Josh Corwin
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
• 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
o 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
• Chest
o Crackles and wheezes at bases
• Consolidation, pulmonary edema
• Heart murmurs
• Pleural rubs
• Hard stool- constipation/impaction may have diarrhea
• Pelvic genital and rectal exam on every patients with severe abdominal pain
• Cervical motion tenderness PID- Shandeliar Sign
•
• Adnex mases of the testicular portion can also present as abdominal pain
• **adhesions ms cause of acute bowel obstruction with surgery
• 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
• 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
• Elderly patients: pain presentation is often atypical in location and severity; may not mount febrile response. We may see hypothermia or nothing at all.
• Immunosuppressed patients; steroids may mask pain and decrease inflammation, immunosuppression leads to opportunistic infections and may cause the following diseases: CMV, lymphoma
• In an obese patients organs are not in place where you think they are there is overall abdominal distortion
• Patients on medication: some medications may change the perception of pain or cause constipation
• 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
• MRI scan- not much use in diagnostic workup of abdominal pain
• EKG- rule out ischemia and mi
• 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
• 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
• 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
• 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
• 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
• 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
• 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
• 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
• 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
• Elevated basal acid output
• Remove tumor
• Vomiting anorexia weight loss abdominal pain worsened by foods- gastric ulcer
• Chronic GERD progressive dysphagia weight loss x6 months diagnostic method- endoscopy and biopsy
• 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
• DM due to endocrine dysfunction
CT 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
• Acute pancreatitis is most commonly associated? Alcoholic gall stones
• 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
• 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 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
• Liver biopsy req for definitive diagnosis
• Ct scan determine extrahepatic spread of disease
Tx:
• 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
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
• Vaccine for Hep B was successufl? HBsAb
• Poor prog sing in alcoholic hep
• 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
• 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
• Conjugated bilirubin- extrahepatic biliary obstruction
• 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
• Typical manifest nation of acute cholecystitis: murphy's
Small bowel obstruction
• Partial vs. complete obstruction
• Partial: able to pass gas or have bowel movements
• 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
• 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
o Iron deficiency anemia
o Hemorrhage
o Malignancy
o Strictures
o Sclerosing cholangitis
o Cholangiocarcinoma
o Electrolyte disturbance, dehydration
IBS
• 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 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
• LLQ pain, fever leukocytosis- diverticulitis
• 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
• Upper GI bleed- PUD, Gerd, esophageal varices, gastric varices, mallor weiss tear, av malformation, endoplasm
• Lower GI bled- diverticulosis, angiodysplasia, IBD, colorectal carcinoma
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