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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