Gastroenterology Flashcards
Common causes of viral gastroenteritis
Norwalk (cruise), Coxsackivirus (summer), Echovirus (summer), Adenovirus (conjunctivitis), Rotavirus (foul-smelling greenish diarrhea)
Mostly self- limited and they get better on their own
n/v/d/abd pain, cramping, myalgia, low-grade fever
Labs: no fecal white blood cells, viral cultures
Treatment: maintain hydration
Bacterial gastroenteritis: Bacillus cereus
Bacillus cereus (fried, reheated rice) vomiting within several hours of eating
Treatment: maintain hydration
Bacterial gastroenteritis: campylobacter jejuni
poultry
2nd most common food-borne bacterial GI infection
bloody or watery diarrhea
rare association with Guillain-Barre syndrome
Treatment: usually self- limiting, so try rehydration and maybe azithromycin
Bacterial gastroenteritis: clostridium botulinum
honey, home- canned foods
n/v/d
flaccid paralysis
don’t allow children
Bacterial gastroenteritis: C. Diff
antibiotic- induced suppression of normal colonic flora “superinfection”
watery or bloody diarrhea
pseudomembranous colitis
Treatment: metronidazole, vancomycin (oral, because Po stays in the GI tract)
Bacterial gastroenteritis: E. Coli (enterotoxigenic)
travelers’ diarrhea
contaminated food and water
watery diarrhea, vomiting, fever
Treatment: often self- limited, hydration
Bacterial gastroenteritis: E. Coli (enterohemorrhagic, O157:H7)
undercooked ground beef bloody diarrhea vomiting, fever ,abdominal pain Hemolytic uremic syndrome -thrombocytopenia -hemolytic anemia -acute renal failure
Treatment: hydration and supportive care
Bacterial gastroenteritis: staph aureus
room-temperature food
it’s the premade toxins that make you sick
Vomiting within hours of eating
Diarrhea
treatment: hydration
Bacterial gastroenteritis: Salmonella
Food-borne -egg salad at picnic -poulty, milk, fresh produce -nausea, abd pain -bloody diarrhea -Treatment: hydration The disease is usually self- limited
fluoroquinolones if immunocompromised or very ill
Bacterial gastroenteritis: Shigella
food or water-borne
overcrowding
“bacterial dysentery”
fever, nausea/vomiting, severe bloody diarrhea, abdominal pain
HUS Treatment: hydration We do use antibiotics here: fluoroquinolones (ciprofloxicin) TMP-SMX
Bacterial gastroenteritis: vibrio cholerate
"rice water" diarrhea seafood abd pain, watery diarrhea, within 24 hours of eating treatment- hydration Tetracycline or doxycycline
Bacterial gastroenteritis: Vibrio parahaemolyticus
seafood (oysters)
abd pain
watery diarrhea within 24 hours of eating
treatment: hydration
Bacterial gastroenteritis: yersinia
pork, produce, puppy feces
abd pain, bloody diarrhea, RLQ pain
Treatment: hydration
Parasitic and protozoan GI infections: giardia lamblia
surface water
greasy, foul- smelling diarrhea
abd pain, malaise
cysts and trophozoites in the stool
Treatment: metronidazole
Parasitic and protozoan GI infections: entameoba histolytica
water-borne
areas of poor sanitation
mild to severe bloody diarrhea
abd pain
cysts and trophozoites in stool
liver abscess
Treatment: metronidazole, paromomycin
Parasitic and protozoan GI infections: Cryptosporidium
food or water-borne immunocompromised patients watery diarrhea, abd pain, malaise acid fast stain- parasites in stool Treatment- nitazoxanide
Parasitic and protozoan GI infections: trichonella
undercooked pork
fever, myalgias, periorbital edema
eosinophilia
CNS and cardiac symptoms also may occur
this is a bendy work
Treatment: albendazole, mebendazole
Parasitic and protozoan GI infections: Taenia solium
undercooked pork
mild diarrhea
CNS symptoms
Call it “taeniasis” if the adult is carrying the tapeworm in the gut
If the person ingests eggs, then these lead to cyst formation in the muscles (cysticercosis) and brain (neurocysticercosis)
Treatment:
praziquantel (GI)
albendazole + corticosteroids (CNS)
Food poisoning as a result of mayonnaise sitting out too long
staphylococcus aureus, salmonella
Rice- water stools
vibrio cholerae, enterotoxigenic e. coli
diarrhea transmitted from pet feces
yersinia enterocolitica
food poisoning resulting from reheated rice
bacillus cereus
MCC “Traveler’s diarrhea”
enterotoxigenic e.coli
Diarrhea after a course of antibiotics
c. difficile
diarrhea and recent ingestion of water from a stream
giardia lamblia
entamoeba histolytica
mild intestinal infection that can become neurocysticercosis
taenia solium
food poisoning from undercooked hamburger
enterohemorrhagic e. coli
diarrhea from seafood
vibrio species
bloody diarrhea from poultry
salmonella, campylobacter
diarrhea and pink eye
adenovirus
bloody diarrhea leading to liver abscess
entamoeba histolytica
diarrhea in an AIDS patient
cryptosporidium
dehydrated child with greenish diarrhea in winter months
rotavirus
Treatment for entamoeba histolytica
metronidazole
Treatment for giardia lamblia
metronidazole
Treatment for salmonella
fluoroquinolones only if pt is immunocompromised or very ill
Treatment for shigella
fluoroquinolones, TMP-SMX
Treatment for campylobacter
erythromycin, but this is usually self- limited
How long does hepatitis last before we call it chronic?
6 months
risk factors for viral hepatitis
IV drug use
alcoholism
travel to developing countries
poor sanitation
history and physical consistent with hepatitis B
asymptomatic or malaise, arthralgias, fatigue nausea/vomiting RUQ pain jaundice, scleral icterus hepatomegaly, splenomegaly lymphadenopathy
Labs: bilirubin increased AST increased ALT (roughly equally elevated) increased bilirubin increased alk phos
hepatitis A diagnostic labs
Anti-HAV IgM abs
-present during illness
Anti-HAV IgG abs
- after illness has resolved
- present with vaccination
HBsAg
active disease
HBcAb
history of active disease
IgM rises early
IgG rises late
HBeAg
active viral replication, high transmissibility
HBeAb signifies low transmissibility
Hep A
characteristics of the virus
ssRNA
spread by fecal- oral route
food/shellfish
treatment: self-limited, supportive care
Hep B
dsDNA
spread by blood, sexual contact
Treatment: hep B vaccine, IFN-gamma
Prevention: hep B vaccine
Complications: chronic hepatitis, cirrhosis, hepatocellular carcinoma
persistent carrier state
fulminant hepatic failure
Extrahepatic manifestations: polyarteritis nodosa (vasculitis of medium and small- sized arteries), glomerular disease
polyarteritis nodosa
vasculitis of medium and small- sized arteries
fever weakness rash joint pain erythematous nodules
associated with hep B
glomerular disease
membranous nephropathy
rarely, membranoproliferative GN (hep B or hep C), proteinuria
adults>children
Hep C
ssRNA
spread via blood
treat: IFN-alpha, ribavirin
there is no vaccine
complications: chronic hepatitis cirrhosis, hepatocellular carcinoma, persistent carrier state extrahepatic manifestations: membranoproliferative GN essential mixed cryoglobinemia lymphoma thyroiditis porphyria cutanea tarda lichen planus DM
Hep D
disabled, requires co-existant hep B in order to be infectious
Treatment: IFN-alpha
prevention: Hep B vaccine
Hep E
spread by facal-oral route, contaminated waters
treatment: self- limited, supportive care
complications: pregnant women
Sialolithiasis
obstructed salivary gland by a stone
swelling, pain with eating
Tx: warm compresses, massage, sour candy, surgery (remove the stones)
antibiotics if infection
Sjogren syndrome
inflammatory disorder that can affect the salivary glands.
Dry mouth, dry eyes (sicca complex)
diminished secretions
What is the most common neoplasm affecting the salivary glands
pleomorphic adenoma, benign
MC site for sialic neoplasm
parotid gland, which can also be a site of extra-pulmonary sarcoidosis
Dysphagia
difficulty or abnml swallowing
(oropharyngeal/transfer disfunction= difficulty initiating swallo)
(esophageal phase is the 2nd phase of the swallow)
Causes: achalasia, scleroderma, food impaction
peptid strictures, cancer, esophageal webs/rings, radiation- induced fibrosis, alkaline fluid-induced fibrosis
odynophagia
pain with swallowing
Plummer Vinson triad
iron def
dysphagia
esoph web
feeling of food stuck in throat with swallowing (immediate discomfort)
cough
choking
Oropharyngeal dysfuntion
delayed discomfort dysphagia
esophageal dysfunction
dysphagia characterized by difficulty with solids
obstructive pathology
dysphagia characterized by difficulty with solids and liquids
neuromuscular dysmotility
diagnostic testing for dysphagia
BARIUM SWALLOW
esophagogastroduodenoscopy (EGD)
manometry
What anatomical structures in the GI tract are evaluated by the barium swallow?
esophagus, LES, stomach
What anatomical structures in the GI tract are evaluated by the gastric emptying study?
stomach, pyloric sphincter, duodenum
What anatomical structures in the GI tract are evaluated by the small bowel follow through (SBFT)
stomach to terminal ileum
What anatomical structures in the GI tract are evaluated by the barium enema?
appendix to rectum
complications of NG tube
esophageal reflux
pressure necrosis
complications of percutaneous endoscopic gastrostomy (PEG) tube
feeding tube directly into the stomach, can occur at the bedside with proper equipment
open gastrostomy allows the same outcome but with a bigger incision, better for longterm
complications of gastrostomy tube
patient may yank the tube
complications total parenteral nutrition (TPN)
nutrition into the veins. prefer to use the gut biostasis acalculous cholecystitis venous line is a potential site for infection
laparascopy
visualization of the peritoneal cavity using a laparoscope
laparotomy or celiotomy
surgical incision into the abdominal cavity
ectomy
surgical removal or something
achalasia
neuromuscular disorder of the esophagus
impaired peristalsis
decreased lower esophageal (LES) relaxation
most commonly affects people 25-60 years old
secondary causes:
Chagas disease
neoplasms
scleroderma
H and P: gradually progressive dysphagia of solids and liquids regurgitation cough aspiration heartburn weightloss
Diagnostics:
Manometry shows increased LES pressure
Incomplete LES relaxation and decreased peristalsis
Barium swallow shows “bird’s beak” sign
Treatment goal is to lower LES pressure pneumatic dilation myotomy (open up the muscle) botulinum toxin injections nitrates dihydropyridine CCBs
Order an EGD to rule out malignancy
Diffuse esophageal spasm
neuromuscular disorder
non-peristaltic contractions of the lower esophagus
H and P:
chest pain
dysphagia for liquids and solids
diagnostic testing: “cork screw” pattern on barium swallow
non-peristaltic contractions on manometry
Treatment:
CCBs, TCAs, nitrates relieve pain but worsen reflux
Zenker diverticulum
outpouching of upper posterior esophagus caused by smooth muscle weakness
immediately above the UES
H and P: bad breath difficulty initiating swallowing regurgitation of food several days after eating occasional dysphagia feeling of aspiration
Radiology: barium swallow shows
outpouching of the esophagys
complications:aspiration
squamous cell carcinoma
perforation may occur with endoscopy
Treatment:
crichopharyngeal myotomy
diverticulectomy via external neck incision
Traction diverticulum- where in the esophagus is it found?
between UES and LES
Where is the epiphrenic diverticulum found
above the LES
GERD
Caused by a lower esophageal sphincter that transiently and intermittently relaxes
Stomach contents reflux back into the esophagus
Risk factors: obesity hiatal hernia pregnancy scleroderma
H and P: burning chest pain 30-90 minutes after eating sour taste in mouth regurgitation dysphagia nausea cough
symptoms worsened by consumption of alcohol or fatty foods, or after lying down
GERD- diagnostic testing
upper endoscopy with biopsy to evaluate for reflux or other causes
ambulatory pH monitoring to confirm acid reflux
manometry can be used to monitor for dysphagia due to neuromuscular dysfunction
CXR to assess for neoplasm
barium swallow can show peptic stricture
GERD treatment
elevation of the head of the bed
weight loss- avoid carbonated bevereges
dietary modifications
Antacids: calcium carbonate aluminum hydroxide milk of magnesia these neutralize stomach acid quickly
H2 blockers
Famotidine, ranitidine, cimetidine
These should be used on select occasions in patients who do not respond to antacids. They should be used in anticipation of reflux (delayed onset of action, longer duration of action).
Reversibly block H2 receptors to inhibit gastric acid secretion
Side effects: headache diarrhea thrombocytopenia gynecomastia and impotence (cimetidine)
Proton-pump inhibitors (PPIs)
omeprazole, lansoprazole
given to patients who don’t response well to H2 blockers
well-tolerated, but block CYP450 enzymes
irreversibly inhibit the parietal cell proton pump (H/K ATPase) to block gastric acid secretion
Promotility agents in GERD
metoclopramide is an example, no longer recommended for GERD
GERD treatments that are safe in pregnancy
antacids, PPIs, H2 blockers
How do we treat refractory GERD?
Nissen fundoplification
GERD complications
Esophageal ulceration Esophageal stricture Barrett esophagus Adenocarcinoma Reflux- induced asthma Laryngeal disorders
Esophageal cancer: 2 major types
Squamous cell carcinoma (more common worldwide)
Adenocarcinoma (more common in the US, less common worldwide)
Barrett’s esophagus
intestinal metaplasia of the distal esophagus secondary to chronic GERD
increases risk of adenocarcinoma
Risk factors for esophageal cancer
alcohol tobacco chronic GERD obesity (adenocarcinoma) nitrates preserved meats
H and P for esophageal cancer
progressive dysphagia weight loss odynophagia reflux GI bleeding vomiting weakness cough, hoarseness
Esophageal cancer diagnostic studies
barium swallow
EGD (biopsy is what makes the diagnosis)
MRI, CT, PET scan
Esophageal cancer treatment
surgical resection
radiation and chemotherapy (non-operative and advanced cases)
neoadjuvant therapy to surgery
poor prognosis because it has often extended by the time it is diagnosed
Mallory- Weiss syndrome
longitudinal mucosal laceration in the distal esophagus and proximal stomach, minor injury
Boerhaave syndrome
perforation or rupture in the distal esophagus, tears all layers of the esophagus; life-threatening
chest pains, uncoordinated contractions, corkscrew pattern on barium swallow
diffuse esophageal spasm
inability to relax the LES; bird’s beak on barium swallow
achalasia
bad breath, regurgitation of food eaten days ago
Zenker diverticulum
Common symptoms of GERD
persistent cough
heartburn
Which is associated with ischemia- sliding hiatal hernia or paraesophageal hiatal hernia?
paraesophageal hiatal hernia
What is gastritis
inflammation of the gastric mucosa, acute (erosive) or chronic (non-erosive), related to NSAIDs, alcohol, corrosive materials, h. pylori, stress
Where is B12 absorbed?
terminal ileum
How do we diagnose H. Pylori?
urea breath test
antral biopsy
serum h.pylori antibodies
Gastritis treatment
stop alcohol or offending medications
H2 blocker or PPI
Vit B12 (type A)
Treat h. pylori (type B): PPI, clarythromycin, amoxicillin or metronidazole for 7-14 days
Peptic ulcer disease: Gastric ulcer
Patients tend to be older,
H. pylori +
chronic NSAID users
25% if ulcers
pain occurs soon after eating due to acid produced to process food; eating worsens the pain and leads to n/v
normal or low gastric acid level
+/- high gastrin level
eating may cause n/v as well
Peptic ulcer disease:duodenal ulcers
Patients:
younger
+H.Pylori
75% of ulcers
pain occurs 2-4 hours after eating
eating improves pain initially, but the pain then worsens
normal or low gastrin level
there may be nausea or vomiting
patient tends to be thinner than patients with other types of ulcers
Ulcer associated with severe burn
Curling’s ulcer
Ulcer associated with intracranial injuries
Cushing’s ulcers
Zollinger- Ellison syndrome
increased gastrin
What findings on barium swallow are suggestive of cancer?
abnormal appearing mucosal folds in the region near the ulcer
Mass near ulcer
Irregular filling defects in ulcer base
Biopsy 4 quadrants around the ulcer
Treat a peptic ulcer
- rule out active bleeding: CBC, EGD, Stool guiac
- decrease gastric acid levels
PPI
H2 antagonist - protect mucosa
Sucralfate
Bismuth subsalicylate
Misoprostol - Treat H. Pylori: PPI, Amoxicilin or metronidazole, clarithromycin
- Surgery
-perforation repair
-parietal cell vagotomy
-antrectomy - COX2 inhibitors (still have some gastric side effects)
complications of peptic ulcer
hemorrhage
perforation
lymphoproliferative disease
Zollinger-Ellison syndrome
gastrin- producing tumor in the duodenum or pancreas
refractory PUD abdominal pain n/v indigestion diarrhea steatorrhea other endocrine abnormalities
- Labs:
fasting gastrin level (>1000)
secretin stimulation test (secretin induces a steep rise in gastrin levels in patients who do have ZE) - Radiology
CT or MRI to look for the tumor
Endoscopic ultrasound to look for small pancreatic tumors
Somatostatin receptor scintigraphy can localize tumors
Angiography can be used to look for the tumor if it is hypervascular - Treatment:
Surgical resection
PPI (stop before gastrin testing to get an accurate reading)
H2 antagonist
Octreotide
If you must pick between PPI and octreotide, then pick PPI
Gastric cancer subtypes
- ulcerating (this is why we biopsy the area around all gastric ulcers)
- polypoid
- superficial spreading
- linitis plastica, involving all layers of the stomach
Gastric cancer risk factors
H. Pylori Family history Japanese person living in Japan Tobacco use Alcohol use Vit C deficiency Preserved foods (nitrosamines) Males>females
Gastric cancer H and P
weight loss, anorexia, early satiety
vomiting, dysphagia, epigastric pain
left supraclavicular node: Virchow’s node
periumbilcal node (Sister Mary Joseph node)
Labs:
increased CEA
Radiology: barium swallow
EGD to visualize ulcers
Treatment:
subtotal gastrectomy in the distal third
Total gastrectomy for lesions in the middle or upper part of the stomach
Adjuvant chemotherapy and radiation
Prognosis >70% if early detection
Surgical therapy for obesity
malabsorption and restriction
sustained weightloss- 30-50%
reduction or cure of DM, HTN, OSA, mortality overall
depression and suicide increase in the first year after surgery, so pre-opping is extensive
complications of surgical therapy for obesity
nutritional deficiencies iron b12 folate thiamine vit D GERD Dumping syndrome: bloating, swelling, steatorrhea, diarrhea
Most effective treatment of a duodenal ulcer not due to cancer?
H. Pylori triple therapy
PPI
Amoxicillin
Clarithromycin (metronidazole if pt allergic to clarithromycin)
Subtotal gastrectomy
subtotal if cancer in the distal 1/3 of the stomach: subtotal gastrectomy
Total gastrectomy if cancer in the middle or upper stomach
add on adjuvant chemo and radiation as needed
Branching rods, oral infection, what bacteria is this?
actinomyces israelii
How does malabsorption present?
weight loss, bloating, diarrhea, steatorrhea, glossitis, dermatitis (zinc deficiency), edema (protein malabsorption)
Where is ethanol absorbed?
stomach
Celiac sprue
reduced absorptive capacity from duodenum and jejunum
Labs:anti-tissue transglutaminase antibody
antiendomysial antibody
antigliadin ab no longer considered reliable
definitive diagnosis via biopsy of duodenum +/- jejunum looking for blunting of the villi
H and P:
FTT, bloating, abnormal stools
diarrhea, steatorrhea, weight loss
5% of Down syndrome patients have this
Associated with dermatitis herpetiformis
Treatment:
removal of gluten (wheat, barley, rye) from the diet
Refractory disease may require corticosteroids
Tropical sprue
similar presentation to celiac sprue, but the autoantibody tests would be negative and removing gluten from the diet will not have any benefits
occurs in patients who have spent time in the tropics, may present years after leaving the tropics
Megaloblastic anemia
Treatment: folic acid replacement
tetracycline, sulfa drugs
Lactose intolerance
lactase deficiency
lactose goes straight to the colon when it is not metabolized, drawing water into the colon, causing osmotic diarrhea
flatulence, bloating, abdominal pain, diarrhea
Treatment: remove lactose from the diet and supplement calcium
Whipple disease
bacterial infection with tropheryma whipplei
RF:white, european ancestry
H and P: abdominal pain diarrhea weight loss arthralgia wasting endocarditis pleural effusions abdominal distention from ascites or adenopathy vision abnormalities dementia
Labs:
jejunal biopsy- foamy macrophages on PAS stain, villous atrophy
PCR
Treatment:
1. IV ceftriaxone
2. TMP-SMX
continue treatment for 12 months to prevent relapse
Sudan stain
if you suspect fat malabsorption
bacterial overgrowth
pancreatic insufficiency
D-xylose
if you suspect carbohydrate malabsorption
PO radiolabelled D-xylose, then
blood and urine are tested. Low levels suggest impaired carb absorption (poor absorption)
Pancreatic insufficiency would be expected to show normal levels of D-xylose
Meanwhile, normal sudan stain but high D-xylose might indicate lactase deficiency
Schilling test
B12 malabsorption
Stage 1: give radiolabeled B12 by itself and see if it is absorbed by detecting it in the urine or the serum
If it is present in high amounts, malabsorption may be due to absent IF or diminished terminal ileum absorption
Stage 2: B12 is administered with intrinsic factor
If B12 is absorbed in the second stage, then IF is probably the problem
If B12 is not absorbed in the second stage, then the problem is likely the terminal ileum, or maybe the problem is bacterial overgrowth
antibiotics or pancreatic enzymes are given in some versions of the Schilling test to further characterize the cause of malabsorption
Acute diarrhea
chronic diarrhea
- inflammatory
- autoimmune disorders
- Crohn disease
- Ulcerative colitis
- Chronic infection - fatty
- pancreatic insufficiency
- Whipple disease - watery
-osmotic
celiac sprue
tropical sprue
lactose intolerance
excess sorbitol
lactulose
milk of magnesia
-secretory irritable bowel syndrome laxative abuse enterotoxic bacteria hormone-mediated (VIPomas, gastrinomas, medullary thyroid cancer, carcinoid tumors)
treatment:ileum resection
history and physical:
FOBT, CBC, metabolic panel, lactose- restricted diet
sudan stain, D-xylose test, stool electrolytes
osmotic gap125= osmotic
colonoscopy with possible biopsy (malignancy, inflammatory bowel disease?)
The formula for stool osmotic gap
290-2(Na+K)= stool osmotic gap
Pediatric diarrhea
infection
- rotavirus (winter)
- adenovirus (plus conjunctivitis)
antibiotic use
-macrolides
immunosuppression
What is the cut-off in osmotic gap for secretory diarrhea
What is the cut-off in osmotic gap for osmotic diarrhea
> 125
Which tumors can cause diarrhea due to hormone excess
carcinoid tumor
VIPoma
gastrinoma
medullary thyroid cancer
most common food-borne bacterial GI infections in the US
campylobacter
salmonella
IBS
idiopathic, women more than men, related to stress
abdominal pain diarrhea constipation bloating nausea mild abdominal tenderness urinary frequency urinary urgency symptoms of fibromyalgia
What are the Rome diagnostic criteria for IBS?
recurrent abdominal pain/discomfort at least 3 days per month in the last 3 months associated with at least 2 of the following:
1. relief with defecation
2. onset associated with a change in frequency of stool
3. onset associated with a change in form of stool
important to rule out other causes
What are the subtypes of IBS?
IBS with diarrhea
IBS with constipation
Mixed IBS
IBS unsubtyped
What symptoms are NOT c/w IBS alone?
anorexia weight loss malnutrition progressively worsening pain pain that prevents sleep rectal bleeding
What lab findings are NOT consistent with IBS alone?
electrolyte disturbances
anemia
increased inflammatory markers
What imaging is helpful in ruling out other diagnoses when you are considering IBS?
abdominal x-ray
abdominal CT
barium studies
Treatment for IBS
physician assurance no higher rate of malignancy goal is to improve symptoms eat a high-fiber diet avoid gas-producing foods avoid lactose and gluten
possible psychotherapy
Constipation predominant:
fiber and hydration, polyethylene glycol
Diarrhea predominant:
anti-diarrheals
TCAs
SSRIs
Treat abd pain and bloating with
antispasmodics
antidepressants
funtional disorder
IBD
inflammatory disease
Crohn
Ulcerative colitis
Crohn symptoms
fatigue
abdominal pain
weight loss
watery diarrhea
PE: fever RLQ abdominal mass Abdominal tenderness Perianal fissures and fistulas Oral ulcers
Features: transmural inflammation skip lesions most commonly affects the distal ileum "gum to bum"
Imaging:
Transmural inflammation and strictures
String sign (not much lumen in some areas)
Skipped areas of bowel
- Barium study with small bowel follow-through
- Colonoscopy: granulomas, colonic ulcers
Complications: malabsorption fissures fistulas strictures obstruction abscess formation
Treatment for Crohn disease:
- steroids +/- abx for acute exacerbations
- azathioprine or mercaptopurine> methotrexate
- anti-TNF-alpha agents (infliximab, adalimumab)
Medical management preferred over surgical resection, as surgery is not curative
distal ileum classically involved
mouth to anus with multiple skip areas in between
entire thickness of bowel wall is affected
distinguishing features of Crohn disease
GIFTS
distal ileum classically involved
mouth to anus with multiple skip areas in between
entire thickness of bowel wall is affected
Granulomas Ileum Fistula and fissures Transmural Skip lesions
Ulcerative colitis
fatigue abdominal pain diarrhea weight loss fecal urgency tenesmus incontinence bloody diarrhea
PE: fever abdominal tenderness gross blood on rectal exam orthostatic hypotension tachycardia
continuous disease of the colon
perianal inflammation
Colonoscopy would show continuous involvement, pseudopolyps, friable mucosa
barium enema would show lead pipe colon, colonic shortening
Complications: hemorrhage, toxic megacolon, perforation
Longterm complications: strictures leading to obstruction
and dysplasia leading to colon cancer
Treatment: topical treatment with suppositories and enema preferred to oral treatment
start with aminosalicylate (mesalamine), then move on to oral glucocorticoids, immunosuppressive agents, supplemental iron
Total colectomy is curative as long as there is no dysplasia
Extraintestinal manifestations of IBD
arthritis ankylosing spondylitis erythema nodosum pyoderma gangernosum uveitis primary sclerosing cholangitis
Serologic markers for IBD
ASCA:anti-saccharomyces cerevisiae abs often positive in Crohn
pANCA- perinuclear anti-neutrophil cytoplasmic antibodies, often positive with UC
Bowel obstruction- common causes
Adhesions (from previous surgeries ~75% of cases)
Bulge- incarcerated hernia (second most common cause)
Cancer (most commonly metastatic colorectal cancer)
Other less common causes:
volvulus, intussusception, Crohn disease, gallstone ileus, bezoar (organic sediment gets impacted in the small bowel), bowel wall hematoma from trauma, inflammatory stricture, congenital malformation, radiation enteritis
What are the classic signs and symptoms of SBO?
abdominal pain and tenderness
n/v
+/- recent flatus/ small BM
hyperactive high- pitched bowel sounds
diagnosis: dilated loops of small bowel proximal to the obstruction seen on plain film abdominal series or CT scan of the abdomen
What is the treatment for SBO?
NPO, IV fluids, monitor electrolytes, Foley catheter to monitor urine output
NG tube to low intermittent wall suction (LIWS) especially if the patient has severe intermittent nausea and vomiting
Partial obstruction might just need bowel rest
Complete might need surgery
Hospital observation with frequent reassessments +/- repeat CT scan
Avoid pain medication if possible, which may interfere with identification of disease worsening, but treat pain
Surgery (laparotomy and lysis of adhesions) if:
no improvement in 12-24 hours
complete SBO
suspected, impending, or ongoing strangulation
What is the most common benign small bowel tumor?
leiomyoma
WHat is the most common malignant small bowel tumor?
carcinoid
Large bowel obstruction common causes:
neoplasm
adhesions
volvulus
diverticulitis
radiology:
bowel distention proximal to the obstruction
treatment:
NPO, maintain hydration, colonoscopy, surgery if necessary
ischemic colitis
ischemia of the colon secondary to vascular compromise
embolus bowel obstruction hypotension medication surgery
RF: diabetes, atherosclerosis, PVD, lupus
presents with acute abdominal pain bloody diarrhea vomiting mild abdominal tenderness pain out of proportion to exam
Barium enema- thumbprint sign 2/2 diffuse submucosal changes from localized bleeding
Sigmoidoscopy- bloody and edematous mucosa
CT- air within the bowel wall- pneumotosis coli, maybe bowel- wall thickening
Treatment: IV fluids, bowel rest, antibiotics, surgical resection of necrotic bowel
Complications: high mortality rate if irreversible damage
Appendicitis
inflammation with possible perforation of appendix
common clinically
lymphoid hyperplasia, more often seen in children
fibroid bands, fecalith
H and P:
dull periumbilical pain that migrates to the RLQ
n/v/anorexia
Tenderness at McBurney’s Point (2/3 of the way between umbilicus and ASIS)
Rebound tenderness due to peritoneal irritation
Psoas sign- pain on passive extension
Rovsing sign- RLQ pain with LLQ palpation
Obturator sign- RLQ pain on passive internal rotation
Severe pain, distention, rebound tenderness, rigidity, guarding, high fever, hypotension, shock
Labs: CBC with left-shift
UA- increased WBC, cystitis, UTI
What radiological studies can be used to diagnose appendicitis?
CT scan with oral contrast
CT scan with rectal contrast +/- IV contrast
CT scan without contrast (fast, higher rate of false neg, but better than no CT scan)
Plain radiograph for fecolith
Ultrasound for pelvic pathology in women
Don’t wait so long for imaging that the appendix perforates
Treatment for appendicitis
Pain control: Morphine or meperidine PCA
Antibiotic administration for mild to moderate inpatient:
- Ampicillin/sulbactam (Unasyn)
- Piperacillin/tazobactam (Zosyn)
- Ticarcillin/clavulanate (Timentin)
- Levofloxacin + metronidazole
- Ciprofloxacin + metronidazole
Antibiotic administration for severe ICU patient:
- Ampicillin + levofloxacin + metronidazole
- Imipenem/cilastatin (Primaxin)
- Meropenem
If presentation within 24-72 hours of symptom onset, then proceed with surgical removal of appendix by laparoscopy or open appendectomy
If symptoms present for more than 5 days and pain is specifically in the RLQ, then antibiotics, IVF, bowel rest–> interval appendectomy about 8 weeks later
If abscess on CT scan, then percutaneous drainage (interventional radiology)
Ileus
paralytic obstruction of small bowel secondary to decreased peristalsis
infection, ischemia, recent surgery, DM
typically less than 5 days. small bowel recovers first (
Gallstone ileus
gallstone impacted in ileum after passing through biliary-enteric fistula
subacute, episodic obstruction in elderly woman with vague, recurrent abdominal pain and vomiting that recurs as the stone repeatedly lodges and dislodges
Average time from symptom onset to hospitalization- 5 days
Volvulus
abnormal rotation of bowel
obstruction, ischemia
double bubble sign on xray
due to air trapped both distal and proximal to the volvulus
barium enema may show bird’s beak at distal volvulus as well
Treatment:
sigmoidoscopy, colonoscopy for decompression, contra-indicated if gangrene due to risk of perforation
If the bowel is gangrenous or sigmoid/colonoscopy is unsuccessful, then laparoscopic resection of the affected colon and colostomy
Once corrected, the recurrence in 40-60% of patients can be prevented with one of the following:
- mesosigmoidopexy
- resection with primary anastomosis
- Hartmann’s procedure (proximal colostomy + stapling but not removal of the distal segment)
Diverticulosis
outpouchings, may erode and cause bleeding, may become inflammed and infected
RF: low- fiber, high fat diet
being older
H and P: occasional cramping bloating flatulence irregular defecation painless rectal bleeding
MCC lower GI bleed in patients > 40 yo
Mild LLQ pain relieved with defecation
Radiology: irregular outpouchings
Colonoscopy can also visualize diverticulosis
Treatment: do not limit seeds, nuts, popcorn
Complications: diverticulitis, GI bleeds
Diverticulis
infection of diverticulum that can lead to necrosis or perforation
H and P:
LLQ pain
older patient
fever
Labs: increased WBC count with or without left shift
CT scan: increased soft- tissue density in the affected area due to inflammation. You will see bowel wall thickening, and possible abscess formation
Treatment: outpatient
bowel rest
fluoroquinolone + metronidazole
TMP-SMX + metronidazole
Amoxicillin- clavulanic acid
When is inpatient admission for diverticulitis treatment indicated?
elderly immunocompromised significant comorbidities high fever with significant leukocytosis unable to tolerate oral intake
What are the steps in inpatient management of diverticulitis
- IV fluids
- broad- spectrum empiric antibiotics (similar to appendicitis)
- If there are signs of peritonitis (guarding, tenderness), then sent the patient for emergency exploration through midline incision
What are the complications of diverticulitis?
Colonic abscesses
fistulas
sepsis
Hemorrhoids
dilated veins
internal- superior rectal veins, above the pectinate line, painless
external- inferior rectal veins, painful if thrombosed
sigmoidoscopy
colonoscopy
anoscopy
Anal exam for fistulas, lesions
Treatment: warm baths, high fiber diet, avoid prolonged straining, sclerotherapy, ligation, surgical excision
Anal fissure
spasm of rectal sphincter may result
treatment:
1. stool softeners + hydration
2. topical nitroglycerin
3. diltiazem, nifedipine, bethanechol
4. botulinum toxin injection
5. sphincterotomy, which carries 10-30% risk of incontinence
Anorectal abscess
infection of anal crypts, hair follicles
H and P:
throbbing rectal pain, fever, tenderness on DRE
Treatment:
Antibiotics
I and D
Rectal fistula (aka fistula in ano)
A tract between rectum and adjacent structures from unknown cause or 2/2 ischemic bowel
H an P:
mild pain during defecation
visible site draining pus
Treatment:
fistulotomy
Pilonidal disease
1 or more curaneous tracts in the midline gluteal cleft
H and P:
asymptomatic
painful cysts
abscesses
Treatment:
I and D
Sterile packing with changing
Surgical closure of sinus tract
Carcinoid tumors
common sources, sites, features
serotonin-secreting tumor, mc arising from ileum, bronchopulmonary tree, appendix, rectum
MC GI site is the small i (ileum)
H and P:
asymptomatic, because the serotonin gets processed in the liver
abdominal pain
Be FDR Bronchospasm (10-20%) Flushing (85%) Diarrhea (80%) Right- sided valvular disease/murmurs
Treatment:
Somatostatin analog octreotide helps shut down serotonin
Other drugs that can be used for symptom relief:
cyproheptadine for diarrhea and/or anorexia
Albuterol and/or theophylline for asthma symptoms
Codeine and/or cholestyramine for diarrhea
If symptoms are refractory to octreotide, give IFN-alpha combined with ocretotide
Surgical resection in certain circumstances of isolated tumors
Valvular surgery for symptomatic carcinoid heart disease
Labs:
you might see an increase in urine 5-HIAA
increased serum serotonin
The biggest risk factor for colon cancer
presence of colon polyps, especially the adenomatous ones
Risk factors for developing colon cancer
adenomatous colon polyps hereditary polyposis syndromes family history previous colon cancer ulcerative colitis and Crohn's disease low fiber/ high-fat diet alcohol smoking diabetes
Familial adenomatous polyposis
hundreds of polyps in the colon due to mutated APC gene
Treatment: prophylactic subtotal colectomy (this requires a colostomy bag, so wait until after high school)
If a patient has an APC gene mutation, you can start doing colonoscopies at a young age
Gardner syndrome
APC mutation
colon polyps
osteomas
soft tissue tumors
Turcot syndrome
APC gene mutation
colonic adenomas
CNS tumors
Juveile polyposis
polyps in colon, small bowel, stomach
Hamartoma, which is an excess amount of normal tissue (not adenomas, so the polyps don’t become tumors, but they can be a source of GI bleeding)
Peutz-Jeghers syndrome
Hamartomas in the GI tract
pigmented lesions on lips and oral mucosa
Hereditary Non-polyposis Colorectal Cancer (HNPCC)
Colon cancer arising from normal- appearing mucosa
without forming polyps
Neoplasms form in the proximal colon (distal is more common)
How does colon cancer present?
distal colon leads to change in bowel habits
left colon changes leads to thinned stool caliber
There may be hematochezia or melena
Iron deficiency anemia (right- sided cancer)
Weakness, fatigue
Weightloss
Labs:
positive stool guaiac test
anemia
increased CEA *not specific but can be used to monitor response to therapy/ recurrence
Radiology: apple-core lesion seen on barium enema colonoscopy CT PET
Treatment:
take out the cancer and at least 12 nodes
How do we stage colon cancer? what characterizes stages 3 and 4?
node involvement: stage III, involves chemotherapy
met’s beyond nodes: stage IV
Colon cancer post- treatment surveillance
CEA every 3 months for 3 years
CT chest/abdomen/pelvis every year
Colonoscpoy at 1, 3, 5, years
Colon cancer screening for avg risk patient
For the average patient, after age 50
- fecal occult blood test annually with guiac (samples from 3 consecutive stools is ideal)
- Colonoscopy every 10 years
- or, flex sig, which goes up to the splenic flexure, with double- contrast barium enema to see proximal to the splenic flexure BOTH every 5 yrs
- CT colonography is not currently used for screening because it does not have adequate sensitivity and specifiticy, followed by colonoscopy if anything is seen
- screening should stop when a patient’s life expectancy is less than 5 years (or at age 75, whichever comes first)
Screen more frequently if you find polyps
Disadvantages to flex sig
contrast enema requires that the patient take in contrast from above and below, and also tolerate air in the colon
Flex sig done without conscious sedation
Better visualization with colonoscopy than with flex sig
Hematochezia- bright red blood in the stool
lower GI bleed
rapid or heavy bleed
could be an upper GI bleed if it is a severe upper GI bleed
Melena- dark blood
upper GI or proximal small bowel blood
Coffee ground emesis
blood that has been sitting in the stomach for some time
Causes of upper GI bleed
peptic ulcer disease Mallory- Weiss tears esophagitis esophageal varices gastritis
Causes of lower GI bleed
Diverticular disease (most common cause of lower GI bleed in anyone over 40yo)
Neoplasms
Ulcerative colitis
Mesenteric ischemia
AV malformations
Hemorrhoids
Meckel diverticulum (bleeding 2/2 acid secretion into the ileum)
imaging of choice for lower GI bleed
colonoscopy
imaging of choice for upper GI bleed
EGD
Where does the EGD end
duodenum
Where does a colonoscopy stop?
terminal ileum
What can you do to visualize the part of intestine that lies between duodenum and terminal ileum?
capsule endoscopy, which sends pictures to a received
Tagged RBC scan
tagged technetium helps localize bowel bleed to quadrant, helpful for intermittent bleeds
Relevant radiology for GI bleeds
EGD- upper GI bleeds
Colonoscopy- lower GI bleeds
Capsule endoscopy
Tagged RBC scan
Angiography- would miss an intermittent bleed
Meckel scan- just for Meckel diverticulum
Management steps for GI bleed
- H and P
- Continuous monitoring of vital signs
- obtain IV access with 2 large bore IVs (18 gauge in both arms) or central line
4, Volume and rescuscitation with NS or LR as needed - type and cross 2 U PRBC
- Labs:CBC, coags (guaiac stool if necessary, to confirm blood)
Treat and determine the cause
- NG tube to rule out massive upper GI bleed
- If colonoscopy is nondiagnostic and not feasible (too much active bleeding may obscure visualization), and bleeding persists, then radionucleotide scan and/or angiogram
How does history of colon cancer in a first degree relative affect screening?
Start at 40 years of age, or 10 years before the age the relative was diagnosed- whichever comes first
The 3 most common causes of acute pancreatitis
gallstones
chronic alcohol use
idiopathic
acute PANCREATITIS causes
hyperParathyroidism Alcohol Neoplasm (backed up enzymes) Cholelithiasis Rx (drugs- HIV drugs and sulfa drugs) ERCP (backflow) Abdominal surgery hyerTriglyceridemia Infection (mumps) Trauma Idiopathic Scorpion sting
pathophysiology:leakage of pancreatic enzymes into surrounding tissue
increased serum lipase and amylase on labs, though these are not prognostic indicators. Lipase is more specific than amylase
Ranson criteria
total 11 values 5, assessed at admission at GA LAW Glucose >200mg/dK AST>250 IU/L LDH> 350 IU/L Age>55 yo WBC> 16,000/mL
6 assessed after 48 hours:
CALvin and HOBBeS
Calcium10%
pO2 4mg/dL
BUN increase >5mg/dL
Sequestration of fluid > 6L
0-2: 0-3% mortality
3-5: 11-15% mortality
6-11: > 40% mortality
H and P findings c/w acute pancreatitis
acute epigastric pain n/v Cullen sign: periumbilical ecchymosis Grey Turner sign: ecchymosis of flank Tachycardia Hypotension Shock- the pt may need fluids
Check labs for Ranson criteria and for elevated amylase
Upright AXR may show Sentinel loop (dilated loop of bowel)
- elevated hemidiaphragm
- the right colon may be distended until you get to the pancreas “colon cut-off” sign
- pleural effusion
CT scan is most sensitive:
-enlarged, inflamed pancreas
-pseudocyst
US-gallstone
Treat pancreatitis
aggressive hydration
NPO
NGT to suction
correct electrolytes
opioids for pain control
morphine causes sphincter of Odi to spasm (meperidine is therefore preferred)
NJ tube for feeding (nasojejunum, so as not to stim the stomach)
TPN
prophylactic abx
debridement
cholecystectomy if they have gallstones causes pancreatitis
ERCP (remove the stones, or this can cause pain, so weight risk and benefits)
Complications of acute pancreatitis
pancreatic abscess pseudocyst pancreatic necrosis fistulas renal failure chronic pancreatitis hemorrhage shock DIC sepsis respiratory failure
treat patients before they get quick
Chronic pancreatitis causes
almost always due to alcoholism
recurrent
Chronic pancreatitis signs and symptoms
recurrent epigastric pain steatorrhea weight loss nausea constipation
Labs: mildly increased amylase and lipase
low fecal elastase (most specific and sensitive test for chronic pancreatitis)
Xrays and CTs: pancreatic calcifications enlarged pancreas pseudocyst MR-CP pancreatic duct
Chronic pancreatitis treatment
stop alcohol use stop smoking opioids pancreatic enzymes vitamin supplements small, low-fat meals surgical repair of ductal damage
Complications of chronic pancreatitis
ductal obstruction pseudocyst malnutrition glucose intolerance pancreatic cancer
Pancreatic pseudocyst- what is it?
enzyme-rich fluids contained in a sac of inflamed membranous tissue
lined with granulation tissue and fibrous tissue, filled with pancreatic juice
usually asymptomatic
incidental finding
epigastric pain
fever
Labs: elevated WBC and amylase
On aspiration, the cyst contents also hold a lot of amylase
Treatment of pancreatic pseudocyst
often resolves on its own
drain for diagnosis
debridement or percutaneous drainage if the cyst persists over 4 weeks
Pancreatic pseudocyst complications
rupture
abscess
hemorrhage
pseudoaneurysm (digests vessels so that they bleed into the cyst)
Exocrine pancreatic cancer
The most common kind
adenocarcinoma
usually in the head of the pancreas, where the bulk of pancreatic tissues lies
Risk factors: chronic pancreaitis diabetes family history tobacco use high- fat diet male>female obesity sedentary lifestyle abdominal pain with radiation to the back anorexia nausea/vomiting weight loss jaundice
Signs and symtoms: palpable, nontender gallbladder -courvoisier sign -splenomegaly -palpable deep abdominal mass
Pancreatic adenocarcinoma tumor markers
CEA
CA 19-9
increased bilirubin and increased phosphatase with biliary obstruction
CT abdomen: mass at the head of the pancreas will be visible
ERCP to locate
Endoscopic ultrasound
Treatment:
- resection (whipple procedure)
- adjuvant chemotherapy
- pancreatic enzymes
- stenting (this would be a palliative measure)
Pancreatic adenocarcinoma- complications:
death, with 1 yr survival less than 2%
Trousseau syndrome: migratory thrombophlebitis classically associated with pancreatic adenocarcinoma
Trousseau syndrome
migratory thrombophlebitis classically associated with pancreatic adenocarcinoma
Gastrinoma- stomach tumor
Gastrin- secreting glandular tumors that cause Zollinger- Ellison syndrome
Insulinoma
insulin-secreting beta-cell tumor that causes hypoglycemia
Labs: increased fasting insulin
elevated C-peptide (produced when the insulin is made)
CT or US can help, but these tumors are often difficult to locate
Treatment: surgical resection
Diazoxide, which reduces insulin release
Octreotide
Glucagonoma
glucagon- secreting alpha-cell tumor that causes hyperglycemia
Elevated glucagon, presents with refractory diabetes
may present with necrolytic migratory erythemarash, erythematous plaques on the face, perineum, extremities
Treatment: surgical resection if you can localize the tumor
- surgical resection
- octreotide
- IFNalpha
- embolization
Frequently malignant
Necrolytic migratory erythema
uncommon presentation of glucagonoma
rash, erythematous plaques on the face, perineum, extremities
VIPoma
tumor that produces vaso-active intestinal peptide, which leads to watery diarrhea
usually non-beta islet cells
labs: increased serum VIP
high stool osmolality
Treatment: hydration and electrolyte replacement surgical resection steroids chemotherapy octreotide embolization
Risk factors for cholelithiasis
fat fertile female forty family history Also, OCP use TPN rapid weightloss
most gallstones are made of cholesterol, calcium, and bilirubin
H and P: pain worse after fatty meals, which cause the gallbladder to contract n/v indigestion flatulence RUQ tenderness to palpation
Dx: see gallstones on ultrasound
cholesterol stones don’t show up on xray or CT; bile stones might
Tx: low-fat diet bile salts lithotripsy cholecystectomy
complications:
more stones
cholecytitis
pancreatitis
acute cholycystitis
inflammation of the gallbladder
Usually, a gallstone obstructs the cystic duct, leading to infection and inflammation behind the obstruction
Acalculous choecystitis
patients on TPN
critically ill patients
inflammation, without obstruction
Murphy sign
inspiration stopped by pain when you put your hand over the RUQ
positive test consistent with cholecystitis
H and P c/w cholecystitis
RUQ radiating to back n/v fever palpable gallbladder \+Murphy sign
Labs:
increased WBC
increased bilirubin and alk phos
Radiology
Ultrasound: gallstones, thickened gallbladder wall, sludge in the gallbladder, sonographic Murphy sign (Murphy sign elicited with an ultrasound probe), HIDA scan (detects obstruction of the cystic duct)
What is a HIDA scan (cholescintigraphy)?
technectium- labeled hepatic iminodiacetic acid given IV, taken up by hepatocytes, excreted into bile for visualization of gallbladder
Inability to visualize the gallbladder with this test indicates cystic duct obstruction, usually from acute cholecystitis or an obstructing stone
How do we treat cholecystitis?
hydration
antibiotics
wait 24-48 hours, then proceed to cholecystectomy
Use ERCP to inject solvent if you can’t stabilize the patient for surgery
Cholangitis
infection of the bile duct, usually due to bile duct obstruction
RUQ pain, chills, jaundice, fever (Charcot triad)
Labs: biliary obstruction increase AST, ALD, amyplase increased WBC count increased bilirubin increased alk phos
Radiology: ultrasound ok, HIDA scan is preferred test (HIDA accumulates in the liver, and then depending on where the obstruction is, it might fill the gallbladder, or fill the gallbladder and not be able to empty)
Treatment: hydration IV antibiotics endoscopic biliary drainage delayed cholecystectomy
Charcot triad- cholangitis
RUQ pain
jaundice
fever
cholangitis until proven otherwise
Reynolds pentad, cholangitis
Charcot triad (RUQ pain, fever, jaundice) + AMS and hypotension or shock
Gallbladder cancer
Adenocarcinoma of the gallbladder
a/w cholilithiasis, biliary tract disease, chronic infection
poor prognosis Symptoms: pain jaundice palpable gallbladder
Labs:
elevated bilirubin
elevated alk phos
Porcelain (calcified) gallbladder, while more suggestive of chronic cholecystitis, is cancer 10-30% of the time.
Treatment: cholecystecomy lynph node dissection removal of adjacent hepatic tissue radiation and chemo
Why do we always do cholecystecomy on porcelain gallbladder?
Porcelain (calcified) gallbladder, while more suggestive of chronic cholecystitis, is cancer 10-30% of the time.
Primary biliary cirrhosis
- autoimmune disease that destroys the intrahepatic bile ducts (cholesterol, bile acids)
- more common in women
- associated with autoimmune diseases
What physical exam and lab findings would lead you to suspect primary biliary cirrhosis as a diagnosis?
Usually women (95% of patients) between ages 30-65
Fatigue and pruritis are the most common presenting symptoms
- excessive daytime somnolence
- pruritis often starts during pregnancy and then not relieved postpartum
- patients are often initially referred to a dermatologist for pruritis and excoriations are common
Skin changes:
- hyperpigmentation due to melanin deposition, xerosis, dermatographism (wheal where you write on them)
- xanthelasma (cholesterol- filled plaques on the medial aspects of the eyelids bilaterally and/or xanthomata
Hepatomegaly that progressively worsens +/- splenomegaly
Malabsorption and steatorrhea from less bile acid secretion
In late stages, cirrhosis, jaundice, ascites, edema, portal hypertension
Labs:
Elevated alk phos, elevated GGT, elevated direct and indirect bilirubin (in late disease), elevated cholesterol
Elevated serum antimitochondrial antibodies (AMA), in >95% of patients: qhallmark finding of PBC
Elevated antinuclear antibodies (ANA) in 70%
Associated conditions: osteoporosis, osteomalacia, other autoimmune disorders (thyroiditis/hypothyroid, sicca syndrome, scleroderma, Sjogren syndrome, arthritis, Raynaud)
Treatment: Ursodeoxycholic acid (UDCA), delays disease progression and enhances survival. The only approved therapy for PBC
Definitive treatment is liver transplantation
What laboratory finding is a hallmark of primary biliary cirrhosis?
Elevated serum antimitochondrial antibodies (AMA)
Primary sclerosing cholangitis
progressive destruction of intrahepatic and extrahepatic bile ducts, leading to fibrosis and cirrhosis.
Presents with fatigue, pruritis, hepatomegaly, xanthomas, maybe jaundice if severe
UNLIKE PBC
PSC is more common in men
Associated with ulcerative colitis
Labs: negative ANA
often with + p-ANCA
ERCP shows “beads on a string”
Treatment: transplant
Associated with increased risk of cholangiocarcinoma
What condition is associated with cholangiocarcinoma?
primary sclerosing cholangitis is associated with cholangiocarcinoma, which is cancer of the bile duct
What are some of the possible etiologies of secondary (as opposed to primary) sclerosing cholangitis?
- intraductal biliary stones
- surgical trauma or blunt abdominal trauma to the biliary tree
- drugs (IV chemotherapy)
- recurrent pancreaitis
- autoimmune pancreatitis
- AIDs cholangiopathy
Gilbert disease
- mild deficiency of UDPGT
- mild jaundice following fasting, exercise, stress
- increased indirect bilirubin (
Crigler-Najjar syndrome type 1
autosomal recessive -severe deficiency of UDPGT present in infancy -persistent jaundice -kernicterus
Icreased indirect bilirubin (>5mg/dL)
fatal if untreated
- phototherapy
- plasmapheresis
- liver transplantation
Crigler-Najjar syndrome type 2
Mildly decreased UDPGT
Mildly elevated indirect bilirubin
Treatment- phenobarbital,
Note, phenobarbital will induce cytochrome p450 as well as production of UDPGT
Deep palpation of RUQ leads to arrest of inspiration due to pain
Murphy sign
Cholecystitis
Charcot triad (fever, jaundice, RUQ pain), hypotension, AMS
Reynold’s pentad
Cholangitis
RLQ pain on passive extension of the hip
psoas sign
appendicitis
RLQ pain on passive internal rotation of the flexed hip
obturator sign
appendicitis
LUQ pain and referred left shoulder pain
Kehr’s sign
splenic rupture
Ecchymosis of skin overlying the flank
acute pancreatitis
Ecchymosis of the skin overlying the periumbilical area
Cullen sign
acute pancreaitis
What are the major stages of liver change due to chronic alcohol use
- hepatic steatosis (Reversible early on)
- steatohepatitis (fat and inflammation)
- cirrhosis
nonalcoholic steatohepatitis (NASH)
mcc: obesity, DM hyperlipidemia, insulin resistance
insulin resistance leads to excess lipid accumulation in the liver
can progress to cirrhosis, lead to hcc, or worsen hep C progression
suspect NASH if chronically elevated LFTs
Diagnose NASH with liver US, CT scan, or MRI
Magnetic resonance spectroscopy (MRS) is the gold standard
liver biopsy can also make the diagnosis, and can be used to identify those at risk for disease progression
Treatment:
- avoid all alcohol
- weight loss: most likely beneficial, but no proven benefit
- Control any diabetes aggressively to keep HbA1C
symptoms and signs of alcoholic liver disease
anorexia n/v abd tenderness ascites splenomegaly
lab: elevated ALT, AST, GGT
unless the liver is so far gone that it doesn’t make enzymes anymore
look for AST>ALT by 2:1 or more
Also, elevated alk phos and bilirubin
Low albumin, prolonged PT and PTT, low triglycerides, LDL, HDL
increased WBC
Treat alcoholic liver disease
stop alcohol use thiamine folate high caloric intake liver transplant (eligible after sober 6 months)
Cirrhosis
alcohol Hep B and C bile duct obstruction, chronic cholestasis- PBC, PSC hemochromatosis Wilson disease A1AT deficiency Non-alcoholic steatohepatitis autoimmune hepatitis
What do hepatocytes do?
conjugate bilirubin
synthesize proteins
metabolize toxins
What hand finding is associated with alcoholic cirrhosis?
Dupuytren contracture
How to treat cirrhosis:
stop all alcohol even if it isn’t the main problem
lactulose to trap ammonia in the gut
rifaximin to kill of ammonia- producing gut bacteria
liver transplant
What are signs and symptoms of Budd- Chiari syndrome, and how does it usually present?
thrombosis and occlusion of the hepatic vein or intrahepatic/suprahepatic portion of the IVC
presentation: ascites (84%)
hepatomegaly (76%)
jaundice
acute presentation: acute RUQ pain and hepatomegaly
rapid development of jaundice and ASCITES
subacute or chronic presentation gradual development of ascietes, LE edema, cirrhosis, portal hypertension over a few months
eventual development of liver failure and hepatic encephalopathy
Best initial diagnostic test: US
Gold standard test: hepatic venography
How do you diagnose Budd- Chiari?
Best initial diagnostic test: US
Gold standard test: hepatic venography
How do we treat Budd-Chiari syndrome?
Thrombolytics to dissolve the clot) Diuretics Anticoagulation Angioplasty Shunting
Where do varices form, subsequent to portal hypertension?
These varices form due to the need for bypassing blood vessels, around the portal venous system (forming where portal venous system interfaces with the systemic circulation)
- esophageal varices
- hemorrhoids
- caput medusae
- renal varices
- paravertebral varices
Serum- ascites albumin gradient (SAAG)
subtract!
measure albumin in the ascites
measure the albumin in the serum
SAAG= serum alb- ascites albumin
Significance of SAAG> 1.1
portal hypertension (low albumin in the ascites) cirrhosis alcoholic hepatitis heart failure/ constrictive pericarditis massive hepatic metastases Budd- chiari syndrome
Significance of SAAG
ascites not due to portal hypertension (high albumin in the ascietes, or low serum albumin)
high albumin in the ascites
-peritoneal carcinomatosis (ovarian cancer)
-peritoneal tuberculosis
-pancreatitis
-serositis
low serum albumin
-nephrotic syndrome
What if you have high albumin and high LDH on paracentesis?
consider cancer as a cause of ascites
do a workup for cancer if this is the case
What if you have elevated WBC on paracentesis?
high WBC
high protein
low glucose
LDH higher in ascites than serum
consider spontaneous bacterial peritonitis
What is the treatment for spontaneous bacterial peritonitis (SBP)?
- Cefotaxime, ceftriazone, or other third- generation cephalosporin for at least 5 days to cover for gut bacteria (E. coli, klebsiella, and enterococcus), staph, and strep
- Give IV albumin because it maintains plasma volume, preserves renal function, and reduces renal impairment and mortality
How do we treat portal hypertension?
- salt restriction and diuretics (spironolactone and furosemide combined each morning)
- beta blockers to reduce risk of bleeding (propanolol, nadolol)
- vasopressin or sclerotherapy
- hepatic shunting
- TIPs procedure (trans-jugular intra-hepatic port-caval shunt) which channels through liver to shunt blood from portal to systemic systems. This increases risk of hepatoencephalopathy while relieving varices
Hereditary hemochromatosis
AR
excess iron absorption, which then gets deposited in the liver, heart, pituitary
H and P: abdominal pain polydipsia polyuria arthralgias lethargy bronze hue of the skin hepatomegaly testicular atrophy/impotence related to infiltration of the pituitary dilated> restrictive cardiomyopathy
Labs: increased iron, increased ferritin, increased transferrin saturation, increased AST, ALT
Bx will help determine extent of damage
Tx:
- phlebotomy weekly until iron levels normalize
- avoid excess alcohol consumption
- deferoxamine
Complications:
- cirrhosis
- hcc
- CHF
- diabetes
- hypopituitarism
Wilson disease
impaired copper secretion
Copper in the brain can yield depression, personality changes, loss of coordination, Parkinsonian-like symptoms like tremor
dysphagia
Copper in the liver:
jaundice
hepatomegaly
cirrhosis
Copper in the cornea:
Kayser- Fleischer rings
Labs: decreased serum ceruloplasmin (binds copper and transports it in the blood)
UNlikely to be Wilson if pt >40
Labs:
- decreased serum ceruloplasmin
- increased urinary copper
- increased AST and ALT
- liver biopsy with increased copper deposits
Treatment:
trientine and penicillamine as copper chelators
zinc supplements
restrict dietary copper
Vitamin B6 supplements
Liver transplant
complications: fulminant hepatic failure, cirrhosis
Alpha1- antitrypsin deficiency
panacinar emphysema
liver disease- mutated form of alpha1- antitrypsin, which polymerizes and accumulates in liver cells, toxic to hepatocytes
Co-dominant disorder (homozygous confers early emphysema; heterozygotes might not get lung disease unless they smoke)
labs:
increased AST and ALT
PFTs: obstructive disease
emphysema
Tx: liver transplant, lung transplant if severe
Autoimmune hepatitis
Autoimmune inflammation of the liver
More common in women than men
Often asymptomatic/subclinical, may result in cirrhosis
2 clinically similar sybtypes: Type 1 (classic): associated with +ANA and anti-smooth muscle antibodies (ASMA)
Type 2- associated with antibodies against liver- kidney- microsomal (LKM) antibodies or liver cytosol antigens
Treat with glucocorticoids
or glucocorticoids + azathioprine (immunosuppressant)
+ANA and anti-smooth muscle antibodies (ASMA)
Type 1 autoimmune hepatitis
anti- liver- kidney- microsomal (LKM) antibodies or liver cytosol antigens
type 2 autoimmune hepatitis
Benign hepatic neoplasms
hepatic adenomas
focal nodular hyperplasia
hemangiomas
hepatic cysts
These benign liver growths are more common in women who use OCP
Asx unless they get really big, usually found incidentally and don’t need to be treated
Can cause RUQ fullness
Hepatic adenoma
most often in women ages 20-44 (OCP years)
risk factors: OCP use, anabolic steroids, glycogen storage diseases types I and III
symptoms: +/- RUQ pain, usually asx
10% with malignant transformation
Treatment: discontinue the OCP, serial imaging and AFP, +/- resection (especially if >5cm)
What should you do if you see a suspicious liver mass on CT?
CT chest/abd/pelvis, since mets are much more common than primary liver tumors
Consider colonoscopy if the patient is at risk or at screening age
Hepatocellular carcinoma
malignant tumor of hepatic parenchyma
risk factors: hepatitis B hepatitis C cirrhosis aflatoxin (corn, nuts)
History and physical: RUQ abdominal pain weight loss malaise anorexia diarrhea jaundice hepatomegaly bruit over the liver ascites
Labs:
increased AST, ALT
increased alk phos and bilirubin
increased alpha-fetoprotein
complications: hemorrhage, so biopsy is risky
Treatment: surgical resection chemotherapy transplant radiofrequency ablation and chemoembolization if the tumor is unresectable
Complications contd..
liver failure
Budd-Chiari
portal vein obstruction
Paraneoplastic syndromes associated with hcc:
- hypoglycemia
- excessive RBC production -increased erythropoietin
- refractory watery diarrhea
- hypercalcemia
- various skin lesions
Erythropoietin increase may be explained by…
Potentially Really High Hematocrit
Pheochromocytoma
Renal Cell Carcinoma
Hemangioblastoma
HCC
What’s the most widely-used screening test for hemochromotosis?
Ferritin (high)
What lab value do you look for with WIlson disease?
serum ceruloplasmin (low)
