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SYSTEMIC PATHOLOGY TEST 1

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GASTROINTESTINAL

THE ESOPHAGUS

NORMAL STRUCTURE:

CONGENITAL DISORDERS:

RINGS and WEBS:

ESOPHAGEAL DIVERTICULA:

MOTOR DISORDERS:

HIATAL HERNIA:

ESOPHAGITIS:

ESOPHAGEAL VARICES: Lower Esophagus. Portal-caval anastomoses of the esophageal arteries, which become dilated in portal hypertension, and often rupture.

ESOPHAGEAL CANCER:

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THE STOMACH

NORMAL STRUCTURE:

CONGENITAL DISORDERS:

GASTRITIS:

MENETRIER'S DISEASE (HYPERTROPHIC GASTROPATHY):

PEPTIC ULCER DISEASE (PUD): Breaks in the mucosa of the antrum, pylorus, or proximal duodenum, caused by gastric secretions.

BENIGN NEOPLASMS:

MALIGNANT NEOPLASMS:

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THE SMALL INTESTINE

CONGENITAL DISORDERS:

INFECTIONS:

VASCULAR DISEASES:

MALABSORPTION:

MECHANICAL OBSTRUCTION: Mechanical obstructions can lead to ischemic bowel disease.

BENIGN NEOPLASMS:

MALIGNANT NEOPLASMS:

THE APPENDIX:

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THE LARGE INTESTINE

CONGENITAL DISORDERS:

INFECTIONS:

DIVERTICULAR DISEASE:

INFLAMMATORY BOWEL DISEASE:

CROHN DISEASE ULCERATIVE COLITIS
Anatomic Distribution Rectal sparing.

Terminal Ileum is often involved and is very important.

Rectum is always involved.

Terminal ileum is rarely involved.

Type of Inflammation Transmural Strictly mucosal
Distribution of Inflammation Periodic Skip-lesions: Discrete ulcers with islands of normal mucosa. No skip lesions. Diffuse inflammation and edema throughout, leading to edema and ulceration.
Microscopic Pathological Features Non-caseating granulomas Crypt Abscesses
Macroscopic Pathological Features Fissures piercing through wall, which can lead to fistulas. Thickened colonic wall early on. Can see thin, atrophic wall in case of toxic megacolon.

Pseudopolyps are common.

Complications May see strictures

Gallstones

Hydronephrosis from ureter involvement.

No strictures are seen.

Toxic Megacolon.

Many systemic complications.

Cancer Intestinal Adenocarcinoma

Overall risk is slim compared to Ulcerative Colitis.

Risk for diffuse Colonic Adenocarcinoma (not arising from discrete polyps)

Increased risk for cholangiocarcinoma

VASCULAR DISEASES:

POLYPS of the COLON:

ADENOCARCINOMA of the COLON:


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THE LIVER

LOBULAR STRUCTURE:

LIVER ENZYMES:

BILIRUBIN METABOLISM:

JAUNDICE DISORDERS:

LIVER ABSCESS: Focal suppurative inflammation of the liver. May be pylephlebitis due to ascending infection that enters the liver through the portal veins, or cholangitis, if the infection had reached the liver through the bile ducts.

HEPATITIS:

Term Abbrev Description
Hepatitis-B Surface Antigen HBsAg Surface antigen present on viral envelope. Its presence indicates acute HBV infection.

Has serotype-makers: (1) a (always found), (2) d or y, and (3) w or r.

Antibodies to Hepatitis-B Surface Antigen Anti-HBs Antibodies to the surface antigen are not detectable during acute infection even though they are being made, because there is way more antigen and it sops it all up, making it undetectable in the blood.

Presence of Anti-HBs indicates immunity to HBV or previous vaccination for HBV.

Hepatitis-B Core Antigen HBcAg Its presence indicates acute HBV infection, and signifies that the patient is currently infective.
Antibodies to Hepatitis-B Core Anti-HBc Its presence indicates acute or chronic HBV infection. Whether it is acute or chronic depends on whether IgM is present or IgG.
Hepatitis B e Antigen HBeAg This is the hepatitis viral polymerase and is present during acute infection. It indicates that the patient is currently infective.
Antibodies to Hepatitis-B e Antigen. Anti-HBe These aren't usually tested but are present during acute or chronic infection.
Antibodies to Hepatitis-A Anti-HAV Indicates acute infection of Hepatitis-A. There is no chronic Hepatitis-A infection.
Antibodies to Hepatitis-C Anti-HCV Indicates acute or chronic infection of Hepatitis-C.

FATTY LIVER:

ALCOHOLIC LIVER DISEASE:

CIRRHOSIS: The destruction of liver architecture. It is replaced by fibrous septa that contain islands of regenerating hepatocytes.

HEPATIC FAILURE: The common endpoint to many liver diseases, and the clinical manifestations of cirrhosis. Presents with the following complications:

PORTAL HYPERTENSION: Sustained increase in portal venous pressure, usually, but not always, due to cirrhosis.

TOXIC LIVER INJURY:

NEONATAL HEPATITIS: In the neonate, prolonged cholestasis, morphologic evidence of liver injury, and inflammation. Multiple etiologies.

BENIGN NEOPLASMS:

MALIGNANT NEOPLASMS:

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THE GALLBLADDER

CHOLELITHIASIS: Gallstones

CHOLECYSTITIS:

GALLBLADDER CANCER:


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THE PANCREAS

CONGENITAL DISORDERS:

PANCREATITIS:

CYSTIC FIBROSIS:

EXOCRINE CANCERS of PANCREAS:

ENDOCRINE CANCERS of PANCREAS: Islet-Cell Tumors


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DIABETES

Diabetes Type I (IDDM) Diabetes Type II (NIDDM)
Mechanism Insulin is defective or is never formed. Antibodies against pancreatic beta-cells. Insulin resistance; down-regulation of insulin receptors; failure of pancreas to release insulin even though it being formed.
Survival Insulin is absolutely required for survival. Patient will survive without insulin
Synonyms Ketosis-Prone Diabetes

Juvenile-Onset Diabetes

Ketosis-Resistant Diabetes

Adult-Onset Diabetes

Onset Sudden, often discovered by ketoacidosis. Childhood polydipsia, polyphagia, polyuria. Gradual, insidious. Often discovered incidentally, or when chronic complications arise.
Nutrition Often thin. Failure of action of insulin. Usually obese.
Ketoacidosis Frequent Seldom or never
Amyloidosis Amyloidosis of Islets occurs Amyloidosis does not occur.
Complications Nephropathy is often cause of death

Microvascular disease does not show up until 20 or more years after diagnosis.

Multiple causes of death (atherosclerosis, nephropathy).

Microvascular atherosclerosis is present at time of diagnosis.

Epidemiology 10% of cases. 50% concordance of disease between twins. 90% of cases. Multifactorial inheritance. Diet with genetic predisposition.
Treatment (order of importance) Insulin always required

Diet

Never oral hypoglycemics

Diet and exercise

Oral hypoglycemics

Insulin

TYPE-I DIABETES: IDDM

TYPE-II DIABETES: NIDDM

COMPLICATIONS of DIABETES:

KETOACIDOSIS: Lack of insulin (i.e. high Glucagon:Insulin ratio) promotes lipolysis, breakdown of proteins, and glycogenolysis.

HYPOGLYCEMIA:

INSULIN:


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THE KIDNEY

Check out the Table of Nephrotic and Nephritic Syndromes for a nice summary of renal diseases.

CYSTIC DISEASES OF THE KIDNEY:

RENAL FAILURE:

NEPHROTIC SYNDROMES: Non-inflammatory nephropathies.

NEPHRITIC SYNDROMES:

TUBULOINTERSTITIAL DISEASES:

RENAL VASCULAR DISEASES:

UROLITHIASIS (RENAL STONES):

RENAL CANCERS:


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Copyright 1999, Scott Goodman, all rights reserved