Causes
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All the changes in the tissues boil down to cell injury
 Cells make up tissues --organs - --body
 Whatever happens to cell
 Cell sick, organ sick, body sick
Causes of diseases
 In all of them, cells injured
 Most common -- biologic causes (microbiology, parasitology)
 Bacteria, fungus, parasites other microbes
 How microbes produce disease
 Toxins, enzymes, some live inside cells
(HIV) and destroys the cell
 Infectious diseases
 Chemical causes
 Toxins, poisons, drugs, meds you take (don't use right
doses)
 Chemicals - poisons act on the cells;
 Composition of the cell
 Membrane, cytoplasm, nucleus
 In between - organelles
(mitochondria, endoplasmic
reticulum (smooth, rough),
lysosomes, golgi apparatus
 Cytoskeleton - filaments,
microtubules - all organelles
 Not seen under microscope
- use electron microscope to
see it
 If affected by chemicals, membrane first (bilipid
bilayer)
 Biochemistry - protects it very well
 Poison attacks membrane first
 Carbs, proteins, sulfhydryl groups -- can
be oxidized (one of the main injurious
agents with NAD)
 Produce toxic lipid radicals and free
radicals
 Free radicals to cells - want to prevent or
cut down free radicals
 Atom at the center of the
molecule; orbits where electrons
(paired) found
 Take away one electron
 Chemical with only 1
electron
 Outer shell/orbit
 Still connected with
molecule
 Unstable, very
reactived
 If it goes inside the cell, it will
injure it specifically the nucleus
and other components

In nucleus, free radical only
has 1 electron -- need to
balance it; plenty of
electrons in the nucleus --hence reaction

How do you block the free
radical damage??
o
Biologic, chemical, free radicals are reactive chemicals derived from
oxygen
 Also derived from halogens, Cl, carbon tetraflouride, liver
 Nitrogen based also
o
Physical
 Environmental biology
 Trauma - Most common
 Physical force applied to tissue
 Traumatize cells they wil be injured
 Pointed, blunt instrument used
 In surgery discussed
 Changes in temperature
 Go high, tissue gets burned
 Low, freezes
 If cell freezes, form icicles inside the cell
(withdraw water); if you thaw that cell, won't go
back to original composition; soggy mess
(watery)
 Pull down tissue---vasoconstriction ---deprive
tissue of blood
 Frost bites --amputate --tissue dies
 Electrical energy passing thru tissues
 Man holding bulb and livewire; bulb opens up;lets go
and bulb closes
 Nothing happens to him
 Current runs thru body (smith
electricity) ; electrical conduction system
 Higher voltage interferes with
voltage in heart
 Electricians --suffer
electricution --men in posts;
find arrhtymia; interfered
with electrico system of
heart
 Electrolytes in body
 In physics, run current in electro solution
 It ionizes
 Positive ions separate; go to negative pole; vice
versa
 People electricuted get burned because where that
current passes out of body, tissues offer resistance,
generating heat --where burns found
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Depends on the voltage

Radiation
 Why harmful? Depends on dosage
 Have people who are being treated with radiotherapy for
tumors
 Cervical cancer; implant radio needles at
cancerous sites of cervix
 Destructive; control the dose
 Why? Radiation can induce injury to the chromosomes
to a degree; sometimes not anymore; to live, mutant
cells develop
 It zeroes in the nucleus (DNA); breaks in DNA, injuries
of DNA
 Cell dies; if it lives and abnormal ---mutant cells
produced

Changes in atmospheric pressure
 Deep sea diver
 Laborors underwater (cables under sea, posts of
bridges)
 Work in pressurized caving (add oxygen inside)
 When divers brought up to surface very fast
 Acclimatiza yourself from high pressure --if very
fast, like opening bottle of cold beer very fast it;
you dissolved CO2; so it fizzes out; fluid has
certain solubility for gases (like blood); dissolve
O2, CO2, nitrogen, sometimes ozone
 But when done fast, you have to adjust body to
pressure; if too sudden, high pressure to normal
too fast --gases will bublle; however O2 and CO2
have good solubility; dissolve back (N2 doesn’t)
 Pt put in special decompression chamber due to
n2 not reverting back
 In blood, if it goes to brain ---has air in his brain;
so brain not receiving O2 ---column of air --in
areas where loose (knees, elbows), air goes out
into the interstitium; could barely bend elbows
due to rigidity --result of sudden change in
atmospheric pressure (air embolism)
 Detached thrombus --99%; sometimes air
Immune System
 Supposed to defend body. How? Produce antibodies; generate
cytokines; thru cytokines --you involve macrophage system;
talk about now as cause of injury
 How can you injure the tissues?
 Acts against you - AIDS
 How else? Inflammation is innate
 4 types of hypersensitivity
 Type 1 - IgE mediated - allergies, anaphylaxis (2nd
time)


Reaction of IgE with mast cells which release
subs that make disease
2nd type hypersensitivity -- Cytotoxic
 Red cells - how destroyed?
 You injure cells by
 You should first have antigen with specific
antibody (IgM or IgG)
 That combination will reacti with
complement; compliment will undergo a
cascade which is destructive (C3b macrophages will eat up the cell)
 When you have an antigen; produce specific
antibody; that antibody has a heavy and light
chain; bounded by disulfide bridges
 FAD portion --binds with antigen
 FC portion- binds to compliment ©
 There are cells with receptors for c; NK
 Now you bind compliment there which cascades;
like the clotting system; if you have stock of
canned goods like Christmas tree, if you remove
one of those cans from below, it won't fall down
at once, but it cascades - have to start from
bottom before you reach the top
 Same with compliment (C9 all in all)
 C3a and C3b

a (anaphylactoid) --induces vasodilatation

b (opsonizing) --opsonine is Greek
meaning sauce; fried chicken with ketchup
(very good); bacteria and produce sauce,
it covers the bacteria so that it can be
recognized by the phagocytes; need
better recognitition for phagocytosis to be
effective
 Therefore, it will lend for better
recognition
 Cascades more, to C5a and C5b - now correlated
with inflammation
 C5 - chemotactic
 Chemotaxis - movement of white
cells towards attractant (bacteria);
already opsonized; so you hasten
the white cells moving towards the
injurious agent
 Neutrophils - 1st line of
defense
 But, when they go to injurious area
and start phagocytosing those
bacteria, they release enzymes
(inflammation); reason why the
more neutros you have, the more
enzyme being leaked out

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Lung abscess; Example of
inflammation with many
neutrophils
 Most prominent cell
seen
 At center of abscess,
too many abscess;
it's digested by them
 No intact
parenchymal
cell anymore
Cascade keeps going on
 5b, 6,7,8,9 forming big
complex
 Role of C5-C9 - memorize
this; membrane attack (C59 membrane attack)
 Acts like enzyme
destroying
membranes
If red cell, C5-9 destroys it
Red cell
 Antibody, antigen, compliment, C5 b
neutrophils
 C5b-9; membrane attack; see how
immune system destroys the cells; not
only red cells, but other cells like in the
skin;destroy cells of the skin (Type II
hypersensitivity aka Cytotoxic;
mechanism --complement cascade
Can destroy thyroid
 Antithyroid antibodies  Cytotoxic hypersensitivity that will
destroy thyroid
Type III
 You have an immune complex (antigen-antibody) <--related to cell
 What if immune complex is floating around in blood?
 It gets deposited; normally in immune complex
hypersensitivt (III), not normal
 Removing bacteria, antigen --antibody against
antigen
 Immune complexes attach to each other
forming lattice becoming heavier going
down and macrophages don't have to run
around looking for complexes; see
complex, engulf and remove it (normal
process)
 But in hypersensitivity (antigen excess), immune
complexes are small, soluble --don't form
lattices; go into circulation get filtered or
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Type
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deposited in walls of blood reaction (inflammation
therefore) attract white cells to area (immune
inflammation)
If immune complexes go to kidney (glomerulus),
they're stuck in capillaries; they diffuse; now in
capillaries ---immune complex is deposited in
wall of capillaries
III --going to bind complement
Young couple just married; went on honeymoon;
mother in law went with them (killjoy);
complement is mother in law (always there with
couple) because compliment will cascade ,
c3a,b,c5a,b,--C5b--9 (membrane attack)
If it deposits in walls of capillaries in kidney
(capillary functin --fillters (selective filtration)
 Now deposit in wall; mother in law is
cascading to C5-9; will attack membrane
in capillary (basement membrane)
 Complaint in pt - it will bleed if bm
destroyed (capillary will bleed -- very thin
wall)
 Red cells come out; pt has blood in
urine (urine red)
 Resulting in destruction of
glomerular capillaries
 Mechanism - type iii hypersensitivity
 Antigen antibody, complement,
complement c5-9 destroys
membrane; why? Complex acts
like an enzyme (lipid; double
layer); proteins going to be
destroyed by enzyme

Aka acute proliferative --when you destroy, you
release growth factors, fibrin, stimulate
proliferation of cells
 Type II -cytotoxic (mother in law stil
there); only antigen attached to cell
 Type II - immune complex in circulation or
deposited on the basement membrane or
blood vessel wall; chemotaxis, membrane
attack

Don't forget immune diseases
Type IV
 Cell-mediated (T lymphocyte)
 Only hypersensitive mediated by T
 1-3 need antibodies (B)
 T lymphocytes produce
 T4 produces cytokines when activated
 Interleukins
 Cytotoxic T cells
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Cyto means cell; toxic to cells
Mediated by T8; how does T8 destroys it by
releasing enzymes (granzyme perforin);
remember immune chapter very well
Enzymes will destroy the wall and then they
insert perforin
 So that cell undergoes apoptosis
(individual cell death)
Type I
 iGE mediated which will attach to mast cell which will
degranulate; from there you have lots of chemicals
going out; histamine, serotonin,
 Then you have inflammation; attracting inflamm
cells to area;
 Effect on smooth muscles
 Spasm - why some pts; if bronchial smooth
muscles (bronchial asthma, wheezing, dyspnea)
 Primary/secondary mediators
 Know the immune mechanisms
Nutrition
 How does it make cell injury
 Deficiency
 Iron deficiency, you have anemia
 Cells are pale (hypochromic)
 Microcytic; small
 Red cells not only pale but also small
 Protein deficiency -- Kwaskiorkor
 Total caloric deficiency (besides protein) - Marasmus
 Seen in starvation
 In vitamins, minerals
 Excess
 Excess cholesterol in diet -- atherosclerosis (excess
cholesterol in blood it will develop in wall of arteries
especially coronaries and cerebros)
 By simple life adjustment (diet), can bring down
incidence of coronary heart disease,
atherosclerosis
 Atherosclerosis
 Cholesterol deposits underneath intima, pushing
up intima, resulting in gradual narrowing of
lumen in that vessel --block (atherosclerotic
block)
 As it narrows, it will diminish the blood supply
 Those cells can't undergo normal metabolic
activity unless have good O2 and nutrient
delivery
 Excess Uric acid in dieet
 Hyperurecemia - going to deposit in soft tissue as
urate deposits (foreign substance); goes inside
foreign body reactin - chronic granulomatous
type of infection; tophus - form nodules near the
joints (soft tissue nodules); tophi (plural)
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Genetic causes of disease
 Excess
 Excess number of chromosome (21)
 Down's syndrome; same characteristics with
anyone in this world with this syndrome
 Trisomy 21
 Mental retardation; some people who look like
they have Down's have normal mentality
 You have 3 chromosome 21; if you remove one
part and transfer it to another, you'll have 3 also
(Translocation Down's)
 3 in chromosome 40 for example
 Mossaic Down's
 2 population of cells
 One normal
 One trisic -ch
 Normal population may give you a good mental
development; why some people look normal
mentally
 Reason why there are nations that don't approve
birth if mother is diagnosed with baby with
Down's --enough reason for having baby aborted
 Classical Down's of elderly woman above 50; incidence
of having baby with syndrome higher
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Tophi around the joints
Uric acid in excess; cut down on uric acid rich
foods
 If diet not stop, have to give meds to
lower uric acid
Obesity
 One of the minor factor in atherosclerosis
(diabetes mellitus)
Diminished number
 Inborn errors of metabolism
 Lack single gene that codes for enzyme; whole
metabolic process goes wrong
 Pt born without gene coding for tyrosinase; in the
production melanin (tyrosinase is key enzyme)
 Without tyrosinase, can't convert tyrosine to
melanin; so baby born not being able to produce
melanin (albino); happens in animals too; white
tigers, white alligators
 Melanin - protection against harmful rays of the
sun; why people in tropics are darker; they need
it; if you see albino in sunlight, heat stroke in 10
minutes
Deprivation of Oxygen
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Remember biochem; you need that oxygen to continue with
cycles producing energy
 ATP,
If diminish amt of o2 to tissue, impair metabolic activity
When you suddenly stop bringing blood to tissuel; no more
blood, no more ATP; cell will die; not at once though
 You shift to anaerobic glycolysis (use glycogen instead of
oxygen)
 Glycogen deposited; if excess glucose (deposited
as glycogen); used for energy; no oxygen so you
use enzymes
 Phosphofructokinase
 Set up anerobic glycolysis and continue to have
ATP until
 Let's say you have blackout -; generator
on --lights on again until the gas runs out
- dark out again
 You occlude the blood supply (thrombus,
embollus); produce ATP (generator from
glycogen, enzymes) until you run out of
glycogen; can't use anything anymore for ATP;
this is the time ATP goes down ---metabolic
activity will stop; you need energy for the cell


Therefore when you gradually diminish O2, plaque
growin and narrowing lumen, diminishing O2 ---hypoxia;
but when you have a thrombus/embolus occluding
vessle, no more O2 goes in; cant set up alternative
detour ---tissue doesn't receive anymore; won't remove
waste products ---cell dies after anearobic glycolysis
 Ischemia  If block main cerebral artery, area supplied will
only live 3-5 minutes because the nerve cell
needs lots of energy; but no oxygen, no glucose,
waste material accumulating;
 Why you see pt in cardiac arrest (drowns);
immediatelh perform CPR --need to get oxygen
to brain; keep heart pumping; someone faints
(hyposic encepalopathy); raise foot so blood goes
down to the head
 In cold temperature -10-15 minutes okay
 At low temp, basal metabolic activity of
cell goes down
 Normal temperature
 Pt breathes, heart pumps, but take EKG
on brain cells (maybe brain dead already);
can't tolerate lack of oxygen
Heart
 Main coronary artery occluded
 How long will heart muscle live?
 20-40 minutes
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How long muscle tolerates lack of oxygen
So won't die immediately if occluded; anerobic
glycolysis goes on
When someone has cardiac arrest, stimulate heart with
pads to pump again
Cause of ischemia is a blood clot, they can try to lyse
the clot by giving enzymes (fibrinolytic enzymes);
destroy clot and resume back blood supply
When you diminish blood supply, cell membrane (double
layer) becomes permeable in ischemia
Cell Setup
 Na outside
 K inside
 Little Ca inside
 In mitochondria and endoplasmic reticulum
 Lots Ca outside
 Cell membrane won't allow it to interchange
 If Na comes into cell, Na pumps cell in
 Water goes in, you pump it out (Na too) to
maintain osmotic balance)
 Ischemia - inc permeability of membrane
 Going to affect sodium pump; if cannot pump out Na; it
will accumulate inside ---you'll imbalance osmotic
pressure;becomes higher concentration inside then out;
water goes from lower concentration to higher
concentration (so cell will swell and cellular swelling is
the first reversible injury you may see under
microscope)
 Reversible because if you can give back (if blood
clot, thrombus, ischemia), but thrombus lysed
due to fibrinolytic system that may lyse the clot;
when lysed; blood comes in again; supply oxygen,
nutrients, produce ATP, renew pump, water goes
out until you have osmotic balance ---cell back to
normal; why swelling reversible;
 Everything will swell; of lysosomes, mitochondria,
e.r., blisters on cell wall/membrane; but can
reverse it by having o2 given to cell; oxidative
phosphorylation in mitochondria (powerhouse of
cell)
 If ischemia, inc permeability of cell membrane; if cannot
reverse it, then calcium (10,000 more outside of cell)
will now come in (Calcium Influx)
 Calcium influx - mitochondria is affected
(poisoned it)
 Activate enzymes which will digest;
increase digestion of what? Protease
activated; substrate is root of word;
digestion of proteins
 When you digest protein (you denature
it); have fresh egg, boil it, after 10
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o
minutes; remove shell; hard; protein
coagulated (denatured by heat)
So when you digest protein, you denature
it
Phospholipase is activated
 Enzyme that acts on phospholipid
(membrane of cell)
Atpases - enzyme that will destroy ATP
 Already lacking in atp
Endonucleases activated (in nucleus)
 It will destroy the cell
 If nucleus digested, it will shrink,
becoming assymetric, dark staining
(Cariopyknosis); further digestion
will fragment it; (Cariorexis); total
digestion (blue staining; lose
basophilism; no nucleus )
(Cariolyses - cell is dead)
So when cells die, they'll have a gross and microscopic appearance
 Morphology
 So the sum of all morphologic changes in cells that die in living
tissues is called necrosis
 In anatomy, tissues shown (called necrosis?)
 No - because there is no more living tissue; so if you
have the heart with coronaries there; you block one of
them; according to anatomy, blood supply of heart are
end-arteries; they'll end; no other blood supply; so area
supplied will become ischemic (no blood); first anerobic
glycolysis; -- no more glycogen, ATP --cell dies
 Ischemia; cell membrane permeable --calcium influx --digestion - so all cells die around that artery;
surrounding area still there; but that area immediately
under that area is necrosis
 What type of necrosis
 Protease, digestion of protein, denaturation of
proetein (coagulates)
 Therefore coagulation necrosis
 Patient will have a heart attack due to MI --that area of
coagulation necrosis is called an infarct
 MI -- myocardial infarction --how? Blood vessel
got clogged and area that was supplied died
 Going back to repair, what type of tissue is
myocardial (permanent) --don't regenerate; only
go into the cycle once; so they grow, going out of
cycle, cannnot stimulate them to come back
 In liver, you can give them growth factors, go
back to cell cycle and grow again
 But brain, heart
 If brain dies, repaired by scar tissue
 If doesn't die, dead part of heart repaired
by scar tissue, the neighbors will do work
of heart; the surrounding portions will

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compensate and take over functions of
heart
If you have 45% of l ventricle infarcted, patient
goes into cardiogenic shock - pump failure (45%
of that heart (ventricle) is not functioning
anymore; it's dead; bringing pt into cardiogenic
shock - heart failure
Kidney - End organs
 Occluded, coagulation necrosis
Intestines
 If one part occluded, whole intestine will be
necrotic
Brain - middle cerebral occluded; where you have motor
area (Sylvian Fissure); infarcted --- pt goes into stroke
 Pt had cerebral infarction
 It won't coagulate but liquify so these infarcs will
undergo coagulation necrosis except the brain
 Brain very soft; if undergoes necrosis, it
rots ---softer--converted into viscous
liquifying material
 If patient doesn't die, a cavity will result in the
brain
Abscess - plenty of neutrophils, enzymes (digest)
 If have abscess and many enzymes, the area
that was originally firm and solid becomes
liquified
 In abscess, from hard it becomes softer
 See whter part; get scalpel, puss comes
out ---viscous, liquid
 Liquifactio necrosis by enzymes (Heterolysis)

Going back to ischemia
 Common in diabetics; in uncontrolled diabetes, one of
the main pathologies is microangiopathy (narrowing of
blood vessels); in the lower extremities (sometimes
hand) narrows ---hypoxia ---eventually ischemia -thrombus formation ----so infarct in foot/toes
 It also gets infected by bacteria (anerobic
bacteria lives in ischemic area) --staph coccus
won't like it; clostridium will (anaerobes)
 Infection of these ischemic areas by
bacteria
 Gas produced; smells badly
 This person has gangrene (gangrenous necrosis)
 Have no choice but to amputate; dead --toxins
being formed there
 Need ischemia plus infection

Last type of necrosis - fat necrosis
 Related to disease of the pancreas
 Inflammation

Acute hemmorhagic pancreatitis
 Pancreas function -- double gland
 Exocrine - produces amylase, lipase,
chemotrypsin
 Carbs, fats, lipids
 Sent thru pancreatic ducts ----into
intestines
 In acute hemo pancrea---bleeds -necrosis --enzymes leak out of
pancreas; not going to intestines
but around pancreas
 Lipase - will digest fat ---end
product is fatty acid (absorbed,
brought to liver, metabolized there,
esterification)
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
Peripancreatic tissue
 It will digest the fat inside
the fat cells producing fatty
acids ---which is in tissue -not brought to liver; will
react with calcium --saponified fat --remains
inside the cell; won't be
absorbed/dissolved
 Morphology --see shadow
outlines of fat cells
containing saponified fat
 Grossly, fatty tissue is
yellowish, greasy
 Saponified --whitish,
opaque, chalky (crumbly)
 Severe abdominal
pain; some surgeons
may suspect it's
acute abdomen
(ruptured appendix,
peptic ulcer ---they
open up) and
omentum,
mesentary seen with
chalky areas ---acute
pancreatitis
In tuberculosis, another type of necrois
 Not solid, liquid but in between
 Like soft cheese --soft, whitish, friable (hold it
and it crumbles --easily breaks and cheesy in
appearance); the white cheese -- caceous/c
 Aka Cassiation necrosis
 Pt with 2ndry tuberculosis in apex of lung
 Chronic granulomatous type of
inflammation enclosing central area which


looks granular (no intact cells; everything
destroyed/digested); but surrounded by
chro gran type of inflammatin ---memorize components of TB
 Plasma, epithelial,giant cells
 At center --necrotic area -cassiation necrosis
Seen in Xray of the lung
 Fibrocassious density; pt complains of
Apex of right lung'
 Operation; no more cassiation; it
healed
In these conditions, tissues destroyed, cells disappear
 What if the pt can adjust to the injury?
 Hypoxia or plaque gets bigger and bigger; lumen
get smaller
 Less O2 to tissue
 In kidney,
 If oxygen gets smaller,
 Less amount can be enough for small
tissue
 Small amt for big tissue --tissue may die
 So it becomes smaller ----Atrophy
 Cells not yet dead but adapted to
lesser amount of food; of oxygen;
once small it has undergone
atrophy
 Atrophy'
 Part of cell destroyed,
digested
 If cell digests its own self,
autophatic vacuole there autophagolysis
 Heterolysis ???
 So if you give additional nutrients, cell
gets bigger again to certain extent
 If you continue to diminish cell, it will die
 Why kidney undergoing ishcemia will
undergo atrophy
 You have a fractured leg put in plaster cast
 Uses cast;
 When fracture healed, cast removed
 Muscle of that leg will become smaller
(underwent atrophy)
 Not used, no need for nutrients,
components
 Not yet dead, therapy -massage,
exercise --eventually leg goes back
to normal; no stimulus for it to use

Polio myolitis
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Marasmus
 You see a child skin and bones
 Muscles have atrophied -not fed, no nutrients
 Give balance diet, exercise --muscles grow back

Menopausal woman
 Uterus becomes smaller
 Mammary gland atrophies
 She doesn't menstruate anymore
 Lack of hormones for which cells
dependent --bring about atrophy
Senile atrophy
 Grandparents 90 and above
 Not as tall as they are; big as they were
 Atrophy of brain, liver, heart
 Atrophy destroys membranes; after digestion membranes thrown out; if membranes stay -peroxidation ---formation of pigment (lipofuxin
pigment); found in atrophic cells
 Look at heart ---colored brown, not only small
 Brown atrophy of the heart --lipofuxin
pigment in heart muscles
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o
Virus affects motor nerve cell in ant horn of
spinal cord
Connection of impulsee from brain to muscles
passing thru horn
If you destroy motor nerve cell, impulse not sent
down to gastrocnemeus won't move anymore
 No more extension of impulse; not
conducted because motor nerve cell dies ---leg gets smaller; no more work for it to
do
Neurogenic atrophy
Hypertrophy
 Adaptive Change in inc workload
 Physiologic
 Exercise in gym -- weight lifting
 Inc seq of exercises;
 Muscles getting bigger
 Having hypertrophy; increase SIZE of cells
(not number)
 Exerting inc workload --need more
myofibers, mitochondria, more ATP --need
bigger cell
 Stop exercising, no more stimulus --goes back to
normal
 With hormonal stimulation
 Muscles of uterus during pregnancy --get bigger
 In uterus also increase in number (HYPERPLASIA)
 And hypertrophy can take place at same time Uterus

Bad when it results in impairment of function or disease
 Hypertensive pt - inc bp; heart pumps harder (inc work
load on l ventricle); rigid arteries, inc peripheral
resistance
 From normal 1.3-1.5 cm
 Now heart muscle (l ventricle) -- 2.5-3 cm)
 Seen in ECG
 Report --l ventricular hypertrophy


If you get report with big heart already, monitor
pt or sooner or later pt goes into heart failure
 Can't hypertrophy continuously -- or inc supply of
demand --need more O2/nutrients but blood
supply of heart remains the same
 Sooner or later --great demand of muscles
--can no longer supply
 If can't contain stongly, contract weakly --heart failure; can't push blood to
systemic circulation
 When muscles hypertrophy, they undergo genetic
alteration; the genes that control protein
synthesis revert back to embryonic function
(when you were fetus, you produced fetile
proteins); so fetile proteins produced which
aren't efficient in function of muscles; why
discrepancy in blood supply, genetic alteration
 Histology of heart
 Each muscle has their own capillaried
 When heart gets bgi, capillaries are compressed;
muscles are very large ----pt goes into heart
failure; treat hypertension so they won't have
increased workload ---newer meds for
hypertension --proved you can revert a big heart
---you'll prevent heart failure
Hypertrophy because they don't undergo mitosis
 If cell undergoes mitosis and inc stimulation, they will
divide ---inc number of cells ----hyperplasia

If you inc size and number, the organ gets bigger --muscles,
uterus all get bigger
 Hyperplasia

Neoplasia - or tumor
 Also increase in number;also grow
 Neo or hyper?
 Neoplasia doesn't stop growing
 No purpose
 Malignant -- cells may vary already (change)
 Benign - grow same cells; inc amt
 Hyper--remove stimulus --stops growing
 Adaptive change
 Grow same cells --inc in number only
Hyperplasia



Physiologic
 Pregnancy - inc in size of mammary gland
 Grow more cells; needed for more milk
 After breastfeeding, baby no longer
feeding, cells fall off, mammary gland
back to normal
 Pathologic - increase hormonal stimulation
of tissues
 Endometrial hyperplasia - very
thick endometrium; the woman
complains of long menstrual period
 Instead of 3-4 days, already 2
weeks --still flowing profusely
 Thick endometrium --prolonged
bleeding --abnormal
 Atypical complex hyperplasia
 If woman with enough children, dr
removes uterus
 If no children yet, dr. scrapes it clean
 Carries high risk of developing
endometrial cancer
 Considered precancerous
Metaplasia - change from one normal tissue to another normal
tissue in case of injurious environment and the new tissue is
resistant to the injury
 Heavy cigarette smoking
 1 pack a day
 100 chemicals in cigarette smoke
 If bronchial tree bombarded, it will adapt -change lining of bronchial tree --pseudo strat
columnar ciliated changed to stratified squamous
 After a while, you lose the cilia (protects you)
 Escalator goes up --continuously
 Smoker -no more cilia
 Very high correlation btw heavy cigarette
smoking and lung cancer
 Metaplasia --precancerous; higher
incidence of cancer
 Esophagus
 Lower part --lined by stratified squamous non
keratinizing
 If sphincter not closing very tight (little bit open)
during processl
 Gastric juice goes up (reflux)
 Lining of esophagus not protected
 Lining changes (not destroyed) to
intestinal lining (Barret's esophagus); not
squamous but columnar secretory
metaplasia -- change so lining not
destroyed by the acid --acidity very
severy (pH 4); not squamous, but
secretory

If tissues can adapt they won't be destroyed

Endocrine - prod of insulin