Liver dysfunction

The most common causes of Cirrhosis in the US are Hep C, chronic alcoholism, nonalcoholic fatty liver
disease, hemochromatosis

Signs of liver dysfunction are

1) Abnormal LFTs
2) Signs of Portal HTN
3) Nonspecific symptoms: fatigue, weakness, nausea

Evaluation of patient with Cirrhosis/Hepatitis

Initial evaluation of a patient with suspected cirrhosis is obtaining a medical history. Ask about
medications, alcohol use, drug use, high risk sexual activity. Ask about family history to exclude
hemochromatosis. The consider obtaining lab studies, obtain viral hepatitis serology and iron studies.

In a patient who presents with hepatitis, after obtaining history, repeat LFTs. IF the LFTS remain
persistently elevated over 6 months then the patient is said to have chronic hepatitis and then you start
testing for Viral hep B, C, hemochromatosis, and fatty liver disease.

Signs like spider angiomata and gynecomastia are very specific for cirrhosis.

All patients with Cirrhosis, should undergo endoscopy to look for VARICES and assess risk of variceal
hemorrhage, and determine strategies for primary prevention of variceal hemorrhage.

Goals of treatment are to treat reversible factors and prevent potential complications such as variceal
bleeding and hepatocellular carcinoma.

If the clinical picture fits cirrhosis, then a liver biopsy is not needed.

If a patient presents with NEW-onset ascites, you have to perform PARACENTESIS to obtain a diagnosis.

Alcohol use is more likely to cause folate deficiency than Vitamin B12 deficiency (due to greater stores
for B12).

B12 is more likely to occur with SIBO or pernicious anemia.

Treatment of Cirrhotic patients

The most important complication from cirrhosis is GI bleeding from an esophageal varices. Cirrhotic
patient who have medium or large varices should be treated with 1) Endoscopic variceal ligation
(preferred for large) or 2) nonselective beta blocker such as propranolol or Nadolol as PRIMARY
prevention.

Lactulose and rifaximin are used to treat hepatic encephalopathy. You do not prophylaxis for hepatic
encephalopathy.

Furosemide and Spironolactone are 1st line treatment for ascites 2/2 to cirrhosis. Large-volume
therapeutic paracentesis is used when the patient has 1) respiratory compromise from ascites or 2)
significant abd discomfort.

Compensated cirrhosis without evidence of complications is not sufficient for a transplant. To be eligble
for transplant need to be abstinent from alcohol for at least 6 months.

A TIPS (transjugular intrahepatic portosystemic shunt) is used as salvage therapy (last resort) in patients
with refractory ascites or esophageal varices who failed endoscopic or medical management.

Alpha-1-antitrypsin deficiency AAT presents with early onset COPD or Liver disease in a young patient
(10-30s).

Nonalcoholic Fatty Liver Disease (NAFLD/NASH)

Px. Asymptomatic, mild hepatomegaly, metabolic syndrome, obesity

Labs: AST/ALT ratio < 1 and elevated

Hyperchoic texture of liver on US

Tx: Diet and exercise, Bariatric surgery if BMI > 35

Plummer Vinson syndromes presents with upper esophageal webs, dysphagia, stomatitis, beefy red
tongue, and iron deficiency anemia. More common in women.

Diverticulosis is the MOST common cause of gross/frank lower GI bleeding in adults. Diverticulosis is
most common in the sigmoid colon but diverticular bleeding is more in the right colon.

Path: hernation of colonic wall that affects blood supply and leads to bleeding in outpouchings
Px: painless bleeding. Low-moderate can present as maroon stools or hematochezia. Large bleeds cause
frank red blood

Dx. With colonscopy

Autoimmune hepatitis

Px: Fluctuating hepatocellar injury elevated transaminits.

Dx: ANA + Anit-Smooth-Muscle

Tx: Glucocorticoids.

Hepatocellular Carcinoma

62 yo man 35 year ppd smoking hx presents with fatigue and weight loss. CT shows multiple lesion in
the liver.

Colorectal cancer is the MOST common cause of iron deficiency anemia in an elderly patient.

Colorectal cancer is the most common source of Liver metastases. Multiple liver lesions on CT points to
metastatic cancer. Next best step is COLONOSCOPY. Lung and breast cancer also metastasize to the
liver.

Primary liver disease presents as a solitary mass. Alpha-Feto-Protein can be used along with imaging
studies to diagnose.

The only time you aspirate and culture liver lesions is when you have a PYOGENIC liver abscess. You
would expect fever, RUQ, anorexia etc.

Prostate cancer commonly metastasizes to the pelvic lymph nodes and BONES (osteoblastic lesions).
Doesnt really metastasize to the liver.

Acute Liver Failure

Is defined as severe acute liver injury in a patient WITHOUT cirrhosis or underlying liver disease.

The diagnosis of Acute Liver Failure requires:

1) Severe acute liver injury evidenced by ELEVATED AMINOTRANSFERASES

2) Hepatic Encephalopathy (asterixis, confusion)
3) Impaired hepatic synthetic function (INR > 1.5)

The presence of hepatic encephalopathy differentiates Acute hepatitis from ACUTE Liver failure.

The most common causes of ALF are Viral hepatitis and drug toxicity.

Tx: Transplant 50% of patients with ALF will die without liver transplant.
Rising Bili, rising PT, acute renal failure, severe hepatic encephalopathy suggest worsening Acute Liver
Failure portend a worse prognosis. Criteria are 1) Grade 3 or higher: (really confused and incoherence),
2) Cr > 3.4 3) PT > 100

Cerebral edema is a complication of ALF and may lead to coma and brain stem herniation. IT IS THE
MOST COMMON cause of death in ALF.

Steroids only treat autoimmune hepatitis not ALF.

A patient can have chronic Hepatitis B and be stable and then develop Hepatitis D as a superinfection
triggering ALF.

Liver cirrhosis is defined as Signs of liver dysfunction (jaundice, ascites),

Hyperestrogenism/Hypognoadism, Portal HTN

OCPs can cause abnormalities in LFTs.

Autoimmune hepatitis px with + ANA (anti-nuclear antibody) and/or Anti-Smooth muscle antibody.

Drug induced Acute hepatitis can be caused by drugs/toxins such as carbon tetrachloride,
acetaminophen, tetracycline, and Amanita phalloides mushroom. Other drugs include Chlorpromazine,
halothane, and Anti-retro-viral therapy.

Isoniazid can cause liver injury that presents similar to viral hepatitis: panlobular mononuclear
infiltration and hepatic cell necrosis.

Chronic epigastric pain that suddenly becomes worse and becomes diffuse with rebound tenderness
and/or guarding and PNEUMOPERITONEUM (air under the diaphragm) should make you think of
PERFORATED Peptic Ulcer Disease.

Perforated gallbladder is uncommon but when it does it occurs SEVERAL days after someone has had
cholecystitis that developed into GANGREONOUS cholecystitis. They would px very septic.

Just because someone has gallstones doesnt mean that they are symptomatic. Many people have
gallstones and are asymptomatic.

Peritoneal inflammation px with rebound tenderness, abd guarding, and decreased bowel sounds.

Ischemic Hepatopathy
Hallamark is a RAPID and MASSIVE increase in ALT/AST with mild elevations in total bilirubin and ALK
Phos.

Acute hepatitis A or B infection can present with LARGE AST/ALT elevations but you would also see it
accompanied with HIGH total bilirubin and other symptoms such as N/V.

Autoimmune hepatitis affects women and with would have HIGH AST/ALT with HIGH total bili.

For Alcohol hepatitis, AST is usually < 300 and remember 2:1 ratio

Alcoholic Hepatitis

Px Jaundice, anorexia, fever with mild RUQ/epigastric pain, some abd distention, potentially hepatic
encephalopathy

Labs: Elevated AST: ALT ratio > 2:1 AST usually < 300

Elevated GGT,Bilirubin, INR, and Ferritin

Leukocyosis with PMNS

Abd imaging may show fatty liver

Spontaneous Bacterial Peritonitis

Path:

Px: Fever > 100F (37.8 C), abd pain/tenderness, AMS that may be represented as failure to timed to
connect the numbers test (Reitan trail test), hypotension, and PARALYTIC ileus with SEVERE infection.

The findings for SBP superimposed on cirrhosis can be subtle (subtle fever, leukocytosis, and AMS).
(slightest hint of a FEVER or AMS in a cirrhotic patient with ascites think SBP)

Patients with cirrhosis are usually hypothermic which is why the FEVER threshold for SBP is set at 100.

Dx: Paracentesis to sample ascetic fluid

PMNS > 250 in fluid, positive culture (E.coli, Klebsiella aka enterics), Protein < 1g, and SAAG > 1.1 g/dl

Tx: Empiric abx eg Cefotaxime (3rd gen Ceph); Fluoroquinolones for SBP prophylaxis.

Reminder: whenever any patient presents with NEW-ONSET ascites, your next best step is
PARACENTESIS to tap it.

Composition of Ascitic Fluid

Color: Bloody = trauma, cancer, TB Milky = chylous, pancreatic Turbid = infection Straw color = benign

PMNS: > 250 = peritonitis or spontaneous bacterial infection < 250 = No peritonitis
Protein: > 2.5 g/dL = high protein ascites eg CHF, Budd chiari, Peritoneal carcinomatosis (fluid of cancer
cells in peritoneum) < 2.5 g/dL = low protein ascites eg Cirrhosis, nephrotic syndrome

SAAG: > 1.1 g/dL = portal HTN (cardiac ascites, cirrhosis, Budd-Chiari) < 1.1 g/dL = no portal HTN so
think TB, peritoneal carcinomatosis, nephrotic syndrome etc

SAAG = Serum to Ascites Albumin Gradient

To figure out whether a patients ascites if from Portal HTN or not take the Serum Albumin and subtract
for Ascitic fluid albumin.

DAM It VW VW HAAPPENS

Giardia

RF: international travel, hiking, contaminated water

Path: incubation period of 1-2 weeks

Px diarrhea with foul-smelling stools, bloating, malabsorption, weight loss, GI distress

Dx 1) Stool antigen assay with ELISA 2) Stoop O and P

Tx: Metronidazole

Acute Pancreatitis

Path: Chronic alcohol use or Gallstone, Hypertriglyceridemia, Drugs, Infections, Cholesterol emboli after
procedure (cardiac cath, ERCP, ischemic)

For hypertriglyceridemia to be the cause, the serum triglyceride levels have to be > 1000 mg/dlL.

Px: epigastric pain radiating to the back that improves by sitting up or leaning forward, n/v, ileus of
nearby small and large bowel due to inflammation (dilated bowel loops)

Severe disease can present SIRS

Dx. 1 Acute epigastric pain radiating to the back 2) Amylase or lipase > 3 times normal limit 3)
Abnormality or imaging consistent with pancreatitis ie diffuse pancreatic enlargement with
enhancement. Lipase is more useful than Amylase.

If dx unclear, can before Abd CT.

Labs: ALT > 150 suggests biliary pancreatitis.

Tx: Supportive care: pain control, IVF, NPO. Most acute pancreatic attacks are self-limiting and resolve
within a week.

For gallstone pancreatitis, ERCP with sphincterectomy is a tx option.

Chronic Pancreatitis

Path: Chronic alcohol use, Cystic fibrosis (especially in children), ductal obstruction (gallstones),
autoimmune disease

Px: 1 CHRONIC epigastric pain relieved by sitting up or leaning forward; with intermittent pain-free
intervals, 2 malabsorption with steatorrhea, diarrhea, weight loss 2/2 to pancreatic enzyme def, 3
Diabetes Mellitus

Dx:

1. CT scan or MRCP showing calcifications in pancreas (white dots in pancreas), dilated ducts, and
enlarged pancreas

Amylase/Lipase can be normal; not helpful

Tx: analgesics for pain, alcohol/smoking cessation, frequent, small meals, pancreatic enzyme
supplements to improve bloating and diarrhea symptoms.

Pancreatic Cancer

Path

RF: Smoking biggest RF, hereditary pancreatitis, Non-hereditary pancreatitis, obesity and lack of physical
activity

Px: painless jaundice with palpable non-tender gallbladder, weight loss, steatorrhea 2/2 to loss of
pancreatic enzymes.

Pt with tumor in body or tail can present with pain and weight loss but NO JAUNDICE.
If someone with chronic pancreatitis presents with worsening symptoms: more frequent pain and
weight loss = think about PANCREATIC cancer.

Labs: show increased serum bilirubin and alka phos

Dx; 1st Try Abd U/S as patient is presenting with jaundice 2nd Abd CT scan 3rd if U/s and CT are non-
diagnostic then consider ERCP

Imaging would show dilated intra and extra hepatic bile ducts.

Tx: Early and isolated to Head of pancreas: Whipple Late: Palliative chemotherapy

Complications: poor prognosis, usually presents late. CA-19-9 is used to evaluate tumor response to
therapy ie track disease
Biliary Colic

Px Episodic RUQ/epigastric pain that radiates to RIGHT shoulder after fatty meals. Pain can be constant
with n/v but resolves within 4-6 hours. No fever, abd tenderness or leukocytosis ie no signs of local or
generalized inflammation.

Acute Cholecystitis

Px: persistent RUQ that radiates to right shoulder, fever, leukocytosis, tenderness to palpation aka
murphy sign. May see mild transamnitis BUT ALk PHOS is normal. Pain lasts longer than 6 hours.

Pain usually starts after ingesting large or fatty meal

Dx RUQ ultrasound

Tx: If no PERF: Admit NPO, IV abx, Analgesics; perform lap cholecystectomy electively

If PERF; perform lap cholecystectomy urgently

Acalculous Cholecystitis

Path: severe illness, recent surgery (Cardiac, pulm, abd) or prolonged fasting or TPN cause gallbladder
stasis leading to ischemia with gallbladder distention, necrosis, and 2 bacterial infection

Px: It presents with UNEXPLAINED fever say in post-op patient, diffuse or Right upper quadrant
tenderness, and Leukocytosis. It can also present with ELEVATED LFTs, Jaundice, RUQ mass but these do
not need to be present. I repeat: do not need jaundice or elevated LFTs to make diagnosis.

Dx: 1st Abd U/S showing signs of acute cholecystitis without gallstones 2nd CT scan or HIDA scan if u/s
unclear

Complications: Gangrene, Perforation, and emphysematous cholecystitis

Subphrenic abscess is rare cause of fever and abd pain and develops 2/2 to peritonitis from a PERF.

Porcelain Gallbladder

Path: chronic inflammation of gallbladder leads to deposition of Calcium.

Px Porcelain gallbladder eg firm, non-tender mass in RUQ with calcifications seen on imaging. Increases
the risk of developing Gallbaldder adenocarcinoma. Described as bluish color and brittle consistency.

Tx: Cholecystectomy to reduce risk

Echinococcal cyst appears as cystic lesion in livr.

Liver abscess is dx by u/s or CT scan.

Risk factors for Gallstone development

Patients on TPN or prolonged fasting are at increased risk for gallbladder stasis because lack of
fat/protein in duodenum decreases CCK so gallbladder doesnt contract to move bile. Increases risk of
gallstones and SLUDGE.

Small bowel resection involving Ileum can also increase risk of gallstones by DECREASING enterohepatic
circulation of bile acids. Ie gallbladder releases bile into duodenum but its no longer reabsorbed at the
ileum so this depletes the bile acid concentration in gallbladder which then allows cholesterol to
precipitate out and form stones.

Estrogen increases cholesterol seceretion and can increase risk of gallstones. Female, Fertile, Forty, Fat.
So women on OCPs, pregnant are at increased risk. During pregnancy, progesterone decrease GB
motility and estrogen increases cholesterol synthesis.

Increased RBC destruction (hemolytic anemia) increases the risk of pigmented gallstones. (more bilirubin
to be converted to bile)

Primary Sclerosing Cholangitis

Path: Sclerosis of extrahepatic bile ducts ie CBD

RF: Male, Ulcerative Colitis

Px: Pruritus, fatigue but may be asymptomatic

Labs: ALT/AST < 300; Elevated Alk Phos, P-ANCA positive

ERCP or MRCP shows multifocal stricutring/dilation of intrahepatic and/or extraphepatic bile ducts

Liver bx shows fibrous obliteration of bile ducts and periductular onion-skin fibrosis concentric
replacement by connective tissue in an onion-skin pattern

Tx:

Complications: Intra or extra hepatic biliary stricture, Cholangitis and cholelithiasis,

Cholangiocarcinoma, decreased fat soluble vitamins, osteoporosis, colon cancer (2/2 to UC)

Primary Biliary Cholangitis (cirrhosis)

Path: Autoimmune destruction of intrahepatic bile ducts

RF: Middle-age female

Px: insidious onset of fatigue and pruritus, progressive jaundice, hepatomegaly, cirrhosis
 Cutaneous xanthomas and xanthelasmas (fat deposits on eyelids)

Labs: High ALK phos, mildly increased ALT/AST (Cholestatic pattern), Anti-Mitochondrial Antibody

Severe Hypercholesterolemia (Increased HDL out of proportion to LDL, does not increase risk of
atherosclerosis)

Tx: Ursodeoxycholic acid delays progression by increasing biliary acid secretion from liver; Liver
transplant for advanced disease

Complications: Malabsortion, Fat soluble vitamin def, METABOLIC BONE disease (osteomalacia,
osteoporosis), and Hepatocellular carcinoma

Associated with other autoimmune diseases

Labs: AMA (anti mitochondrial antibodies)

Carcinoid syndrome

Path: tumor in small intestine that produce serotonin

Px: Right sided valvular disease (TR), secretory Diarrhea, Bronchospasm, Episodic Facial flushing,
telangiectasias

May develop pellagra from NAD (Vit B3) deficiency

Dx. 1) 24 hour urinary collection of 5-H1AA

2) CT/MRI to localize tumor

3) Octreotide scan to detect metastases

Tx: 1) Octreotide for symptomatic patients 2) Resect

Achalasia

Px: chronic dysphagia to solids and liquids, regurgitation, heartburn, and mild weight loss. Patients
typically are diagnosed after 5 years of having symptoms so its really CHRONIC.

Symptoms improve by being upright position: increases pressure in the esophagus (gravity)

Dx: Manometry = showing increased LES resting pressure and incomplete LES relaxation, and decreased
peristalsis of the distal esophagus

Barium swallow shows smooth Bird-Beak pattern

EGD to exclude malignancy

Tx: lap myotomy or pneumatic balloon dilation, for poor surgical candidates: Botulinum injection,
nitrates, and CCB.
Diffuse Esophageal Spasm

RF: See in association with emotional factors/functional GI disorders

Path: random spasm or contraction of esophagus (uncoordinated,simulanteous contractions)

Px: Intermittent Chest pain and Dysphagia for solids and liquids

Dx: 1) Manometry showing multiple simultaneous contractions of the middle and lower esophagus 2)
Barium swallow aka Esophagram showing corkscrew esophagus

Tx: short term: CCB, NO, TCA

Prinzmetal Angina (Variant angina) is a due to coronary artery spasm. Px with episodic chest pain at rest.
Patients have normal EKG and variable ST abnormalities during events.

Costocondritis (costosternal syndrome) occurs after repetitive activity. Px with pain that is reproducible
with palpation and worsened with movement or position changes.

Eosinophilic Esophagitis px with food impaction, dysphagia, or heartburn that does not respond to
standard medications. Endoscopy reveals esophageal rings or strictures.

Globus hystericus or sensation px with a sensation of foreign body in the throat. Worse when
swallowing saliva and associated with anxiety.

Zenkers doesnt usually cause chest pain.

Esophageal Stricture

RF: long-standing hx of GERD, scleroderma, radiation, or caustic damage

Px: progressive dysphagia to SOLID foods without anorexia or weight loss. Hx of GERD that has improved
recently.

Dx: Barium swallow will show symmetric, circumferential, narrowing on barium swallow. Best dx step
is EGD w bx.

Esophageal Cancer

Types: Adenocarcinoma is lower 1/3. SCC in upper 2/3s/ anywhere.

RF: GERD (long-standing, > 20 years) , Obesity (Adenocarcinoma), Smoking, Alcohol, Caustic injury for
SCC

Px Chest pain, weight loss, dysphagia for solids

Dx 1) EGD w bx 2) CT/PET to stage Barium swallow shows asymmetric narrowing of the esophageal
lumen.

If a patient is older > 55 or has alarm symptoms: bleeding EGD is 1st line. If they are younger can
consider Barium swallow.

Carefully chewing his food before swallowing = dysphagia

ALARM SYMPTOMS = CANCER do EGD

Gastric cancer

RF: Asians, Nitrosamines, H. pylori, chronic gastritis

Px: vague abd pain, weight loss, +/- GI bleeding.

Dx. 1) EGD w bx

2) CT scan to stage

Tx: if early: resection

Staging of Gastric Adenocarcinoma

1. Dx with EGD w bx
2. CT abdomen and pelvis to stage disease and look for metastasis (especially in Liver)
3. Additional staging procedures such as PET, endoscopic U/s, chest CT may be used.

If a patient presents with Gastric ADENOCARCINOMA, treating their H. Pylori does nothing for them. If it
was MALToma then treating H.pylori would be curative.

No markers for gastric cancer.

IBS

Path: idiopathic, related to stress and co-morbid psych issues

RF: Woman with comorbid psych issues, stress

Px: chronic crampy abd pain or discomfort relieved by defecation and alternating bowel patterns.

ABD pain/discomfort for > 3 days for 3 months with 2/3 of

1) Abd pain relieved by defecating

2) Changes in bowel habit
 3) Changes in form of stool: size, shape, or consistency

If the patient has alarm symptoms: rectal bleeding, nocturnal abd pain, or weight loss = NOT IBS

Tx

Toxic Megacolon

RF: IBD (ulcerative colitis), C. Diff infection, volvulus, diverticulitis,

Dx: SIRS (fever, tachycardia, hypotensive, leukocytosis), bloody diarrhea, Abd distention/peritonitis, and
non-obstructive marked colonic distention on imaging

Dx

1. AXR to see dilation and exclude perf

a. Colonscopy/endoscopy is contraindicated due to risk of PERF

Tx: NPO (bowel rest), NGD, IV abx, +/- IV corticosteroids if patient has IBD. If condition does not improve
then Surgery

Acute Diverticulitis

RF: hx of straining eg constipation or hernia, low fiber-diet but high fat diet

Px: abd pain in (usually LLQ), fever, leukocytosis, n/v, ileus

Dx. Abdominal CT with CON C Diverticulitis

Complications; Abscess, obstruction, fistula, perf

Colovesciula Fistula

Path: Diverticulitis, Crohns disease, Cancer (colon, bladder, pelvic organs)

Px. Air in urine, stool in urine, and recurrent UTIs

Dx 1) Abd CT with ORAL or rectal CONTRAST 2) Colonscopy to exclude malignancy

C. Diff colitis

Px develops watery diarrhea and abd pain after taking fluoroquinolones or other abx. Febrile. Even
without diarrhea you should consider C. Diff.

Dx Stool studies Toxin gene PCR

If studies negative then 1) Colonscopy or sigmoidoscopy to look for pseudomembranous colitis.

Tx

If patients WBC < 15,000 give empiric oral metro while awaiting stool studies.

Severe colitis treat with oral Vancomycin +/- IV metro. If recurrent C diff colitis or patient unable to take
Vanco, can give FIDAXOMICIN.

C Diff colitis approach

Mild to moderate colitis is defined as WBC < 15,000 or Cr < 1.5x baseline treat with oral metro

Severe colitis defined as WBC > 15,000, Cr > 1.5x baseline and Serum albumin < 2.5 g -- oral vanc +/-
IV metro, or switch to rectal vancomycin

IF WBC > 20,000 or Lactate > 2.2, or Toxic megacolon or severe ileus Surgery, subtotal colectomy

Hepatitis B

To diagnose, Acute Hepatitis B infection, look for HbsAg and anti-HBc.

Hepatitis B viral DNA is used to evaluate eligibility for anti-viral therapy or to monitor response to
treatment. It is not used in diagnosis.

Mallory Weiss Tear

Path: sudden increase in abdominal pressure from forceful vomiting causes a mucosal tear at the GE
junction of the stomach causing bleeding

RF: Alcoholism and Hiatal Hernia

Px. Hematmesis and epigastric pain after vomiting/retching

Dx: 1) Endoscopy to visualize longitudinal laceration

Tx: 1) Most heal spontaneously 2) Endoscopic therapy with epi or electrocautery if persistent bleeding

Boerhave syndrome rupture of esophagus. Px as acute chest pain, subQ emphysema, pleura effusion
etc

Hemobilia is bleeding in the biliary tree. Occurs after abdominal trauma or surgery

Esophageal varices are submucosal veins that bleed

Insulin decreases lipolysis in fat cells. Therefore insulin resistance, actually increases LIPOLYSIS.

Evaluation of Minimal Bright Red blood per rectum

Minimal bright red blood is defined as small amounts of bright red blood on toilet paper after wiping or
a few drops of blood in the toilet bowl after defecation,

This is usually caused by HEMORRHOIDS or rectal fissures.

Risk factors for malignancy such as weight loss, anemia, blood mixed with stool should undergo

Patients age > 50 or a patient with RED FLAGS for malignancy: weight loss, anemia, blood mixed with
stool etc are high risk for colon cancer should undergo colonoscopy unless they have had a normal
colonoscopy within 2-3 years.

Patients age 40-49 with no red flags are intermediate risk and should undergo sigmoidoscopy or
colonscopy.

Patients age < 40 with no red flags should are low risk and should undergo ANOSCOPY or proctoscopy. If
this doesnt show anything then you can consider Colonscopy or Sigmoidoscopy.

If you see a palpable abnormality in the rectum, ANOSCOPY should be used.

A negative FOBT does not rule out occult GI blood loss. Still perform colonoscopy/endoscopy in any
elderly adult that presents with Iron-Def anemia.

Herpes Zoster

In a patient who underwent cancer treatment.

Pain from shingles may precede onset of vesicular rash.

More common after age 50.

Triggered by physical stress such as cancer treatment, immunosuppressed states, or spontaneous.

No rebound, guarding or tenderness but rubbing skin elicits intense pain

Malabsorption

Malabsorption px as chronic diarrhea, steatorrhea, and weight loss.

D-xylose test is used to differentiate malabsortipn due to MUCOSAL disease eg Celiac disease from
enzyme deficiency (lactose intolerance).

D-xylose is absorbed in the small intestine and then filtered into urine.

In Muscosal disease, less D-xylose is absorbed and less ends up in the urine.

With enzyme def, D-xylose is normally absorbed and an adequate amount ends up in the urine.

Crohns Disease patients have steatorrhea but decrease BILE acid resorption at the ileum.
SIBO

When colonic bacteria are present in the small intestine.

RF: underlying motility disorder eg. gastroparesis from DM or anatomic abnormality (jejuno-colic fistula)

Px Greasy diarrhea

Exocrine Pancreatic insufficiency

RF: chronic pancreatitis, Cystic fibrosis, or hx or bowel or pancreas resection

Path: impaired digestion of fat and protein

Px: steatorrhea

For familial adenomatosis polyposis

Start screening at age 10, followed by annual colonscopies. Should also undergo increased screening for
upper GI tumors.

Tx is increased screening and elective proctocolectomy.

UC px with chronic abd pain, bloody diarrhea, and systemic symptoms

C. diff

Px watery diarrhea, fulminant colits with pseudomembranes, and toxic megacolon

Dx stool PCR for toxin gene

Tx mild : Oral metro or ORAL vancomycin

GI notes

Celiac disease

Immune mediated destruction of intestinal villi

Px with severe diarrhea, flatulence, Fe def anemia

Dx Typically IgA anti-tissue transglutaminase and IgA anti-endomysial antibodies are positive but can be
NEGATIVE since some patients can have associated igA deficiency.
If suspicious of Celiac disease is strong with biopsy showing villous atrophy, then SERUM testing is not
needed for diagnosis. Can measure total IgA to confirm IgA def or use IgG testing.