Tissue Response to Injury

Question 1

“scorched earth strategy”

Answer 1

body responds by heaps of WBC can lead to lesions
trigger tissue destruction

Question 2

what is this process called: “body responds by heaps of WBC can lead to lesions
trigger tissue destruction” ?
Demonstrate understanding of the relationship between injury and homeostasis

Answer 2

Question 3

important principle?
Claud. B & Virchow theory?

Answer 3

any injury= can dirve cell away from homeostasis, response is mostly good
- C.B coined homeostasis
Virchow= any alteration of homestasis= disease

Question 4

define homeostasis

Answer 4

Answer 5

stress to cell = changes:
good: efficient, adequate adapt, healthy cells return
bad: failure to adapt= cell injury= die
- cells die= complex healing, cells replaced by other cells (see lecture 4 wound healing, fibrosis)
- goal is homeostasis

Question 6

death of living tissues is called?
- first organ to die after pt dies?
- organ that lives long?

Answer 6

necrosis

notes:
- first organ to die is pancreas bc strong enzyme in pancreatic cell
- cells long live: hair follicles

Question 7

Identify the many types of cellular injuries, using example

Answer 7

• heat, radiation, trauma, chemical, infection, immunological,, nutriton, ageing,

Question 8

types of changes you can see in cell

Answer 8

hypertrophy= big size, hypo, atrophy (smaller size, sometimes by autophagy which is when cell eats itself), hyperplasia (more cell numbers), mtaplasia (mod. of aspect of cell) dysplasia, anaplasia (cancer)

Question 9

Electron mag shows what

Answer 9

bad: acc. of water (hydropic degeneration?), pale mitochondria, lots of tiny vacoules, blebs on plasma membrane, can reverse.

Question 10

Answer 10

blbs beginning. changes in nuclei.
C) def. irreversivle, cells dies, loss of nuclei structure, cell fragmented

Question 11

Answer 11

liver
right: white bubbles are areas fat was stored and accumulated (can happen in heart and other tissues)

this is an e.g. of excess fat accumulation

Question 12

Answer 12

see further: chronic obstructive pulm. disease: heart pump more, to push blood with more force, so size increase in contrast when cell dies (acute myocardial infarction= white not red tissue due to fibroblast and pus)

Question 13

acinar hypertrophy vs serous atrophy

Answer 13

non inflamm non neoplastic pathology= enlarged acinar cells

acinar hypertrophy: only cells responsible for secreting hypertrophy
VS
serous atrophy= infection in glands

Question 14

apoptosis vs autophagy

Answer 14

autophagy: cell eat itself. abn. activation of lysosomes. can be protective mechanism when severe nutrient deprivation (cells eat yourself :O)

Question 15

normal conditions in heterophagy

Answer 15

eating something diff from cell itself

e.g. monocyte engulfing bacteria then fusion btw vacoul and lysosome= become phagolysosome, structure destroyed, debris removed in exocytosis (kicked out of cell)

autophagy: so existing structure of cell progressively destroyed, residue, heavily stained

Question 16

Answer 16

overworked muscle

Answer 17

happens in plasma cells, when they make too much Ig molecules, there are heaps of pink hyaline structures

Question 18

Answer 18

Question 19

Answer 19

proliferation of cells

Question 20

Answer 20

aspect of cell changed

e.g.columnar cell progresses to squamous, no microvilli and several layered. still reversible and can be protectivetective

Question 21

dysplasia

Answer 21

alt. of size or organisation of cell. reversible. mostly resolves on its own.

Question 22

Answer 22

em progressively eroded. some cells can migrate. cancer transformation complete. migration of cells -> metastatic lesion

Question 23

anaplasia

Answer 23

Question 24

summarise using image

Answer 24

Question 25

Metaplasia is replacement of

Answer 25

= replacement NOT gradual

Question 26

2 ways to die

Answer 26

necrosis + apoptosis, irreversible

Question 27

gen types of necorsis

Answer 27

irreversible - coagulant: thrombus - pyknosis: fat nucleus (density) - liquefactive: pus e.g when tissue becomes liquid. - caseous N: chronic inflammation lecture. specific to TB

Question 28

caseous necrosis is diagnosis of what?

Answer 28

TB

Question 29

fat necrosis is numerous in where?

Answer 29

pancreas

Question 30

Apoptosiss vs necrosis main diff

Answer 30

necrosis= inflammatory surrounding apoptosis= NO

Question 31

apoptosis pathological process?

Answer 31

Question 32

what is involution of breast medaited by

Answer 32

apoptosis

Question 33

growth of fingers are created by

Answer 33

triggering of apoptosis

Question 34

Answer 34

explosion of cancer cell

Question 35

Answer 35

Question 36

Answer 36

cxhanges in cell, leading to progressive destruction, triggering inflammatory cells (neutrophils are first cells. blebs progressively leave cell

Question 37

Differentiate between different types of cell death, using examples

Answer 37

cells get larger in apoptosis

Question 38

Answer 38

loss of structures, plama membrane destroyed, integrity bad so leaky, nmucleus condense progrssively shrinking

Question 39

Answer 39

necrosis of pulp= see nucleus structure and most of limit of cells GONE.

Question 40

Multiple pathways towards morphology of injury

Answer 40

Question 41

SUMMARY cellular morphological responses to injury

Answer 41

Question 42

Identify morphological changes associated with cellular injury

Answer 42

Question 43

Lists the multiple pathways to the morphology of cellular injury

Answer 43

Question 44

Describe processes which affect the macroscopic changes in organs

Answer 44