Vous êtes sur la page 1sur 9

MODIFIABLE FACTORS

• Diet (↑fats, ↓fiber, ↓Calcium Intake)


NON-MODIFIABLE
• Smoking (2packs/day) FACTORS

• Alcohol Consumption (since 14 yearsold, • Age (66yrs old)


at least 2x/wk)

Fats will enter the Ingestion of carcinogens in the Inherited mutated genes
Signals the duodenum intestine (nitrosamines,
gallbladder to polycyclic hydrocarbones, iso
secrete nile ↑ Bile secretions in the cyclic amines)
intestine

Signal the ↑ Secondary bile


↑ Colonic
gallbladder to acids to concentrate ↓ the ability to
epithelial cells
secrete bile bile detoxify the
carcinogens due to ↓
Promotes binding Ca + that binds to
↑ biliary Modification of of carcinogen in carbonic acid to
secretion cell membrane the epithelial cells etoxify the
by the liver of the colon carcinogens
to emulsify
the excess
fats Mutation of the
Induce cellular
normal cells
proliferation Negatively Prevent Continues Cannot
Bile pasess thru
affects the apoptosis DNA stop DNA
biliary duct
A and
DNA repair
Mutation of the Tumor replication replicatio
sphincter of oddi
DNA mismatch suppressor of the
Activation of n
Activation of Mutated ↓ Function Mutated K-
and secreted to
APC gene is not able repair genes are mutated cell
duodenum mutated APC the mutated HNPCC of CK2 RAS gene
to release APC protein turned off Inactivation
gene P53 gene gene is (protein is activated
of C-MYC activated substance)
↑ cell Natural self-
A growth gene
Invades and
thedivided
destruction
very quickly/
epithelial lining↑Hyperplasia of
mechanism
proliferation is the mutated
of mutated
of the colon
Beta
catenin Cannot stop
enters DNA replication
the
nucleus

↑ Survival of the
mutated cell

Springs out from the epithelial


cells of the colon
(ADENOMA/POLYPS IN THE
SIGMOID)
Continues
hyperplasia
mutated cell
↑WBC to
reduce further Inflammati
Tissue E
Hypo function ↑↓ absorption
infection (10.4 on of the
Forms epithelium Transformation takes damage goblet cell of water in the
x 109) – sept. tissue
composed of place among the stem colon
13,2007
genetically altered cell population at the
cell located in the crypts base Angiogenesi
superficial portions of Mutation/ina
Loss of methyl Activated s of the
Transformed Causes Abnormal
one in
mucosa ctivation of D Continuou
group DNA of oncogenes
stem cell adenoma ALTERATION
obstructionIN BOWEL function of
Otherthetumor
adenoma the MOVEMENT s
Abnormal cells spread replicated the colon
cells enters suppressor (DIARRHEA/CONSTIPATI peristalsis
laterallyto
Connects
Continues and
pre- Monocial
the lymphatic ON) -2 yeays prior to
downward
existing
hyperplasia to form
crypts
of conversion
system or the hospitalization
theand new
tumor crypts
replace
cell them produces the
blood stream
Loss of proliferation Abdominal
control of the mutated spasm
cell (sept. 03 ,
2010)
D

ADENOCARCINOMA IN THE
SIGMOID

Tumors E
Hypo function
become goblet cell
ulcerated due
to continuous Epithelial
passage of lining of the
colon tends Inflammation noccicepto
Tumors tend to to bleed of the r send
bleed due to due to epithelial signals to
ulcerating mass continouos lining the brain
iritation Brain interprets the
and signals coming
Metastasis to the Continuous PALLOR (september
BLOOD IN THE STOOL
↑ O2 (1 years PTA) from nocciceptors FATIGUE
other epithelial but slow loss Easy
16,2010) demand Bone marrow release
cells of the of blood over moreTrigger
platelet for tiring of
ABD PAIN (7/10) – (sept. 7
different organ a long period tissuethe
by repair the cells PTA)
ANEMIA TACHYPNEA SEPTEMBER
body of time MALAISE (1 EASY ↑ CO2 in respirato
↓ O27,2010
on
year PTA) FATIGABILI the lungs count
ry center (SEPT.
↑ platelet – 504x10) – sept.
TY (1 year of the cells
13,2010 07,2010)
PTA) brain
Liver Hypo function of Nephron
metastasis the hepatocytes damage
Elevated
CEA Ploriferation of
Glycogen restore in Protein breaks F ↑ hydrogen
(325ng/mL) adenocarcinoma
hepatocytes and into amino acids ion
– september in the liver
15,2010 does not released
C
Amino acids
Heart is Invasion of the Some H bind Some H bind
Gluconeogenesis does not convert into keto
being hepatoctes and with CO3 = with HCO3 =
occur acids and
affected angiogenesis of HCO3 H2CO3
ammonia
due to the Glucose does not release Ammonia
adenocarcinoma in to the blood Unable to excrete H
combined with ↑ H in the
the arteries of the by the kidney
CO2 by the lungs
HYPOGLYCEMIA- 60mg/dL (september process of Unable to
Na retention
17,2010) oxydative synthesize to Respirator
and water
y center in
reabsorption
↑BV ↓ Glucose in the body tends to use H back to the brain
cell the excess fats Accumulation of triggers
peritubular
HPN in portal vein ammonia in the
↓ ATP spaces
blood
production MODERATE Fat METABOLIC
metabolism ACIDOSIS H combined HYPERVENTILATIO
Excess fluid
↓ Perfusion of Accumulation Unable
with NH3toto N (september 17,
pulls into the ↓ Energy of ASCITES occurs
(september 17,2010)
hepatocytes with of fluid in the secrete
become 2010)
peritoneal the cell (SEPTEMB
portal peritoneum ↑ fatty acids NH4NH4due to
spaceblood ER 15,
kidney
2010)
Compensatory mech is FATIGUE malfunction
NH4 cannot go
activated by shifting fluid (september
↓ Cardiac output back into
Heart tends 17,2010)
intravenously to H justspace
peritubular
to reserve
extracellularly andrepeat
remainthe
in the
the Water will
cycle
remaining reabsorbe
Catecholamines
Blood RAASblood d back in
Release of release
volume in
vessels in (compensati Ccirculating ADH
↓ systemic F
↓ opening and (compensation)
the on)the blood
(compensatio
blood
↑ O2 ↑ preload, ↓ supply in
proximal closure of
volume
circulation the
peripheral demand SV, andheartHR valve ↑ SVR
organs of peripheral
Damage Inability of
of the the kidney to
glomeruli secrete urea,
hydrogen
ions,crea,uric
Inability to acid
filter
macromole Acummulation
cules like of creatinine
protein in the blood
OLIGURIA
(<50ml/shift)
↓ blood volume – sept 16. PROTEINURIA ↑ creatinine
in the 2010 (+1) – sept. level
peripheral area 13,2010 (153.1umo/
L) – sept.
16.2010)
HYPOTENSI ↓ O2↓ of
ON (80/60) Temperature
the cell
– sept. of the cell WEAK THREADY
17,2010 PULSE(SEPT.
COLD
17,2010)
CLAMMY SKIN
↓ Cellular
(sept.17,2010 Trigger
TACHYCARDIA –
metabolism thus
by142bpm
the (SEPT.
decreased) production ↓ CO2 in
TACHYPNEA
respirato
17,2010)
of heat by the cell (37cpm)
the lungs ry center
of the (SEPT. 17,2010)
brain
Review of system

Cardiovascular system

• Anemia – prolonged slow blood loss due to ulcerating mass

• Tachycardia – compensatory mechanism due to reservation of the remaining blood into the proximal organ

• Weak thready pulse – decreased pressure to the peripheral area due to decreased blood flow/volume and vasoconstriction

• Hypotension – due to decreased blood volume


Gastrointestinal system

• Altered bowel movement (diarrhea/constipation) – due to obstruction, abnormal function of the colon, altered function of the goblet
cells, ↓ absorption of water

• Abdominal spasm – due to obstruction of the mass, accumulation of fecal materials, water, gas in the colon

• Moderate ascites – due to plasma pulling in the blood and secrete it into the abdominal space

• Blood in the stool – due to ulceration of mass and contiuous passing of stool; thus irritating the ulcerated mass that cause bleeding

• Abdominal pain – due to inflammation of the colon caused by invading cancer cells or ulcerated mass

Metabolism

• Hypokalemia – decreased absorption in the colon

• Hypoglycemia – glycogen stores in the hepatocytes thus glucogenolysis is not occur; decreased production of glucose by the liver that
result in decreased glucose in the blood

• Metabolic acidosis – inability of the kidney to secrete hydrogen and toxic materials; use of fatty acids by the body to use as a source of
energy

Renal system

• Oliguria – compensatory mechanism of the body increasing reabsorption of water and retention of sodium by the kidney

• ↑BUN – inability of the kidney to excrete the creatinine due to altered function of the kidney

• Proteinuria – inability of the glomeruli to filter macromolecules

• Metabolic acidosis - inability of the kidney to secrete hydrogen and toxic materials; use of fatty acids by the body to use as a source of
energy
Integumentary system

• Pallor – due to anemia, decreased O2 supply

• Cold clammy skin – compensatory mechanism of the body by decreasing blood in the peripheral area to reserve the remaining blood
volume to the proximal organ of the heart; thus decreasing O2 supply to the cells; thus decreased workload of the cell that leads to
decreaed temperature

• Hypothermia - compensatory mechanism of the body by decreasing blood in the peripheral area to reserve the remaining blood volume
to the proximal organ of the heart; thus decreasing O2 supply to the cells; thus decreased workload of the cell that leads to decreaed
temperature

Respiratory system

• Tachynea – compensatory mechanism of the body due to metabolic acidosis; thus exhaling the hydrogen in the body in form of carbonic
acid

• Hyperventilation – of the body due to metabolic acidosis; thus exhaling the hydrogen in the body in form of carbonic acid

General

• Malaise – increased O2 demand

• Fatigue - increased O2 demand

BSU-BSN- IVA- GROUP1

BATCH 2010-2011
ALL STARS GROUP1...MIKE,MAROH,RORRE,JACOB,DAH,TUBZ,GRE,MAU,JOVS,LORRAINE + BABY BOY.. :8)