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patho exam1

cancer, stress, fe, a/b, hematology

TermDefinition
sodium normal level 135-145
hyponatremia level <135
hypovolemic hyponatremia causes renal (adrenal insufficience, osmotic, diuresis, diuretic use); nonreal (GI tract losses w excessive sweating, diarrhea, vomiting)
hypervolemic hyponatremia causes excess water, sodium is diluted
hypovolemic hyponatremia symptoms thirst, hypotension, tachycardia
hypervolemic hyponatremia symptoms headache, lethargy, confusion, muscle cramps; cell swelling (leading to seizure and coma)
hypernatremia level >145
hypernatremia causes water loss or intake of salt wo water
hypernatremia symptoms cells become dehydrated and shrink, edema, weight gain, hypertension (water retention), dec salivation, tachycardia, flushed skin, dec reflexes, weak pulse (water loss)
most at risk for hypernatremia elderly and infants
potassium normal level 3.5-5
hypokalemia level <3.5
hypokalemia causes diuretic therapy, dietary deficiencies, vomiting, diarrhea, hyperaldostronism, salt wasting kidney disease, GI surgery, alkalosis and laxative abuse
hypokalemia symptoms anorexia, nausea, vomiting, sluggish bowel, cardiac arrhythmias (prolonged PR interval, flattened T wave, prominent U wave), postural hypotension, muscle fatigue, weakness, leg cramps
potassium is found in orange juice, banana, dried fruits, meat
hyperkalemia level >5.2
hyperkalemia causes excess intake of K, aldosterone deficieny, Na depletion, acidosis, tissue trauma, burns, extreme exercise, renal failure, addison's disease (dec cortisol), hemolysis, potassium-sparing diuretics ACE inhibitors
hyperkalemia symptoms nausea, vomiting, diarrhea, intestinal cramping, numbness, tingling of extremities, muscle weakness/cramping, dizziness, apathy, mental confusion, ecg changes (tall peaked T wave, wide QRS complexes)
calcium normal range 8.5-10.5
where is calcium found/functions bone/teeth, blood clotting and neuromuscular signaling
hypocalcemia level <8.5
hypocalcemia causes hypoparathyroidism, malabsportion syndrome, hypomagnesia, hyperphosphatemia, renal failure, insufficient vitamin d, hypoalbuminemia, diuretic therapy, diarrhea, acute pancreatitis, gastric surgery, massive blood transfusions
hypocalcemia symptoms porethesias around mouth, hands and feet, muscle spams (tetany), laryngeal spasm, seizures, hypotension, arrythmias, chronic hypocalcemia (bone pain and fragility), chrosteks sign and trousseaus sign
chrosteks sign cheek/facial spasm
trousseaus sign wrist/carpal spam T
tetany muscle spasms
hypercalcemia level >10
hypercalcemia causes hyperparathyroidism, cancer, excessive Ca in diet, excessive vitamin d, immobility, hypophosphatemia, diuretics, ace inhibitors, lithium therapy, malignancy of bone or blood
hypercalcemia symptoms muscle flaccidity, proximal muscle weakness of lower extremities, bone tenderness and weakness, dec neuromuscular activity of bowel (constipation), high ca in urine, hyperreflexia (muscles twitch), tongue fasciculations
phosphate normal level 2.5-4.5
phosphate found/function bone, rbc, enzymatic processes, formation of atp, acid-base balance
hypophosphatemia level <2.5
hypophosphatemia causes ingestions of excess antacids (al + ca), severe diarrhea, lack of vitamin d, hypercalcemia, alkalosis, hyperparathroidism, diabetic ketoacidosis
hypophosphatemia symptoms tremors, lack of coordination, paraesthesias, hyporeflexia, anorexia, dysphagia, confusion, ataxia, muscle weakness, joint stiffness, bone pain, osteomalacia
hyperphosphatemia level >4.5
hyperphosphatemia cause kidney failure
hyperphosphatemia symptoms hypocalcmemia, paraesthesia, muscle cramps, tetany, hypotension, cardiac arrhythmias
magnesium normal range 1.8-3
magnesium found in bone
hypomagnesemia levels <1.5
hypomagnesemia causes prolonged diarrhea, malnutrition, malabsorption, alcoholism/cirrhosis, laxative abuse, inc renal excretion of mg, dka, sepsis, burns and wounds need debridement
hypomagnesemia symptoms neuromuscular manifestations like tetany, chvosteks sign, trousseaus sign, cardiac arrhythmias, ecg changes like hypokalemia (u wave), respiratory muscle paralysis, heart block, coma
hypermagnesemia level >2.5
hypermagnesemia causes kidney failure, excessive use mg in antacids and laxatives, untreated diabetic ketoacidosis, and excessive mg infusion
hypermagnesemia symptoms inhibits acetylcholine release and cause diminished neuromuscular function, hyporeflexia, muscle weakness, cardiovascular effects (hypotension and arrhythmias), severely high mg levels can cause cardiac arrest, lethargy and confusion
pH normal ranges 7.35-7.45
dec pH acidosis
inc pH alkalosis
pCO2 range 35-45
HCO3- range 22-26
carbonic acid/bicarbonate equation CO2 + H2O<->H2CO3<->HCO3- + H+
inc co2 shifts toward inc h and inc carbonic acid (more acidic)
buffer systems protein, phosphate, carbonic acid-bicarbonate
respiratory tract as buffer for regulating co2 maintains pH of blood and adjusts co2 (outgasses)
role of kidneys as buffer for regulating H+ and HCO3- cells reabsorb HCO3- from urine back to blood and secrete H+ into urine
respiratory failure bc of respiratory acidosis failure of lungs to remove or exhale co2 from body fluids as fast as it is produced by cells pH<7.35, PCO2>45, HCO3-<22
anxiety leads to hyperventilation syndrome leading to repiratory alkalosis loss of co2 from lungs faster than produced by cells pH>7.45, PCO2<35, HCO3->26
metabolic acidosis causes lactic acidosis, ketoacidosis of diabetes, renal failure causing failure acid waste build up pH<7.35, PCO2<35, HCO3-<22
compensation that occurs in metabolic acidosis by respiratory compensation hyperventilation to dec arterial PCO2
chemoreceptors affect respiratory rate and depth inc rates of firing that cause inc inspiratory activity and inc pulmonary ventilation
metabolic alkalosis causes excess loss of acids, unrelated to CO2, kidneys and GI tract loss, inc bicarb levels, post-code excess bicarb iv pH>7.45, PCO2>45, HCO3->26
respiratory system and kidneys compensate for metabolic alkalosis lungs dec ventilation to inc co2, kidneys, excrete hco3-, retain h+, kidney reabsorb h+ instead of usual K+
effects of acidosis h+ into cells k+ out of cells
effects of alkalosis k+ into cells leading to hypokalemia
normal anion gap range 8-16
anion gap only in metabolic acidosis, ketoacidosis, lactic acidosis, chronic kidney disease
adult body weight is water 60%
where is fluid located intracellular fluids and extracellular fluids
extracellular fluid found in saline as Na and H2O in plasma, and interstitital fluids bw cells and capillaries
extracellular fluid is more easily lost
albumin responsible for movement of water into and out of vessels
osmolarity measures particle per L of solution
isotonic equal distribution of sodium and water in ICF and ECF
why give isotonic solution to patient raise blood pressure
ringer's lactate similar physiological constituents as found in blood
hypotonic lower sodium level/more water than what is found inside the cell
why give hypotonic solution to patient avoid dehydration
hypertonic higher sodium level/less water than what if found outside cell in blood vessel
why give hypertonic to patient shift fluids into bloodstream to dilute electrolytes
filtration solid particles in liquid or gas fluid removed by filter that permits fluid to pass thru but retains solid particles
sodium-potassium pump atpase pump to maintain na as ecf and k as icf
na fluid balance and osmotic pressure
k neurotransmitter excitability and acid-base balance
hydrostatic pressure pressure from heart in arteries that pushes water out of capillaries into isf
osmotic and oncotic pressure help pull water back into vessels from isf on venule side of capillary
capillary hypertension condition caused by excess fluid left in interstitial space due to problem with hydrostatic, oncotic, or osmotic pressures
raas hormones renin, angiotensin 1, angiotensin 2, and aldosterone
angiotensin 1 to angiotensin 2 where blood pressure regulation starts
natriuresis excretion of large amount of na and h2o by kidneys in response to excess ecf volume
antidiuretic hormone hormone stimulated by posterior pituitary gland when blood pressure is low and causes kidney to retain water in blood to help elevate blood pressure
atrial natriuretic peptide (anp) hormone released when there is too much fluid sensed in right atrium of heart which stimulates diuresis
diuresis release of fluid in form of urine from kidneys
brain natriuretic peptide (bnp) hormone released when blood vessels in brain and left ventricle of heart sense excess fluid in vessels which stimulates diuresis (diagnoses left-sided heart failure)
edema swelling when there is excess fluid in isf and icf
hypoalbuminemia liver failure, protein malnutrition
dependent edema collection of venous blood in lower extremities
pitting edema pressure is applied to small area and an indentation persists after release of pressure, measured +1,+2 or +3
transudate serious filtrate of blood (blister and clear)
exudate contains blood, lymph, proteins, pathogens, inflammatory cells (puss)
hypervolemia bloodstream has excessive amount of water-->heart failure
testing for hypervolemia dilutional hyponatremia (<130)
hypervolemia symptoms rapid weight gain, swelling in arms legs face or abdomen, cramping, headache, stomach bloating, shortness of breath, crackles in lungs, high blood pressure, bounding pulse, heart failure
dehydration or hypovolemia diminished water volume in body
body's reaction to dehydration osmoreceptors stimulate thirst and adh released, vasoconstriction and inc heart rate, raas activated
hypovolemia causes reduced fluid intake, reduced adh or kidneys not responsive to adh, burns, fever, respiration, osmotic diuresis (elevated blood glucose), hypernatremia (inc osmolarity of blood and dec circulating blood volume)
hypovolemia symptoms thirst, dry mucous membranes, sunken eyes, poor skin turgor, hypotension, low urine output, dark-colored urine, weight loss, tachycardia
testing for hypovolemia high blood urea nitrogen (6-24), oliguria, hypernatremia
most at risk for hypovolemia or dehydration older adults and babies
volatile acid co2 combines with water forming carbonic acid
nonvolatile (fixed) acids not converted to co2 (ketones, lactic acid)--> secreted thru kidneys
protein buffer system largest in body
phosphate buffer system regulate intracellular pH
carbonic acid buffer system involves co2, h2co3, h+, hco3, lungs and kidneys utilize to maintain blood pH
anion gap measure gao bw neg and pos charged electrolytes, measured cations minus anions
eustress stress that stimulates a person positively
distress stress that stimulates a person negatively
acute stress response to intermittent, intensity varies in response to stimuli and ends after threat is avoided
chronic stress prolonged activation of stress response to a perceived threat that does not abate rapidly-->illness
short term (neural) protective effect
prolonged exposure (endocrine) diminishing effectiveness
alarm stage activation of cns, sns, and adrenal glands
we see this in alarm stage increased alertness, cardiorespiratory stimulation, pupil dilation, dec gi tract activity, inc blood flow to muscles, inc sweating, dec blood flow to urinary tract
hpa axis hypothalamus, pituitary, adrenal gland
hypothalamus releases crf (cortico releasing factor)
anterior pituitary releases acth (adrenal cortico tropin hormone)
adrenal cortex releases cortisol--> inc blood glucose
short term and long term of cortisol short=enhances immune response long=immunosuppression
posterior pituitary releases adh (antidiuretic hormone)
adrenal medulla releases epinephrine and norepinephrine
resistance stage parasympathetic system tries to stop cortisol and get body back to normal
exhaustion stage stress overwhelms body-->can lead to infection
allostatic overload stress exceeds bodys ability to adapt
allostatic load wear and tear on body systems caused by stress rxns
tachycardia fast heart rate
hypercapnia high co2
epinephrine dilates bronchioles, elevates blood pressure and heart rate, dec production of urine, dec gi tract
cortisol inc glucose, inc blood pressure, dec immune response
antidiuretic hormone (adh) stops water being pulled out of blood
norepinephrine raises heart rate, constricts blood vessels
catecholamines in both hormones and neurotransmitters that are stimulated from sns (adrenal gland)
aldosterone tail of raas system, acts in renal tubules to reabsorb na into blood, h20 follows inc volume
ischemia loss of oxygenated blood flow
hem(o) or hemat(o) blood
erythr(o) red
leuk(o) white
an- without
immun immunity
necr death
-ology study or science of
-rrhage excessive flow
-oma tumor or specified by base
-poiesis production or making
-penia deficiency
-cytes cells
-emia condition of blood
-globin protein
-osis abnormal conditions
-philia abnormal attraction (love of)
% of blood is water 92%
% of blood is solute 8%
whole blood is composed of plasma and serum
plasma aqueous liquid with electrolytes and organic elements
serum clear liquid that remains after blood clots
plasma proteins are produced in liver
what plasma protein is not produced in liver immunoglobulins (plasma cells)
what % do plasma proteins make up weight of plasma 7%
role of plasma proteins regulate processes in the body
albumin carriers, control plasma oncotic pressure (hydrophilic)
globulins- alpha bilirubin and steroids
globulins- beta fe and cu
globulins-gamma immunoglobulins
rbc function oxygen and co2 transport
normal range rbc male 4.5-5.5 million
normal range rbc female 4.0-4.9 million
rbc life cycle 120 days
rbc shape biconcavity or reversible deformity
biconcavity shape provides sa and volume ratio that are optional for gas diffusion and deformity
reversible deformity enables erythrocyte to assume more compact torpedo-like shape, squeeze thru microcirculation, and return to normal
rbc contain hemoglobin
rbc is released from _________ and destroyed in ___________ bone marrow and liver
wbc function defend against infection and remove debris
wbc normal range 4000-10,000
wbc life cycle 13-20 days
wbc contain granulocytes and arangulocytes
granulocytes neutrophils, basophils, eosinophils
neutrophils function phagocytosis, degranulation, release of nuclear material
basophil function inflammation
eosinophils allergic reaction
agranulocytes monocytes and macrocytes
monocytes function defend against bacteria
complete blood count measures number of rbcs, wbcs, platelets and indices
hemoglobin protein on rbc that carries oxygen to the body's cells ande co2 from organs to the lungs and is measured by the hemoglobin level
hbg (hemoglobin) normal range male 13-18
hbg (hemoglobin) normal range female 12-16
hct (hematocrit) normal range male 45-52
hct (hematocrit) normal range female 37-48
hematocrit volume or proportion of rbc in the blood
mean corpuscular volume (MCV) measures size of rbc; tells what type of anemia is present in the blood
elevation of mcv means person has macrocytic anemia which is caused by low folate or vitamin b12 deficiency or pernicious anemia
mean corpuscular hemoglobin count measures amount of hemoglobin a single rbc as relates to volume of the cell
low mchc means patients anemic
high mchc means patient has high elevation of hbg in blood
mean corpuscular hemoglobin measures average amount of hemoglobin contained in each rbc
if low mch iron deficiency anemia
if high mch rbcs are too big from pernicious anemia
hemostasis pooling of blood
hemostasis roles vasculature (endothelial cells and subendothelial matrix), platelets, blood proteins (clotting factors)
pt (prothrombin time) range 10-13
prothrombin time measurse how quickly bleeds and clots (extrinsic and common pathway)
inr (international normalized ratio) range 1.1 or below
inr measures bleeding and clotting w pt for anticoags
aptt (activated partial thromboplastin time) range 30-40
aptt measures response to anticoagulant therapies, measures intrinsic and common pathway
clotting leads to blockage of blood flow
bleeding loss of blood
stage 4 of hemostasis 4. clots retract (shrink)
stage 5 of hemostasis 5. clots dissolute (clot is destroyed)
stage 3 of hemostasis 3. coagulation cascade is activated by tissue factor
stage 2 of hemostasis 2. platelets form a plug @ site of injury
stage 1 of hemostasis 1. injury to blood vessels leads to narrowing of blood vessels (vasoconstriction)
when vessel tissue is damaged platelets are called to are of damage by the release of van willebrand factor
3 steps of platelet plug or clot formation adhesion, activation, aggregation
adhesion binding of platelet surface receptor glycoprotein (GPIb to van willebrand factor)
activation smooth spheres change to spiny projections and degranulation (platelet-release rxn) resulting in biochemicals
aggregation facilitated by fibrinogen bridges bw receptors on platelets
extrinsic pathway forming a clot when superificial damage occurs to the epithelial tissue; stimulated by release of x factor; less clotting factors in this branch to get to the common pathway; lab values are used to determine hw long this pathway to respond is inr and pt
common pathway final leg both pathways travel to form a clot; starts w production of phospholipids then combines w platelets to form a scab. starts w factor x stimulating factor v that stimulates prothrombin to thrombin, then fibrinogen to fibrin that forms clot
intrinsic pathway responsible for forimg a clot when damagae occurs thru wall of blood vessel; starts w release of hageman (xii) factor which cascades thru multiple clotting factors until reaches common pathway. lab test that determines how long it takes is aptt
lysis clots must be broken down, otherwise they will continue to grow and block a blood vessel
embolus clots break off and travel in blood to cause a blockage elsewhere in body like brain, heart, or lungs
fibrinolysis clot dissolution
if clot is inside blood vessel, ______ is released to begin fibrinyolysis tpa (tissue plasminogen activator)
if clot is extracellular, then _________ is released to start breakdown process upa (urokinase plasminogen activator)
upa and tpa activate plasmin
plasmin along w fibrin degradation products breakdown fibrin
d-dimer test checks the blood for clots
hypercoagulability inc in blood clots
causes of hypercoagulability pregnancy, oral contraceptives, post-surgery, immobility, congestive heart failure
atrial fibrillation cause hypercoagulability in venous and arterial circulation
causes of bleeding dec # circulating platelets, impaired platelet function
thrombocytopenia dec platelet production, inc platelets in spleen, dec platelet survival
3 types of thrombocytopenia drug-induced, idiopathic pupura, thrombotic purpura
thrombocytopenia symptoms bleeding in nose, mouth, gi track, and uterine cavity
vitamin k in clotting cofactor in synthesis of clotting factors, if no vitamin k liver produces inactive clotting factor, resulting in abnormal bleeding
hemophilia a deficiency in factor viii, x linked recessive disorder, bleeding occurs w local trauma in soft tissues, gi tract, hip, knee, elbow and ankle joint; leads to swelling and pain in synovium of joint
von willebrand hereditary bleeding disorder from deficiency or defeat in vwf; symptoms: bleeding from nose, mouth, gi tract, excessive menstrual flow, prolonged bleeding time w normal platelet count
disseminated intravascular disorder (DIC) widespread coagulation and bleeding in vascular compartment, complication from pregnancy, sepsis, cancers, shock, trauma, or surgery and hematologic conditions; symptoms: bleeding from all orifices, petechiae, purpura, oozing from punctures to hemorrhage
erythropoiesis rbc production; bone marrow, body needs oxygen; hypoxia
bilirubin protein that breaks down old rbc, liver gets rid of it
conjugated bilirubin water soluble
unconjugated bilirubin insoluble in plasma and attaches to proteins for transport
jaundice yellowing of skin and whites of eyes and indicates dysfunction of bilirubin (too much)
anemia abnormally low number of circulating rbs or hemoglobin, or both; diminished oxygen carrying capacity
anemia occurs from excessive loss of blood (stab wound) or destruction of rbcs (cancer of medicines), deficient rbc production (diet-low iron, b12 deficiency), and inherited disorders (sickle cell)
anemia symptoms fatigue, weakness, dyspnea (difficulty breathing), angina, headache, faintness, dim vision, pallor of skin, nail beds, tachycardia, palpitations, leg cramps
leukopenia dec in leukocytes
neutropenia dec in neutrophils
agranulocytosis absence of neutrophils
neutropenia symptoms fever, mouth ulcer, sore throat, susceptibility to infection
hodgkin disease lymphoma in single node or chain of nodes *Reed-sternberg cells
who do you see hodgkin disease in 15-40 or >55
hodgkin disease symptoms painless nodes above diaphragm, cough, dyspnea, fever, night sweats, weight loss, pruritis
non-hodgkin disease lymphoma originates @ extranodal sites and spreads to contiguous nodes >60
non-hodgkin disease symptoms fever, drenching night sweats, and weight loss
proliferation constantly replicating
primary hemostasis platelet aggregation
secondary hemostasis fibrin formation
purpura blood collecting under skin
petichiae blood speckles
labile cells hair cells that rapidly divide
stable cells only replicate when necessary liver
permanent cells never return to cell cycle neuron
etiology original cause of cell alteration or disease
cellular adaptation protective mechanism to prevent cellular and tissue harm bc of stress
biopsy extraction of cell samples from an organ or mass of tissue to allow for histological examination
atrophy shrinkage of cell
hypertrophy enlargement of cell
hyperplasia inc # of abnormal cells in response to a stimulus
ex hyperplasia excessive estrogen production--> abnormal menstrual bleeding
metaplasia reversible change where one cell is replaced by another in response to chronic irritaition
ex metaplasia esophagus exposed to reflux from gastroesophageal overtime replaced by stomach cells
dysplasia deranged cell growth of tissue resulting in cells varying in size and shape and organization
ex dysplasia abnormal pap smear w cluster of cells
anaplasia cells that divide rapidly and have little to no resemble to normal cells
neoplasia new growth// cancerous
infarction death of tissue, ischemic necrosis (lack of oxygenated blood to tissues)
necrosis cell death due to injury
gangrene occurs from bacteria that grow in dead tissue
wet gangrene odor, swells, oozes
dry gangrene no blood supply, tissue dries, turns black
angiogenesis formation of new blood vessels
cancer 65+ more @ risk bc more run down, less replication of cells and weaker
causes of cancer viruses, chronic inflammation, radiation, chemicals that contain highly reactive oxygen species (ros)
tumor suppressor genes genes that guard against cancer formation
proto-onco genes control normal cell growth and proliferation
oncogenes mutate from proto-onco genes and allow unrestrained cell division
benign well differentiated cells that resemble normal cells, well defined borders, progressive and slow, do not invade surrounding tissues, does not spread by metastasis
malignant undifferentiated cells that do not resemble normal cells, poorly defined borders, rapid growth rate, invades into other tissues, gains access to blood and lymph channels to metastasize other areas of the body
initiation initial damage to dna
promotion alerted cell divides and passes on abnormal dna
progression benign lesions proliferate and invade adjacent tissue or metastasize
T extent of primary tumpr
n nodes
m metastasis
tx, nx, mx cannot be assessed
t0,n0,m0 no evidence
tis cells only found in area where formed
n1,n2,n3 inc involvement of nodes
t1, t2, t3, t4 inc size
m distant metastasis
gx cannot be assessed
g1, g2, g3, g4 well-->moderately-->poorly-->undifferentiated
cancer cells impact almost all body functions bc tumor cells replace noramally functioning tissues
initial symptoms of cancer reflect primary site of involvement, and as grows it impacts other functions (metastasizes)
adenoma benign tumor, glandular tissue or organ
lipoma derived from fat cells
hemangioma collection of blood vessels in skin or internal organ
desmoid tumor highly invasive but dont metastasize
nevi non-cancerous moles on skin
myomas muscle tumor
carcinoma malignant epithelial cells
adenocarcinoma cancer of glandular or ductal tissue
sarcoma mesenchymal origin (connective tissue, cartilage, and bone)
leukemia cancerous changes in leukocytes
lymphoma cancerous lymphocytes in lymph tissue
cachexia loss of body fat and lean body/weakness
anorexia loss of appetite
paraneoplastic syndrome clinical effects at a body site distant from primary or metastatic cancer caused by tumor (unrelated)
3 ways for cancer to metastasize in blood, lymph system, surgery
primary prevention focuses on preventing or delaying the onset of cancer -education, minimize exposure, sunscreen, preventative surgeries, and medications
secondary prevention early detection thru screening -pap smears, colonoscopy, psa, annual dermatology screens, history, physical exams
tertiary prevention treatment, management, or prevention of progression to later stages
diagnosis of cancer done thru screening test like pap smear, mammogram, psa, mri, ct scans
breast cancer at risk 1/8 women and men
risks for breast cancer prolonged reproductive life, family history, age >50, hormone replacement theory, obesity, late childbirth, nulliparous (no pregnancies), ashkenazi jewish women, brca 1 and 2 genes, epithelial cell tumors lining ducts or lobules
symptoms of breast cancer singular, nontender firm mass, irregular borders, adhere to skin or chest wall, upper outer quadrant of breast, nipple discharge, swelling of one breast, nipple/skin retraction, peau d'orange=orange swelling, paget's disease of breast=red, crusting nipple
biopsy most definitive way to diagnose cancer (direct visualization of cells)
breast cancer diagnostics mammogram, ultrasound, fine-needle or excisional biopsy, ductogram (nipple discharge), PET scan (dye)
screen for breast cancer thru mammogram and screen for prostate cancer around 50
prostate cancer classified with gleason and tnm system
prostate cancer greatest risk man >65
no early symptoms for prostate cancer, but late symptoms are hematuria (blood in urine), azotemia (blood urea nitrogen inc), anemia, anorexia, back pain in vertebra
prostate cancer metastasizes to lymph nodes and bones
prostate cancer diagnostics digital rectal examination (dre) and prostate screening antigen (psa)
s phase division or replication occurs
G0 phase resting phase
G1 phase cell grows larger
G2 phase cell grows again for 2nd time
Created by: cat9210
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