Path 2, 4: Cell Injury I And Ii

Front 1

define labile cells

Back 1

cells that are continuosly dividing (hematopoietic ,surface epithelia)

Front 2

definte stable cells

Back 2

aka quiescent, minimally replicative, proliferate in responses to injury (parenchyma of solid organs, endothelial cells, fibroblasts, smooth muscle cells)

Front 3

define permanent tissues

Back 3

non-proliferative (neurons, cardiac muscle cells)

Front 4

define hypertrophy. In which type of cells does it take place?

Back 4

increase in the size of cells  by increaseing the amount of proteins and organelles. Occurs in cells that have limited or no capacity to divide

Front 5

Given an example of physiologic hypertorphy

Back 5

an increase in functional demand or homonal stimulation leads to an increase in cell/ organ size-weight lifting=bigger muscle

Front 6

Give an example of pathologic hypertrophy

Back 6

cardiac muscle hypertrophy in response to hypertension

Front 7

Define hyperplasia. In which type of cells does it occur?

Back 7

increase in cell number, occurs in cells capable of division (labile and stable)

Front 8

Give an example of physiologic hyperplasia

Back 8

hormonal hyperplasia of female breast at puberty/ pregnancy, compensatory hyperplasia of liver after partial resection

Front 9

Give an example of pathologic hyperplasia

Back 9

excessive stimulation by growth factors or homones, imbalance=endometrial hyperplasia, release of GF's due to HPV=squamous hyperplasia

Front 10

define atrophy

Back 10

decrease in cells size and function due to loss of cells substance, decrease in protein synthesis and increase degradation, there is a loss of fxn but no cell death

Front 11

give an example of physiologic atrophy

Back 11

loss of hormonal stimulation -endometrium @ menopause

Front 12

give some examples of pathologic atrophy

Back 12

broken arm=decreased functional deamand, loss of innervation, inadequate nutrition

Front 13

define metaplasia

Back 13

one adult cell type is replaced by another adult cell type. adaptive response to chronic stress/ injury

Front 14

Give an example of epithelial and mesenchymal metaplasia

Back 14

epithelial-in smoker lung ciliated=> squamous,in barrett esophagous squamous=> glandular;  mesenchymal-bone formation in soft tissue

Front 15

what are the two key features of irreversible cell death

Back 15

1. inability to reverse mitochondrial dysfunction (lack of ox phos and ATP generation) 2. disturbance of membrane fxn

(explain death at M&M)

Front 16

Compare necrosis, apoptosis, and reversible injury in terms of: cell size

Back 16

necrosis-enlarged,
apoptosis-reduced,
reversible- enlarged (hydropic or vacuolar)

Front 17

Compare necrosis, apoptosis, and reversible injury in terms of: nucleus

Back 17

necrosis-pyknosis, karyorrhexis, karyoLYSIS;
apoptosis-fragmentation into nucelosome size fragments; reversible-clumping of chromatin

Front 18

Compare necrosis, apoptosis, and reversible injury in terms of: plasma membrane

Back 18

necrosis-disrupted;
apoptosis-intact but altered structure;
reversible-swollen but intact

Front 19

Compare necrosis, apoptosis, and reversible injury in terms of: cellular contents

Back 19

necrosis-enzymatic digestion, may leak; apoptosis-intact but released in apoptotic bodies, eosinophilia, blebs; reversible-vacuoles distend ER, lipid vacuoles in cytoplasm

Front 20

Compare necrosis, apoptosis, and reversible injury in terms of: adjacent inflammation

Back 20

necrosis-frequent; apoptosis-no; reversible-maybe

Front 21

Compare necrosis, apoptosis, and reversible injury in terms of: phys vs. path role

Back 21

necrosis-always path; apoptosis-often phys, can be path; reversible-path

Front 22

What is the difference between hypoxia and ischemia? Which is "worse"?

Back 22

Hypoxia=inadequate oxygenation of the blood, ischemia=lack of blood. Ischemia is worse because not only does the tissue lack oxygen, it also lacks nutrients required to continue anaerobic metabolism

Front 23

Cellular swelling and fatty change are characteristics of the morphology of reversible cell injury. WHat causes these features?

Back 23

Cellular swelling resutls from failure of membrane pumps to maintain homeostasis, vacuoles appera in the cells corresponding to a distended ER. Fatty change refers to lipid vacuoles in the cytoplasm of cells dependent on fat metabolism, occurs a result of toxic/ hypoxic injury

Front 24

Describe the morphological features of necrosis

Back 24

increased eosinophillia (result of increased binding of eosin to denatured cytoplasmic protiens and loss of basophilia that is normallly imparted by RNA in the cytoplasm), nuclear shrinkage and fragmentation, breakdown of plasma and organelle membranes

Front 25

What is the cause of coagulative necrosis

Back 25

hypoxic or anoxic injury due to ischemia in solid organs (except brain)

Front 26

Describe the morphology of coagulative necrosis

Back 26

persistence of dead cells with intact outlines but with loss of cellular details (ghosts), injury denatures proteins and enyzymes but no proteolysis takes place, contrast to liqeufactive and caseous necrossis where there is a loss of tissue architecture

Front 27

What is the cause of liquefactive necrosis

Back 27

bacterial or fungal infection, infarct in the brain

Front 28

Describe the features of liquefactive necrosis

Back 28

release of digestive enzymes from WBCs leads to complete digestion of the cells, acute inflammation and pus (note that in the brain, acute inflammation is usually not present the tissue is soft and soupy but there is no pus)

Front 29

What is the cause of caseous necrosis

Back 29

tuberculous infection

Front 30

describe the features of caseous necrosis

Back 30

resemebles cheese, fragmented and coagulated cells with loss of tissue architecture (no cell outlines), usually surronded by a boarder of inflammatory cells forming a granuloma

Front 31

Describe gangrenous necrosis

Back 31

a specific type of ischemic coagulative necrosis of the extremity. can be dry or wet (bacterial infection), also used for severe necrosis of other organs

Front 32

What is the cause of fat necrosis? Where does it occur?

Back 32

Typically seen in the pancrease in acute pancreatitis when injury to the pancreases releases lipases which liquefies fat and splits TGs The FA's combine with Ca to form chalky white substance. Can also occur as a result of trauma to fatty itssue (breast)

Front 33

What is the cause of fibrinoid necrosis

Back 33

deposition of immmune complexes (antigens+ antibody) in the vascular wall. Occurs in vasculitis syndromes

Front 34

Describe the features of fibrinoid necrosis

Back 34

"fibrin-like", bright pink amorphous appearance in vascular wall

Front 35

Where does fibrinoid necrosis occur?

Back 35

vascular wall as a result of deposition of immune complexes

Front 36

What is lipofusin? Where is it found?

Back 36

indigestible material resulting from lipid peroidation, a "wear and tear" pigment th eoccurs predominately with aging found esp. in heart, liver, brain

Front 37

Describe anthracosis in the lung

Back 37

carbon particles inhaled and phagocytosed by alveolar macrophages, transported to region lymph nodes

Front 38

Hypertrophy of the smooth ER in the liver can be a result of..

Back 38

adpative response to increased demand for toxin removal i.e. alcohol, barbiturates

Front 39

"parking lot inclusions" are a sign of damage to which organelle

Back 39

mitochonria. changes include atrophy (starvation), enlargement (toxin, alcohol), myopathy (respiratory chain enzyme abnormality)

Front 40

Give two examples of change that can occur to the cytoskeleton as a result of cell injury

Back 40

1. accumulations-toxins like alcohol-Mallory hyaline liver, Alzheimer's and  NF tangles
2. abnormal organization-Kartagener Syndrome-immotile cilia = sterility and lung infections

Front 41

List 4 specific targets of cellular injury

Back 41

1. mitochondria 2. calclium homeostasis 3. cellular membrane 4. DNA & cellular protiens

Front 42

What are the major causes of ATP depletion in a damaged mitochondria

Back 42

decreased oxygen, decresed nutrients, specific toxins

Front 43

Describe the effects of incrased intracellular calcium that occurs with cell injury

Back 43

too high of intracellular Ca activates cell enzyems which leads to breakdown of phospholipids, disruption of the membrane and cytoskeletal proteins, and nuclear damage. Additionally, the high Ca increases mitochondrial permeabiliyt which decreases the avaiability of ATP.

Front 44

Explain how cell damage can lead to accumulation of ROS and oxidative damage

Back 44

Cell injury leads to production of ROS in the mitochondria which can cause lipid peroxidation= membrane damage, protein modifications= breakdown and misfolding, and DNA damage= mutations

Front 45

Describe the mechanism of reperfusion injury

Back 45

restoration of blood flow to ischemic tissue may increase injury because the new oxygen allows for generation of free radicals. Additionally the arriving leukocytes, plasma proteins, and complement can lead to inflammation and the proudction of ahdesion molecuels and cytokines that  attract more inflammatory cells that increase the extend of the injury

Front 46

What is the difference between a direct toxin and a toxic metabolite

Back 46

direct toxin-bind to cellular organelle or molecular component, no modification is necessary for toxic effect; toxic metabolite-non toxic substance is "activated", often by P450 in the liver

Front 47

List three key morphologic features of apoptosis

Back 47

1. eosinophilic cytoplasm 2. cell shrinkage 3. condensed nucelus

Front 48

What are the two ways in which apoptosis can be initiated. What is the common end pathway

Back 48

1. intrinsic pathway-cell injury leads to activation of the Bax proteins which increase the perm. of the mitocondria and allow cyt C to enter the cytoplasm.

2. extrinsic pathway-death receptor is engaged (Fas, TNF),

common feature is the activation of capases

Front 49

How do dystrophic and metastatic calcification differ in terms of tissues invovled?

Back 49

distrophic-non-viable, damaged or dying tissues. metastatic-normal tissues

Front 50

How does the serum calcium level differ in dystrophic vs. metastatic calcification

Back 50

dystrophic-normal serum calcium

metastatic- hypercalcemia (high PTH, destruction of bone, D intox, renal failure)

(Hint: Metastatic "forces" Ca into normal tissue so need excess Ca)

Front 51

Describe the morphology of dystrophic calcification

Back 51

gross=white, gritty deposites, microscopically=basophilic

Front 52

Describe the changes that occur with aging that lead to decreased cellular replication and defective protein homeostasis

Back 52

progressive shortening of telomers and lack of telomerase=progressive replicative senescence

Front 53

This is an example of endometrial hyperplasia, not ehte increased number of cells and the convolution of the glands

Back 53

-

Front 54

This is skeletal muscle atrophy with compensatory hypertrophy

Back 54

-

Front 55

An example of metaplasia of the endocervix, note the transition from normal columnar epithelial to squamous

Back 55

-

Front 56

A kidney tubule showing blebs, swelling and eosinophilia of vacular cahnge, transitioning to necrosis. Note the absence of nuclei

Back 56

=

Front 57

What type of necrosis is shown on the right

Back 57

coagulative
Note the persistence of dead cells with intact outlines but loss of cellular details

Front 58

What type of necrosis is this

Back 58

coagulative

Front 59

What type of necrosis is this

Back 59

liquefactive

Front 60

What type of necrosis

Back 60

caseous

Front 61

What type of necrosis

Back 61

coagulative

Front 62

What type of necrosis

Back 62

fibrinoid

Front 63

Lipofuscin pigments in cardiac muscle, indeigestible material resuing from lipid peroxidation, a "wear and tear" pigment, occurs predominatly with aging particualry in heart, liver, brain

Back 63

-

Front 64

dystrophic calcification within an atherosclerotic plaque
(occurs in damged tissues but normal serum calcium levels) Dystrophic=Damaged

Back 64

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