Download Patient`s history Chronological sequence of events Pain then N/V

Patient’s history
 Chronological sequence of events
o Pain then N/V= appendicitis
o N/V then Pain= gastroenteritis
 Sudden or gradual onset of pain
 Character of pain
o Autonomic nerves innervate the viscera
 Visceral pain- dull, cramp like, insidious
o Somatic nerves innervate parietal peritoneum
 Somatic pain- localized sharp constant
 Duration of pain
o Pain for hours to days is often more severe than pain lasting for weeks
 Location of pain
o May not be specific
o Referred pain diaphragmatic irritation- kehr's sign
o Periumbilical going to the right lower quadrant- appendicitis
o Changes in location marker of progression
 Palliation
o Use of heat or ice- musculoskeletal origin
 Medications: ASA, ibuprofen
 Relation to food- duodenal ulcer- pain 2 hours after meals relieved by eating
 Relation to food- worse with eating- gastric ulcer
 Movement- peritonitis, fatty food- billiary colic comes with cholithiasis
 Severity of pain scale 1/10
o Single rating is not much clinical help
 Serial determinants of pain severity- useful
 Temporal nature of pain
o Awaken patients at night?
 Post prandial- cholelithias or gastric ulcer
 Randomly through day vs at a certain time
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Fever chills- infection
Nausea, vomiting, diarrhea, constipation
History of severe retching/vomiting- mallory-weiss (tear) or boerhaave's syndrome
(triad- vomiting, subcutaneous emphysema and LLQ pain)
Urinary and bowel habits- change in caliber of stool- cancer makes it pencil thin
Last menstrual period, sexual and pregnancy hx
Upper resp tract symptoms- lower lobe pneumonia as cause of abdominal pain
Family social medical history
Cardiac history-atypical acute MI- stomach pain in women or silent MI in elderly and
diabetics
a-fib-abdominal vascular infarction- mesenteric ischemia
o test is mesenteric angiography
o FOB is positive
Exposure history- corrosive esophagitis
o Caustic chemicals, lead
o Alcohol or narcotic withdrawal
o Mushrooms ticks (deer tick) spiders (black widow)
o Travel
Appearance
Pain constant (parietal, lying still) vs. crampy (gall bladder, cant sit still)- still
vs. writhing
o Diaphoresis- acute MI sepsis or shock
o Pallor anemia shock
Vital signs
o Orthostatics- 3rd spacing or volume depletion- acute pancreatitis
Heent and neck
o Sclera icterus (jaundice greater than 2.5)
o Fundoscopic signs of emboli (A-Fib)
o Carotid bruits
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Chest
o Crackles and wheezes at bases
Consolidation, pulmonary edema
Heart murmurs
Pleural rubs
Hard stool- constipation/impaction may have diarrhea
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Pelvic genital and rectal exam on every patients with severe abdominal pain
Cervical motion tenderness PID- Shandeliar Sign
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Abdomen palpate from area of least pain to areas with most pain
Inspection: scars (adhesions, rash (herpes zoster), visible pulsatile masses AAA
o **Adhesions are the most common cause for acute small bowel obstructions
in patients without virgin abdomens
o MCC of SBO without surgeries is hernia
Auscultation: bowel sounds- least revealing! Abdominal bruits
Percussion: identify ascites- shifting dullness to percussion
Palpation
o Obtaining rebound tenderness is most often unnecessary and unkind to the
patient pain with cough has similar specificity and sensitivity
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Adnex mases of the testicular portion can also present as abdominal pain
**adhesions ms cause of acute bowel obstruction with surgery
 CBC with diff: inflammation like IBD which would be UC and Crohn’s or infection
Serum electrolytes
 BUN and Creatin, urinalysis (UTI), UCG (pregnancy)
o Metabolic causes, dehydration, UTI, pregnancy
 Liver function tests: AST (alcohol), ALT (viral)
 Pancreatic enzymes- amylase, lipase (more specific)
 Cardiac enzymes- CKMB, troponin
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Elderly patients: pain presentation is often atypical in location and severity; may not
mount febrile response. We may see hypothermia or nothing at all.
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Immunosuppressed patients; steroids may mask pain and decrease inflammation,
immunosuppression leads to opportunistic infections and may cause the following
diseases: CMV, lymphoma
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In an obese patients organs are not in place where you think they are there is overall
abdominal distortion
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Patients on medication: some medications may change the perception of pain or
cause constipation
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Pregnancy: distorted abdomen may be difficult to examine, variable organ location.
Symptoms of preg my mimic those of some gasteroenteritis i.e. N/V, electrolyte
disturbances and dehydration
Imaging studies:
 Upright supine
o Intraperitoneal free air obstruction
o Air fluid levels and dilated loops of bowels specific for bowel obstruction
o Colon cutoff sign is acute pancreatitis
Abdominal pelvic ultrasound- modality of choice for RUQ pain and Gyn disease
CT scan- evaluates intrabdominal infections vasculature inflammation and solid organs
 Diagnostic test of choice Appendicitis, diverticulitis, pancreatitis
 Not good for gall bladder and pelvic organs
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MRI scan- not much use in diagnostic workup of abdominal pain
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EKG- rule out ischemia and mi
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Diseases of esophagus
GERD
 Recurrent reflux of gastric contents due to
 Weak or incompetent lower esophageal sphincter
 Decreased resting pressure of LES
 Prolonged or transient relaxation of LES
 Conditions pregnancy scleroderma
 Drugs: anticholinergics, b-adrenergic, CCB
 Substances: nicotine alcohol
 Foods: chocolate, peppermint, and nitrates.
 All Aggravate the lower esophageal sphincter pressure and promotes reflux
 Delayed gastric emptying in gastroporesis in diabetics
 Esophageal will begin to occur in a pH less than 4
Clinical manifestations
 Heartburn- MC
 Regurgitation
 Anemia
 Cough hiccups
 Dysphagia to solids- because you have mucosal damage
 Recurrent laryngitis
 Reflux induced asthma
 Diagnosis
o Barium swallow upper gi series
o Endoscopy with biopsy
o Esophageal manometery: evaluates LES pressure- motility disorders
o Esophageal 24 hour pH monitoring- diagnostic test of choice
 Treatment: lifestyle changes
 Avoid eating prior to sleep weight loss
 Avoid aggravating acidic foods
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Avoid tight fitting clothes
Antacids: calcium, mg, bicarbonate. Taken before meals and at bedtime
H2 receptor antagonists: cimetidine, pepsid
*Proton pump inhibitor: omeprazole. Most potent*
Promotility agents: metoclorpramide
Surgery: nissen fundoplication. Indicated in Barretts esophagus when PPI doesn’t
work or when we have extra esophageal signs of GERD
Complications:
o stage one is hyperemia, stage two is linear non-confluent lesions, and stage
three is circular confluent erosions (Barretts Esophagus)
o persistent reflux can produce cycle of mucosal damage that causes hyperemia
edema and erosion to surface leading to strictures PUD gi bleed
Barretts esophagus
o Normal squamous mucosa replaced by columnar epithelium
o Premalignant state
o Dx: endoscopy with biopsy
o Tx: same as Gerd, serial biopsies for high grade dysplasia
Corrosive esophatitis
 Chemical burn to upper gi mucosa due to ingestion of alakaline or acidic substances,
bleach or detergents, assc. with suicide attempts
 Clinical manifestations
o Burning oropharyngealk and or retrosternal pain
o Poropharyngeal erythema burns erosions ulcers. Even if you don’t see burns
in the mouth does not mean that they don’t exist further down in the
esophagus
o Excessive gagging dysphagia odynophagia, drooling
o hematemesis, melena
o Diagnosis clinically established. Within 24 hours make sure you do an upper
endoscopy to check for grade of damage
 Treatment supportive (IV fluids) no inducing emesis
o Steroids and broad spectrum antibiotics initially
 Steroids given to prevent stricture
o Surgery esophagogastrectomy, colon interposition
 Complications stricture, formation cancer risk
Esophageal cancer
 There are 2 types; in the past SCC accoutered for more than 90% of cases
Squamous cell carcinoma
 Incidence higher in African men
 MC location upper and mid thoracic esophageous
 Risk factors
o Alcohol and tobacco use
 HPV **achlasia** plumner vinson syndrome (esophageal web, iron deficiency
anemia, and glossitis)
 Caustic ingestion, nasopharyngeal carcinoma
Adenocarcinoma
 Incidence higher in white men
 Mc location distal 1/3 esophagus gastroesohpageal junction
 Risk factor
o Gerd, barretts
o Alcohol and tobacco
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Prognosis is very poor
Clinical features
 Dysphagia (difficulty): mc symptoms; initially solids and then liquids
 Anorexia wieght loss- 2nd MCC
 Odynophagia (painful) late finding
o Suggests mediastinum invasion
 Hematemsis chest pain
 Hoarseness
 Aspiration pneumonia and resp symptoms once the cancer has spread to the tracheal
bronchial tree
Diagnosis
o Barium swallow- outline a diverticula
o Upper endoscopy with biopsy: definitive dx***
o Full metastic workup
o Ct scan of chest and ab
Treatment
 Palliation is goal
 Surgery; esophagetctomy may be curative
 Chemotherapy and radiation before surgery
Mallory-Weiss syndrome
 Inadequate relaxation of the esophageal sphincter during vomiting with subsequent
mucosa tearing of the gastroesphageal junction
 Hematemesis status post retching episode
 Amount may vary- from blood streaked to massive frank blood
 Risk factors: alcoholics bulimics
 Diagnosis: upper endoscopy but may not be necessary because 90% self resolve
o If not, then you will do endoscopy: local injection, sclerotherapy or cautery or
surgery if we need to repair the tear
Boerhaves syndrome
 Complete full thickness longitudinal rupture of distal esophagus usually above
gastroesohpageal junction- stomach contents empty into the peritoneal
 Triad: vomiting, chest pain, subcu emphysema
 Homan’s Crunch
 Risk factors: sudden increase in intra abodminal pressure caused by retching
vomiting heavy lifting childbirth
 Dyspnea diaphoresis
 DX: upright CXR- air in mediastinum, esophagram- usually don’t do because pt is not
stable
 Tx: surgical repair broad spectrium antibiotics
Benign esophageal stricture
 Sequelae of prolonged reflux esophagitis
 s/s heart burn solid food dysphagia
 Dx: barium swallow endoscopy
 Tx: balloon dilation catheters
Esophageal web: plummer vinsons syndrome
 Located in upper 1/3 of esophagus
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Higher risk factor for squamous cell carcinoma (10% will develop into oral and
esophageal carcinoma)
Causes: dysphagia, iron deficiency anemia, atrophic oral mucosa, coroenichia (spoon
shaped finger nails)
Treatment esophageal dilation that will break the web and iron supplements
Esophageal rings: schatzki rings
 A circumferential ring in the lower esophagus, usually accompanied by a sliding
hiatial hernia
 MC occurs at the squamous columnar junction
 Usually asymptomatic
 Mild to moderate dysphagia and reflux can occur if you have that hernia
 If there is no reflux all you have to do is dilate the esophagus. If theres reflux you
have to dilate the esophagus and Anti-reflux surgery which is the Nissan
fundopigation
Esophageal diverticula
Three types: traction, zenker’s, and epiphrenic
 Most esophageal diverticula are saved by an underlying motility disorder
Zenker's diverticulum: (pulsation, failure of the cricopharengeal muscles to relax
during swallowing) mc esophageal diverticula
o Mucosal herniation found in upper 1/3 of esophagus
 S/S: dysphagia regurge (solid food) halitosis weight loss cough
 Tx: surgery. Be careful with endoscopy because you don’t want to perforate
Traction diverticulum (traction, being pulled on by lymphadenopathy) asymptomatic
no treatment
 Located at mid-point of esophagus near tracheal bifurcation
 Traction from continuous mediastinal inflammation and adenopathy causing
retraction of esophagus pulmonary TB or sarcoidosis
Epiphrenic diverticulum (pulsation) often asymptomatic
 Mucosal herniation found in lower 1/3 of esophagus
 Assc with spastic dysmotlity or **achlasia**
 Dx: barium swallow
 Tx: surgery
Achlasia
 Acquired disorder of esophageal smooth muscle
 LES fails to completely relax with swallowing
 Abnormal peristalsis of the esophageal body in the lower third because the
neuroplexus is missing
 Causes: idiopathic, assc. with gastric cancer
 Ss: dysphagia odynophagia CP weight loss nocturnal cough recurrent bronchitis or
pneumonia
 Equal difficulty in swallowing solids and liquids
 Wash food with lots of water, twist their necks to help the food to go down
Diagnosis
 Barium swallow: birds beak narrowed distal esophagus with large dilated proximal
esophagus
 Endoscopy required to exclude malignancy because achlasia is risk factor
 Esophageal manometry confirms Dx. Because manometry is the best test for motility
disorders
Treatment adaptive measures: chew food better, don’t eat before bed
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medical therapy includes CCB, sublingual nitroglycerin, and injection of botulism into
the LES, dilation to the LES ring and surgery
Diffuse esophageal spasm
 Non peristaltic spontaneous contraction of esophageal body
 Several segments contract simultaneously preventing appropriate advancement of
food bolus
 Complain of both chest pain and dysphagia
o Nutcracker esophagus more complaint on chest pain** because the spasm is
of higher amplitude
 In contrast to achlasia LES function is normal. Food will go to stomach
 Ss non cardiac chest pain that mimic angina, dysphagia is common, regurgitation of
food is uncommon
 Diagnosis esophageal manometry: simultaneous repetitive contraction that occur
after swallowing with normal LES response
 Barium swallow cork screw: multiple spontaneous contractions
 Treatment nitroglycerin CCB TCA
Hiatal hernias
 Sliding account for greater 90 of cases
 Both gastroesophageal junction and portion of the stomach herniate into the thorax
through the esophageal hiatus
 Les is above the diaphragm
 Medical- antacids, small meals, elevation of trunk
o 10% require nissen's
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Presents with a several month history of intermittent dysphagia foods such as steak
seem to get stuck
He is able to clear these foods by drinking extra liquids symptoms are not getting
worse: lower esophageal ring shitake’s ring
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A 65 y/r male. Trouble swallowing for 5 weeks. At first only meat stuck in his
through now trouble with soft foods. No hx of similar problems or of any gi problems.
He is a moderately heavy drinker and has smoked 1 pack per day for 40 years
Esophageal cancer
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Presents sp having dry heaves after drinking- mallory weiss
Acute gastiritis
 Diffuse or localized inflammation of gastric mucosa
Etiology
 Aspirin nsaids alcohol smoking
 H. pylori infection, severe illness/stress
 Ss: epigastric burning and pain n/v gi bleed
 Diagnosis: endoscopy with or without biopsy
 Gastric mucosa may appear congested friable with superficial ulcerations or petechia
 Treatment remove offending agent
 Antacids h2 receptors antagonist PPI
 Antibiotics for h. pylori
Chronic gastritis
 Autoimmune gastritis assc with
o Parietal and gastric cell antibodies pernicious anemia
 Low chloride levels
Etiology
 Helicobacter pylori infection
 Diag: endoscopy with biopsy
 Tx: h. pylori, irradication
PUD
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Areas of discrete GI tissue destruction occurring mostly in the proximal duodenum
and stomach
 More common in men
 MCC: h. pylori and nsaids
 Acid hypersecretion states: zolinger elisson syndrome
 Caused by combination of impaired mucous defense and acid gastric contents
Clinical manifestation
 Epigastric pain
 Duodenal ulcers: caused by increase in offensive 70-90 of patients low very rare,
younger patients, nsaids, eating relieves pain
 Gastric: older patients, smoking, more complications higher recurrence
Diagnosis: endoscopy most accurate
 Barium swallow: less reliable
 Upright x-ray for perforation
 Lab tests for h. pylori infection
Treatment: supportive alter all risk factors
 Acid suppression
 Eradicate h. pylori infestation
 Cytoprotection
 Misoprostol
 Surgery required for complications
Gastric cancer
 Rare in the us
 MC: adenocarcinoma
 Risk factor severe atrophic gastritis gastric dysplasia
 Gastric polyps
 H. pylori infection
 Pernicious anemia
Clinical manifestation
 Abdominal pain, unexplained weight loss
 Early satiety*
 N/v, anemia, melena
Diag: endoscopy with multiple biopsies most accurate
Gastric lymphoma
 Type of non hogdkins lymphoma
 Stomach is the most common extra nodal site
 Similar to adenocarcinoma
Zolinger ellison syndrome
 Pancreatic gastric secreting islet cell tumor
 Causes: refractory PUD
Clinical manifestiontion: similar to PUD but worse
 Secretin injection test
 Elevated fasting gastrin level
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Elevated basal acid output
Remove tumor
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Vomiting anorexia weight loss abdominal pain worsened by foods- gastric ulcer
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Chronic GERD progressive dysphagia weight loss x6 months diagnostic methodendoscopy and biopsy
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What are two causes of PUD? H pylori, nsaids
Treatment: Misoprostal
Acute pancreatitis
 Inflammation of the pancreas resulting from prematurely activated digestive
enzymes
 Invokes pancreatic tissue auto digestion
 Causes
o Alcohol abuse (40%)
o Gallstones (40%)
o Bluntabdominal trauma: MCC in children
o Post- ERCP, pancreatic cancer
o Viral infections: mumps, coxsackie
o Scorpion bite
Clinical manifestations
 Epigastric abdominal pain radiates to back
 Nausea vomiting anorexia
 Fever tachycardia hypotension
 Decreased or absent bowel sounds
 Hemorrhagic pancreatic: grey turners, Cullen, fox
Diagnosis:
 Serum amylase and lipase
 LFTs
 Hyperglycemia, leukocytosis
Abdominal x-ray: calcifications- chronic disease
 Sentinel loop
 Colon cut-off sign
 Abdominal ultrasound
 CT scan or MRI
Ransons's criteria- determine prognosis and mortality
 Tx: bowel rest NG tube, IV fluids pain control
 Complications: pancreatic necrosis pseudocyst or absecess
Chronic pancreatis
 Persistent continual p\pancreatic inflammation
 Fibrotic tissue replaces pancreatic parenchyma
 Alteration ort stricture of pancreatic ducts
 Altered endocrine and exocrine functions
Causes: chronic alcholism (>80) hereditary pancreatitis, idopathic chronic pancreatitits
 Severe epigastric pain recurrent or persistent
 Often accompanied by NV
 Pain radiates to the back
 Aggravated by drinking episodes or by eating
 Steatorhea and weight loss due to malabsorption
 Anemia and signs of alcohol abuse
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CT
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DM due to endocrine dysfunction
scan initial study of choice
Calcifications
Abdominal x ray
ERCP gold standard
Serum amylase and lipase levels
Non operative
o Narcotic analgesics
Operative
 Pancreaticjejunostomy: most common
o Pancreatic duct drainage; ductal decompression
 Pancreatic resection: whipples procedure
Pancreatic cancer
 Most common in elderly patients
 75% of patients over 60
 Rare before 40
 More common among African Americans
 Anatomic locations: pancreatic head, body, tail
 Smoking’s most established risk
 Chronic pancreatitis heave alcohol
 Diabetes
 Jaundice more common with head involvement
 Abdominal pain
 ERCP is most sensitive test
o Also differentiates pancreatic head cancer from tumors of CBD
 CT scan is preferred test for diagnosis and assessment of disease spread
 Tumor markers CA19-9 CEA- used for monitoring and test for reoccurrence of colon
cancer
 Treatment: surgical resection: whipple's procedure only hope for cure
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Acute pancreatitis is most commonly associated? Alcoholic gall stones
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Suspected of having pancreatic disease. Ultrasound is inconclusive. Which test would
be the next most appropriate? ERCP
Viral hep
 A clinical syndrome with lab evidence of liver cell necrosis preceded or accompanied
by malaise fever and jaundice
 All types of viral hep produce clinically similar
 No virus directly cytopathic to hepatocytes
 Acute liver injury is caused by immunologic response of the host cytotoxic t cells
recognize and destroy host cells
 Panlobar inflitration loss of lobar pattern
 asymptomatic infection only serological markers
 acute hepatitis
Fulminatent hep massive liver cell necrosis
o MC with B, D, E viruses
o Rapidly shrinking liver size and rising bilirubin level
o Tx. Liver transplant
Chronic hep
 Persistent minimal cell necrosis
 Active gradual cell necrosis leading to failure
Clinical manifestation
 Onset abrupt or gradual
 URI symptoms
 Myalgias and arthalgias
 Malaise, fatigue
 Anorexia n/v
 Fever and chills
 Epigastric, RUQ pain
 Jaundice, pruritis, dark urine
 Tender hepatomegaly, averison to smoking
Risk factors:
 Travel
 Inmates
 Homos
 Overcrowding
 Poor sanitation
 Contaminated foods
 Infected blood
 Daycare
Hep B
 Window period- no HBsAg, no HBsAb ,+HBcAb
 Resolving infection- +HBsAb, +HcAb, +HBeAb
 Infectivity- high= +HBeAg, Low= +HBeAb
Hep C
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May diagnose with PCR serology RIBA ELISA
Assays for HCV RNA are most sensitive- gold standard
In addition to serological markers
CBC- wbc normal or decreased
Urinalysis- + bilirubin
Liver function tests= elevations of LFTs does not correlate with severity
o AST and ALT increase 10-1,000 times normal level
o Lower enzymes elevation in chronic hepatitis
 Alkaline phosphate= mild elevation
 Conjugated bilibruin- moderately elevation
 Liver biopsy
 Acute illness resolves over 2-3 weeks
 5-10% if cases have a protracted course
 Avoid hepatotoxic agents
 Supportive therapy
Chronic hep B- interferon
Hep D- treat hep b
Alcoholic hep
 Chronic and excessive alcohol ingestion
 Fatty liver steatois
 Alcoholic hep: precurorsor to cirrhosis
 Hepatocyte injury and necrosis fibrosis
 Potentially reversible with cessation of drinking
Clinical manifestation
 Hepatomegaly
 RUQ pain
 Anorexia NV
 Fatique fever and chills
 Jaundice
 Spider nevi
 Ascitis
CBC- macrocytic anemia leukoctrosis
 Impaired liver function
 High bilirubin
 High alakaline phosphates
Diag:
 Liver function tests
 Bilirubin elevated
 Liver biopsy- confirms diagnosis
 Treatment: complete abstinence from alcohol
 Nutritional and psychological
Portal hypertension
 Normal pressure in portal vein is low because vascular resistance in hepatic cells is
minimal
 Portal HTN results from increase resistance to blood flow
 System lacks valves- portal HTN leads to retrograde transmission of pressure
 Splanchnic vasodilation, portal systemic collateral formation
Major sites of collateral formation involves veins at:
 Cardioesophageal junction- esophageal varices
 Rectum- hemorrhoids
 Abdominal wall- caput medusa
Occurs at 3 levels relative to hepatic cells:
 Pre sinusoidal: proximal to cells so liver si not exposed to elevated pressure
commonly portal veins
 Sinusoidal: cirrohisis
 Post sinusoidal
Clincal manifesetation
 Hepatomegaly splenomegaly ascities varicies
 CBC: anemia leukopenia thrombyocytopenia
Diag: markers of hepatic dysfunction
 Portal venous pressure may be measured by percutaneous transhepatic
catheterization
 Fiberoptic endoscopy- esophageal varices
 MRI or CT scan to detect collateral circulation
Tx: reduce pressure in portal venous system
 Tips: transjugular intrahepatic partosystemic shunt
 B-blockers: cause vasocontstriction splanchnic arterease decrease cardiac output
 Liver transplantation
Cirrhosis
 Irreversible chronic injury to hepatic parenchyma fibrosis in assc. with regenerative
nodules
 Disruption of liver architecture decreased blood flow through liver and hepatic
dysfunction/failure
Clinical manifestations
 Malaise fatigue
 Anorexia weight loss jaundice pruritis hepatic nodularity
 Abd pain
 Edema ascitis hypotension
 Coagulopathy
 Splenomegaly
 Spider elangiectasias
 Palmar erythema
 Portal HTN
 Gynecomastia
 Testicular atrophy
 Types of cirrhosis
Alcohol: MC type in US
Post hepatic: MCC chronic hepatitis infection
 Bilary: MCC injury or prolonged obstruction of biliary ducts
 Cardiac: MMCC by prolonged severe right heart failure
 Metabolic/ drug: ehemochromtosis, wilson's disease tylenol, methotrexate
Diag: liver biopsy
 Treatment: treat underlying cause
 Ascites: sodium restriction diuretic paracentesis
 Coagulopathy: vitamin K injections
 Liver transplantiation- only care
Complications: hepatic encephalopathy
 Acute reversible chronic irreversible mental status changes
 Affects behavior intellect neuromuscular function and LOC
 Caused by liver dysfunction and shunting of portal blood into systemic circulation so
liver is bypassed
 Various toxic metabolites ** ammonia are absorbed
Hepatic encephalopathy
 Clinical man: all those cirrhosis plus
 Decreased mental status confusion coma
 Asterexis: flapping tremor
 Fetor hepaticus: musty breath
 Reflexes symmetrically hyperactive rigidity
Diag:
 Elevated ammonia levels markers of hepatic insufficiency
 Distinction EEG changes
Spontaneous bacterial peritonitis
 Occurs in pts with ascities caused by chronic liver disease
Clinical manifestation: abd pain rebound tendernes fever vom
 Diag: paracentesis with ascites fluid analysis increase WBC increase PMN
 Treatment emperic antibiotics
Hepatocellular carcinoma
 primary malignant tumor of liver arising from the hepatocyte or blood vessels within
the liver
 Excludes: gall bladder and biliary passages
Signs
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and symptoms of cirrhoisis
Unexplained deterioration in stable cirrhosis
Diag: abd liver function tests
Alpha fetoprotein screening and diagnosis of HCC
Ultra sound best test to diagnoses HCC when AFP is normal
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Liver biopsy req for definitive diagnosis
Ct scan determine extrahepatic spread of disease
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Curative conditions: no metastasis, 3 or fewer nodules, each nodule less than 5 cm
Ablation with x ray radiation chemotherapy
Embolization of supplying artery
Surgical resection of nodules with 2cm
Tx:
Hemochromatosis
 Idiopathic autosomal recessive disorder where small intestine absorbs excessive iron
 Stored in glands and busmcels
 Excess hemosiderin deposition affects primarily
 Liver pancreases heart joints skin thyroid gonads hypothalamus
 Must be differentiated from iron overload
Clinical manifestations
 Weakness ascites peripheral edema DOE cardiac arrhythmias
 Hepatomegaly cirrhosis fibrosis jaundice splenomegaly
 DM symptoms abdominal pain
 Artharalgia increased skin pigmentation
 Gynecomastia loss of libido amenorrhea loss of body hair
Diagnosis: liver biospy with iron concentration gold standard
 Increased LFTs hyperglycemia
 Transferrin staturation over 70%
 Decreased TIBC
 Increased serum ferritin and iron
 Decreased FSH LH testosterone
Treatment: removal of excess iron: repeated phlebotomy 1-2x weekly
 Lifelong phlebotmomy to keep iron stores at normal levels
 Iron chelating agent: deferoxamine
 Lisons disease
 Idiopathic autosomal recessive defect in copper transport
 Toxic accumulation in brin leiver skin kidney and bones
 Normally copper excreted billiary system
 Defect in chromosome 13: low ceruloplasmin
 Hep dis: hep portal HTN
Diagnosis: liver biopsy hepatic copper measurement- goldstandard
 Low levels of serum ceruloplplasmin
 Elevated urinary copper levels
 Coppor chelation- d penicillamine
 Zinc therapy
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Vaccine for Hep B was successufl? HBsAb
Poor prog sing in alcoholic hep
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Tumor marker for primary liver cell carc: alpha
Evaluation of jaundice
 RBC breakdown
 Heme- heme oxygenase- biliverdin
 Biliverdin- biliverdin reductase- bilirubin
 Unconjugated indirect insoluble
 Bound to albumin- liver
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Indirect bilirubin- glucuronosyltransferase- conjugated bilirubin
Conjugated, direct, soluble
Bile channels- ATP pump
Excreted via feces and urine
Overproduction of bilirubin
Impaired uptake or
Prehepatic increase heme production
Spherocytosis sickle cell anemia G6PD deficiency
Hemolytic uremic syndrome increase marrow production
Hepatic decrease liver uptake or conj
Drug induced: Tylenol INH probenecid
Gilbert syndrome- mild unconj
Hyperbilirubenemia
Dubin johnsons syndrome- mutated ATP pump
Rotors syndrome- impaired hepatic storage
 Impaired excretion of conjugates
Understanding lab LFTs' ast and ALT
 Alt is more sensitive and specific for liver damage
 In cirrhosis and chronic liver disease may be normal
 Alkaline phosphate
o Not specific to liver also found in bone GI
o Elevated in obstruction to bile flow
 Albumin
o Decreased in chronic liver disease, nephritic
Cholestasis
 Blockage of bile flow
 Increased conjugated
 Jaundice gray stools dark urine
 Pruritis bile salt deposit in skin
 Elevated serum alkaline phosphatase
 Elevated serum cholesterol cant excrete
 Skin xanathomos
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Conjugated bilirubin- extrahepatic biliary obstruction
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Unconjugated hyper bilirubinemia (pre hepatic jaundice) casued by- hemolytic
anemia
Gallbladder disease
 Cholelithiasis- galls stones
Three types
 Cholesterol stones
 Pigment stones
 Mixed
Clinical manifestiations: biliary colic
Diagnosis: RUQ ultrasound, CT or MRI as alternatives
Treatment
 Non if asymptomatic
 Elective cholecystectomy for patients with recurrent episodes of bilary colic
Acute cholecystitis
 Prolonged obstruction of the cystic duct with gall bladder wall inflammation
 Happens in absence of infection
 Epigastric RUQ abd pain and tenderness
 Radiates to the right shoudler or scapulat
Diagnosis:
 RUQ ultrasound best of choice
 RUQ CT scan
 HIDA scan
 If gall bladder not visual after 4 hours confirmed
Acalculous cholecystitis
 Acute cholecystitis without stones obstruction the cystic duct
 Usually idiopathic assc. with severe illness
 Same clinical manifestation
Choledocholoithiasis
 Gallstones in the common bile duct
 Asymptomatic jaundice epigastric RUQ pain
 Total and direct hyper bilirubinemia
 Elevated alkaline phosphates
 RUQ ultrasound initially
 ERCP gold standard
 Diagnositic and therapeutic
 Sphincterectomy with stone extraction
Acute cholangitis
 Life threatening infection of the biliary tract due to obstruction
 Leads to biliary stasis bacterial overgrowth
 Caused by choleducholitiasis in 60% of canes
Clinical manifestation
 Charcot's triad: RUQ pain, jaundice and fever
 Reynolds pentad: plus septic shock and AMS
 RUQ ultra sound: initial study
 Hyperbilirubinemia
 Leukocytosis, mild elevation LFTs
 Cholangiography: ERCP
Gall bladder carcinoma
 Most are adenocarcinoma
 Most in elderly
 Risk factors: gallstones, porcelain gallbladder
Clinical manifestation
 Non-specific suggest bile duct obstruction
 Jaundice biliary colic weight loss
 Palpable gall bladder- sign of advanced disease
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Typical manifest nation of acute cholecystitis: murphy's
Small bowel obstruction
 Partial vs. complete obstruction
 Partial: able to pass gas or have bowel movements
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Complete: any gas or bowel movement is residual from a Point distal to the
obstruction
Closed loop vs. open loop obstruction
 Closed loop: bowel is occluded at 2 points by adhesive ban or hernia ring comprising
blood supply
Proximal vs. distal obstruction
 Distal: distention of proximal bowel, late vomiting
 Proximal: early vomiting and minimal distention
Pathophysiology- intestinal distention causes: reflex vomiting increase intestinal
secretion proximal to obstruction decreased absorption
Etiology: adhesions from abdominal surgery MCC adults
 Incarcerated hernia: second MCC
 Malignancy
 Intrasusception
 Inflammatory bowel disease
Clinical features:
 Abdominal pain: cramping severe continuous
 Nauseas and vomiting, abdominal distension
 Altered bowel sounds, obstipation
Diagnosis
 plain abdominal x ray
o Dilated loops of bowel, air fluid levels
 Barium enema- identifies site of obstruction
 Upper GI series
Treatment
 Nonoperative if SBO is incomplete without fever tachycardia leukocytosis peritoneal
signs
o Iv fluids ng tube antibiotics
 Surgery for complete obstruction
Paralytic ileus
 Peristalsis is decreased or absent
 Without the presence of mechanical obstruction
 Causes: post operative state shock hypokalemia, medications spinal cord injury
 Diagnosis: abdominal xray; uniform distribution of gas in bowel colon and rectum
 Barium enema failure to pass contrast beyond a fixed point is diagnostic
 Treatment IV fluids NPO correction of electrolytes
Celliac sprue
 Hypersensitivity to gluten (wheat products)
 Clinical manifestations:
o Weight loss abdominal distension
o Bloating, diarrhea
 Diagnosis:
o Biopsy: flattening of the villi, malabsorption
 Treatment
o Strict adherence to gluten-free diet
IBD
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Inflammation of GI tract subsequent tissue damage
More common in white and jews
Mean age of onset 15-35
 Chron's disease
 Chronic transmural inflammatory disease
 Affects any part of the GI tract MC small bowel
 Terminal illeum and cecum most common
Pathology:
 Terminal ileum is hallmark location
 Transmural thickening and inflammatoun**
 Skip lesions- discontinuous involvement
 Fistula luminal strictures non casseating granulomas
Clinical manifestation
 Diarrhea malabsorption
 RLQ abd pain
 NVF weight loss
 Extra intestinal manifestation
 Arthritis MC extra intestinal manifestation anklyosing sspondylitis sacrolitis
 Hyper coagulablility
 Diag: endosocophy with typical findings:
o Apthous ulcers
o Cobblestone appearance, skip lesions
 Barium enema
 Treat: surgery- reserved for complications
 Antidiarrheal agents
 Sulfasalazine- blocks prostaglandin reduces inflammation
 Metronidazole- if no response to sulfasalizine
 Systemic steroids- for acute exacerbations
 Immunosuppressants: azathiprine
Complications
 Fistula formation
 Anorectal disease
 Small Bowel Obstruction- MC indication for surgery
 Maligancy- risk for colon cancer UC>>crohn's disease
 Cholelithiasis
 Nephrolithiasis
 Aphtous ulcers
 Narcotic abuse
Ulcerative colitis
 Chronic inflammation disease of colon or rectal mucosa
 Dist: involves rectum in all cases
 Path- uninterrupted involvement, inflammation limited to mucous and submucosa,
PMNs accumulate in colon crypts
Clinical feat:
 Hematochezia, bloody diarrhea, tenesums
 Abd pain
Diagnosis: stool cultures: R/O- c. dificile ova and parasites
 Fecal leukocytes
o Appear in UC ischemic colitis infectious diarrhea
 Colonoscopy
Treat: surgery can be curative
 Systemic steroids- for acute exacerbations
 Sulfaslalazine- mainstay of treatment
 Immunosuppressants- azathiprine
Complications
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Iron deficiency anemia
Hemorrhage
Malignancy
Strictures
Sclerosing cholangitis
Cholangiocarcinoma
Electrolyte disturbance, dehydration
IBS
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Idiopathic functional disorder
MC presents in teenage years females??males
50% have comorbid psychiatric disorders
Depression anxiety high stress occupation
Abd pain irregular bowel
Discontinous involvement- crohns
Acute
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appendicitis
Obstruction of the appendix lumen caused by:
Hyperplasia of lymphoid
Fecalith
Foreign body, tumor or parasite
Leads to stasis, bacterial growth and inflammation; distension may compromise
blood supply
 Necrosis may result in appendix perforation and ultimately peritonitis
 Peak incidence; teenager to mid 20s
 Rarely lasts greater than 72 hrs
 Abd pain periubmilical to RLQ pain
 Anorexia
 Nausea and vomiting
 Low grade fever
 RLQ tenderness; mcburnery
 Rebound tenderness
 Rovsings sign
 Psoas sign
 Obturator sign
Diagnosis:
 Mild leukocytosis
 CT scan abd ultrasound
 Treatment: appendectomy
Colorectal cancer
 3rd most common cancer in US
 Virtually all tumors arise from adenomas
Risk factors
 Age greater than 50 family history
 Adenomatous polyps
 History colorectal cancer polyps
 Screening: fecal occult blood digital rectal examination
 Colonoscopy most sensitive and specific test
o Diagnosis study of choice for positive FOB test
 CEA tumor marker baseline and recurrence
 Pattern of spread: direct extension, hematogenous- to liver, lymphatic-regional
spread, transperitoneal
Clinical manifestiation may be asymptomatic
 Abd pain- MC presenting symptom
 MCC of large bowel obstruction in adults
 Weight loss blood in stools
 Colonic perforation
 Left sided- smaller lumen diameter hematochezia more common
o Obstruction constipation
o Narrow stool
 Right sided- larger lumen diameter
o Fecal occult blood, melena
o Iron deficiency anemia
o Triad- anemia, weakness, RLQ mass
 Treatment
o Surgical resection of tumor and regional lymphatics
o Post operative chemotherapy
o Stool guiac test
o Annual ct abdomen and pelvis x ct for five years
Diverticulosis
 Due to increase intraluminal pressure inner layer of colon bulges through focal area
of weakness in colon wall
 MC location- sigmoid colon
 Risk factors: age, low fiber diet, constipation, family history
 Clinical features:
o Usually asymptomatic and discovered incidentally on barium enema or
colonoscopy
o Vague LLQ pain, bloating constipation
o 10-20 symptomatic
Diag: barium enema is best of choice
 Treat: high fiber foods, psyllium
Complications
 Painless rectal bleeding- usually clinically insignificant and stops spontaneously no Tx
 Bleeding may be sever in 5 of cases
Diverticulitis- feces become impacted in diverticulum leading to erosion and
microperforation
 Ss: fever LLQ pain leukocytosis
 Dx: ct scan is test of choice barium enema and colonscopy are contraindicated in
acute disease
 Tx: iv antibiotics no low residue diet iv fluids surgery
Complications
 Abscess formation
 Colovescicual fistula
 Bowel obstruction
 Colonic perforation with peritonitis
Recurrence: diverticulitis
Angiodysplaisia of the colon
 Torturous dilated veins in submucosa of colon
 Common cause of lower GI bleed in patient>60
 Low grade bleeding, unless veins rupture
 In 90% patients, bleeding stops spontaneously
 Dx: colonoscopy
 Tx: colonoscopy coagulation, right hemicolectomy
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LLQ pain, fever leukocytosis- diverticulitis
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Upper GI bleed refers to source of bleeding proximal to the duodenal ligament of
Treitz
 Lower GI bleed refers to source of bleeding distal to the duodenal ligament of treitz
Types of bleeding
 Hematomeis
 Coffee ground
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Upper GI bleed- PUD, Gerd, esophageal varices, gastric varices, mallor weiss tear, av
malformation, endoplasm
Lower GI bled- diverticulosis, angiodysplasia, IBD, colorectal carcinoma