CUSHINGS DISEASE -metabolic disorder;excessive anterior pituitary secretion of ACTH -hypersecretion of cortisol, androgens & aldosterone ETIOLOGY: -ACTH production by nonpituitary tumors(Ectopic tumors-prim lung tumors) -ACTH production by pituitary tumors -Adrenal tumors producing cortisol S/S(commonly caused by hypercortisolism)
 weight gain(buffalo hump)

(*Na&h20 retention due to mineralocorticoid effects of cortisol,exhibited when high cortisol)
  -glucose intolerance (due to cortisol-induced insulin resistance and increased gluconeogenesis and glycogen storage by liver Elevated Cortisol, glucocorticoids results in muscle wasting, accumulation of adipose tissue, in face and trunk and increased blood proteins and glucose levels.

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Elevated mineralocorticoids … aldosterone in conjunction with the increased androgens promotes edema, a form called “pitting edema”. Hyperpigmentation … POMC …ACTH&MSH.

*elevated cortisol levels, vascular sensitivity to catecholamines is increased significantly, leading to vasoconstriction and hypertension. PATHOGENESIS: • Without treatment 50% of the patients die within 5 years of onset. Due to: • Overwhelming Infection • Suicide • Complications from arteriosclerosis and Hypertensive disease TREATMENT: Medication;radiation therapy and surgery IDIOPATHIC ADDISON’S DISEASE(ORGAN-SPECIFIC AUTOIMMUNE) -Adrenal atrophy and hypofunction ETIOLOGY:
   Abnormally low levels of Cortisol and Aldosterone Hypocortical Functioning, Dysfunction of the adrenal cortex, caused by an autoimmune

Adrenoleukodystrophy and adrenomyeloneuropathy are other causes. the % increases in younger patients and those with other autoimmune diseases. POMC …ACTH&MSH. Requires long-term daily glucocorticoid replacement therapy. hypotension PATHOGENESIS: • Other autoimmune diseases predispose one to Addison’s.mechanism. anorexia. diarrhea.  Amyloidosis and Familial adrenal deficiency. hypoglycemia.. fatigue. ****May be inherited as an autosomal recessive trait S/S • Failure of negative feedback causes an increase in ACTH • Possible hyperpigmentation . • Weakness.   • . autoimmune destruction of the adrenal cortex Primarily women. Autoantibodies are present in 50%-70% of the individuals with idiopathic Addison’s disease. 30 – 60 years of age … Associated with TB (tuberculosis)…adrenals are attacked by the TB …irreversible and progressive loss of the adrenal cortex.. apathy.

drug therapy(can reverse thyroid) S/S PATHOGENESIS HASHIMOTO’S THROIDITIS(AUTOIMUNE THYROIDITIS)    HYPOTHYROIDISM destruction of thyroid tissue by infiltration of lymphocytes and circulating thyroid autoantibodies (antithyroid peroxidase and antithyroglobulin antibodies).mental retardation  Hormone replacement therapy(T4 hormone) POST GASTROECTOMY SYNDROME -S/S that occur after gastric resection -caused by changes in motor and control functions of the stomach and upper small intestines CELIAC SPRUE W/ DUODENAL AND JEJUNAL INVMNT(AUTOIMMUNE) ETIOLOGY:  damages the small intestinal villous epithelium when there is ingestion of gluten (gliadin).GRAVES(THYROTOXICOSIS)(TYPE V AUTOIMMUNE DISEASE) ETIOLOGY:        HYPERTHYROIDISM (elevated TH & suppressed TSH) occurs more commonly in women producing an antibody that looks like TSH enlarged thyroid gland(goiter) opthalmopathy (bulging eyes) dermopathy (pretibial edema) surgery. the protein component of cereal grains. Failure of negative feedback S/S  Goiter  Baggy edema  Pharalaryngeal  Gain weight PATHOGENESIS:  Female-fetus…. . radiation.

Jewish ethnicity. associated with genetic factors alterations in epithelial cell barrier functions immunopathology related to abnormal T-cell reactions to commensal microflora and other luminal antigens Risk factors include family history. tobacco use. • Gene therapy is promising for the future. greater curvature of the stomach is connected to the first part of the jejunum in a side-to-side manner. • Hypoxia. pulmonary failure is the most common cause of death. CROHN’S DISEASE(TYPE IV-CELL MEDIATED) ETIOLOGY:       idiopathic inflammatory disorder that affects any part of the gastrointestinal tract but commonly on the distal small intestine and proximal large colon elevated IgG-caused severity of disease.*gluten-sensitive enteropathy BILROTH I & II GASTRECTOMY BILROTH I:  pylorus is removed and the distal stomach is anastomosed directly to the duodenum. when compared with high death rates when it was described in 1936.000 • Chronic cough. labored ventilation. • Maldigestion and malabsorption PATHOGENESIS: • CF is a multiorgan disease. BILROTH II:  EXOCRINE DISEASE CYSTIC FIBROSIS (Autosomal recessive inherited disorder) ETIOLOGY: • Intrinsic … genetic …chromosome 7 … affects chloride ion channels …resulting in enhanced sodium resorption and dehydrated secretions S/S • Caucasian 1/3500. urban residency. clubbing of the fingers and cyanosis. nonwhite 1/12. sputum production. • Mean life expectancy is now about 30 years. and the CARD15/NOD2 (nucleotide-bindingoligomerization-domains) gene mutations PATHOGENESIS .

CHRONIC ANTRAL GASTRITIS  Involves in antrum only  Factors that are associated: 1.nausea. pylori-major causative factor  activation of T and B lymphocytes w/ infiltration of neutrophils  CagA(H. and intrinsic factors. and NSAIDS 2.w/ chronic H. Immunomodulatory agents Surgery TNF delta blocking agents-tx of fistulas and maintain remission GASTRITIS A. pylori infection Combinations of antibiotics(treat h.diminishes secretion of pepsinogen. pylori gene)-produces vacuolating toxin S/S      Anorexia.cant facilitate vit B12 absorption B. Lactose remains in the intestinal lumen because it is not digested or absorbed . and epigastric pain Gastric bleeding Gastric carcinoma.    overly aggressive response to normal flora bacteria in genetically predisposed individuals. with the gene located on the long arm of chromosome 17. pylori) Vit B12 supplement for pernicious anemia PATHOGENESIS: POST GASTRECTOMY MALTASE DEFICIENCY     autosomal recessive disorder. CHRONIC FUNDAL GASTRITIS(AUTOIMMUNE) ETIOLOGY:  Gastric mucosa degenerates extensively in the body and fundus of the stomach.  Elevated plasma levels of gastrin. use of alcohol. or lactose. HCl. accumulation of glycogen in the lysosomes of muscle cells and the cells of other tissues absence of the enzyme acid maltase is responsible for the abnormality in glycogen metabolism LACTASE DEFICIENCY(INTESTINAL LACTASE)     common cause of osmotic diarrhea and loss of pancreatic enzymes Nonabsorbable substance is milk sugar.acid secretion is insufficient(achlorydia)  Pernicious anemia.fullness. tobacco..leading to gastric atrophy  Loss of chief cells & parietal cells…. *****H. vomiting.

and infliximab(chronic UC) Broad spectrum antibiotics/ probiotics can modulate intestinal flora Surgical resection of the colon/ colostomy may be performed PATHOGENESIS: * crohns have skip lesions while UC has continuous colonic invmnt. SOLELY JEJUNAL INVMNT CELIAC SPRUE. S/S         Loss of absorptive mucosal surface.CELIAC SPRUE W/ DUODENAL AND JEJUNAL INVMNT BILROTH I & II GASTRECTOMY MALABSORPTION CYSTIC FIBROSIS CROHNS ULCERATIVE COLITIS ETIOLOGY:    chronic inflammatory disease that causes ulceration of the colonic mucosa and extends proximally from the rectum into the colon. W/ DUODENAL AND JEJUNAL INVMNT BILROTH I& II GASTRECTOMY . tacrolimus. beginning in rectum GASTRITIS POST GASTRECTOMY MALTASE DEFICIENCY LACTASE DEFICIENCY CELIAC SPRUE. individuals between 20 and 40 years of age. w/ small amts of blood Therapy-5-aminosalicylic acid (mesalazine) Steroids and salicylates-suppress inflammatory response Immunosuppresive agents. cyclosporine. Risk factors: jewish descent and prevalent to white populations & Northern Europeans.diarrhea Mucosal destruction-bleeeding. cramping pain & urge to defecate Most common*** frequent diarrhea.