Intrinsic: P53 and Bcl pathways
b. Extrinsic: Fas/FasL
c. Common: Caspase
7. A 64-year-old man with long-standing angina pectoris and arterial hypertension dies of spontaneous intracerebral hemorrhage. At autopsy, the heart appears globoid. The left ventricle measures 2.8 cm on cross section (shown). This adaptation to chronic injury was mediated primarily by changes in the intracellular concentration of which of the following components? DNA ,Glycogen ,Lipid, mRNA, Water
a. mRNA because you have to have more protein made
6. What are the initiator pathways for apoptosis? Common?
a. Intrinsic: P53 and Bcl pathways
b. Extrinsic: Fas/FasL
c. Common: Caspase