Gender Age Hereditary Smoking Alcohol Diet Stress

Testosterone mutation of P53 gene stomach changes hyperinsulinemia hyperlipidemia CNS

APC gene food into glucose (compensation) stimulation of
Testosterone produced TP53 fat cholesterol hypothalamus
Conversion doesn’t produce glucose enters abnormal deposition in
APC protein kills monitor the blood stream growth in artery hypothalamus
Dihydrotestosterone cell division smooth stimulate the
No brakes of defects pancreas makes muscular narrowed CNS response
Prostate cell the production insulin muscles diameter of
Of B-catenin but a clone arteries increase CNS
DNA replication Retention cells gets a insulin enters structural response
And cell second the blood stream hyperthropy
Binds to DNA mutation epinephrine
Rapid cell and activates glucose can’t get vasoconstriction norepinephrine
Proliferation more protein transforms into the cells of production
A large the body increase cardiac
Cell proliferation adenoma output increase
Glucose builds vasoconstriction
Causes enlargement invasive up in the increase BP (increase
Of prostate carcinoma/colon cancer blood vessels peripheral
Resistance
Possible BPH or diarrhea,
Cancer constipation, inadequate blood fewer nephrons
Blood in stool supply to the
Constricting the organs rennin (kidney) decrease filtration
Urethra function of kidneys
Ischemia angiotensin(liver)
Interfering with the possible necrosis angiotensin I Na retention
Normal flow of
Urine angiotensin II attracts H20

Urinary retention adrenal cortex H20 retention

Stimulation
Breeding site of
Bacteria release of
aldosterone
Infection in
Bladder Na and H20
Retention
Weak stream of
Urine,
Painful urination increase fluid volume

Increase preload and afterload

Increase cardiac output

Increase BP

References: Too much increase in BP

Medical Surgical 11th edition by Suzanne C. Smeltzer p.1033
Anatomy and Physiology by Seeley pp.541-549 Tendency blood vessels to rupture
Medical Surgical by Joyce M. Black pp.2143-2144
Stroke, hypertension, HACVD