Anorectal Disorders

Anorectal Disorders
Presenteation by: Carrie Lotenero, DO

Anatomy
Hemorrhoids: MCC rectal bleeding
Hemorrhoids
Anorectal abscesses
Anal fistula
Anal Fissure
Anal Fissure
Venereal Proctitis
Rectal prolapse = procidentia
Anorectal tumors
Anal crypts, columns of morgagni, dentate line
Surgery-partial sphincterotomy and excision of fissure

Anorectal Disorders.ppt

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Acute Appendicitis

Acute Appendicitis
Presentation by:Stephen Cluff D.O.

Acute Appendicitis

Begins as a Lumen obstruction
…mucosal secretion increases pressure
…overcomes perfusion pressure
…obstructs venous/lymphatic drainage
…epithelial breakdown
…invasion by bowel flora
…eventual arterial stasis and necrosis
…spillage of infected contents into peritoneum

Pain Presentation
History
Physical Exam
Labs
Imaging
Special Cases
Treatment

* Appendectomy
* NPO, IV fluids, pre-op antibiotics

Disposition

QUIZ
Acute Appendicitis.ppt

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Diseases of the Exocrine Pancreas

Diseases of the Exocrine Pancreas
Presentation by: Emre Conklu, DO

Anatomy

* Divided into 4 parts: head, neck, body, and tail, located retroperitoneally.
* The head of the pancreas attaches firmly to the duodenum.
* The head rests posteriorly on the IVC, and R renal artery/vein.
* Sphincter of Oddi- is composed of smooth muscle that controls the flow of bile and pancreatic juice into the duodenum.

Blood Supply

* Derived mainly from branches of the splenic, gastroduodenal, and superior mesenteric arteries.
* The head is supplied by the superior and inferior pancreaticoduodenal arteries, branches of the gastroduodenal and super mesenteric arteries.

Lymphatics

* Follow the blood vessels
* Efferent vessels drain to the celiac, hepatic, and superior mesenteric lymph nodes.

Nerve Supply

* Derived from the vagus and thoracic splanchnic nerves passing through the diaphragm.
* Symp/Parasymp fibers reach the pancreas by the celiac and superior mesenteric plexus.

Physiology

* Bulk of the pancreas is composed of pancreatic exocrine cells and their associated ducts.
* Embedded within this exocrine tissue are the Islets of Langerhans, endocrine cells that secrete insulin and glucagon.
* Flow of exocrine juice acinar cell-> acini->intralobular ducts-> main pancreatic duct.
* Packages of zymogen granules have an acidic ph and low calcium concentration. Also packaged with protease inhibitors.
* 2 major pancreatic proteases are trypsin and chymotrypsin-Digest proteins.
* Lipase digests dietary fat.
* Amylase digests starch to maltose

Lipase

* In acute pancreatitis, reaches a max level in 24 hours and remains elevated for 8-14 days.
* Superior sensitivity and specificity than amylase in detection of acute pancreatitis.
* At levels 3X normal, has 100% sensitivity and specificity for detection of acute alcoholic pancreatitis.

Amylase

* Max level reached in 12-20 hours, maintained levels for 2-4 days.
* Activity in human tissues: Pancreas, salivary glands, tonsil, fallopian tube, lung, thyroid, malignant neoplasms.
* Rises in many conditions such as bowel obstruction/perforation, parotitis, ectopic pregnancy, radiation, cirrhosis, hepatitis.

Acute Pancreatitis

* Most common cause is EtOH consumption, followed by gallstones. Other causes include post-ERCP, certain meds, and hypertryglyceridemia.
* Blacks have 3x higher rates than white Americans, HIV/AIDS due to increased pancreatic infections and medication history.

Etiology

* Biliary tract Dz
* Drugs
* Abdominal Trauma
* Abdominal Surgery
* ERCP
* Viral Infections
* Penetrating gastric or duodenal ulcers
* Pancreatic CA
* Renal Failure
* Occupational exposure to chemicals such as methanol, mercuric chloride, naphthalenes, lead, and organophosphates
* Scorpion bites, obstruction at ampulla by carcinoma or Crohns disease
* Hypotensive shock.
* Idiopathic

Differential Dx

* PUD
* Acute Cholecystitis
* AAA Rupture
* Intestinal Obstruction
* Early Acute Appendicitis
* Mesenteric vascular obstruction
* DKA

Prognostic Signs in Acute Pancreatitis
During initial 48 hours


Enzyme Markers

* Amylase rises quickly but returns to normal in 3-4 days.
* Lipase- more accurate than amylase in diagnosis.
* Absolute level of serum amylase or lipase does not correlate with severity.

Major Adverse Factors

* Hypotension
* Need for massive fluid replacement
* Respiratory failure
* Hypocalcemia
* Hemorrhagic peritoneal fluid
Physical

* Epigastric tenderness and guarding, pain may lessen with leaning forward.
* Tachycardia, shock->vomitting and dehydration
* Fever
* Delirium
* Hypoactive bowel signs
* Hypocalcemia
* Cullen’s and Grey Turner Signs
* Jaundice

Labs

* Amylase Increase
* Lipase Increase
* Lipase/Amylase ratio increase=Alcoholic pancreatitis
* Serum trypsin level most accurate indicator of acute pancreatitis.
* Leukocytosis, Increase/Decrease in Hct
* BUN increase due to dehydration
* Liver tests may be abnormal due to hepatic involvement.
* Hypocalcemia-Free fatty acids chelate calcium, causing saponification in the retroperitoneum.
* Hypernatremia due to dehydration

Diagnostic Imaging Studies

* Abdominal CT Scan-Contrast-enhanced
* Abdominal US for gallstones
* Abdominal X ray for ileus and calcifications
* ERCP for recurrence of unknown cause, preoperative planning, or trauma to ducts.
* MRCP
* CT guided fine needle aspiration for infected acute necrotizing pancreatitis.

Treatment


* Increase intravascular volume with hydration, measure UO
* NPO
* NG suction
* Control pain-- -> caution with morphine
* Correct metabolic abnormalities.
* TPN for prolonged cases.

Complications

* GI Bleeding- DIC , liver diseases
* Renal Failure- hypovolemia
* Hypoxemia – ARDS
* Abdominal Hemorrhage

Pancreatic Divisum
Pancreatic Adenocarcinoma
Cancer of the Exocrine Pancreas
Risk Factors
History
Physical Findings

* Abdominal mass
* Ascites
* Jaundice
* Palpable gallbladder
* Supraclavicular lymphadenopathy
Initial Presentation

* Varies according to tumor location
* Tumors in the pancreatic body or tail usually present with pain and weight loss.
* Tumors in the head present with steatorrhea, weight loss, and jaundice.

Diagnostic Imaging Studies
Serum Tumor Markers
Other Risk Factors
Molecular Pathogenesis
Cholecystitis
Calculous Cholecystitis
Ascending Cholangitis
Gallstone Ileus
Pneumobilia
History
Exam
Studies

Treatment

Diseases of the Exocrine Pancreas.ppt

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