Final Exam Pathophysiology

  Major endocrine glands

–      Pituitary

–      Thyroid

–      Parathyroid

–      Adrenal cortex and medulla

–      Pancreatic islets

–      Ovaries and testes

The endocrine system is

a collection of glands that secrete hormones into the bloodstream.

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–      maintaining homeostasis.

Hormones are chemicals

–      that act on target organs to increase or decrease the target’s activity level.

–      Controls cellular activity

HORMONES ARE TRANSPORTED IN

–      THE BLOOD

Hormones…..

Come in contact with all cells, but only have an effect on those cells that have specific receptors (target cells)

Hormones in the body are

–      Control via negative feedback

Normally, hormones are inactivated by the target cell enzymes (degraded) or

–      inactivated by the liver

__Panhypopituitarism__

•       Anterior lobe fails to secrete all hormones

•       Tumor or disturbance of its blood supply

•       Can be congenital

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Function of thyroid, adrenal, and gonads are impaired due to loss of stimulation

It may selectively involve one type of pituitary cells

__Panhypopituitarism__

identify underlying cause and Hormone replacement

Pituitary tumors

–      Many pituitary endocrine disturbances caused by anterior lobe pituitary tumors

•       Pituitary adenoma is most common

Functional tumors:

produce hormones that cause clinical manifestations

Nonfunctional tumors:

do not produce hormones but exert other effects

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–      May encroach on important structures adjacent to optic chiasm; disrupt hormone-producing functions of anterior lobe cells

__Growth hormone overproduction__

–      Caused by pituitary adenoma

–      May cause visual disturbances from tumor encroachment in optic chiasm

__Growth hormone overproduction -__–      Causes gigantism in children

•       Before epiphyseal closure, increase height ( 8- 9 ft) with proportionately large body

•       If left untreated, tumor can completely destroy gland

__Growth hormone overproduction--__–      Causes acromegaly in adults

•       Incr. GH after epiphyseal closure

•       Results in incr. bone diameter . Most evident involving  facial bones and hands and feet.

•       Thickened skin

•       TX: surgical removal/radiation of tumor

__Hypothyroidism__

•       In adults --secretion of thyroid hormone is chronically reduced

–      Condition is called Myxedema

•       Name refers to hydrophilic mucopolysaccharide accumulation in connective tissue in body

•       Most pronounces around eyes and lips and fingers

–      Causes metabolic slowing

__Hypothyroidism--__Clinical presentation

–      Decrease heart rate

–      Slow, dull reflexes

–      Constipation

•       The digestive system works sluggishly, so the patient suffers from constipation

–      Feeling of being cold

–      Weight gain

\-        Dry skin, alopecia

\-        Lack of thyroxine increases the amount of circulating lipids, which leads to the development of atherosclerosis.

__Hypothyroidism-__Etiology

–      thyroid gland dysfunction

•       Iatrogenic (radiation therapy, surgery) or congenital

–      Iodine deficiency

•       Most common cause worldwide

–      Hashimoto thyroiditis

•       Most common cause in US; autoimmune disease

secondary to pituitary disease.

–      If the pituitary gland does not secrete thyroid-stimulating hormones, the thyroid gland ceases to function—rare

__Hashimoto thyroiditis__

•       Autoantibody destroys thyroid tissue

–      Autoimmune disease

•       Most common cause of hypothyroidism

•       An immunologic reaction, not from an infection

–      T lymphocytes destroy gland

•       Cellular infiltration from an immunologic reaction between antigen and antibody

__Hashimoto thyroiditis--__Treatment

•       hypothyroidism is treated by administering thyroxine.

•       The condition generally responds well to treatment, and the symptoms disappear

__Thyroid hypofunction in an infant__

–      Known as Cretinism

__Thyroid hypofunction in an infant--__Etiology:

error in fetal development if the thyroid gland fails to form or the gland is nonfunctional or may be endemic where the mother suffers from an inadequate iodine supply

__Thyroid hypofunction in an infant--__Clinical manifestations

–      include mental retardation, hypothyroidism, and varying degrees of other growth and developmental abnormalities.

•       Thyroid hormone is particularly important in the development of the central nervous system during the fetal and early postnatal periods.

•       Thyroid enlargement (goiter) is usually the earliest clinical feature of iodine deficiency.

•       From overstimulation of TSH (TSH levels are high)

stocky stature and a

\-    characteristically protruding abdomen. The sexual organs do not develop

        -     the face is typically misshapen:

¤   a broad, sunken nose, small eyes set far apart, puffy eyelids, and a short forehead.

\-     A thick tongue protrudes from a wide-open mouth-difficulty swallowing

\-      the face is expressionless.

__Thyroid hypofunction in an infant--__Treatment

The earlier this condition is diagnosed and treated with thyroxine, the more optimistic is the prognosis.

Lifelong hormonal therapy will be required.

__Hyperthyroidism__:

Toxic goiter or Graves disease

•       Caused by antithyroid antibody that stimulates gland

–      Autoimmune disease

•       Mimics effects of TSH but not subject to normal control mechanisms

•       Goiter develops from stimulation of TSH autoantibodies

–      Low levels of TSH and high t3 and t4 levels

•       More common in women than in men and usually affects young women

__Hyperthyroidism__:Clinical Manifestations

¤  The person has a tremendous appetite but loses weight to the point of appearing emaciated, as calories are burned up at a rapid rate.

¤  Thyroxine speeds the passage of food through the digestive tract. There is no time for the normal reabsorption of water from the large intestine, so diarrhea frequently accompanies the disease.

¤  Tachycardia, rapid pulse rate, and palpitation are also among the symptoms.

¤  The person is extremely nervous, excitable, and is always tired but has difficulty sleeping because of the hyperactivity of the body.

¤   The high metabolic rate causes excessive heat production, which results in profuse perspiration. The skin is always moist, and an insatiable thirst follows the loss of water

¤  Exopthalmos

¤  The eyeballs protrude outward, a condition called exophthalmos.

¤  Caused by infiltration of T lymphocytes in the fat, connective tissue, and muscles of eye movement

¤  Leads to inflammation and edema and pushes eye anteriorally

¤  This symptom generally persists even when the hyperthyroidism is corrected.-immunosuppresive therapy may alleviate swelling

__Hyperthyroidism__:¤  Treatment

¤  Antithyroid drugs, thyroidectomy, large doses of radioactive iodine (irradiation destroys part of the gland)

__Addison’s disease/hypoadrenocortism__:

adrenal cortical hypo-function

¤  Deficiency of hormones

¤  Glucocorticoid deficiency

¤  Mineralocorticoid deficiency

__Addison’s disease/hypoadrenocortism__: Etiology:

destruction or damage to the adrenal glands by cancer, infections (tuberculosis),autoimmune (most common), or idiopathic

__Addison’s disease/hypoadrenocortism__:  CLINICAL MANIFESTATIONS

¤  General presentation: Slow developing weakness, fatigue, decrease appetite, weight loss

¤  Cortisol deficiency leads to low blood glucose, impaired protein and carbohydrate metabolism, and generalized weakness.

¤  Aldosterone deficiency leads to Hyponatremia, Hyperkalemia, dehydration, hypotension

¤  Hyperpigmentation: bronzed or sun tan appearance

¤  Pituitary gland produces more adrenocorticotropic hormone (ACTH) in response to a deficiency of corticosteroids.

¤  Precursors (pro-opiomelanocortin) of ACTH stimulate melanocytes to produce melanin

¤  Seen especially in areas of the body exposed to sunlight

¤  Lack of cortisol results in vulnerability to stress

¤  Stress can result in an addisonian crisis

¤  Characterized by an acute presentation of  abdominal pain, nausea, vomiting, diarrhea hyponatremia, hyperkalemia, hypotension, and dehydration, and unconsciousness

¤  Can lead to circulatory shock

__Hyperadrenocortism/Cushings syndrome__:

excess glucocorticoid production

__Hyperadrenocortism/Cushings syndrome__:Etiology

¤  Hormone-producing pituitary microadenoma

¤  Most common

¤  Hormone-producing adrenal cortex tumor

¤  Can be benign or malignant

¤  Administration of large amounts of corticosteroid

¤  Iatrogenic cushing syndrome

¤  Other tumors Non-pitiuitary ACTH secreting tumor (e.g. small cell carcinoma of lung)

__Hyperadrenocortism/Cushings syndrome__:Clinical Manifestations

* Hyperglycemia (adrenal diabetes)
* Cortisol induce gluconeogenesis and inhibit the uptake of glucose by cells
* This results in glucosuria and polydyspsia and polyuria
* Altered fat metabolism
* Mobilization of lipids (trunk obesity, buffalo hump but the arms and legs remain normal, moon shaped face)
* atherosclerosis-circulating lipid
* muscular weakness and fatigue
* polyuria/polydipsia-osmotic diuresis
* Signs and symptoms from protein synthesis:
* -skin becomes thin resulting in bruises, striae (stretch marks) develop on the abdomen, buttocks and breasts, poor wound healing, bones especially the vertebrae and ribs, are likely to fracture, loss of collagen and bone resorption results in osteoporosis, cortisol inhibits immune and inflammatory response , increases susceptibility to infections, cortisol limits gastric acid secretion, increased risk of ulceration

__Hyperadrenocortism/Cushings syndrome__:Treatment:

surgical removal of the enlarged glands or tumor can correct the condition.

•       Hormonal therapy is then required to replace the hormones normally secreted by the adrenal cortex.

__Hyperadrenocortism/Cushings syndrome__: treatment

surgical removal of the enlarged glands or tumor can correct the condition.

•       Hormonal therapy is then required to replace the hormones normally secreted by the adrenal cortex.

Liver anatomy:

largest organ in body, right upper abdominal area, beneath the diaphragm

Bile:

aqueous solution with various dissolved substances

bilirubin

–      blood passes through liver, bilirubin is removed by conjugation by combining bilirubin with glucuronic acid

–      Most of the bilirubin is excreted in conjugated form

•       More soluble and less toxic than unconjugated bilirubin

Bile salts:

major constituent of bile; derivatives of cholesterol (lipid) and amino acids

•        emulsify fats, function as detergents

Other substances present in bile

•       Lecithin: lipid that also functions as a detergent

•       Water

•       Minerals

•       Other materials that have been detoxified by the liver

Bile is secreted

continually…

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•       Concentrated and stored in gallbladder

•       During digestion, gallbladder contracts, releasing bile into the duodenum

•       Bile does not contain digestive enzymes, but acts as a biologic detergent-emulsifies fats

Jaundice

•       Yellow discoloration of skin and sclera from increase bilirubin in blood and then accumulation of bilirubin in tissues and body fluids

•       Caused by hemolytic anemia, primary liver disease and obstruction in biliary systemt

•       Bilirubin has affinity for elastic connective tissue (sclera)

–      Hepatitis

•       Inflammation of the liver

–      Acute or chronic

–      Hepatitis-Etiologies:

•       viral (50% of cases), drug (acetaminophen) and alcohol toxicities, autoimmune

Fatty liver:

–      nonalcoholic; idiopathic, but linked to obesity and insulin resistance

–      Cirrhosis

•       Chronic liver cell injury from any cause followed by diffuse scarring

Alcoholic Liver Disease

•       Refers to a group of structural and functional changes in the liver resulting from excessive alcohol consumption

•       Severity depends on amount and duration of alcohol consumption

Alcoholic fatty liver:

mildest form-reversible

Alcoholic hepatitis:

–      causes degenerative changes and necrosis of liver cells

•       Degenerative changes along with fatty deposits in cell

•       Mallory bodies-irregular pink deposits in the cytoplasm-characteristic feature

•       Denotes irreparable damage to cell

•       -neutrophils accumulate in response to necrosis

•       Followed by fibrous scarring

•       Diffuse distribution

Alcoholic cirrhosis:

most advanced, diffuse scarring, disturbed liver function

    Associated with a history of repeated bouts of alcoholic hepatitis

Cirrhosis:

chronic progressive and irreversible condition

–      Diffuse scarring of the liver from any cause with derangement of liver function  and regeneration

–      Liver is converted into mass of scar tissue containing nodule of normal and degenerating cells along with inflammatory cells

–      Complete disorganization of liver

–      Intrahepatic branches of the hepatic artery and portal vein are constricted by scar tissue

–      Decrease in liver cell function by scarring  death

Cirrhosis:Etiology:

–      Alcoholic liver disease

–      Chronic hepatitis-HBV or HCV

–      Severe liver necrosis

–      Repeated liver injury: drugs and chemicals

–      Longstanding bile duct obstruction

Cirrhosis:Clinical Manifestations

Weight loss (sometimes masked by ascites)

•       Weakness

•       Anorexia

•       Diarrhea or constipation

•       Hepatomegaly initially, then decrease in size

•       Jaundice

      Abdominal pain

Cirrhosis:•       Clinical manifestation in men

–      Estrogen elimination is reduced b/c of livers inability to inactivate it

–      Leads to increase in estrogen levels

•       Testicular atrophy, decrease sex drive and mammary gland hypertrophy

Cirrhosis clinical manifestations:women

–      Irregular menses (irregular menstration)

Cirrhosis:Pathophysiology

Hepatic insufficiency

– Impaired bile synthesis

–      Increase bilirubin in blood  jaundice

–      Increase bile salts in blood skin  itching

–      Excreted in urine dark urine

– Impaired detoxification

From accumulation of toxic substances in the blood that are normally detoxified and excreted by the liver

•       Toxic products include ammonia from deamination of amino acids and bacterial decomposition products of colonic fecal material-protein digestion

•       Leads to hepatic encephalopathy (nervous system disorder brought on by severe liver disease): Deterioration of brain function characterized by impaired consciousness, confusion, disorientation, and eventually coma

 

– Clotting defects

– Reduced plasma proteins

Portal hypertension

–      Scar tissue obstructs portal vein leading to increase pressure

–      Increase pressure affects capillaries and leads to a leakage of fluid from the capillaries

•  increase hydrostatic pressure in abdominal capillaries leads to fluid leaking into peritoneal cavity (ascites)

–      Ascites

      Low albumin from hepatocytes inability to produce it

•       Leads to decrease colloid osmotic pressure and fluids leaks from the portal capillary beds

•       Edema

 -increase blood pressure in the hepatic circulation leads to blood backing up into collateral venous circulation

•  Results in splenomegaly

•  Results in dilation of esophageal veins

•        leads to varices and risk of upper gi hemorrhage  

•       Results in rectal vein varices and risk of lower gi hemorrhage

 

Cholelithiasis:

–      Formation of stones in the gallbladder  

         Predominantly composted of cholesterol

Cholelithiasis:     Pathogenesis

•       Cholesterol (lipid) is insoluble in aqueous solution and Bile salts and lecithin increase its solubility in solution

•       Anything that disrupts the relative ratio between cholesterol and bile salts and lecithin can lead to precipitation of cholesterol –crystals form

•       Factors influencing solubility of cholesterol in bile

•       Solubility of cholesterol depends on ratio of cholesterol to bile salts and lecithin

•  Increase cholesterol  precipitates

•  Decrease in salts/lecithin precipitates

•       Supersaturated bile can lead to gallstones

Cholelithiasis:Incidence

•  Higher in women than men

•  Higher in women who have borne several children

•  Twice as high in women who use contraceptive pills

•       ABOVE ARE FROM INCREASE OF ESTROGEN PROMOTES INCREASED EXCRETION OF CHOLESTEROL into the bile

•       Higher in obese women-increased cholesterol in blood

•       Infection can lead to gallstones (uncommon)

Cholelithiasis:         Manifestations

•       Asymptomatic

•       Biliary colic if stone is extruded into ducts

•  Pain in upper right quadrant; may be referred to upper back / right shoulder

•  Common duct obstruction: obstructive jaundice

•       No bile enters into duodenum

•       Reduced bile clearance from liver  bilirubin and bile salts accumulate in liver and then in blood

•       Bilirubin in blood causes jaundice

•       Bile salts in blood are carried to peripheral tissue and produce pruritus (intense itching)

•  Cystic duct obstruction: no jaundice, acute cholecystitis may occur with preexisting infection in gallbladder

–      Bile can neither leave nor enter the gallbladder

–      Bile still can flow from the liver into the duodenum

Cholelithiasis:•       Treatment

•       Cholecystectomy-laparoscopic surgery

•       Chenodeoxycholic acid dissolves gallstones

cholecystitis

•       Inflammation of gallbladder

•       Chronic infection is common

•       Gallstones may predispose to cholecystitis

•       Impaction of a stone in neck of gallbladder may cause acute cholecystitis

Pancreatitis:

inflammation of the pancreas

Pancreatitis: etiology

•  Gallstones (stones in the common duct)

•  Alcohol abuse

•  Hyperlipidemia

•  Hyperparathyroidism

•  Infections (particularly viral)

•  Abdominal and surgical trauma

•  Drugs such as steroids and thiazide diuretics

Pancreatitis: •       Pathogenesis

•       Escape of pancreatic juice from the ducts into the pancreatic tissue

•  This leads to destruction of the pancreatic tissue by the activated enzymes in the fluid

•  This leads to acute inflammatory reaction of the affected tissue

Pancreatitis: •       Presentation

•       Acute abdominal pain in left upper abdominal quadrant, fever, tachycardia, respiratory distress

•       Severe form can lead to hemorrhagic pancreatitis

•       Elevated serum pancreatic enzymes-lipase and amylase

•       Ultrasound and CT scans to evaluate structure

}  Anorexia

}  Loss of appetite

}  Nausea

}  The awareness of  an unpleasant sensation referred to the epigastrium and abdomen

}  Vomiting

}  Sudden and forceful oral expulsion of contents (vomitus) of the stomach

}  Rids GI tract from noxious agents

}  Pallor (paleness) and increased salivation precede vomiting

}  Result of altered CNS output

}  Retching: unproductive vomiting

}  Diarrhea

}  Increased fluidity of fecal matter/increase frequency (motility diarrhea)

}  Caused by increased colonic fluid volume, which increases distention and activates the defecation reflex.

Constipation:

difficulty defecating

Diseases of the Esophagus--}  General Symptoms/Signs

◦       Sub sternal discomfort or pain

◦       Difficulty swallowing (dysphagia)

◦       Inability to swallow (complete obstruction)

◦       Regurgitation of undigested food

}  A backward flow of undigested food

}  Choking and coughing can result and food particles can enter the trachea

__Hiatal hernia__:

protrusion or herniation (projects from its normal cavity) of the stomach through the esophageal hiatus of the diaphragm

}  Axial-hernia  (sliding)

}  Characterized by a bell shaped  protrusion of the stomach above the diaphragm

}  Common and of no significance in asymptomatic individuals

Non-axial-hernia (paraesophageal)

Portion of the stomach enters through a widened opening

–  Hernia Progressively enlarges and can lead to the entire stomach within the thoracic cavity ; require surgery

__Hiatal hernia__: Etiology:

Muscle weakness common with increase age, trauma, congenital

__Hiatal hernia__:Ø  Signs and Symptoms

o   asymptomatic

o   heartburn related to gastroesophageal reflux

o   Dull burning ache that may radiate to neck

o   Large paraesophageal hernias  can result in difficult, painful swallowing, chest pain, and vomiting.

__Gastroesophageal reflux__

Ø  Backward movement of gastric contents (acid) into the esophagus

Ø  Results in heartburn (pyrosis)

o   Usually occurs soon after eating and short lived

o   Rarely cause serious problem

Ø  Transient relaxation of the LES after meals is common

Ø  Increased occurrence after gastric distention and meals high in fat

o   Pressure is higher within the stomach and exceeds LES pressure

Ø  Normally refluxed material is returned to the stomach by a 2nd peristaltic wave in the esophagus and saliva (bicarbonate) will neutralize the stomach acid

 __Gastroesophageal Reflux Disease__ (GERD)

}  Persistent reflux of gastric contents

◦        signs and symptoms occur at least twice a week      interfere with your daily life

◦        damage to the esophagus

A chronic digestive disease

Factors that predispose to GERD

–  Hiatal hernia

–  Weakened lower esophageal sphincter

–  Food or alcohol ingestion, cigarette smoking that lower LES pressure

–  Increased abdominal pressure (obesity or pregnancy)

–  Delayed gastric emptying

 __Gastroesophageal Reflux Disease__ (GERD)--Signs and Symptoms

Heartburn

}  Severe and occurs 30 – 60 minutes after a meal

}  Is worsened with bending at waist or when lying down

}  Usually relieved by sitting up

}  Antacids give prompt relief (transient)

}  Usually at night

Chest pain

–  Epigastric region or retrosternal area that may radiate to throat, shoulder, or back

–  Confused with Angina

 __Gastroesophageal Reflux Disease__ (GERD)--Treatment

Avoidance of predisposing factors

–  Decrease size of meals

–  Eat sitting up instead of lying down

}  Avoid lying down for several hours after a meal

}  Bending should also be avoided (increases intra-abdominal pressure)

–  Avoid ingestion of foods that reduce LES tone

}  Caffeine, chocolate, fats, alcohol, and smoking

–  Sleep with head elevated

–  Weight loss

–  Antacids, H2 blockers, proton pump inhibitors

–  Surgical treatment

Complications: Result from persistent reflux

◦       Hyperemia ( xs blood ), edema (swelling caused by excess fluid), and erosion of the mucosal surface of the esophagus

–  Can lead to strictures of the esophagus

–  , edema, spasms, scar tissue formation during healing

–  Narrowing of the esophagus  dysphagia

Barrett’s\*\* esophagus

–  Normal Squamous mucosa is replaced by columnar epithelium (metaplasia-conversion of cell type)

–  Prolonged gastroesophageal reflux inflammation ulceration healing occurs in low pH environment gastric/intestinal epithelium, which is more resistant to acid

–  Predisposes to malignant neoplasia

Acute Gastritis

}  Inflammation of the gastric lining

◦       Results from sudden disruption of the normal barrier

◦       Can be from increased acid secretion, decrease bicarbonate buffer, decreased blood flow, disruption of mucous lining, direct damage to epithelium

Acute Gastritis--Etiology

Idiopathic

       Commonly associated with local irritants:

}  Alcohol: a gastric irritant

}  Bacterial toxins

}  Non-steroidal anti-inflammatory drugs (NSAID) aspirin\*\*, ibuprofen, naproxen

Acute Gastritis--}  Clinical manifestations

◦       Asymptomatic

◦       C/O Heartburn or ‘sour’ stomach

◦       Vomiting

◦       Diarrhea

◦       Mucosal ulcerations and hemorrhage

}  May present with massive hematemesis (“coffee grounds”), melena, and fatal blood loss

Acute Gastritis---  Treatment

}  Self limiting with complete healing in several days of removal of inciting agent-most common scenario

}  stop NSAIDS

}  Acid reduction (H2 blockers, proton pump inhibitors)

}  Used as first line medication in trauma pts

}  Antacids that neutralize stomach acid.

Chronic Gastritis

}  Characterized presence of chronic inflammatory changes and occurs slowly over time

◦       Leads to atrophy of glandular epithelium of stomach and metaplasia

 __*Helicobacter pylori*__

}  Small, curved, gram-negative organisms that colonize surface of gastric mucosa

◦       Antrum of the stomach

 Most common cause of chronic gastritis in U.S

}  In the United States, approximately 35% of adults are infected with *H pylori*

}  Infects more than ½ of world’s population

}  The infection is usually acquired during childhood

}  Socioeconomic differences are the most important predictor of the prevalence of the infection in any group— better sanitation

}  Spreads via person-to-person through close contact (mouth –mouth) and fecal-oral route

}  Possible environmental reservoirs

__*Helicobacter pylori*__---Pathogenesis:

◦       Grow within layer of mucus covering epithelial cells

– Able to move through the mucosa because of their multiple flagella

 __*Helicobacter pylori---*__Clinical manifestations

}  are dependent on both host factors and virulence of microbe

◦       Acute infection

}  Nausea and abdominal pain –may last for days

}  Usually progresses to asymptomatic chronic mucosal inflammation

◦       Chronic infection

}  Leads to gastric atrophy and peptic ulcers

}  associated with increased risk of adenocarcinoma and low grade gastric lymphoma

 __*Helicobacter pylori---*__Treatment

◦       Combination of 2 antimicrobial agents

◦       Proton pump inhibitors/H2 blockers/peptobismol

helps alleviate ulcer-related symptoms (i.e., abdominal pain, nausea)

Enteritis  =

inflammation of any part of the small intestinal tract

Colitis=

inflammation of colon

Bowel inflammation =

any part of intestinal tract

Inflammatory Bowel Disease: 2 types

}  Crohn’s disease: any area of GI

}  Chronic ulcerative colitis: colon and rectum

Inflammatory Bowel Disease:Etiology:

}  Alterations in host interactions with intestinal micro biome

}  Intestinal epithelial dysfunction

}  Alteration in microbiome composition

}  Inappropriate immune response

}  Genetic predispostion

__Crohn disease__

◦       Slowly progressive Recurrent Granulomatous inflammation that can affect any area of the GI tract

◦       Most common locale is terminal ileum and cecum, but can involve other areas of the small intestine

◦       Granulomatous lesions may be scattered with normal intervening areas or “skip areas”

◦       Submucosal layer is mostly involved

◦       Over time the bowel wall becomes thickened and inflexible

__Crohn disease---__Symptoms and Signs

periodic with diarrhea and cramping, weight loss, fever and fecal urgency

◦       May mimic appendicitis with lower right abdominal pain, fever and bloody diarrhea

◦       Asymptomatic periods can last for weeks to month

◦       Symptoms associated with physical or emotional stress, diet or smoking