FINAL EXAM – SEMESTER NOTES COMBINED
Week1
Cellular adaptation, injury, and death
diabetes 1 prob in beta cell
type 2 cells resist insullin
measles in cells
any disease trace down to cells - depends on the activity of cell
cell - all have 8 function
3 types of tissues specialize and don’t divide - neurologic or spinal cord; cardiac muscle tissue
when infart part dies and that’s it; 3 is skeletal muscles can’t regenerate.
- Apoptosis Vs necrosis
-normal cells live in equilibrium. Blood sugar 70-110, potassium 3.5 -5, sodium 136-145,
bicarbonate 22-26. cells are at ease but when these change you live in a disease state
● Glucose: 70–110 mg/dL.
● Specific gravity: 1.010–1.030.
● BUN: 7–22m g/dL.
● Serum creatinine: 0.6–1.35 mg/dL (< 2 in older adults)
● LDH: 100–190 U/L.
● CPK: 21–232 U/L.
● Uric acid: 3.5–7.5 mg/dL.
● Triglyceride: 40–50 mg/dL.
● Glucose: 70–110 mg/dL.
● Specific gravity: 1.010–1.030.
● BUN: 7–22m g/dL.
● Serum creatinine: 0.6–1.35 mg/dL (< 2 in older adults)
● LDH: 100–190 U/L.
● CPK: 21–232 U/L.
● Uric acid: 3.5–7.5 mg/dL.
● Triglyceride: 40–50 mg/dL.
● Activated partial thromboplastin time — 25-35 s. ...
● Ferritin, serum — 15-200 ng/mL (15-200 mg/L) ...
● Albumin, serum – 3.5-5.5 g/dL (35-55 g/L) ...
● Troponins, serum. ...
● Albumin–creatinine ratio – less than 30 mg/g. ...
● Gastrin, serum — 0-180 pg/mL (0-180 ng/L) ...
● Forced expiratory volume in 1 second (FEV1) — greater than.
stress - any alteration in what is expected is stress or injury. cell tries to adapt
-using 5 mechanisms: atrophy, hypertrophy, hyperplasia, dysplasia, and/ or metaplasia
atrophy, - is reversible - 6 weeks arm in a cast and muscles atrophy -this is disuse atrophy;
hormonal atrophy when the endometrium is deprived of the support of estrogen and you will get
dystonia which is painful sex due to atrophy. With cast removal, muscles can come back. shrink
1
,is a term used if you loose water. if proteins or lipids or cellular matter it is called atrophyr.
Shrinkage is not adaptation and is loss of water; inadequate nutrition all cells lose cellular stuff.
hypertrophy, - actual water gained it swells, but increase in cellular mater is hypertrophy;
pregnancy is physiological. All gets bigger - also hyperplasia- smooth muscle can also increase
in number. pregnancy is a stress. uterus is more stress and effort so gets bigger and multiple;
muscular exercise. skeletal muscle cells get bigger. going to gym doesn’t increase cellnumber
because cell muscles don’t increase in number only in size
hyperplasia, - injured cells can increase in number BPH - benign prostate hyperplasia is an
example; hypertension causes a 24 7 left ventricle workout so it gets big and hypertrophies
under the pathological stress. increases in size but not number. increase in size encroaches on
the cavity so the amount of blood pumped out is reduced. not enough cardiac output eventually
and then heart failure. With kidneys when one doesn’t work the other compensates and gets
bigger.
metaplasia- meta = different, plasia means shape. cells exposed to stress sometimes change their
shape and is reversible unless too injured. a normal cell can be replaced with immature differnt
normal cell type; example callous walking barefoot this is dysphagia. prostate cells increase in
number fro elderly mean that's BPH. Uterus bleeding or growth that is bleeding hormonal but
not cycle; lungs ciliated columnar epithelium - burn glucose to make ATP to clean using cilia.
exposed to smoking injures cells . when smoking coverts to stratified squamous cells without
cilia and can’t clear airway. so cough up to clean air passages and this is metaplasia which is
not reversible
dysplasia, - the irreversible version of metaplasia- bad shape and considered by most bad
premalignant growth. classic is cervical under HPV infection. adapt by dysplasia. acquire
different shape size arrangement. This is why annual pap smears are needed. check how bad the
dysplasia is. low grade is not bad. high grade is bad. low grade keep an eye on th patient. high
grade remove because it’s on the verge of malignacy
inschemia leads to hypoxia. hypoxia is hte most common type of cell injury. Blood
carries oxygen to tissue. stopping blood to tissues leads to lack of oxygen and then cell/tissue is
hypoxic and is injuried.
chemical/drugs injure cell, ultraviolent injury from sun, virus or bacteria injury. genetic
injury, nutrition deficiency vit B12, folate. most common injury hypoxia
adapation ends in 1 of two ways. adaptation wills and person recovers. adaptation fails and then
the organism dies.
- Role of Na + and Ca ++ in hypoxic cell injury
- Aerobic Vs anaerobic metabolism: effects in cell injury
- Adaptation (Metaplasia)--once cell is injured will resist and adpat to stressor -may develop
signs and symptoms of disease have disease and are sick but are alive. either causiative agent is
mild and you get rid of it or treatment will help this. or injury so severe and persistent and cells
fail. Then whole tissue fails, organ fails, the system fails, and the organism dies
- Dysplasia
injury - hit- capillaries bust and oxygenated blood extrovasates andnext morning turns to
blue/bruise and when healing yellow due to bilirubin. manifestation of cell injury is an acculmate
stuff inside. mot common thing to accumulate in injured cell is water and usually accumulates
wih hypoxia. cell stored in water vaculoe in cell. tacy-sac disease the brain of young babies
2
,accumulate lipids and can’t metabolize in the brain. manefests by age of 2 and lipids accumulate
and will stop walking and talking and breathing and put on ventilator and then die.
first stage of alcohol disease is alcoholic fatty liver. its the way liver shows injury but showing up
shinny in ultrasound and shows injury by collecting lipids. pigments from in disease;
atherosclerosis calcium. gout arthritis accumulate urate in the synovial membrane;
shows up by : fever, pain, leukocytosis, increased enzyme levels
Cancer
molecular mechanism of injury - ie cardia infaction. hypoxia from ischemia deprives tissue of
oxygen. coronary arteries (L.A.D.) blocked with cholesterol from that part above will not see
blood supply. lower down less tissue affected. cells need oxygen to metabolize glucose, burn
glucose to get ATP. it’s metabolism it’s cellular respiration. 1 glucose gives you 32 to 36
AA].T.P.s. from aerobic metabolism. if blood supply cut must do anaerobic. glycolysis can only
provide 2 A.T.P.s. the other bad thing is this produces lacticacid. lactic acid denatures, damaging
cells. causes extreme deficiency of energy The sodium-potassium pump sodium is normal. For
every 3 sodium pumped in 2 potassium moves out. 135-145 mEq. K is 3.5-5. sodium is always
outside the cell. the pump keeps K in and sodium out. The pump is protein. if surrounded by
lactic acid the proteins of the pump are denatured. more sodium gets in and water follows so the
cell swells full of water vaculoes. all the cell stuff sweats mitochondria, endoplasmic reticulum.
Cell membrane still in tack so you’re still ok. once cell membrane breaks up and loses integrity
and stretches and breaks and now it’s the point of no return. The killer gets in and it’s calcium.
Calcium is not allowed into the cells and is strictly regulated and not allowed in big
amounts. Calcium is a catalyst for all chemical reactions. increases all enzymatic activities
in the cell. All proteases - digest proteins. When calcium goes in all the proteases activate
and digests all proteins inside the cells -proteins, lipids, lipoproteins will all be metabolized.
necrosis. cell eats itself up. We measure troponin and ckb if see in great amount in cell
escaped form cardiac cells and no longer intracellular and know there are heart problems.
When you see alt and ast shows injury and death of liver. These are signs of cell death and
cell losing integrity.
Reperfusion injury - the troponin level initially shoots up due to reperfusion injury immediately
following the infarct. wait too long for reperfusion and open the coronary and provide
mitochondria they have been waiting too long for oxygen so instead of producing A.T. P
produces oxygen free radicals and then gets much worse with reperfusion injury. Don't delay
perfusion as fast as possible.
Apoptosis - is normal, preprogrammed sying for death and doing a good service for the whole
body. in utero early weeks web between fingers, but about 20 or so weeks these cells go through
apoptosis. blood cells go to spleen after 120 days and it’s organized and iron is recycled. no fever
normal physiologic same with regen of skin cells. cells shrink. in necrosis cell swells but in this
cell shrinks. Nucleus condenses and fragments into nucleochromatin bodies and forms fragments
that are membrane-bound. in apoptosis neve lose cell membrane it’s always there and not messy
and not associated with elevated enzyme levels in the blood. in necrosis the cell membrane loses
it’s integrity chaotic and unprogrammed and messy. Necrosis with cell function and function of
tissue and organs. apoptosis serves a function.
in Cancer - natural killer cells are lymphocytes and keep checking on your cells. cells have ID
natural killer cells convince cells through enzyme release to die to protect the tissue. apoptosis is
3
, selective. necrosis is not selective. Like atherosclerosis. all cells affected will die. necrosis starts
by swelling. apoptosis not messy membrane intact no increased enzymes in blood.
Types of necrosis:
when tissues die kidney, adrenal glands, and heart look yellowish and firm and swollen.
liquified necrosis Liquified in brain in CNS and whenever any necrosis dead part is invaded by
bacteria.
Caseous necrosis - lungs look cheesy white and is seen in TB can be in intestines too.
fat necrosis - pancreatic cells look fatty and when calcium and magnesium get together you get
soap. also seen in trauma to breast
gangrene - is massive necrosis mass death of a part of a body, millions of cells die
dry - seen in excessive smokers when arteries in burger disease get peripheral arterial disease an
tips of toes affected most and toes will get darker and get black and shrink because dying. you
have a clear mark of demarcation. it’s bad but wet is worse. messes up the venous drainage of the
lower limb and venous return is obstructed seen in diabetics and kidney failure patients.
accumulates fluid and bacteria affect tissue and smells foul and associated with systemic and
causes liquefaction necrosis a
Body has a repair mechanism and if these don’t work they convince the cell to go through
apoptosis. Also social control genes meaning it’s too crowded and tell cells not to divide
anymore adherence so notices when too close to the next cell and stops dividing
*malignant cells have 3 criteria. 1-normal cells can’t divide unless instructed too but malignant
cells do what they want.2- immortality. normal body cells divide 10 to 50 times and stops or dies
to be replaced. cancer cells can keep going millions of times. 3. anaplasia - don’t resemble their
mother the tissue from which they came. can be highly anoplastic, or poorly differentiated and
it’s bad but not as bad as highly differentiated.
tumor markers - certain chemicals in the blood become elevated. hepatoma can detect alpha-feta
protein; PSA (is questionable) no longer considered a marker for prostate. not a tool of diagnosis
and screen for this either. markers warrant further investigation. So tumor markers only help with
follow up. If decreases after treatment indicate treatment is doing fine. prognostic factors.
Japanese ladies low incidence of breast cancer but in US almost the same as us. Same for
Japanese men and prostate. but they have the highest incidence of stomach cancer
- cancer? environment and genetics
Protein growth factor- instructions given to cell for cell proliferation. protein is coded for my
genes and genes can get mutations. mess up with gene and mess up code you get defective
protein.
signal transduction pathway 100s and 1,000s of proteins that reach inside the cell. anyone
incorrect can lead to abnormal cell proliferation. if abnormal receptor gave growth order if is
abnormal mutation and lead to abnormal cell proliferation.
Normal cell proliferation - cycle. Cell gets order, and through to completion it takes about 25
minutes. G zero is cell resting page. check proliferation during division 3 times. very precise
What’s CIS?
3 good genes when coded as normal (this is essence though 100 times more complicated)
1) Proto-oncogene mutation - any protein that initiates and accelerates cell division. These
are good. When you have a wound, the proto-oncogenes make sure you have adequate
repair. Help to heal wounds. at 3 checkpoints stops.
4
Week1
Cellular adaptation, injury, and death
diabetes 1 prob in beta cell
type 2 cells resist insullin
measles in cells
any disease trace down to cells - depends on the activity of cell
cell - all have 8 function
3 types of tissues specialize and don’t divide - neurologic or spinal cord; cardiac muscle tissue
when infart part dies and that’s it; 3 is skeletal muscles can’t regenerate.
- Apoptosis Vs necrosis
-normal cells live in equilibrium. Blood sugar 70-110, potassium 3.5 -5, sodium 136-145,
bicarbonate 22-26. cells are at ease but when these change you live in a disease state
● Glucose: 70–110 mg/dL.
● Specific gravity: 1.010–1.030.
● BUN: 7–22m g/dL.
● Serum creatinine: 0.6–1.35 mg/dL (< 2 in older adults)
● LDH: 100–190 U/L.
● CPK: 21–232 U/L.
● Uric acid: 3.5–7.5 mg/dL.
● Triglyceride: 40–50 mg/dL.
● Glucose: 70–110 mg/dL.
● Specific gravity: 1.010–1.030.
● BUN: 7–22m g/dL.
● Serum creatinine: 0.6–1.35 mg/dL (< 2 in older adults)
● LDH: 100–190 U/L.
● CPK: 21–232 U/L.
● Uric acid: 3.5–7.5 mg/dL.
● Triglyceride: 40–50 mg/dL.
● Activated partial thromboplastin time — 25-35 s. ...
● Ferritin, serum — 15-200 ng/mL (15-200 mg/L) ...
● Albumin, serum – 3.5-5.5 g/dL (35-55 g/L) ...
● Troponins, serum. ...
● Albumin–creatinine ratio – less than 30 mg/g. ...
● Gastrin, serum — 0-180 pg/mL (0-180 ng/L) ...
● Forced expiratory volume in 1 second (FEV1) — greater than.
stress - any alteration in what is expected is stress or injury. cell tries to adapt
-using 5 mechanisms: atrophy, hypertrophy, hyperplasia, dysplasia, and/ or metaplasia
atrophy, - is reversible - 6 weeks arm in a cast and muscles atrophy -this is disuse atrophy;
hormonal atrophy when the endometrium is deprived of the support of estrogen and you will get
dystonia which is painful sex due to atrophy. With cast removal, muscles can come back. shrink
1
,is a term used if you loose water. if proteins or lipids or cellular matter it is called atrophyr.
Shrinkage is not adaptation and is loss of water; inadequate nutrition all cells lose cellular stuff.
hypertrophy, - actual water gained it swells, but increase in cellular mater is hypertrophy;
pregnancy is physiological. All gets bigger - also hyperplasia- smooth muscle can also increase
in number. pregnancy is a stress. uterus is more stress and effort so gets bigger and multiple;
muscular exercise. skeletal muscle cells get bigger. going to gym doesn’t increase cellnumber
because cell muscles don’t increase in number only in size
hyperplasia, - injured cells can increase in number BPH - benign prostate hyperplasia is an
example; hypertension causes a 24 7 left ventricle workout so it gets big and hypertrophies
under the pathological stress. increases in size but not number. increase in size encroaches on
the cavity so the amount of blood pumped out is reduced. not enough cardiac output eventually
and then heart failure. With kidneys when one doesn’t work the other compensates and gets
bigger.
metaplasia- meta = different, plasia means shape. cells exposed to stress sometimes change their
shape and is reversible unless too injured. a normal cell can be replaced with immature differnt
normal cell type; example callous walking barefoot this is dysphagia. prostate cells increase in
number fro elderly mean that's BPH. Uterus bleeding or growth that is bleeding hormonal but
not cycle; lungs ciliated columnar epithelium - burn glucose to make ATP to clean using cilia.
exposed to smoking injures cells . when smoking coverts to stratified squamous cells without
cilia and can’t clear airway. so cough up to clean air passages and this is metaplasia which is
not reversible
dysplasia, - the irreversible version of metaplasia- bad shape and considered by most bad
premalignant growth. classic is cervical under HPV infection. adapt by dysplasia. acquire
different shape size arrangement. This is why annual pap smears are needed. check how bad the
dysplasia is. low grade is not bad. high grade is bad. low grade keep an eye on th patient. high
grade remove because it’s on the verge of malignacy
inschemia leads to hypoxia. hypoxia is hte most common type of cell injury. Blood
carries oxygen to tissue. stopping blood to tissues leads to lack of oxygen and then cell/tissue is
hypoxic and is injuried.
chemical/drugs injure cell, ultraviolent injury from sun, virus or bacteria injury. genetic
injury, nutrition deficiency vit B12, folate. most common injury hypoxia
adapation ends in 1 of two ways. adaptation wills and person recovers. adaptation fails and then
the organism dies.
- Role of Na + and Ca ++ in hypoxic cell injury
- Aerobic Vs anaerobic metabolism: effects in cell injury
- Adaptation (Metaplasia)--once cell is injured will resist and adpat to stressor -may develop
signs and symptoms of disease have disease and are sick but are alive. either causiative agent is
mild and you get rid of it or treatment will help this. or injury so severe and persistent and cells
fail. Then whole tissue fails, organ fails, the system fails, and the organism dies
- Dysplasia
injury - hit- capillaries bust and oxygenated blood extrovasates andnext morning turns to
blue/bruise and when healing yellow due to bilirubin. manifestation of cell injury is an acculmate
stuff inside. mot common thing to accumulate in injured cell is water and usually accumulates
wih hypoxia. cell stored in water vaculoe in cell. tacy-sac disease the brain of young babies
2
,accumulate lipids and can’t metabolize in the brain. manefests by age of 2 and lipids accumulate
and will stop walking and talking and breathing and put on ventilator and then die.
first stage of alcohol disease is alcoholic fatty liver. its the way liver shows injury but showing up
shinny in ultrasound and shows injury by collecting lipids. pigments from in disease;
atherosclerosis calcium. gout arthritis accumulate urate in the synovial membrane;
shows up by : fever, pain, leukocytosis, increased enzyme levels
Cancer
molecular mechanism of injury - ie cardia infaction. hypoxia from ischemia deprives tissue of
oxygen. coronary arteries (L.A.D.) blocked with cholesterol from that part above will not see
blood supply. lower down less tissue affected. cells need oxygen to metabolize glucose, burn
glucose to get ATP. it’s metabolism it’s cellular respiration. 1 glucose gives you 32 to 36
AA].T.P.s. from aerobic metabolism. if blood supply cut must do anaerobic. glycolysis can only
provide 2 A.T.P.s. the other bad thing is this produces lacticacid. lactic acid denatures, damaging
cells. causes extreme deficiency of energy The sodium-potassium pump sodium is normal. For
every 3 sodium pumped in 2 potassium moves out. 135-145 mEq. K is 3.5-5. sodium is always
outside the cell. the pump keeps K in and sodium out. The pump is protein. if surrounded by
lactic acid the proteins of the pump are denatured. more sodium gets in and water follows so the
cell swells full of water vaculoes. all the cell stuff sweats mitochondria, endoplasmic reticulum.
Cell membrane still in tack so you’re still ok. once cell membrane breaks up and loses integrity
and stretches and breaks and now it’s the point of no return. The killer gets in and it’s calcium.
Calcium is not allowed into the cells and is strictly regulated and not allowed in big
amounts. Calcium is a catalyst for all chemical reactions. increases all enzymatic activities
in the cell. All proteases - digest proteins. When calcium goes in all the proteases activate
and digests all proteins inside the cells -proteins, lipids, lipoproteins will all be metabolized.
necrosis. cell eats itself up. We measure troponin and ckb if see in great amount in cell
escaped form cardiac cells and no longer intracellular and know there are heart problems.
When you see alt and ast shows injury and death of liver. These are signs of cell death and
cell losing integrity.
Reperfusion injury - the troponin level initially shoots up due to reperfusion injury immediately
following the infarct. wait too long for reperfusion and open the coronary and provide
mitochondria they have been waiting too long for oxygen so instead of producing A.T. P
produces oxygen free radicals and then gets much worse with reperfusion injury. Don't delay
perfusion as fast as possible.
Apoptosis - is normal, preprogrammed sying for death and doing a good service for the whole
body. in utero early weeks web between fingers, but about 20 or so weeks these cells go through
apoptosis. blood cells go to spleen after 120 days and it’s organized and iron is recycled. no fever
normal physiologic same with regen of skin cells. cells shrink. in necrosis cell swells but in this
cell shrinks. Nucleus condenses and fragments into nucleochromatin bodies and forms fragments
that are membrane-bound. in apoptosis neve lose cell membrane it’s always there and not messy
and not associated with elevated enzyme levels in the blood. in necrosis the cell membrane loses
it’s integrity chaotic and unprogrammed and messy. Necrosis with cell function and function of
tissue and organs. apoptosis serves a function.
in Cancer - natural killer cells are lymphocytes and keep checking on your cells. cells have ID
natural killer cells convince cells through enzyme release to die to protect the tissue. apoptosis is
3
, selective. necrosis is not selective. Like atherosclerosis. all cells affected will die. necrosis starts
by swelling. apoptosis not messy membrane intact no increased enzymes in blood.
Types of necrosis:
when tissues die kidney, adrenal glands, and heart look yellowish and firm and swollen.
liquified necrosis Liquified in brain in CNS and whenever any necrosis dead part is invaded by
bacteria.
Caseous necrosis - lungs look cheesy white and is seen in TB can be in intestines too.
fat necrosis - pancreatic cells look fatty and when calcium and magnesium get together you get
soap. also seen in trauma to breast
gangrene - is massive necrosis mass death of a part of a body, millions of cells die
dry - seen in excessive smokers when arteries in burger disease get peripheral arterial disease an
tips of toes affected most and toes will get darker and get black and shrink because dying. you
have a clear mark of demarcation. it’s bad but wet is worse. messes up the venous drainage of the
lower limb and venous return is obstructed seen in diabetics and kidney failure patients.
accumulates fluid and bacteria affect tissue and smells foul and associated with systemic and
causes liquefaction necrosis a
Body has a repair mechanism and if these don’t work they convince the cell to go through
apoptosis. Also social control genes meaning it’s too crowded and tell cells not to divide
anymore adherence so notices when too close to the next cell and stops dividing
*malignant cells have 3 criteria. 1-normal cells can’t divide unless instructed too but malignant
cells do what they want.2- immortality. normal body cells divide 10 to 50 times and stops or dies
to be replaced. cancer cells can keep going millions of times. 3. anaplasia - don’t resemble their
mother the tissue from which they came. can be highly anoplastic, or poorly differentiated and
it’s bad but not as bad as highly differentiated.
tumor markers - certain chemicals in the blood become elevated. hepatoma can detect alpha-feta
protein; PSA (is questionable) no longer considered a marker for prostate. not a tool of diagnosis
and screen for this either. markers warrant further investigation. So tumor markers only help with
follow up. If decreases after treatment indicate treatment is doing fine. prognostic factors.
Japanese ladies low incidence of breast cancer but in US almost the same as us. Same for
Japanese men and prostate. but they have the highest incidence of stomach cancer
- cancer? environment and genetics
Protein growth factor- instructions given to cell for cell proliferation. protein is coded for my
genes and genes can get mutations. mess up with gene and mess up code you get defective
protein.
signal transduction pathway 100s and 1,000s of proteins that reach inside the cell. anyone
incorrect can lead to abnormal cell proliferation. if abnormal receptor gave growth order if is
abnormal mutation and lead to abnormal cell proliferation.
Normal cell proliferation - cycle. Cell gets order, and through to completion it takes about 25
minutes. G zero is cell resting page. check proliferation during division 3 times. very precise
What’s CIS?
3 good genes when coded as normal (this is essence though 100 times more complicated)
1) Proto-oncogene mutation - any protein that initiates and accelerates cell division. These
are good. When you have a wound, the proto-oncogenes make sure you have adequate
repair. Help to heal wounds. at 3 checkpoints stops.
4
