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00 - path-review again crds


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2 common chronic injury cell type changes
smoker:ciliated epithelium - stratified squamous. Cervix - glandular to squamous epithelium
4 systems in cell vulnerable to injury
membrane pump, genetic apparatus, aerobic respiration, structural-enzymatic proteins
4 mediators - cell death
02 and 02 free radicals, intracellular Ca+, ATP depletion, membrane permeability defects
2 energy mechs affected in cell injury
aerobic respiration (oxydative phosphorylation), glycolysis (anaerobic respiration)
result when each energy mech. injured
aerobic - ATP production lost. glycolysis - depletion of glucogen, byproducts and acidity
byproducts - glycolysis
lactic acid, reduces intercellular pH
4 mechanisms free radical injury
peroxidation of membrane lipids, DNA breaks, X-linking of proteins destroys function, damage to mitochondria.
6 free radical injuries
reperfusion/hypoxia, aging, radiation, 02 toxicity, chemical injury, INFLAMMATION
2 mechanisms chemical injury
direct (chemotherapy), toxic reactive metabolite reaction (in liver)
2 methods necrotic cell removal
denaturation, enzymatic digestion
nuclear shrinkage
many cytoplasmic proteins denature - result?
cytoplasmic eosinophilia (incr. staining)
markers of infarct in brain
cyst, tissue debris, fluid, inflamm. cells, bacteria
normally seen in caseous necrosis
granulomatous inflammatory border with giant cells, epitheloid histiocytes
2 conditions assoc. w apoptosis
viral infections, radiation injury
fast necrosis dev. in organs with?
high met. rate (int. mucosa), cytolytic enzymes(pancreas), vital organs - high O2 (brain, heart, lungs)
physiologic hyperplasia 2 types, examples
compensatory (liver regen) hormonal (breast/uterus - pregnancy)
inflammation mediators
chemicals derived from host
inflammatory changes occur where
terminal vascular bed, blood, conn. tissue
main cells involved in inflammation
monocytes, neutrophils, macrophages
purpose of inflammation
eliminate injurious agent and initiate repair, restoring continuity if not function
characteristics acute inflam.
short duration, fluid exudate, plasma proteins (edema), neutrophil and leukocytes to tissue, then macrophages.
chronic inflam. char.
long duration, lymphocytes, plasma cells, macrophages, vascularization, fibroblasts.
following vascular chgs
blood tissue barrier chgs - widen endothelial gaps - histamine reaction - edema
swelling of inflammation bc of
capillary leakage - blood plasma and leukocytes to tissue
inflammatory exudate
cellular debris, plasma proteins, fluid
cellular events of inflamm
margination, pavementing w/in vessel wall, emigration from vessel to interstitium, chemotaxis-site, phagocytosis
inflamm cell types
Neutrophils first 24 hrs, then monocytes 24-48 hrs
5 host derived main mediators inflammation
vasoactive amines, plasma proteases, cytokines, adhesion molecules, arachiodonic acid metabolites
2 vasoactive amines
histamine, seratonin
purpose, origin vasoactive amines
vascular chgs inflammation
what produces vasoactive amines
mast cells, platelets
3 systems of plasma proteases
kinin, clotting, complement systems
cytokine, peptide source
cytokine purposes
inflammatory mediators (IL1, TNF), activate polymorphs, macrophages to incr. killing, incr. vasc. permeability
ICAM1 def
cytokine - initiated production by endothelium
ICAM1 purpose
facilitates inflam cell binding to vessel endothelium
AA metabolites are?
arachiodonic acid - degraded phospholipids of cell membranes
AA’s cause?
inflammation - vasodilation, chemotaxis, increase vasc. permeability
aspirin function
blocks prostaglandin synthesis
prostaglandin function
pathogenesis of pain and fever - hyperalgesic
steroid function
blocks prostaglandin, leukotrines
chemotactic, activate neutrophil aggregation, adhesion
chronic inflam cells
MNL, lymphocytes, plasma cells
main processes, chronic inflam
healing and repair and tissue destruction cycle
define granuloma
form of chronic inflam w/ lots of histiocytes, giant cells, LANGHANS cells
granuloma forms bc
bacterial or fungal infection, foreign materials
3 examples persistent infections causing chronic inflam
tuberculosis, syphilis, fungi
2 autoimmune disorders assoc w chronic nflamm
rheumatoid arthritis, thyroiditis
chronic inflammation: granuloma histology
activated macrophages, large squamous cell epitheloid appearance
pyogenic organism example
3 systemic effects inflam
fever, elevated WBC count, neutrophylia, lymphocytosis
exudate with RBCs
inflammation is
response of VASCULARIZED tissue to injury
inflammation designed to
bring plasma proteins to site of injury in fastest poss.time
main chgs in inflammation
blood flow changes, formation of fluid and cellular exudates
3 functions fluid exudate
bring plasma proteins, dilute toxins, loosen conn. tissue to allow diffus-migration of cells to injury site
cell type assoc w/ parasitic infection
polymorphonuclear leukocytes: NEUTROPHILS
chemical attractants at injury site
host factors - plasma proteins, and infectious agents
protein expressed on infectious agent
OPSONIN - labels agent for phagocytic destruction
3 conditions lysosomal enzymes released inadvert. during inflamm.
during phagocytosis, trying to digest on flat surface (frustrated phagocytosis), cytotoxic release
system: removes AgAb complexes in spleen, liver, bone marrow
reticulo-endothelial system
tissue destruction from cytotoxic release
4 agents of chronic inflammation
microorganisms, foreign bodies, toxins, auto-immune reactions
chronic inflam main events
cellular infiltrate, tissue destruction, repair by scar
chronic infection, macrophages differentiate - epitheloid cells, cluster
4 disorders assoc w granulomatous inflam
tuberculosis, syphilis, leprosy, crohns
2 modes of destruction AbAg complex
direct lysis, complement activation
cells with FC receptors
macrophages, NK cells, eosinophils, neutrophils
direct lysis of AgAb complexes how
cell with FC receptor engages FC fragment, releases lysosomes - destroys complex
2 basics of complement system
hydrolytic enzymes directly lyse infectious agents or chemical mediators initiate acute inflammation, attract neutrophils to phagocytose
2 main classes Tlymphocytes
CD4s assist others, CD8s kill directly
3 types of antigen presenting cells
dendritic(skin), macrophages, langerhans
distinguish self from non-self
major histocompatibility protein (MHP)
two types of MHP & locations
Class I - all cells, Class II - ONLY antigen-pres. cells
MHC protein recognition
CD4s recognize class II, CD8s only class I
cytokine, source activates Bcells
interleukin produced by Type2 CD4s
cytokine source - activates macrophages
Interferon Gamma, produced by Type1 CD4s
macrophage activation results
increased size, lysosomal enzymes, ability to digest/kill, secretion of growth factors(endothelial cells, fibroblasts), hydrolytic enzymes
macrophages kill what and how
TB, parasites, fungi, tumour cells, organ trans. direct lysis or phagocytosis
CD8s kill antigens how
proteolytic enzymes -- osmotic lysis
CD8s mostly kill
virus infected cells, tumour cells, organ trans (non-self)
stimulates scar repair in chronic inflam
activated macrophages secrete growth factors
Type I hypersensitivity mediated by Ig?
2 cell types central to Type I hypersensitivity
mast cells and basophils
mast cells - what and where
from marrow, wide dist. in body, esp. around nerves, vessels, subepithelial where Type I reacts occur
Mast cells/basophils activated how?
crosslinking IgE receptors
diff btwn mast cells and basophils
basophils in blood, small numbers
type of helper cell assoc. w Type I hypersens
Type 2 CD4s
What is produced by Type 2 CD4s
Interleukins 4 and 5
genetic predisposition to type 1 hypersensitivity called
atopic disease (allergy) IgE diseases
other IgE mediated diseases
asthma, dermatitis, gastrointestinal food allergy
released upon exposure to allergen?
histamines, leukotrines
slow-reacting substance of anaphylaxis
eosinophil chemotactic factor of anaphylaxis
type 1 mediators act on what?
vessels, sm. musc, secretory glands
Type 1 mediators cause what?
edema, cellular infiltrate, clinical features of allergy
IL4 is what
IgE switch factor, produced by Th2, activates Bcells
HDN example of what type hypersensitivity
Type II
produced in mother in HDN following second child?
IgG antibodies, which cross placenta
problem with IgG crossing placenta?
attack fetal erythrocytes - hemolytic anemia
natural antibodies reactive with AB blood groups
IgM - can’t cross placenta
2 examples of Type II hypersensitivity
organ rejection, myasthenia gravis
define RA (rheumatoid arthritis)
chronic systemic inflamm.autoimmune disease - joints
what histocompatibility complex assoc. with rheum arth
HLA-D4, and HLA- DR4
what are rheumatoid factors
immunoglobulins specific for FC fragment of IgG - an antibody against ones own antibody Immunoglobulin
2 examples Type III hypersensitivity
serum sickness, arthus phenomenon
inflammatory factors associated with rheumatoid arthritis
histamine release, cytokine production (neutrophils, monocytes), white cells to synovial space
define pannus
vascular mass of lymphocytes around area of necrosis where bone and cartilage have degraded
cause of tuberculosis
mycobacterium tuberculosis (or mycobac.T.bovine)
TB inflammation type
focal granulomatous with central caseous necrosis
tuberculosis vaccine
BCG - bacille Camette Geurin
Test for TB
PPD purified protein derivative
endogenous infection
from interior - ones own flora attacking system
how well an organism can produce symptoms
how severe symptoms are that are prod. by organism
poisons secreted by bacteria
examples of 3 exotoxins
diptheria, tetanus, enterotoxin
diptheria pathology
sore throat - death. destroys epithelium and mucous memb, leaving fibrous necrotic tissue, esp. in throat.
tetanus pathology
neurotoxin, interrupts motor nerve signals, causes spasm
food poisoning - staphylococcus
endotoxins released when
when bacteria destroyed
3 bacterial metabolic examples - contrib. to disease
hyaluronidase, streptokinase, coagulase
metabolite - dissolves conn. tissue
metabolite - demineralizes tooth enamel
plaque acid
metabolite - breaks down fibrin
metabolite, breaks down DNA
3 examples where foreign organisms multiply - prod. inflammation
shigellosis(dysentry), Salmonella Typhi (Typhoid Fever), Spirochete(necrotizing ulcerative gingivitis)
organism in bloodstream from infection called
another name for blood poisoning
3 main factors - infection resistance
patient factors(immunity, nutrition, biochem, secretions), organism virulence, site of infection, level of blood supp.
atrophy caused by plasma protein deposition in tissue
autoimmune disease where antibodies clog acetylcholine receptors
myasthenia gravis - causes generalized muscular weakness
chronic rheumatic fever can lead to risk of
infective endocarditis - heart valve deformity, incompetency
mast cell histamine release-mucous hypersecretion-more goblet cells - bsmt. memb. thickening-sm. vessel constriction
5 HIV related infections
fungus in meninges, cytomegalovirus - gigantic langhans cell, lung yeast infection, carposis sarcoma, lymphoma
proteins that regulate cell cycle
continuously regenerating cells
labile, from stem cells, eg: marrow, epithelia
cells which can but don’t normally divide
stable- divide if injured, eg: liver, fibroblasts, sm. musc
cycle stage cells at
G0 - resting(quiescent)
matrix btwn cells - origin, composition
interstitial matrix:fibroblasts-amorphous gel, collagen, elastin, proteoglycan, glycoproteins
bsmt membrane composition
platelike mesh, type IV collagen, glycoproteins
extracellular matrix active in tissue repair how
mech support, determine orientation, control regulate growth and differentiation, pres: regulatory molecules
collagen - describe
fibrous structure proteins from fibroblasts Xlink by VitC in triple helix
source of cell growth factors
activated macrophages
3 examples growth factors
epidermal, fibroblast, cytokines
basic substrate extracell. matrix forms on and timing
granulation tissue at abt. 3 days
char. of first intention healing
more epithelial regen than fibrosis
1st intention - process
neutrophils, mitosis; epithelial migration, new bsmt memb.; macrophages, granulation tissue, collagen fibres; epidermis - collagen fibre bridge
char. of 2nd intention healing
fibrosis rather than epithelial regen
example 2nd intention
ulcer (eg Diabetes)
process 2nd intention
big inflamm. reaction, lots of granulation tissue, wound CONTRACTS
3RD intention
delayed closure to allow some natural disinfection
exuberant collagen production in 1st intention wound
types of factors effecting healing
local(infection, foreign body, blood supp, temp.) Systemic(immunosup.,vasc.disease, nutrition, alcohol)
key characteristics neoplasia
autonomous cell division persisting post cessation of initiating stimuli
2 components of tumours
parenchyma (prolif. neoplastic cells) stroma (conn. tiss & vessels)
benign tumour of epithelial origin
papilloma (eg squamous or transitional)
malignant tumour of epithelium
benign tumour of glandular origin
malignant tumour of glandular origin
age effected carcinoma versus sarcoma
carcinoma 55+, sarcoma usually children
3 categories of hereditary cancers
mutant gene inheritance (autosomal dominant - eg:retinoblastoma), familial (uncommon CA type, prevolent in family), autosomal recessive (need both parental alleles)
well differentiated versus poorly differentiated
Grade I (less agress) - Grade III(v.aggress)
highly UNDIFFERENTIATED tumour cells called
variation in size and shape of tumour cells called
tumour cell nuclei with lots of DNA - dark staining
6 morphologic chgs in anaplasia
pleomorphism, hyperchromasia, lg nuclei, incr. mitosis, giant cells, disturbed orientation
disorderly growth type that doesn’t nec. lead to CA
type of benign tumour not well defined
hemangioma (tum. of blood vessels)
spread through blood
hematogenous - usually sarcomas
tumour (benign or malig) effects depend on what 6?
location, impingement; functional activity; bleeding; 2ndary infections; ulcerations; initiation of acute symptoms: rupture or infarct
example of local effect of benign tumour
adenoma of pituitary destroying pit. function, causing endocrinopathy
hormonal effect example - benign tumour
pancreatic islet tumour, overproduction of insulin, causes deadly hypoglycemia
wasting syndrome associated with cancer
cachexia - usually a result of cytokines
example of substance imbalance assoc. w cancer
cushings syndrome - lung or pancreatic CA producing ACTH
histologic features, squam. cell CA
sheets or solid nests “mosaic” pattern, intercellular bridges, sometimes keratinized
term: sm. muscle
examples of acquired pre-neoplastic disorders
chronic wound - cell regeneration, so potential for cancer; smokers - chronic bronchial dysplasia; chronic gastritis (pernicious enemia) - all can become malignant
risk factor for oral CA
leukoplakia - incr. risk squamous cell CA
risk for colorectal CA
villous adenoma (glandular)
basis of carcinogenesis
non-lethal genetic damage (chem, radiation, viral)
targets of genetic dmg in cells
genes: promote or inhibit growth, or apop.regulators
growth promoting gene
oncogene is what
a mutant allele of a proto-oncogene
oncogene does what
promotes autonomous cell growth
example tumour supressor gene
Rb gene - usually prevents cell cycle which otherwise causes retinoblastoma
Most common genetic disorder in cancer
TP53 gene - regulates apoptosis, senses DNA damage and initiates repair
HER2 gene does what
protooncogene - produces growth factor. commonly damaged in 20 - 30% of breast cancer cases.
Type I hypersensitivity
mast cells, basophiles release vasoactive amines, provoke an immediate (anaphylactic) response - eg food allergy, hay fever - IgE antibodies
Type II hypersensitivity
mediated by humoral antibodies which predispose cells to phagocytosis, lysis - complement mediated cytotoxicity - (hemolytic disease of newborn, transfusion reactions) - IgG antibodies
Type III hypersensitivity
Immune complex mediated (rheumatoid arthritis, serum sickness) --acute inflammatory response initiated, causing cell injury (in Rheum - fc fragment of IgG antibody)
type IV hypersensitivity
cell mediated (delayed hypersensitivity reaction) TCells rather than antibodies. eg tuberculosis.
what might accompany a type II transfusion reaction
what is the last stage in wound healing?
what type of cancer is xeroderma pigmentosum
autosomal recessive CA-probs w genetic repair mechs
in what vessels does the exudate occur
post-capillary venules
what percentage of patients have paraneoplastic syndromes associated with cancer

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