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73 Cards in this Set

  • Front
  • Back
two mains mechanisms for cell death
cell necrosis and apoptosis
Cell necrosis
irreversible change in cellular architecture, manifested by:
nuclear pyknosis,
karyolysis
karyorrhexis
nuclear permeability to vital dyes such as trypan blue
Apoptosis
physiological cell death,
programmed cell death
3 main manifestations of disease following cell injury
inflammation
repair
neoplasia
4 sequelae of inflammation
granuloma
abscess
chronic inflammation
repair
2 sequelae of post inflammatory repair
regeneration, leading to tissue restitution

Fibrosis leading to scar
3 sequelae to chronic inflammation
resolution

organ failure

Fibrosis leading to scar
2 sources of fibrosis
post inflammatory repair

post inflammatory chronic inflammation
6 principal types of cellular agents of injury
genetic, nutritional, physical (e.g., hypoxia, radiation), chemical, immune and infectious
How radiation causes injury
Direct: macromolecules ionized (most susceptible in S and G1)

Indirect: water or solute molecules are ionized and produce free radicals
What cells i liver metabolize alcohol
centrilobular hepatocytes
What liver cells metabolize alcohol to
acetaldehyde
Effect of acetaldehyde
impaired fatty acid oxidation, causing fatty liver

inhibition of microtubule-directed protein traffic out of hepatocytes, leading to accumulation of ER and balooned hepatocytes

synthesis of abnormal cytokeratin filmanets (Mallory bodies) that attract neutrophils

stimlation of lipocytes in the space of Disse to becoome myofibroblasts that synthesis collagen
Sequelae of alcoholism
alcoholic hepatitis, which leads to:

- progressive fibrosis
- regeneration of hepatocytes as nodules that lead to cirrhosis
Type of infiltrating cell in actue inflammatory response
neutrophils
type of infiltrating cell in parasitic infections
eosinophils
type of infiltrating cell in drug toxicity
eosinophil
type of infiltrating cell in allergy
eosinophil
type of infiltrating cell in viral infections
lymphocytes
type of infiltrating cell in chronic inflammation
lymphocytes and plasma cells
Type of infiltrating cell in granuloma
closely apposed macrophages that deal with agents that are not readily degraded
Response to bacteria
acute inflammation with neutrophils
Response to viruses
cytopathic changes in infected cells

or

lymphocyte attack
Response to fungi, parasites
granuloma formation
four ways for substances to enter cell
passive diffusion

active tansport

enzyme carriers (microfilaments)

pino or phagocytosis
Cell's four defenses against injury
Vascular space

extracellular space

cell structure and differentiation

Capacity for division
postmitotic - def and example
remain in G phase; once divided that's it

heart and nerve
intermitotic - def and example
constantly dividing

intentinal epithelium, skin, bone marrow
reverting postmitotic - def and example
usually resting, but capable of division after injury; quiescent for long periods

hepatocytes, renal tubular epithelium
pyknosis
condensation of chromatin
karyolysis
dissuolution of chromatin and nuclear membrane
karyorrhexis
breakdown of nucleus into clumbs
atrophy
decrease in size and/or number of cells
hypertrophy
increase in size of cells or tissue
hyperplasia
increase in number of cells
metaplasia
change from one mature cell population to another (e.g. bronchial pseudostratified columnar to squamous)
neoplasia
new growth

includes benign and malignant
benign vs metastatic
limited vs. unlimited growth potential
most diseases can be considered examples of:
inflammation
repair
neoplasia
cause of splenic infarct
endocarditis
repair mechanism after coagulative necrosis for postmitotic cells
fibrosis
color of amyloid in H&E
pink
primary sites of adenocarcinoma
pancreas, lungs, colon
bacteria in facial abscess
actinomycetes
bacteria in pharyngitis
streptococcus
bacteria in pneumonia
pneumococcus pneumoniae
bacteria in bacterial meningitis
meningococcus
bacteria in pyelonephritis
escherichia coli
bacteria in syphilis
spirochetes
bacteria in lymphogranuloma venerium
chlamydiae
bacteria in osteomyelitis
staphylococcus
bacteria in TB
mycobacteria?
fungus in meningitis
crytococcus
fungus in oral thrush
candida
fungus in pneumonia
aspergillus
fungus in athlete's foot
dermatophytes
virus in polio
enterovirus
virus in encephalitis
herpes
virus in stomatitis
herpes simplex
virus in shingles
herpes zoster
virus in measles
rubeola
virus in hepatitis
hepatitis virus
dysplasia
cancer precursor

abnormal arrangement or appearance
anaplasia
bad dysplasia
invasion
tumor grew through the Basement membrane
are changes in RER reversible or irreversible
reversible
are changes in nuclear chromatin reversible or irreversible
reversible
are changes in cell surface reversible or irreversible
reversible
are changes in membrane reversible or irreversible
irreversible
are changes in mitochondria reversible or irreversible
irreversible
are changes in lysosomal Ca++ reversible or irreversible
irreversible
Traits of necrosis
Eosinophilia (denatured protein)

swelling (permeability altered)

Glass cytoplasm (loss of glycogen)

Vacuolated cytoplasm (loss of organelles)

Nuclear decay (pyknosis, karyorrhexis, karyolysis)

Inflammation
is inflammation characteristic of apoptosis? necrosis?
necrosis only