GIT

Diarrhea

Inflammatory Diarrhea

• >1 month + abdominal pain + weight loss

• Signs of inflammation (Reactive leukocytosis & thrombocytosis & normocytic anemia)

• Characterized by intestinal wall injury → systemic inflammatory response → leakage of inflammatory cells & blood in stool → Occult stool/hematochezia

• Causes:
• IBD (Crohn’s - UC)
• Invasive GI infections
• Ischemic colitis [preceded by sudden hypotension]
• Radiation colitis [preceded by prostate cancer radiation]

• Shiga Toxin-producing E.coli (STEC)
• Presents as watery diarrhea → bloody diarrhea 1-3 days after with NO FEVER or low-grade fever (<38.5) + diffuse abdominal pain
• Resolves in a week, but can be complicated by HUS 1-2 weeks after
• AVOID abx & give aggressive IV hydration

Secretory Diarrhea

• Can occur in patients with ileocecal resection (can be referred to as “patient shot in abdomen + got multiple surgeries)

Laxative Abuse

• Presentation → Large volume water stools + abdominal cramping (that may wake patient up from sleep)

• CAUSES METABOLIC ALKALOSIS (VS normal diarrhea that causes metabolic acidosis)
• This is due increased loss of K, causing disruption of Cl reabsorption → decreased Cl-HCO3 exchange → Metabolic Alkalosis
• Patients can also have hypermagnesemia if Mg-containing laxative is abused

• Dx → Screening Stool for Laxatives
• CHARACTERISTIC → Colonoscopy shows Melanosis Coli [Dark Brown mucosal pigmentation with pale lymphoid follicles]
• If not seen → Microscopic examination can show PIGMENT IN MACROPHAGES OF LAMINA PROPRIA
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Bile Acid Diarrhea

• 10% of patients post cholecystectomy

• Secretory diarrhea due to irritation of intestinal mucosa

• Labs, ESR and everything is NORMAL

• ttt → Bile Acid resins

Chemotherapy-related Diarrhea

• Due to direct cytotoxic effect on intestinal mucosa → secretory diarrhea

• ttt → Loperamide +/- IV hydration & electrolyte replacement

• All patients on chemotherapy that get diarrhea, should undergo Labs and stool testing (including Cl. difficle) prior to dx of CRD

Esophagus

Eosinophilic Esophagitis

• Diagnosis: endoscopy (trachealization) → biopsy (≥ 15eosinophil/hpf)

• TTT → Stop allergens (via diet modification), PPIs, topical steroids

• If not treated ⇒ fibrosis & esophageal stricture

Vascular Ring

• Abnormal 2ry arch of aorta compresses:
• posterior aspect of the esophagus ⇒ Solid-Food dysphagia leading to food impaction
• Trachea ⇒ Biphasic Stridor OR recurrent aspiration infections

• Associated with failure to thrive due to all-liquid diet

• Dx → Barium esophagoscopy THEN CT or MRI Angio

Dysphagia Approach Algorithm

Achalasia

• Manometry is required for diagnosis

• buzzy sentences are “Swallowing improved with standing” and “regurgitation of undigested food”

• If achalasia like presentation in an older male with significant weight loss ⇒ THINK ESOPHAGEAL CANCER (pseudo achalasia) ⇒ DO ENDOSCOPY

Pill-Induced Esophagitis

• Sudden onset Odynophagia + Retrosternal Chest pain

• Caused by Tetracyclines (acid effect), NSAIDs (decreased mucosal protection), Bishphonates, Iron, Potassium Chloride (Osmotic effect)

• Endoscopy shows Mid-esophageal circumferential ulceration

Esophageal Perforation

• Severe chest/back/epigastric pain + systemic signs (fever, hypotension)

• Crepitus and Hamman Sign

• Pleural Effusion with atypical green fluids
• Pleural Analysis would show Low pH, high amylase, and food particles

Esophageal Rupture (Boerhaave Syndrome)

• Vomiting/Forceful retching → increased intraesophageal pressure → full thickness rupture → gastric content & air into mediastinum:
• Air → Pneumomediastinum & Suprasternal crepitus crunching sound/subcutaneous emphysema with each heart beat (Hamman sign)
• Gastric content → Pain (Chest/Upper abdominal/back) & peritonitis → sepsis

• Dx → Esophagography or CT scan with water-soluble contrast (NOT BARIUM)

• TTT → abx, PPIs, NPO then → surgery

Mallory-Weiss Syndrome

• Vomiting/Forceful retching → mucosal tear → hematemesis & epigastric/back pain

• Is often seen in association with alcohol use disorder and hiatal hernia

• Dx → upper GI endoscopy

• ttt → PPIs. Heals spontaneously
• if ongoing → electrocoagulation or local epinephrine injection (endoscopically)

TEF with Esophageal Atresia

• First Step → Place NGT

• 2nd Step → CXR

Stomach

Gastric Cancer

• Epigastric pain + nausea/vomiting + weight loss + IDA → Gastric Cancer
• Especially if from Eastern Asia

‘If cancer is at proximal stomach ⇒ presents as dysphagia and postprandial nausea and vomiting’

• Liver metastasis is common & causes hepatomegaly, signs of liver failure (hypoalbuminemia), elevated ALP/AST/ALT

• Dx → Upper GI endoscopy + biopsy followed by CT for staging
• H.pylori testing is AFTER EGD as biopsy in patients with alarming signs

Autoimmune Metaplastic Atrophic Gastritis

• Increases risk of gastric adenocarcinoma and neuroendocrine tumors so Routine Surveillance endoscopy is indicated

Acute Erosive Gastropathy

• Exposure to irritants (alcohol, cocaine, aspirin) followed by acute abdominal pain & hematemesis

Hiatal Hernia

• Paraoesophageal Hiatal Hernia
• Retrocardiac Air-Fluid Level is buzzy (can also be seen in sliding hiatal hernia)
• Confirmed by barium or endoscopy
• ttt → surgical repair due to risk of gastric volvulus & IO

H.pylori Infection

• Dyspepsia + occult bleeding ⇒ Endoscopy + Biopsy is indicated
• If NO occult bleeding ⇒ Non-invasive diagnostic testing (Stool antigen & Urea breath testing)
• 2 week AFTER stopping PPI
• Serology can’t between active and cleared infection, so not preferred nor used.
 

• Duodenal Ulcers
• Most common causes are H.pylori and NSAIDs
• If patient has no other risk factors and hx of NSAIDs use, the cause is H.pylori
• ttt → abx (amoxicillin & clarithromycin) + PPI

Perforated Peptic Ulcer

• First → CXR
• If CXR is negative, we can do a CT scan with contrast to visualize the smaller amounts of air/fluid under the diaphragm
• OR IF NO OR availability, we can also do a CT scan to localize the perforation site

• If perforated, endoscopy is C.I

Stress-Induced Ulcer

• Common in ICU patients

• Causes painless bleeding hours-days after period of stress

Intestinal Disorders

Intussusception

• Recurrent

• Atypical location

• Atypical age

• persistent bleeding despite reduction

• If negative → CT or Colonoscopy

Small Bowel Obstruction (SBO)

• Change of pain character

• Fever

• Hypotension

• Metabolic Acidosis

• +/- guarding & leukocytosis

Small Intestinal Bacterial Overgrowth (SIBO)

• Risk Factors:
• Ileocecal resection (as ileocecal valve acts as physical barrier)
• Motility Disorders (DM, Scleroderma)
• Chronic Pancreatitis, Hypochlorhydria, PPI use

• Causes watery diarrhea +/- malabsorption

• Vitamin B12 is DECREASED, while Vitamin B9 is INCREASED

• Dx
• Gold Standard is Jejunal Aspirate (Invasive)
• Carbohydrate Breath test

Ascaris SBO

• 1st sign is Peripheral Eosinophilia

• Dx → visualization of ascaris eggs or worms in stool/resp secretions

• ttt → Conservative (NGT + fluid/electrolyte replacement) + Albendazole/Mebendazole

Colon

Colon Cancer

• Anemia + occult blood in stool + solitary liver nodule ⇒ CRC metastatic to liver
• Asymptomatic CRC is possible → spread to liver as a solitary mass or multiples
• if Colonoscopy reveals the CRC, LIVE BIOPSY IS NOT NEEDED

• Microcytic Anemia + multiple liver nodules ⇒ CRC metastatic to liver
• Colonoscopy must be performed
• If unrevealing, upper endoscopy is done next to assess other cancers and sources of blood loss

• Right-Sided Cancers ⇒ IDA and occult bleeding

• Left-Sided Cancers ⇒ Obstructive Symptoms + change in bowel habits +/- hematochezia

• Rectal Cancers ⇒ Hematochezia or bright red blood + tenesmus + sensation of rectal mass

• NEW-ONSET changes in stool frequency & consistence in high risk patients (age>50 years, family hx of CRC), especially if the changes are persistent & significant
• Other indications for colonoscopy are Red Flags (anemia, weight loss, hematochezia, change in pain severity)

• Infection with Streptococcus Bovis (group D streptococcus) Warrants a colonoscopy as it is associated with CRC

• Clostridium Septicum Bacteremia/Infection is also associated with CRC, so colonoscopy is indicated

• Lynch Syndrome (CRC + Endometrial Cancer + Ovarian Cancer)

• Normal Patients → START COLONOSCOPY AT 45 years
• Repeat colonoscopy every 10 years OR
• gFOBT or FIT every year OR
• FIT-DNA every 1-3 years OR
• CT colonography every 5 years OR
• Flexible Sigmoidoscopy every 5 years (or every 10 years if done with annual FIT)
 

• Patient with Family hx of CRC or high-risk adenomatous polyp → START COLONOSCOPY AT 40 YEARS (OR 10 years prior to age of diagnosis in FDR)
• Repeat colonoscopy every 5 years (or every 10 years if FDR diagnosed at > 60 years)
 

• Patient with UC → START COLONOSCOPY 8-10 years after diagnosis
• Repeat colonoscopy every 1-3 years
• IF PATIENT HAS UC + PSC THEN THE SCREENING IS ANNUAL
 

• Hx of abdominopelvic radiation → 30-40 years (x4 risk)

• Family hx of FAP or colon cancer → earlier age (???)

• Adenomatous Polyps ⇒ Repeat in 1 year

• Consumption of processed/red meats, smoking, alcohol, DM, obesity

• Family hx or Px hx of FAP, colon cancer, adenomatous polyps, Lynch Syndrome

• UC, Prior abdominopelvic radiation

• CRC in <50 years with absence of major risk factors → look for obesity/DM as hyperinsulinemia increases ILGF-1 which decreases apoptosis & promotes progression of GI epithelial cells → adenocarcinoma

• High Fiber diet & NSAIDs/Aspirin use

• Resection is almost always indicated (Primary Tumor + Liver Metastasis)
• Chemotherapy is noy indicated unless liver metastasis is unresectable due to size or number of lesions
• Resection of primary tumor is also indicated regardless of stage for relief or prevention of obstruction

FAP

• Starting puberty → annual colonoscopies

• Significant symptoms → GI bleeding

• High Risk Features → large polyps (>1cm), high grade dysplasia, or innumerable polyps.

Ogilvie Syndrome (Colonic pseudo-obstruction)

• Causes
• Electrolyte derangement (hypokalemia & hypomagnesemia due to diuretics + diarrhea)
• Major Surgery / Trauma / Sepsis / Meds (opioids / anticholinergics)

• Imaging → Colonic Dilation with normal haustra without obstruction

• Management → NPO, NGT, Rectal Tube
• if 48hr with no improvement OR cecal diameter > 12cm (impending perforation) → Neostigmine

Diverticular Disease

Acute Diverticulitis

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• Acute diverticulitis diagnosis is via CT showing focal/localized colonic thickening AND peri-colonic fat stranding
• Seeing the diverticulum is not diagnostic or essential for diagnosis
• CT is diagnostic & endoscopy is C.I in the acute phase due to risk of perforation
• Endoscopy is done 6-8 weeks after to exclude colonic adenocarcinoma
 

• Complications:
• Abscess:
• Small (<4cm) → IV abx WITHOUT drainage
• Large (≥4 cm) → IV abx AND drainage

 

• Associated with sterile pyuria due to irritative of bladder from adjacent inflamed sigmoid colon

• ACUTE DIVERTICULITIS CAN PRESENT AS TENDER LEFT SIDED ABDOMINAL MASS

 

Diverticular Perforation

• Micro → medical ttt (abx & NPO)

• Macro (Free air on CT) → surgical (washout & resection)

Sigmoid Volvulus

• Perforation or peritonitis ⇒ Laparotomy + Sigmoid Colectomy

• NO Perforation or peritonitis ⇒ Therapeutic Flexible Sigmoidoscopy (if successful allows for elective surgery to prevent recurrence)

Cecal Volvulus

• More common in younger adults & they often report self-resolving similar episodes due to a congenitally mobile cecum

• AXR shows a large single dilated loop

• CT is diagnostic (Twirl Sign)

• ttt ⇒ Emergency Laparotomy with right colectomy
• Detorsion IS NOT advised (VS sigmoid volvulus)

Ulcerative Colitis (UC)

• Mild UC:
• < 4 watery bowel movements per day + NO/RARE/Intermittent hematochezia
• NO Anemia
• NORMAL ESR & CRP
• Colonoscopy shows shallow ulcers & erythema of the rectum & sigmoid
• ttt → 5-ASA (mesalamine, sulfasalazine, balsalazide)
 

• Mod-Severe UC:
• >6 watery bowel movements + frequent Hematochezia
• ANEMIA
• HIGH ESR & CRP
• ttt → TNF-alpha inhibitors

• Toxic Megacolon if suspected (Worsening of pain, distention/tenderness, leukocytosis, fever, hypotension, tachycardia)
• CT scan to confirm (DO NOT COLONOSCOPY AS IT CARRIES RISK OF PERFORATION)
• Followed by IV steroids
• If Fails → Surgery may be required

Irritable Bowel Syndrome (IBS)

Algorithm

Pseudomembranous Colitis

• Peritonitis (diffuse tenderness, rebound tenderness)

• Megacolon (>6 cm + decreased diarrhea “loss of tone”) ⇒ [systemic toxicity (fever, hypotension, tachycardia), distention & pain (maybe even ceasing of diarrhea), leukocytosis]

• Increased serum lactate (marker of colonic ischemia)

• Abx use or hospitalization

• Advanced age > 65

• Gastric Acid suppression (PPI. H2 use)

• IBD

• Chemotherapy

• Non-severe (classic symptoms) & Severe (+ leukocytosis>15,000 + serum creatinine 1.5) ⇒ Fidaxomicin or vancomycin

• Fulminant CDI (severe + hypotension/shock OR ileus/megacolon) ⇒ Oral Vancomycin & IV Metronidazole

Microscopic Colitis

• Gross Colonoscopy is NORMAL

• Histology:
1. Collagenous Colitis: Thickened Subepithelial Collagen Bands
2. Lymphocytic Colitis: High levels of Intraepithelial Lymphocytes

• Management:
• Smoking Cessation + Withdrawal of meds (NSAIDs)
• If fails → Oral budesonide and anti-diarrheal

Colovesical Fistula

• Caused by Diverticular disease (most common), Crohn’s, Malignancy

• Presents as pneumaturia, fecaluria, and recurrent UTIs

• Dx → CT scan of the abdomen with oral/rectal (NOT IV) contrast
• Followed by colonoscopy to exclude colonic malignancy

Rectum & Anal Canal

Proctalgia Fugax

• Spastic Contraction of anal sphincter (most commonly in women) that causes short episodes of pain (<30 mins) with painless periods between attacks

• Pain is unrelated to anything, but can be stimulated by sitting, intercourse, or stress

• Diagnosis of exclusion (Normal Examination & Labs)

Gonococcal Proctitis

• Transmission → Anal intercourse OR spread from vagina

• Presentation → Mucopurulent discharge + tenesmus + Pruritis
• +/- bleeding, urgency, pain, constipation, rectal fullness

• Dx → PCR of rectal swap

• ttt → Ceftriaxone + Doxycycline for chlamydia co-infection (Azithromycin is NOT studied for proctitis)

Radiational Proctitis

• Chronic ⇒ > 3 months to a year
• Obliterative endarteritis and Fibrosis
• Severe bleeding
• Endoscopy shows multiple telangectasias with mucosal pallor and friability

• Acute ⇒ <3 months
• Direct mucosal injury
• Minimal Bleeding, but diarrhea + mucus + tenesmus are present
• Endoscopy shows severe erythema, edema, and ulcerations

Evaluation of Rectal Adenocarcinoma (diagnosed by sigmoidoscopy)

• Do a full colonoscopy as patients with left-sided tumors are at a high risk of having synchronous left sided tumors

• Then CT scans for pelvis, chest, and abdomen are required for staging

• CEA can be done for prognosis

Thrombosed External Hemorrhoids

• Thrombosis presents as excruciating anorectal pain that is exacerbated by sitting

• Direct visualization of a bluish (or purplish) bulge at the anal verge confirms the diagnosis

• Management ⇒ sitz baths, stool softeners, lidocaine
• If fails OR EXTREMELY PAINFUL WITHIN 72 HOURS OF PRESENTATION → External Hemorrhoidectomy
• After 72 hours, clot formation causes decrease of pain

Fecal Incontinence 2ry to Fecal Impaction

• Risk Factors ⇒ Decreased motility, inadequate fiber/fluid intake, chronic constipation, and decreased sensation in rectal vault (dementia/spinal cord injury patients)

• Obstruction causes backup of stool ⇒ Abdominal distention & diffuse tenderness
• Passage of liquid stool around the impaction ⇒ Fecal Incontinence

GI Bleeding Disorders

Angiodysplasia

Variceal hemorrhage Bleeding

 

 

• Either Octreotide or Terlipressin can be used

 

• Blood transfusion is typically performed for a hemoglobin <7 g/dL in most patients with variceal hge
• OR <9 g/dL in high-risk patients (unstable CAD)
 

• PLT transfusion is for PLTs < 50,000 AND Bleeding patient

Ischemic Colitis

• Presents in watershed area, causing Lower GI bleeding + crampy left-sided abdominal pain within 24 hours of hypotension

Bleeding Patients on Warfarin

1. Stop Warfarin Immediately

2. Prothrombin Complex Concentrate (PCC) Should be given ⇒ Normalizes INR in ≤ 10 mins; however effects are transient
1. if PCC is unavailable, Fresh Frozen Plasma can be administered, however, less effective as it needs more units & risks volume overload

3. IV Vitamin K

Occult GI Bleeding Algorithm

New-Onset IDA in elderly

• Endoscopy + Colonoscopy MUST be performed

• EVEN IF a single FOBT is negative

Minimal Bright Red Blood per Rectum (BRBPR)

• Associated with benign disorders like hemorrhoids or fissures ⇒ Anoscopy
• Can sometimes also be caused by proctitis, ulcers, polyps, or cancer
• Symptoms here would include increased amount of blood mixed with mucus, systemic symptoms, and change in bowel habits/caliber

Liver

Cirrhosis

• Management
1. Treat underlying cause
2. Prevention (Avoid alcohol & hepatotoxic meds + Vaccination of HBV and HAV)
3. Complications
1. Screen for varices (endoscopy)
2. Screen for HCC (US +/- AFP every 6-12m)
3. Frequent assessment of ascites and encephalopathy

• Varices Primary Prevention (in medium-large nonbleeding varices) & Repeat EGD every YEAR
• Nadolol & Propranolol → used in decompensated cirrhosis
• Carvedilol → used in compensated cirrhosis
• If Beta blockers are contraindicated, band ligation can be used as a primary prevention
• Contraindications are hypotension, AKI, serum sodium < 130 mEg/L
 

• New-Onset Ascites
1. SAAG
1. If ≥1.1 g/dL ⇒ Portal HTN
1. Protein < 2.5 g/dL ⇒ Cirrhosis
2. Protein ≥ 2.5 g/dL ⇒ Right-Sided HF causing hepatic congestion
2. If <1.1 g/dL ⇒ Peritoneal Inflammation (Malignancy, TB, Pancreatitis) OR Nephrotic Syndrome
 
2. Cell Count & Differential
1. Lymphocyte predominance ⇒ TB or Malignancy
2. Neutrophils predominance (≥250) ⇒ SBP
 
• Management Of ascites in cirrhosis:
• Medical: Spironolactone with furosemide + STOP alcohol & Salt intake + AVOID ACEIs, ARBs, and NSAIDs.
• If Refractory → Paracentesis OR TIPS

Acute Liver Failure (ALF)

• Diagnosis Requires:
1. Elevated aminotransfereases (> 1000) OR
2. Signs of hepatic encephalopathy OR
3. Impaired synthetic function (INR≥1.5)

Hepatic Encephalopathy

1. ttt of cause (Hypokalemia/Metabolic alkalosis are major HY causes that are caused by frusemide + spironolactone intake)

2. decreased blood ammonia levels
1. Nonabsorbable disaccharides (lactulose & lactitol) → metabolized by bacteria into lactic & acetic acid → decrease pH → ammonia to ammonium (trapping) & causes bowel movement
2. Rifaximin
3. If above measures fail → oral neomycin

Toxic-Metabolic Encephalopathy

• Most Common → Reye Syndrome
• Mitochondrial dysfunction → Impaired FA metabolism → Acute hepatic (Microvesicular) Steatosis
• Hyperammonemia → Cerebral Edema & Encephalopathy
• ttt → Supportive

• INH (idiosyncratic reaction) causes hepatocellular injury that looks similar to viral on histology (panlobular mononuclear infiltration & cell necrosis)
• Others → INH, Chlorpromazine, and HIV drugs

Acetaminophen Toxicity

• Causes ALF, characterized by:
• AST/ALT > 1000
• Hepatic Encephalopathy
• Synthetic Liver Dysfunction

• ttt → Liver Transplantation
• Indications are Grade 3/4 hepatic encephalopathy, PT > 100 seconds, serum creatinine > 3.4

Ischemic Hepatopathy

• Hallmark is rapid and significant increase in LFTs (up to >10,000) following episodes of septic shock, hypotension, or HF

• If they survive, LFTs return to normal after 1-2 weeks.

Autoimmune Hepatitis

• More common in middle-aged women

• Antibodies
• + SMA (Smooth-muscle antibodies) OR Anti-Liver/Kidney Microsomal Type 1 antibodies ⇒ Specific
• + ANA ⇒ Commonest

• Hepatocellular pattern of injury → Persistent high LFTs (20x UNL of ALT & AST) + variable bilirubin levels (asymptomatic woman + persistent high AST/ALT + high gamma gap)

• Large gamma gap (total protein - albumin > 4 g/dL) [NOT SEEN IN ALL CASES]

• treatment
• Immunosuppression (by glucocorticoids) +/- Azathioprine
• If ALF [Hepatic Encephalopathy, prolonged PT] or Decompensated Cirrhosis [Varices, Ascites] ⇒ Liver Transplantation

Metabolic Diseases

• Labs → Increased indirect bilirubin; EVERYTHING ELSE NORMAL

• NO ttt required

Alcoholic Hepatitis

• ALT & AST levels are usually >300 but almost always <500

• Macrocytic Anemia

• AST:ALT ration is >2
• When in doubt of cause of Hepatocellular pattern injury, look at ratio

• GGT & Ferritin levels are also increase (Ferritin as APR)

Nonalcoholic Fatty Liver Disease (NAFLD)

• AST:ALT ration < 1

• Hepatomegaly & Increased echogenicity on U/S (steatosis) OR course echotexture (fibrosis)

• Pathophysiology is Insulin Resistance, which causes Increased Peripheral Lipolysis + Triglyceride synthesis ⇒ Increased Hepatic Accumulation of FAs and TAGs (Steatosis)

Hepatic Hydrothorax

• Transudative Pleural effusion 2ry to passage of ascites fluid into the pleura through diaphragmatic openings/defects.
• Usually on the Right Side

• Dx → CXR to show effusion THEN exclusion of other causes

• TTT:
• Conservative → Salt Restriction + diuretics +/- Thoracocentesis if needed
• AVOID chest tube placement as it can cause complications (Protein loss, electrolyte loss, renal failure)
• Definite → Liver Transplantation

Infections

Hepatitis A

• ALT/AST > 1000

• ttt → Conservative

Spontaneous Bacterial Peritonitis (SBP)

• Classical Triad → Fever, AMS, and abdominal pain in a patient with ascites

• To confirm dx → Cell count & differential: neutrophils ≥ 250
• culture: E.coli & klebsiella (50%) THEN streptococci

• ttt → Ceftriaxone

• prophylaxis → in patients with prior SBP OR patients with cirrhosis + Upper GI bleeding

Liver Transplant Rejection

Acute Cellular Rejection

• First 3 months

• Can present as fever, fatigue, jaundice, or be asymptomatic, so ACR is suspected by labs

• Dx → Biopsy (shows mixed infiltration of portal tracts, Interlobular bile duct destruction “nonsuppurative cholangitis”, and Endothelitis [most reliable sign])

• ttt → High dose steroids
• If fails → thymoglobulin, sirolimus, and other immunosuppressants
• If fails → Repeat Transplantation

Cancer

HCC

• Normal AFP does NOT rule out HCC

• MOST COMMON CAUSE OF BLOODY ASCITES
• If first sample is bloody ⇒ Repeat.
• If repeated samples are bloody ⇒ Malignancies

• Patients with cirrhosis + new-onset ascites or any sign of liver decompensation (varices bleeding) ⇒ THINK HCC

• Asymptomatic Patients with cirrhosis should undergo screening for HCC via AUS every 6 months

• Most Common Origin is CRC ⇒ DO colonoscopy EVEN IN ABSENCE OF CRC SYMPTOMS
• Followed by Breast & Lung
• NOTE THAT Prostate Cancer likes Bone & Lymph Nodes, in comparison to liver

Hepatic Adenoma

• US shows well-demarcated hyperechoic mass & CT shows early peripheral enhancement

• Young women on COCs
• if asymptomatic & <5 cm → stop COC
• if symptomatic OR >5 cm → Surgical Resection
• Needle biopsy IS NOT recommended due to risk of bleeding

• Solid Tumor
• Complications ⇒ Malignant Transformation or Rupture & Hge (more common)

FNH

• NOT associated with COCs

• Due to anomalous arterial formation

• Imaging shows increased arterial flow and central scar

Hepatic Hemangioma

• spontaneous rupture is super rare apparently.

Biliary Disorders

Acute Cholangitis

• Presents as Fever, Jaundice, RUQ pain (Charcot’s Triad) +/- hypotension & AMS (Reynold’s Pentad)

• Caused by ascending infection due to biliary obstruction (stone - malignancy - stricture [PSC])

• Labs → Increased direct bilirubin & ALP + mild increase in AST/ALT

• Imaging → CT/US show biliary & intrahepatic dilation

• TTT: Supportive → abx → ERCP with sphincterotomy
• other options: Percutaneous transhepatic cholangiography & open surgery

Approach to asymptomatic patient with elevated ALP and direct bilirubin levels:

1. Abdominal U/S (to differentiate site of cholestasis)
• Normal sized common bile duct ⇒ Intrahepatic Cholestasis
• Think PBC
• So, next step is → AMA
• Dilated common bile duct ⇒ Extrahepatic Cholestasis
• Think Pancreatic head tumor, PSC, or choledocholithiasis
• So, next step is →
• CT for pancreatic tumor
• MRCP for PSC

Primary Sclerosing Cholangitis (PSC)

• MALES

• Presents as recurrent AC attacks + hematochezia
• Fibrosis & Stricture of intrahepatic & extrahepatic bile ducts ⇒ recurrent AC
• associated UC ⇒ hematochezia

• Labs → Cholestatic pattern

• Diagnosis → MRCP

• ttt → endoscopic intervention for strictures, abx, ttt of UC, and +/- ursodeoxycholic acid

Cholangiocarcinoma

• Presentation → Malignant Biliary Obstruction [Weight loss, Jaundice, Dark Urine, RUQ pain, Acolic Stools, Cholestatic Liver Enzymes]
• Associated Metastasis → Liver (Hepatomegaly)
• Usually intrahepatic duct dilation, but can also be extrahepatic depending on level of obstruction

• Greatest Risk Factor is PSC with underlying UC (~90%)

• LABS ⇒ Elevated CEA/CA 19-9 with NORMAL AFP [VS HCC normal CEA/CA 19-9 with high/normal AFP]

• CT/US shows dilation but not biliary mass always, so BEST IS ⇒ ERCP or EUS

Primary Biliary Cholangitis (PBC)

• FEMALES

• Rarely associated with AC & UC, because it affects intrahepatic biliary ducts

• Antimitochondrial antibodies

• Presentation: Fatigue + Pruritis are super HY + xanthelasmas & hepatomegaly

• Labs → Cholestatic pattern

• Complications:
• Fat-Soluble Vitamins Deficiency (this is why, regular bone densitometry screening should be preformed + calcium & Vitamin D supplementation; if osteoporosis develops, biphosphonate therapy is started)
• HCC

• ttt → Ursodeoxycholic acid if asymptomatic OR noncirrhotic (if cirrhosis → liver transplant)

Hemobilia

• Bleeding into the biliary tract

• Common after “hepatobiliary procedures”: liver biopsy, cholecystectomy, ERCP

• Presents as: RUQ pain, Jaundice, BLEEDING (usually Melena) ~ 5 days post-op
• Additional findings: anemia/reactive thrombocytosis/reactive leukocytosis/ direct hyperbilirubinemia

• ttt → conservative unless bleeding is persistent → embolization or surgery

Biliary Cyst

• Cystic Dilation of Biliary tree

• Presentation:
1. Asymptomatic (Incidental Finding)
2. Classical Triad: Abdominal Pain, RUQ mass, Jaundice
3. Neonates: Jaundice, Acolic stools, dark urine, hepatomegaly

• Complications:
• Cholangiocarcinoma, GB Cancer, Pancreatic Cancer
• Acute Cholangitis
• Pancreatitis (due to associated anomalous pancreaticobiliary junction)

• Dx → US followed by MRCP or CT

• ttt → Cystectomy +/- Roux-en-Y-hepaticojejunostomy
• Cystectomy is at the time of the diagnosis
• If patient presented with a complication, ttt of complication is done first
• After surgery, serial labs and imaging are done as there is still a small chance of cancer

Emphysematous Cholecystitis

• Risk Factors → Old age/DM & vascular disease (cystic artery compromised or atherosclerosis)

• Cl / E.coli

• Crepitus in abdominal wall can sometimes be seen

• Gas in gallbladder with no gas in biliary tree (most of the time)

• ttt → Emergency cholecystectomy & IV abx (Piperacillin-taobactam)

Cholecystitis

• ttt → IV fluids, abx, and cholecystectomy within 72 hrs. (better than delayed)
• the abx of choice is empirical Piperacillin-Tazobactam

• Dx → US (if undetermined → HIDA scan)

• PAIN OF CHOLECYSTITIS IS THE SAME AS THE PAIN OF BILIRARY COLIC, THE ONLY DIFFERENCE IS THAT CHOLECYSTITIS THE PAIN LASTS LONGER THAN 6 HOURS.

Acalculous Cholecystitis

• Seen in patients with severe trauma, recent surgery, critical illness, TPN, prolonged fasting ⇒ Gallbladder Stasis & Ischemia
• This causes distention, necrosis, and 2ry bacterial infection
• Associated with adynamic ileus (”decreased bowel sounds, retention of gastric contents, and gaseous distention of bowels with NO air-fluid level”)

• Dx → GB distention, wall thickening, and pericholecystic fluid in ABSCENCE of gallstones

• ttt → Abx + percutaneous cholecystostomy followed by interval cholecystectomy

Suspected FB Ingestion

Why is battery ingestion dangerous?

• Current → Corrosion

• Leaking of alkaline battery → Liquefactive Necrosis

• + like any other FB → pressure necrosis

• Prolonged Impaction In esophagus: ulceration → perforation → hemorrhagic shock → death

 

How to differentiate between battery & coin on X-Ray?

• Battery has Halo Sign/Double-Ring Sign around the circular battery

• Battery has a Step-off or beveled edge

 

 

Administering honey soon after ingestion in an asymptomatic patient may provide a partial protective barrier but should not delay definitive management

 

• Fish Bone is a “sharp item”

Spleen

Splenic Infarction

• Sickle Cell Disease (will have associated anemia) ⇒ DO electrophoresis

• Embolism (AF, IE, Atheroma)

• Thrombosis due to hypercoagulable state (cancer, SLE, APLS)
• SLE → Joint Pain, Thrombocytopenia, young female ⇒ DO ANA
• Can be associated with NBTE (MR murmur) ⇒ DO ECHO
• Can be associated with APLS ⇒ TEST FOR IT

Splenic Abscess

• Triad → Fever, Leukocytosis, LUQ pain (due to splenic fluid collection)
• +/- splenomegaly, left pleural effusion, left pleuritic chest pain

• Risk Factors
• IE (especially with patients with structural HD like MVP) → septic emboli
• Sickle Cell disease
• Trauma
• HIV & IV drug usage

• Dx → CT

• ttt → abx + splenectomy

Atraumatic Splenic Rupture

• Caused by:
• Hematological Malignancies (Leukemia, Lymphoma)
• Infection (EBV, CMV, Malaria)
• Splenic Congestion (Cirrhosis, Pregnancy)
• Medications (Anticoagulation, G-CSF)

• People with these increase the risk of splenic rupture, so should be avoided for 3-4 weeks.

• Dx → Acute anemia + Intraperitoneal free fluid

• ttt:
• Stable → Embolization
• Unstable → Emergency Splenectomy

Post-Splenectomy

• Vaccinations & prophylactic abx (Amoxicillin-Clavulanate is DOC)
• If allergic → Levofloxacin

Pancreas

Pancreatic Cancer

Always think of pancreatic cancer in patients with history of smoking & weight loss

• If with Jaundice (the most likely head of pancreas mass) ⇒ US

• If with NO jaundice (most likely tail/body mass) ⇒ CT

Pancreatic Cysts

• If risk of malignant transformation is low → Reassurance

• If risk of malignant transformation is high ⇒ US-guided FNA + Cytological examination
• Large size ≥ 3 cm
• Solid components OR calcifications
• Main pancreatic duct involvement
• Thickened or Irregular cyst walls

Acute Pancreatitis

• Management is NPO and IV fluids

• Dx: (requires 2+) → Acute epigastric pain radiating to the back, Amylase or Lipase > 3x UNL, Imaging consistent with pancreatitis

• Causes → Stones, Alcohol, Hypertriglyceridemia, or Cholesterol Embolism, Drugs
• Hypertriglyceridemia-induced pancreatitis is managed by insulin infusion or apheresis
• Cholesterol Embolism happens in patients with risk of atherosclerosis who underwent cardiac cath or vascular surgery → Cholesterol in artery gets launched off:
• Skin → Livedo Reticularis
• Kidney → Acute Kidney Injury (high creatinine)
• GI → Acute Pancreatitis or Mesenteric Ischemia
• Drugs:
• analgesics: NSAIDs, Acetaminophen, Opioids, Mesalamine, Sulfasalazine
• abx: INH, Tetracyclines, Metronidazole, TMP-SMX
• anti-eplipetics: Valproate & Carbamazepine
• HTN: Thiazides, Loops, ACEi, ARBs
• Viral: Lamivudine & Didanosine
• immuno: AZA, MCP, Steroids
• others: Estrogens & Asparaginase

• Worse Prognosis Prediction:
1. Patient Factors:
• Older age > 55
• Comorbidities, including obesity (BMI > 30)
2. Clinical Factors:
• AMS
• SIRS (Leukocytosis > 12,000 OR Temp > 38)
3. Lab Factors:
• High BUN (>20), High Cr (>1.8), high Hct (>44)
4. Radiological Factors:
1. CXR: pulmonary infiltrates/effusion
2. CT: Severe pancreatic necrosis

Pancreatic Ascites

• Rare complication of chronic pancreatitis

• Ascitic Fluid analysis is serosanguinous/straw-colored + high levels of amylase + high protein with low SAAG

Pancreaticopleural Fistula

• Exudate pleural fluid by Light’s Criteria that is amylase-rich:
• pleural LDH/serum LDH > 0.6 OR
• pleural protein/serum protein > 0.5 OR
• pleural LDH >2/3 UNL of serum LDH

• Commonly due to attacks of acute or chronic pancreatitis or even iatrogenic after percutaneous drainage of pancreatic cysts or abscesses

Gallstone Pancreatitis

• Stone causing pancreatitis
• Presents as acute pancreatitis (epigastric/back pain + high amylase/lipase) + high serum ALP, ALT >150, elevated direct bilirubin.
• Next Step ⇒ RUQ US to confirm
• Can be complicated by cholangitis (Charcoat triad [fever, RUQ pain, jaundice] or Reynold’s pentad [+ hypotension & AMS]
• ttt → IV hydration + abx + ERCP
• Cholecystectomy is indicated after resolution of acute pancreatitis attack

Acute Necrotizing Pancreatitis

• Patient with pancreatitis + 7-10 days after develops sepsis.

• Presents as → Fever, AMS, Sepsis

• Dx → CT Scan (gas + necrotic tissue collection) ⇒ IV ABX
• If CT scan uncertain ⇒ Aspiration & Culture
• After patient stabilizes on abx + necrotic tissue becomes capsulated ⇒ SURGICAL DEBRIDEMENT

Gastrinoma

Algorithm for suspected Gastrinoma

• If Gastrinoma is confirmed, patients should be screened for PTH, Calcium, and PRL.

• The cause of the steatorrhea is inactivation of pancreatic enzymes & mucosal injury

Appendix

Management of Suspected Appendicitis

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Atypical Presentations

1. Postpartum: The periumbilical pain is masked, especially if delivery was CS

2. Pregnant: The pain site is on the right flank (mid-upper) as it is displaced by the gravid uterus
1. Maternal Fever → Fetal Tachycardia
2. Peritoneal Irritation → Uterine contractions

Pseudoappendicitis

• Caused by Campylobacter jejuni and Yersinia entercolitica

• Predilection for infection ileocecal region → Infectious ileocecitis

• Presents as fever, leukocytosis, peri-umbilical abdominal pain that migrates to RLQ
• However, mucus and bloody diarrhea is present +/- history of other sick contacts

Appendix Abscess

• Psoas Sign: RLQ pain that increases with right hip/thigh extension (Psoas Abscess OR retrocecal appendicitis)

• Obturator Sign: RLQ pain that increases with internal rotation of the right thigh (Pelvic Abscess or Appendicitis)

• Rectal Tenderness Sign: Right Pelvic pain during rectal examination, especially when pressure is on the right rectal wall (Pelvic abscess or Appendicitis)

• Management → IV abx, bowel rest +/- percutaneous drainage of the abscess
• 6-8 weeks later, an interval appendectomy can be done

Subphrenic Abscess

• Post Laparoscopic Appendectomy

• Patient develops fever, RUQ pain, SOB, right pleural effusion, hiccups

• Dx → CT scan

• ttt → abx + drainage

Nutrition

Roux-en-Y gastric bypass

• Classically causes KEDA & B12 deficiencies

• Vitamin C can occur due to poor post-op diet ⇒ Ecchymosis, Petechiae, Poor Wound Healing, Perifollicular hemorrhage, coiled hair, gingivitis WITH NORMAL PT, PTT, PLT count

• Complications:
• Anastomotic leak is seen usually in the first WEEK
• MOST SENSITIVE INDICATOR → HR >120
• Other features: Fever, Pain, Tachypnea, Leukocytosis
• Dx → CT with contrast → Surgical Repair
 
• Stomal Stenosis is usually seen in the first YEAR
• Present as progressive dysphagia (solids → liquids), postprandial vomiting, and GERD
• Diagnosis is via EGD

Celiac Disease

• next step → Anti-tissue transglutaminase antibody assay

• If biopsy shows atrophy, however, anti-tissue transglutaminase is negative ⇒ Think of concurrent Selective-IgA deficiency

• Associated with other autoimmune diseases (hx of maternal hypothyroidism or DM)

• Can be diagnosed using D-xylose test
• D-xylose in absorbed in the duodenum, and excreted in urine
• Celiac disease → less duodenal absorption and less urine excretion
• If other disease etiologies, like Pancreatic insufficiency, Urinary D-xylose would be NORMAL (Not a defect in intestinal mucosa)
• Can be false positive in delayed gastric emptying, impaired GFR, and SIBO (trial of rifaximin resolved SIBO)

• Unique Presentation ⇒ Atrophic Glossitis (Red smooth tongue) + Peripheral Neuropathy (seen in 50% of patients) + IDA + normal celiac GI symtoms

Vitamin B12 Deficiency

• Usually seen in patients on long term PPIs, due to achlorhydria (increased activation of IF)

• Causes Pellagra

• Can be caused by corn intake (binds to niacin), heavy alcohol intake, INH (decreases tryptophan which makes niacin), carcinoid syndrome (depletion of tryptophan → serotonin), and Hartnup disease (congenital disorder of tryptophan absorption)

Vitamin B2 Deficiency

• Angular Cheilosis, Stomatitis, and Glossitis

• Normocytic Anemia

• Seborrheic Dermatitis

Vegan Diet Deficiencies

• Common: Vitamin D, Calcium, Vitamin B12

• Possible: Iron & Zinc in children & young women

Trauma

Rectal Sheath Hematomas

• Follows Abdominal Trauma or Excessive contraction (cough in asthma exacerbation), especially those on anticoagulants.

• Phys Exam → Old lady on anticoag + risk factor above + lateral abdominal mass that doesn’t cross midline + tenderness/gaurding/rigidity + doesn’t change with LL movement

• Labs → Anemia + Leukocytosis

• Imaging → CT

• management:
• Stable → conservative
• Unstable → Angio + embolization

Duodenal Hematomas

• Epigastric pain, nausea, and worsening bilious emesis approximately 1 day after blunt abdominal trauma (BAT)
• Rapid compression of duodenum against vertebral causes rupture of mucosal & submucosal layers, causing hematomas formation and progressive expansion ⇒ Duodenal Obstruction

• Dx → Abdominal CT

• management → NPO, NGT, parenteral nutrition followed by serial CTs or US
• If they persist beyond few weeks → percutaneous drainage or surgery

PENETRATING ABDOMINAL TRAUMA MANAGEMENT:

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Blunt Abdominal Trauma

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• Free air in the retroperitoneum → duodenum/Ascending or Descending colon (as they are hollow viscus)

• Free fluid in the retroperitoneum → pancreas or kidney

• Free air in intraperitoneal space (under the diaphragm) → Stomach/Transverse colon (hollow viscus)

• Retroperitoneal inflammation is delayed & may present as flank pain

• BAT + initial CT is normal + few days later → Nausea/Vomiting, Upper Abdominal Pain, Large amount of free fluid in upper abdomen
• Dx → Pancreatic Duct Injury

• BAT + Initial CT is ABNORMAL → Large amount of free fluid in upper abdomen
• Dx → Liver OR spleen

Surgery

Nissen Fundoplication post-op complications

1. Dysphagia → clinical dx & resolves spontanously

2. Gas/Bloats Syndrome → Bloating & inability to belch (clinical dx & managed with simethicone & avoidance of carbonated drinks)

3. Gastroparesis → dx is EGD to rule out obstruction & gastric scintigraphy

Bariatric Surgery

• Indications
• BMI > 35
• BMI > 30 with T2DM
• BMI > 30 with unsuccessful attempts at weight loss or comorbidities
• IF BMI < 30 (25-29.9) ⇒ Weight-loss medications

Laparoscopic Surgery

• Side effects:
1. Co2 inflation causes stretching of peritoneum → vagal stim → bradycardia → HB → asystole
2. injection into vein → embolism (Hypotension & obstructive shock)
3. Injection into artery → embolism (infarction)
4. CO2 absorption → increases pCO2 → vasodilation → increase in HR

1. Superficial Dehiscence: Skin & subcutaneous tissue WITH intact rectus muscles
1. Management is conserbative with careful dressing changes
 

2. Deep Dehiscence: Involvement of Rectus muscles and evisceration of abdominal contents
1. Management is EMERGENCY SURGERY

Peds

Algorithm of Bilious Emesis in the Neonates

Food Protein-Induced Allergic Proctocolitis

• non-IgE mediated reaction to proteins that cause bloody stools in a well appearing infant

• Usually <6 months of age (peak 1-4 weeks after initial exposure)

• CAN ALSO OCCUR WITH BREAST MILK

Algorithm

Straining Infant Algorithm

Necrotizing Enterocolitis

• Always suspect it in a premature neonate or LBW neonate ≤1.5 kg

• Can present as bloody stools OR bilious vomiting

• Management:
• Bowel Rest, NGT, Paretral nutrition, IV fluids and EMPIRICAL ABX + Blooc Clultures
• If Failure OR Perforation ⇒ Laparotomy

Colic

• Diagnosis of exclusion characterized by ≥ 3hours a day for ≥ 3 days a week in a healthy <3 months infant.

• Management is soothing techniques & parental reassurance

• Physiological regurg in an asymptomatic (growing well) “Happy spitter” baby

• Management is Reassurance & Reposition (hold the infant upright 20-30 mins after feeds & prone when awake)

Pediatric Functional Constipation

• Presents in children >6 months of age with hard stools +/- blood streaks (in case of anal fissure) [THIS IS IN CONTRAST TO MILK-ALLERGY SEEN IN CHILDREN <6 months with mucus and blood MIXED IN THE STOOLS]

• Initial ttt → diet changes and laxative

• If fecal impaction (stool ball on PR) → enema followed by laxatives
• However, if patient has anal fissure ⇒ MORE TRAUMA.

Intussusception

• Typical presentation is sudden episodic abdominal pain in a child that lasts 15-20 mins
• Pain causes the child to be irritated and fussy

• Saline/Air Enema is diagnostic/therapeutic
• If failed ⇒ Surgery
• Surgery is also indicated if a mass lesion was found

Cystic Fibrosis

• Pancreatic Insufficiency present as ~1 year of age

• Chronic multiple respiratory diseases would be expected

• Associated with Meconium Ileus
• Inspissated stools (THICK STICKY STOOLS) causes obstruction AT TERMINAL ILEUM + Microcolon
• Presents as failure to pass meconium within 24 hours of birth +distention + no stool in rectum/vault +/- bilious emesis

Biliary Atresia

• Symptoms start from 2-8 weeks (not the rigid 6 weeks in textbooks)

• Hepatomegaly & Cholestatic Pattern: Increased direct bilirubin & GGT & ALP

• Abdominal US → Triangular Cord Sign (fibrous remnants above porta hepatis) OR a small/absent gallbladder

• Definitive Diagnosis ⇒ Intra-operative cholangiography OR Liver biopsy (fibrosis and obliteration of EXTRAHEPATIC bile ducts)

Approach to Neonatal Cholestasis

Lactation Failure Jaundice

• Presents in neonates < 1 week of age with INDIRECT hyperbilirubinemia

• Presents as a neonate with inadequate intake & signs of dehydration
• Signs of dehydration are weight loss (≥ 10% of bw) & decreased urine output (normally number of wet diapers = age in days in first week)
• Signs of inadequate intake are infrequent feedings (normally it is every 2-3 hours) & delayed milk production (normally maternal milk supply increases by day 5)
• Other Risk Factors are exclusive breastfeeding and ineffective latch

• Management is breastfeeding every 2-3 hours & follow-up in 1 day (This maintains hydration and promotes bilirubin excretion)
• If this fails → Formula supplementation and/or phototherapy may be necessary

Hirschsprung Disease

• Increased rectal tone with squirt sign + Stool is NORMAL in consistency & obstruction at level of rectosigmoidal region

• Initial step ⇒ Barium Enema with contrast shows “transition zone”

• Confirmation of Diagnosis is via ⇒ Rectal Suction Biopsy

• AXR shows complete bowel obstruction (absent rectal air + dilated bowel loops)

Congenital Umbilical Hernia

• If small → spontaneous growth

• if larger (>1.5cm) → Elective surgery at 5 years
• OR sooner if complications arise/associated with other medical conditions

Beckwith-Wiedemann Syndrome (BWS)

• At birth → Macrosomia, Macroglossia, hemihyperplasia, omphalocele & umbilical hernia

• Wilms Tumor → Serial AUS until 8 years of age

• Hepatoblastoma → Serial AFP until 5 years of age

Dehydration

• Mild → decreased intake with no clinical signs

• Moderate → delayed capillary refill time (2-3 seconds) & decreased urine output

• Severe → cool clammy skin, delayed capillary refill time (>3 seconds), sunken eyes and fontanelles, hypotension, and signs of shock

• ttt
• mild-moderate ⇒ ORS
• moderate-severe ⇒ IV fluids 20ml/kg normal saline

Gastroschisis VS Omphalocele

 

• Gastroschisis is usually an isolated defect associated with oligohydramnios
• Chronic inflammation of intestines exposed to amniotic fluid causes intestinal thickening & reduced mobility
• This may lead to IO & polyhydramnios instead.
• After Birth, the lower half of the infant is placed in a sterile bag to prevent fluid loss & heat loss + NGT is used until surgery

 

• Omphalocele is usually associated with Beckwith-Weidmann syndrome

 

OBGYN

Acute Fatty Liver of Pregnancy (AFLP)

• Defect in maternal-fetal fat metabolism → intrahepatic microvesicular fatty infiltration → Acute onset Fulminant Liver Failure
• Profound Hypoglycemia
• Mildly elevated LFTs
• Hyperbilirubinemia
• Thrombocytopenia

• management → IMMEDIATE DELIVERY

• 3rd Trimesteric (due to increased estrogen and progesterone cause hepatobiliary tract stasis and decreased bile excretion) generalized pruritis (more on hands & feet) + NO rash + RUQ pain

• Labs show: Increased total bile acids (≥10) + High liver enzymes +/- high direct bilirubin

• Complications → IUFD, Preterm, NRDS, Meconium-stained amniotic fluid

• Management → Ursodeoxycholic aci + antihistamines + delivery at 37 weeks

Post-menopausal Female with Constipation & Early Satiety

• Post-menopausal females with new-onset constipation and early satiety with NEGATIVE colonoscopy findings should be explored for Ovarian Cancers
• Do Pelvic U/S

Misc

• Diagnosis is via Stool Antigen OR PCR testing

• Diagnosis via HFE genetic testing

• If patient has hyperferritinemia (Ferritin > 1000ng/mL) ⇒ URGENT Phlebotomy BEFORE genetic testing to prevent irreversible end-organ damage

1. Nonpharm ⇒ Fluids, Fiber, Exercise, Early ambulation

2. Pharm ⇒ Laxatives (1st line are osmotic & stimulants)
1. IF FAILED → Methylnaltrexone or Lubiprostone

• Increase fluids and fibers

• Then Exclude Hypothyroidism, DM, and hypercalcemia

• As DS patients are at increased risk of endocrine abnormalities

1. Galactosemia in the newborn

2. Maternal HIV infection in developed nations where formula is available

3. Herpetic breast lesions

4. Most chemotherapy and radiation therapy

5. Active tuberculosis until no longer contagious (ie, 2 weeks of antituberculin therapy)

6. Active substance use disorder without enrollment in a methadone or buprenorphine treatment program

Pilonidal Disease

• Management:
• Drainage of abscess and debris followed by excision of sinus tract
• Open closure is preferred due to decreased recurrence rates, despite the longer healing time

Cyclic Vomiting Syndrome

• A recurrent, predictable pattern of acute and frequent vomiting that resolves spontaneously with no symptoms between episodes.

• Growth, examination, and eating patterns are also normal

• Dx of Exclusion

• The pathogenesis is unknown, but most patients have a personal/family history of migraines.