3240 Midterm 1

Front 1

physical signs vs clinical symptoms

Back 1

measured vs described

Front 2

morbidity

Back 2

impaireness

Front 3

motality

Back 3

cause death

Front 4

leading cause of death in Ca

Back 4

1. cardiovascular disease, 2. cancer, cerebrovascular (stroke)

Front 5

most frequent cancer in women/men

Back 5

breast and prostate

Front 6

leading cause of death cancer

Back 6

lung

Front 7

etiology

Back 7

cause of disease process

Front 8

pathological and morphological sequelae

Back 8

secondary consequence

Front 9

prognosis

Back 9

aniticipated course and final outcome

Front 10

epidemiology

Back 10

with population, we look for pattern and study risk

Front 11

incidence/prevalence

Back 11

number of new cases in a pop.

total number of cases in a pop.

Front 12

Iatrogenic disease

Back 12

result from a treatment by physician

7.5% in canada

Front 13

alternative classification of disease

Back 13

injury, inflammation, infection, immunological reaction, neop[lasia, metabolic or endocrine, nutritional, vascular disease, phychological factors.

Front 14

injury cause

Back 14

physical, chemical, biological, nutritional, immune reaction, genetic defects, cellular aging

Front 15

vulnerable cell components

Back 15

1. cell membrane
2. mitochondria
3. protein synthesis
4. DNA

Front 16

change in cell size

Back 16

atrophy
hypertrophy
hyperplasia
metaplasia
dysplasia

Front 17

atrophy

Back 17

decrease in mass due to shrinkage in cell size

Front 18

cause of atrophy

Back 18

ischemia
low nutrient
new steady state for the cell to survive

Front 19

how is atrophy achieved (mechanism)

Back 19

lysosome digestive enzyme degrade molecules inside
ubiquinitin-proteasome pathway:degrade proteins by ubiquitin binding

Front 20

can atropy be physiological or patho.

Back 20

can be both
aging in physio

Front 21

hypertrophy

Back 21

increase in size of cell, can by physiological or path.

due to increase function demand or hormonal stimulation

Front 22

hyperplasia

Back 22

increse # of cell
can act with hypertrophy

can be due to functional demand, hormonal and cell injuries repair

Front 23

metaplasia

Back 23

change into different cell type, if stimulus removed, goes back
may be loss of function

Front 24

two types of cell death

Back 24

necrosis and apoptosis

Front 25

features of hydropic swelling/hydropic change

Back 25

increase size
pale cytoplasm
impaired ion conc.
membrane pump inpaired, Ca accumulation
water increase
swell
mito swell
belbs

Front 26

fatty change

Back 26

accumulation of triglycerides

Front 27

necrosis

Back 27

cell death that cell cannot adapt to an enviornment

Front 28

necrosis is characterized by structural changes including: (4)

Back 28

intense eosinophilia (pink)
pyknosis (shrink)
karyorrhexis (fragment in pyknotic nucleus)
karyoloysis (dissolution of nucleus)

Front 29

types of necrosis

Back 29

coagulative
liquefactive
fat
caseous

Front 30

cagulative necrosis

Back 30

most common
all the stuctral change
"ghost"
eg. ischemia

Front 31

liquefactive necrossi

Back 31

rapid loss of architecture
most CNS by bactera damage

Front 32

fat necrosis

Back 32

adipocyte
fat complexes with ca form chalkywhite deposit

Front 33

caseous necrosis

Back 33

cheesy soft materia,
TB.

Front 34

gangrenous necrosis

Back 34

web gangrene
a coagulative necrosis and liquefactive
when they dry, they black and mummified and turn dry gangrene

Front 35

Apoptosis features

Back 35

energy dependent, organized
physiological or pathological

Front 36

proteins invovled in apoptotic cells

Back 36

caspase
endogenous endonuclease :break nucleus and cytoskeleton

Front 37

apoptotic cell will turn into

Back 37

apoptotic bodies with enclosing organelles be eaten by phagocytic cellls

Front 38

what causes apoptosis or necrosis

Back 38

necrosis: severe damage stimuli
lower grade and immune mediated damage: apoptosis

critical factor ATP

Front 39

reversible or irreversible cell injury depends on

Back 39

type of injury (duration +severity)
injured cell (lots of featurres)

Front 40

ROS can cause cell injury. can be formed by?

Back 40

ionizing radiation: water hydrolysis
during reperfusion 偶发tissueafterischemia头哦牧场oxygeninflammatorycells
惨initiatelipid培荣喜达提哦你lead痛damageinmembrane， DNAorform2你的damagingROS.

Front 41

what do we stop ROS

Back 41

spontaneous decay
catalase: convert H2O2 to water
glutathione peroxidase: reduce H2O2 to water
antioxidants: give protection

Front 42

ischemia

Back 42

causes coagulative necrosis,
-loss of blood, no oxygen
NO O2-->no ATP-->no pump-->water acucmulation-->swell-->rapture-
-more lactic acid (higher pH) cause reduction in protein synthesis

longer:
proteolytic enzyme release
Ca release to cause different pathways
leakage of protein into peripheral circulation can be detected

Front 43

ischemia and reperfusion injury can cause injury by (4)

Back 43

restoration can cause injury.
1. high ca and might not be regulated
2. damaged mito create ROS
3. local inflam. cell release ROS
4. injured cell have compromised antioxidant defense mechanisms

Front 44

lipofuscin

Back 44

intra. accumulation
degraded phospholipid
godlenbrown

Front 45

melanin

Back 45

brown-black pigment in skin

Front 46

hemosiderin

Back 46

iron rich brown pigment from break down of RBS

Front 47

hemosiderosis

Back 47

too much iron storage

Front 48

most common oxogenous pigment

Back 48

carbon from air
deposite into lung tissue and lymph node in lung

Front 49

Fatty change and steatosis

Back 49

intracellular accumulation of fat due to increased delivery of fat
-impairment of fat metabolism in liver
-low synthesis of apolipoproteins ( can not transfer out of the cell)
-small vacoule form large vacoule fat

Front 50

fatty change is mostly caused by

Back 50

alcohol

Front 51

fatty change reversible or no

Back 51

entirely reversible

Front 52

inflammare

Back 52

to excite

Front 53

features of inflammation

Back 53

dynmic process start with injury and healing then repair
defense mechanism can be harmful
stereotyped repair process
intesnsiry and duration and outcome is depend on host factor and etiological agent
must be nonleathal injury

Front 54

infection is

Back 54

a type of inflammation due to biological agents

Front 55

what do we have to protect ourself
defense mechanisms

Back 55

lysozyme
cerumen
anatomical barrier
stomach low pH
mucus cilia
lysozyme in urine
immune system

Front 56

injury defeinition

Back 56

excess stimulation or
effect of an excessive stimulus upon cell and tissues

Front 57

exudation

Back 57

outpouring of fluid and proteins and cells from vessels into intersitium or body cavidties

Front 58

exudate

Back 58

extravascular fluid rich in protein and cell
implies alternation of permeability of BV in area of injury

Front 59

transudation

Back 59

oupouring of fluid with little protein

Front 60

transdate

Back 60

ultrafiltrate of plasma and due to hydrostatic imbalance
permeability

Front 61

pus exudate or transdudate?

Back 61

purulent (hua nong de) exudate
by cell debris of PMNs
has powerful lysosomal enzymes

Front 62

Cardinal signs
-Rubor
-Tumour
-Calor
-Dolor
functio

Back 62

redness
swelling
heat
pain
impaired function

Front 63

two types of inflammation

Back 63

acute and crhonic
acute: short and exudation
PMNs present

Chronic: long, with lymphocytes macrophages and involved tissue repair

Front 64

what causes inflammation (6)

Back 64

1. anoxia (lack of oxygen)
2. Trauma: penetrating injury
3. immunologic reactions (humoral-B, cellular-T)
4. biologic agent
5. physiocal agent
-metabolic injury

Front 65

events in acute inflammatory reaction

Back 65

1. Vascular event (changes)
2. Cellular events
3. phagocytosis
4. mediator of inflammation

Front 66

Vascular events

Back 66

vascular flow , calibre and permeability change

Front 67

triple responses of lewis

Back 67

refer to vascular flow and calibre
1. pale line along area of stroke
2. flare
3. swelling and branching

Front 68

actual change of vascular in inflammation

Back 68

1. transient vasoconstriction (vascular contraction) of arterioelse: smooth muscle at arteriolar walls
2. vasodilation: open arterioles, capillaries, arterial venous shunts: result in blood flow and appears red and heat
3. permeability change with exudation: outpouring of liquid of protein from BV
4. slow blood flow cause cellular event take place
5. period: more severe faster

Front 69

two events to increase vascular permeability

Back 69

1. hydrostatic pressure in microcirculation (allow passive transport into interstitium)
2. widening of endothelial cell junctions: myofibrils within the cytoplasm of endothelial cells

Front 70

Starling's hypothesis

Back 70

fluid balance maintained by two opposing set of forces
1. flows out by
-osmotic pressure of interstitial fluid
-intravascular hydrostatic pressure
2. move in by
-osmotic pressure in plasma proteins
-tissue hydrostatic pressure

Front 71

transudate is caused by

Back 71

increase in intravascular hydrostatic pressure (vasodilation)
or decrease intravascular osmotic pressure (decreased albumin)
pg 24

Front 72

Patterns of increased vascular permeability
5 mechanisms

Back 72

1. immediate transient
2. junctional retraction
3. immediate sustained or delayed prolonged leakage
4.leukocyte dependent endothelial injury
5. increased transcytosis

Front 73

Immediate trasient

Back 73

contraction of endo. lead to gaps mediated by histamine, reversible. only in small venules not capi. or arterioles.

Front 74

junctional retraction

Back 74

cytokine mediated
reorganization of cytoskeleton and disruption of endo. cells junctions of venules

Front 75

immediate sustained response

Back 75

under severe injury
right after injruy and persist for hours
-direct endo. injury and end. cell necrosis and detachment
may induce delayed prolonged leakage: involves cap. and venules

Front 76

Leukocyte dependnent endothelial injury

Back 76

inflammatory cell release toxic oxygen and cause endo. cell detachment
mostly in venules, pumonary capi.
late in inflammatory

Front 77

increased transcytosis

Back 77

with presense of vascular endo. GF and mediators
increase venular permeability via a vesculovacuolar intracellular pathway

Front 78

most clinically significant injuires is

Back 78

immediate-sustained

Front 79

Cellular event in inflammatory

Back 79

most important feature
accumulation of leuk. at affected tissue

Front 80

what will Leukocyte do

Back 80

1. engulf, degrade things
2. release lysosomal
3. release chemical mediators
4.release toxic radicals

Front 81

migration of leukocyte is called

Back 81

exudation

Front 82

Sequence of events of cellular events

Back 82

1. margination
2. pavementing and rolling
3. adhesion and emigration
4. chemotaxis and activation

Front 83

margination:
(1st step in cellular event under inflammation)

Back 83

under viscous blood, WBSc are small and pushed to periphery

Front 84

pavement and rolling
(2nd step in cellular event under inflammation)

Back 84

adhesion molecules and leukocyte at endothelial cell surface
cell adhesion molecules CAMs are expressed by chemical mediation.

Front 85

CAM families

Back 85

cell-surface glycoprotein CAMs in response of chemotatic agents.
they are the selectin family
adhesion molecule L-selectin are on phagocytes' surface. and P-selectin those are leuk adhesion molecules and the number increases with cytokines.

Front 86

adhesion & emigration
(3rd step in cellular event under inflammation)

Back 86

adhesion: mediated by ICAM1 and VCAM both upregulated. integrins are only activated under chemotactic factors

after binding, leuocyte move between cell gaps called diapedesis

Front 87

PMNs are usually first to at the site of infection except?

Back 87

viral infections, lymphcoytes first

Front 88

Chemotaxis & activation
(last step in cellular event under inflammation)

Back 88

attracting cells toward infection site
chemokinesis: accelerated random locomotion cells
WBCs respond to this
PMN and monocyte most sensitive

Front 89

Chemotactic factors for PMN

Back 89

1. bacterial products
2. complement fractions (C5a)
3. arachidonic acid metabolites
4. cytokines (chemokines)

Front 90

how do WBC sense chemotatic factor

Back 90

some are cell surface receptors
once binding Ca2+ is involved and cause locomotion

Front 91

locomotion

Back 91

pseudopods have actin/myosin which is Ca2+ dependent

Front 92

Phagocytosis has 3 steps

Back 92

1. recognition and attachment
2. engulfment
3. killing/degradation

Front 93

1. recognition and attachment
(phagocytosis)

Back 93

two well known opsonins: IgG and C3b
IgG: Fc fragment receptor
C3b: opsonin receptor

Front 94

2. engulfment
(phagocytosis)

Back 94

complete enclosure by fusion with lysosomal granules in phagolysosome.
-leakage of H2O2 in to medium increasing tissue damage
requires!! Ca2+ and MG2_ to initiate microfilament and microtubules movement
note that: any intracellular movement involves Ca2+

Front 95

3. killing and/or degradation
(phagocytosis)
what are the two types

Back 95

a) oxygen dependent mechanism
b) oxygen independent bactercidal mechanism

Front 96

oxgeyn dependent mecahnism for killing

Back 96

oxidative burst using NADPH oxidase producing O2-. two ways of killing:
1) H2O2 myeloperoxidase halid system. producing HOCL which is highly antimicrobial
ii) MPO (myeloperoxidase) independent killing: requires O2
producing OH- free radical using H2O2+ O2-

Front 97

oxygen-independent bactericidal mechanisms

Back 97

H+ ion from increased lactate and carbonic anhydrase lower pH.

extracellular release of leukocyte products:
1. lysosomal enzyme
2.oxygen derived metabolites
3. products of arachidonic acid metabolism

Front 98

when monocyte turn into macrophage what does it lose

Back 98

MPO function

Front 99

Mediators of inflammation

Back 99

inc. neurogenic mechanisms and chemical mediators of inflammation

Front 100

chemical mediators include (2)

Back 100

1. cell derived vasoactive mediators
2. plasma derived vesoactive mediators

Front 101

cell derived vasoactive mediators includes 4

Back 101

1. arachidonic acid metabolites
2.platelet activating factors
3.amines: serotonin, histamine
4. endothelins

Front 102

plasma derived vasoactive mediators includes 2

Back 102

kinins and coagulation cascade

and

complement system

Front 103

arachidonic acid metabolites drived from?
two end products?
what do they do?

Back 103

derived from phospholipids of cell membrane
end products are Porstaglandins and Leukotrienes which
produce vasodilatation and increase permeability, and increase permeability and chemotactic

Front 104

PAP platelet activating factor
what is generated by
what does it do

Back 104

by all inflam. cells, endo cells
vasodilator, permeability, stimulate platelets, inflam cells, endo cells. produce aggregation of platelets.
chemotactic function

Front 105

vasoactive amines includes :2

function?

Back 105

histamine: found in grounules of mast cell/basophils/platelets

serotonin: only in platelets

effect: vesodilation, permeability

Front 106

endothelins

Back 106

peptide produced by endothelial cells, powerful vasoconstrictive effect.

Front 107

does chronic trigger relies on acute?

Back 107

no. low toxicity may incite a chronic

Front 108

clinical difference between acute /chronic

Back 108

duration of more than 2 weeks.

Front 109

in chronic what is different in terms of tissue

Back 109

chronic have more proliferation of cells and CT, less exudation.

Front 110

chronic can be caused by 3

Back 110

persistent infections
exposure to non degradable material
autoimmune reactions

Front 111

chronic inflam cells

Back 111

macrophage
lymphocyte
plasma cell
eosinophils

Front 112

chronic divided into two forms

Back 112

1: non-specific chronic inflam. : no pattern of tissue reaction, participating cells are mononuclear cells and CT cells
2. granulomatous inflammation is by a special tissue reaction, cells invovled are reticuloendothelial cells, largely macrophages (creating a wall off)

Front 113

special case of chrnoic?

Back 113

granulomatous inflammation
-presence of granulomas, are collection of epitheliloid macrophages and resemble epithelial cells (TB case)
-inner cells are giant cells.

Front 114

morphologic patterns in inflammation: serous

Back 114

mild injuries
albumin-containing exudate
secretion of serosal mesothelial cells

Front 115

morphologic patterns in inflammation: fibrinous

Back 115

more sever inflammation, deeply acidophilic
-have fibrin
-incrased permeability allow fibrinogen to escape

Front 116

morphologic patterns in inflammation: suppurative or purulent

Back 116

large amount of pus with neutrophils and liquified tissue debris and bacteria

Front 117

morphologic patterns in inflammation: sanguinous

Back 117

exudate with large number of RBS, serious damage to vessels, mixed form with other exudate.
often in TB
NEVER PURE that can have such as
fibrino-purulent
sero-sanguineous etc.

Front 118

location and special forms of inflammation or out come: abscess

Back 118

localized pus in tissue

Front 119

location and special forms of inflammation or out come: Paronychia

Back 119

infection extends around base of finger nail
hurts!!

Front 120

location and special forms of inflammation or out come: felon

Back 120

deep-seated infection at anterior portion of the distal phalanx of finger, cause osteomyelitis

Front 121

empyema

Back 121

localized pus in the pleural cavity

Front 122

location and special forms of inflammation or out come: Ulcer

Back 122

local defect or excavation of surface of an epithelium

Front 123

location and special forms of inflammation or out come: pseudomembranous inflammation

Back 123

a false membrane created by powerful necrotizing toxin. fibrin, necrotic epithelium and WBCs are on the mucosal surface.
happens in the intestine when ppl receive oral antibotics

Front 124

location and special forms of inflammation or out come: fistula

Back 124

abnormal communication betwen 2 hollow organs lined by endo. or epith.

Front 125

location and special forms of inflammation or out come: : sinus

Back 125

abnormal tract (communication) between solid organ to epithelium covered surface (skin)
eg.muscle with skin

Front 126

Bacteriemia

Back 126

micro-organism circulate in blood but no illness

Front 127

septicemia

Back 127

bacteriemia with illness

Front 128

toxemia

Back 128

illness due to bacterial toxin in blood rather than bacteria

Front 129

what can defect the leukocyte function 6

Back 129

1. number of circulating cells (less)
2. adherence (cant adhere)
3. chemotaxis: can not attract, the chediak0higashi syndrome the lazy leuokocyte
4 defect in phagocytosis
5. defect in microbicidal acvity
6. mixed defects

Front 130

what produce fever`

Back 130

Pyrogen
also prostaglandins
it increase metabolic rate and it is good.
high temp are lethal to denature bacteria proteins

Front 131

how is tissue restored to structural and functional integrity? 3 steps

Back 131

1. removal of exudate
2. removal of cellular and tissue debris
3. replacement of cell and tissue lost

Front 132

regeneration vs repair

Back 132

regeneration replace identical cells
repair replace cells either same kind or different/simpler type

Front 133

three groups base on regenerative capacity

Back 133

1. labile: throughout life
2. stable: lower normal level, reponse to stimuli
3. permanent: can not divide

Front 134

variation in the ability of diff. kinds of cells and tissues to regenerate. which regenerate the best?

Back 134

supporting tissues eg. c.t. fibrous, cartilage, BV, epithelium, epidermis, intestinal etc.

Front 135

Atypical regeneration of an organ

Back 135

restoration not only upon the parenchymatous tissue's ability to regenerate
(parenchymatous tissue means functional part of tissue)
restoration also depend on if the framework was destroyed.

Front 136

which organ in mammals regenerate best

Back 136

liver and lung
kidney and spleen are good too

Front 137

what are the mechanisms involved in generation andd repair (2)

Back 137

1. control of cell proliferation
2. collagenization of acquisition of wound strength

Front 138

Control of cell proliferation(1st step of generation/repair)

Back 138

-labile cells follow cell cycles and form mitosis
-stable cells stimulated to G1.
-stimulatory hormones and growth factors are released
hormones: estrogen progesterone somatotropin insulin
GF includes
PDGF
EGF
bFGF
VEGF
IL I IL II
TNF
nerve GF
macrophage derived GF

all GF are mitogenic

you have cell-interactions next
receptors interact and a group is called the integrins.

Front 139

if stable cells arrest at G2 before entering mitosis, what does it appears like

Back 139

polyploid cells (hypertrophy)

Front 140

integrins

Back 140

group of receptors includes
fibronectin R
platelet surfae R
Leuk. adhesion molecules

they recognize a specific AA sequence

Front 141

ECM includes

Back 141

collagen, glycosaminoglycans, proteoglycans, glycoproteins and fibronectins

Front 142

fibronectin are what and found where

Back 142

high molecular weight glycoprogeins can be found in
1. cell surface
2. basement membrane
3. pericellular matrix (ECM)

Front 143

fibronectin can be produced by

Back 143

fibroblast
endothelial cells
monocytes

Front 144

what do fibronectin do in wound healing (5)

Back 144

-facilitate migration of epithelium (glue)
-chemotactic for monocyte
-chemotatic for fibroblast
-stimulate endothelial migration and organization
-release bFGF from monocyte (make more)

Front 145

Collagenization and wound strength (2nd step in regeneration)

Back 145

involves proliferation of endothelial cells, fibroblast, and deposition of collagen in wounds.

Front 146

under severe damage, parenchymnal cells and framework are disrupted, how can healing be done? regeneration?
repair?

Back 146

can not use regeneration alone,
first forms granulation tissue

Front 147

granulation tissue features
made up of what

Back 147

pink soft granular and painless, resist to infection
made up of capi. fibroblast, inflammatory cells and ECM

later scar will form, cell will dimish cap will disappera and CT will laid down

Front 148

Steps involving process of repair (3)

Back 148

angiogenesis
fibrosis
maturation and organization of the scar

Front 149

Angiogenesis (repair 1)

Back 149

new vessle budding off from preexisting ones. they are immature and leaky.
edematous appearance (like a water blob)

Front 150

what are the chimical mediators for angiogenesis

Back 150

VEGF b-FGF
vascular endo GF
fibroblast GF

Front 151

Fibrosis (repair 2)

Back 151

proliferation of fibroblast
deposition of ECM
depends on GF

Front 152

maturation and organization of scar (repair 3)

Back 152

collagen and ECM degraded by metalloproteinases.
collagens 1234/fibronectin are also cleaved.
injured site is debrided and remodeled at CT

Front 153

what is metalloproteinases

Back 153

this thing degrades collagen and ECM, they cleave colagen 1 2 3 4 and fibronectin.
produced by inflam. cells and epi. cells.

they aid the debridement and remodeling of CT

Front 154

what can digest Collagen fibers (2)

Back 154

1. collagenase (by fB, macrop. PMN, epi cells)
2. metalloproteins

Front 155

components of BM

Back 155

type IV V, laminin, fibronectin, heparin sulfate proteoglycan

Front 156

what are the Extracellular CT components (4 categories)

Back 156

elastic fibers
laminin
glycosaminoglycan and proteoglycans
fibronectin

Front 157

elastic fibers are produced by?
what are the two components
how is the life time
what digest this

Back 157

fibroblast produces this
two components: elastin (amophours) and elastic microfibril (fiber like)
long half-life
elastase (bacteria, macrophage, PMN)

Front 158

where is laminin
what are they
what do they do

Back 158

(in ExtraC CT and BM)
they are large glycoproteins
they mediate attachment of epi. cells to IV collagen
attachment of epi. cell to BM

Front 159

what do glycosaminoglycan and proteoglycans in Extracellular CT do

Back 159

arrange orientation of Collagen Fib.

Front 160

fibronectin is what kind of molecule
associated with what
produced by what
what is it called in blood
what is the primary function

Back 160

is a large glycoprotein
associated with surface of the cell, BM and matrix
produced by fibroblast, monocyte and endothelial cells
in blood is called cryoglobulin
it interact cells and matrix

Front 161

how would wound strength compare to the original strength
why?

Back 161

never gain intitial strength
70=80% restored at 3 months

due to diff. type of collagen and organized not that well

Front 162

what type of collagen is found on
1. adult skin
2.granulation tissue
3.cicatrization (yu he)

Back 162

1
3
replacement of 3 to 1

Front 163

for skin wounds, what are the 3 steps.

Back 163

1) crust formation: quick provisional closure
2) removal of dead tissues, debris exudate
3)replacement of lost cells and tissue

Front 164

(skin wounds crust 1)what is closing up the wound forming a crust?

why do we need the crust?

what condition is required for forming a crust

Back 164

coagulated blood that dries and become the crust or scab

1. stop leaking 2. stop infection

1. blood 2. permit drying

Front 165

(remove dead tissue, skin wounds 2)
two ways of removing

Back 165

1. slough off at zone of demarcation
2. phagocytosed by lymphatics
-liquefaction first

Front 166

what is a zone of demarcation

Back 166

the zone that dead tissue slough off

Front 167

(Replacement of lost cells and tissues, skin wounds 3)
two major processes
what kind of cells under go these processes

Back 167

1. cell migration
2. cell division (proliferation)

fibroblast, endothelium, epithelium

Front 168

in skin wound, in order for epithelium to migrate in sheet it requires what

Back 168

a substratum made up off granulation tissue and fibronectin

Front 169

cicatrization what is.

Back 169

conversion of granulation tissue to scar by closing small vessels

Front 170

keloid

Back 170

the repaired skin that has no skin appendages, they are homogenous and haylinized made up of basophilic collagen fibers.
more fibroblast are found here.

Front 171

two types of repair and intension

Back 171

primary and secondary

primary refers to superficial wound
secondary repair is when a lot of tissue is loss and wound can not be approximated

Front 172

restitutio ad integrum
what does it mean

Back 172

means restore to original conditions in primaryr epair

Front 173

primary repair features

repair takes up what (repair or regen or both)

Back 173

only epidermis is gone, dermis is intact
NO BLEEDING
only regeneration of epithelium
small or no scar
in deeper cuts, surgury required

Front 174

in secondary repair, whats the feature

Back 174

loss of tissue, edge won't approximate

this requires granulation tissue forming a scar
can not regenerate only

Front 175

3 periods for secondary repair

Back 175

1. latent period (size of wsound no change)
2. period of contraction( shrinkage of granulation tissue, pulling edges)
3. epidermization (after contraction the process of epidermals)

20-25 cm or more requires skin grafting

Front 176

what are the factors (4) affect rage of healing

Back 176

age
size of wound
secondary infection
dietary statues (vitamin, protein intake)

Front 177

Dysplasia

Back 177

abnormal in size and organization called cellular pleomorphism
ncuelus shape and size are different too called nuclear pleomorphism

Front 178

cellular pleomorphism
nuclear pleomorphism

Back 178

size and shape are different in cells, and nucleus

Front 179

what kind of plasia is pre-malignant lesion??

Back 179

dysplasia

Front 180

what does it mean to be pre-malignant

Back 180

no invasions.

Front 181

Neoplasia/neoplasm

Back 181

new and abnormal growth of tumour

abnormal mass of tissue, growth exceed and uncoordinate with normal tissue and remains the same after cessation.

Front 182

cancer means what kind of plasia

Back 182

cancer is malignant Neoplasm, malignant means it is invasive and spreads
and metastasis means it is maligant

Front 183

benign tumour

Back 183

does not invade/spread

Front 184

Nomenclature
benign tumour
suffix of:
majority are named suffix of:

Back 184

-oma
tissue type-
eg: adenoma: B tumour form glands
eg: papilloma: B tumour form finger-like projections

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two exceptions for B tumours

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melanoma
lymphoma

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malignant tumours nomenclature
when they are involved with mesenchymal cells they are :
when they are involved with epithelial cells they are:

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-sarcoma
-carcinoma

eg: adenocarcinoma: M tumour that is an epithelial and found in glandular growth pattern
eg: squamous cell carcinoma: M epithelial tumour made of squamous cells
eg: Fibrosarcoma: M tumour made of fibrous tissue

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Mixed tumour

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can either be benign or malignant

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Teratoma

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2 or more germ layers arising from mesnchymal cells
can be mixed tumour

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Choristoma

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ectopic rest
normal tissue at wrong area
B tumour

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Hamartoma

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disorganized tissue in normal location
B tumour

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Cyst

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a fluid filled space

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differentialtion levels
B tumour is?
lack of differentiation is called

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well moderately poor
well
anaplasia

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anaplasia

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lack of differentiation
cellular/nuclear pleomorphism
hyperchromatic nuclei
increase mitosis
loss of polarity
tumour giant cell

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rate of growth with:
B tumour
M tumour
correlates with
inversely orrelates with

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slow
fast (except leiomyoma during pregnancy is slow)
blood supply (nutrients)
differentiation, poorly=faster

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central necrosis

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fast growing tumours dies cus grow 2 fast

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carcinoma in situ

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when carsinoma localize on basement membrane, situ=origin spot

this is a severe dysplasia

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Metastasis

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tumour implant discontinuous from primary tumour.
sign of malignancy!

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Metastasis can have 3 pathways

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1)seeding via body cavity
2)lymphatic spread
3)hematogenous spread

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seeding via body cavity
where most common

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peritoneal cavity
can be on pericardial pleural subarachnoid cavities

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lymphatic spread

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initial dissemination is common, follow natural draiange

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hematogenous spread favours which type of tumour

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sarcoma
liver and lung are frequent

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four phases of M tumour

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1. transformation (carcinogenesis)
2. growth of transformed cell
3. local invasion
4. distant metastases

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Transformed cell are usually how many
what is transformed

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1
no normal growth/differentiation
0no inhibitory signal
-resistant to apoptosis
-defect DNA repair
-unrestricted proliferation
-angiogenesis, invasion, metastasis

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time required for tumour double in volume depends on

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growth fraction: cell cycles/total cells
cell loss factor (if many restrictions are loss)
cell production over cell loss
similar cell cycle phase

tumour with high growth fractions can be chemotheraprized

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minimum size for detection tumour
how many cells
how many doublings
how many more doubling is lethal

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1 cm^3, 1gm

10^8-9

30

30 x 10

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Tumour angiogenesis
what does it do

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tumour secrete angiogenic factors and inflammatory cells (tries to kill tumour)
induce many growth factors
fBGF VEGF PDGF H1F1a

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Tumour progression and heterogeneity

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means tumour metastasis into subgroups varies in antigencity and others. and the stronger one survives

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how tumour invade and metastasis

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secrete proteolytic enzyme degrading ECM and bind to ECM by the interaction of numbers of adhesion molecules like laminin receptor and intergrins.

penetrate BV and lymphatic by same mechanism, move via binding to platelets and WBC and bind endothelium

extravaste ad metastaic site and grow

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local effect of tumour on host

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depends on location and infrigement (invasion)

@leiomyoma: bleeding (B tumour)
neoplasm in gut: obstuction (hard to move)
pituitary adenoma: growth destruction of the gland
GI tumour: bleed
ovarian: torsion

also: infraction, rupture, ulceration secondary infection

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Hormonal effects of tumour on host

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B cell adenoma in pancrease affects insulin and cause hypoglycemia, low sugar
adrenal cortex adnoma loses steroid and have 2ndary effect
carcinoid tumour: carcinoid syndrome

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cancer cachexia

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severe cancer
loss of fat/lean body mass with weakness, anorexia (doesnt wanna eat) anemia.

caused by :
reduce food intake
reduce synthesis/storage of fat

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paraneoplastic syndrome

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symptom complex cancer cause but cant explained. due to local or distant spread of cancer. or different hormones

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we categorize cancer in two main parts

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grading and staging

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grading:

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estimate aggressiveness of neoplasm base on differentiation level.

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stagin: clinical importance

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base on tumour size, lymph noe spread and metastasis of other oragans
clinical staging: base on evidence acquired prior to the decision as to odefinitive treatment
pathological stagin: include info obtained at surgery and from examination of tissue by patholgist

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systems of staging (2)

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TNM by union
Tumour nodes metastases
american joint commitee divid stages O to IV similar to TNM