Gastroenterology Flashcards

(284 cards)

1
Q

Common causes of viral gastroenteritis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Bacterial gastroenteritis: Bacillus cereus

A
Bacillus cereus (fried, reheated rice)
vomiting within several hours of eating

Treatment: maintain hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Bacterial gastroenteritis: campylobacter jejuni

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Bacterial gastroenteritis: clostridium botulinum

A

honey, home- canned foods
n/v/d
flaccid paralysis
don’t allow children

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Bacterial gastroenteritis: C. Diff

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Bacterial gastroenteritis: E. Coli (enterotoxigenic)

A

travelers’ diarrhea
contaminated food and water
watery diarrhea, vomiting, fever

Treatment: often self- limited, hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Bacterial gastroenteritis: E. Coli (enterohemorrhagic, O157:H7)

A
undercooked ground beef 
bloody diarrhea
vomiting, fever ,abdominal pain
Hemolytic uremic syndrome
-thrombocytopenia
-hemolytic anemia
-acute renal failure

Treatment: hydration and supportive care

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Bacterial gastroenteritis: staph aureus

A

room-temperature food
it’s the premade toxins that make you sick

Vomiting within hours of eating
Diarrhea
treatment: hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Bacterial gastroenteritis: Salmonella

A
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Bacterial gastroenteritis: Shigella

A

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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Bacterial gastroenteritis: vibrio cholerate

A
"rice water" diarrhea
seafood
abd pain, watery diarrhea, within 24 hours of eating
treatment- hydration
Tetracycline or doxycycline
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Bacterial gastroenteritis: Vibrio parahaemolyticus

A

seafood (oysters)
abd pain
watery diarrhea within 24 hours of eating
treatment: hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Bacterial gastroenteritis: yersinia

A

pork, produce, puppy feces
abd pain, bloody diarrhea, RLQ pain
Treatment: hydration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Parasitic and protozoan GI infections: giardia lamblia

A

surface water
greasy, foul- smelling diarrhea
abd pain, malaise
cysts and trophozoites in the stool

Treatment: metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Parasitic and protozoan GI infections: entameoba histolytica

A

water-borne
areas of poor sanitation
mild to severe bloody diarrhea

abd pain
cysts and trophozoites in stool
liver abscess

Treatment: metronidazole, paromomycin

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Parasitic and protozoan GI infections: Cryptosporidium

A
food or water-borne
immunocompromised patients
watery diarrhea, abd pain, malaise
acid fast stain- parasites in stool
Treatment- nitazoxanide
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Parasitic and protozoan GI infections: trichonella

A

undercooked pork
fever, myalgias, periorbital edema
eosinophilia
CNS and cardiac symptoms also may occur

this is a bendy work
Treatment: albendazole, mebendazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Parasitic and protozoan GI infections: Taenia solium

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Food poisoning as a result of mayonnaise sitting out too long

A

staphylococcus aureus, salmonella

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Rice- water stools

A

vibrio cholerae, enterotoxigenic e. coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

diarrhea transmitted from pet feces

A

yersinia enterocolitica

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

food poisoning resulting from reheated rice

A

bacillus cereus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

MCC “Traveler’s diarrhea”

A

enterotoxigenic e.coli

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Diarrhea after a course of antibiotics

A

c. difficile

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
diarrhea and recent ingestion of water from a stream
giardia lamblia | entamoeba histolytica
26
mild intestinal infection that can become neurocysticercosis
taenia solium
27
food poisoning from undercooked hamburger
enterohemorrhagic e. coli
28
diarrhea from seafood
vibrio species
29
bloody diarrhea from poultry
salmonella, campylobacter
30
diarrhea and pink eye
adenovirus
31
bloody diarrhea leading to liver abscess
entamoeba histolytica
32
diarrhea in an AIDS patient
cryptosporidium
33
dehydrated child with greenish diarrhea in winter months
rotavirus
34
Treatment for entamoeba histolytica
metronidazole
35
Treatment for giardia lamblia
metronidazole
36
Treatment for salmonella
fluoroquinolones only if pt is immunocompromised or very ill
37
Treatment for shigella
fluoroquinolones, TMP-SMX
38
Treatment for campylobacter
erythromycin, but this is usually self- limited
39
How long does hepatitis last before we call it chronic?
6 months
40
risk factors for viral hepatitis
IV drug use alcoholism travel to developing countries poor sanitation
41
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 ```
42
hepatitis A diagnostic labs
Anti-HAV IgM abs -present during illness Anti-HAV IgG abs - after illness has resolved - present with vaccination
43
HBsAg
active disease
44
HBcAb
history of active disease IgM rises early IgG rises late
45
HBeAg
active viral replication, high transmissibility HBeAb signifies low transmissibility
46
Hep A | characteristics of the virus
ssRNA spread by fecal- oral route food/shellfish treatment: self-limited, supportive care
47
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
48
polyarteritis nodosa
vasculitis of medium and small- sized arteries ``` fever weakness rash joint pain erythematous nodules ``` associated with hep B
49
glomerular disease
membranous nephropathy rarely, membranoproliferative GN (hep B or hep C), proteinuria adults>children
50
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 ```
51
Hep D
disabled, requires co-existant hep B in order to be infectious Treatment: IFN-alpha prevention: Hep B vaccine
52
Hep E
spread by facal-oral route, contaminated waters treatment: self- limited, supportive care complications: pregnant women
53
Sialolithiasis
obstructed salivary gland by a stone swelling, pain with eating Tx: warm compresses, massage, sour candy, surgery (remove the stones) antibiotics if infection
54
Sjogren syndrome
inflammatory disorder that can affect the salivary glands. Dry mouth, dry eyes (sicca complex) diminished secretions
55
What is the most common neoplasm affecting the salivary glands
pleomorphic adenoma, benign
56
MC site for sialic neoplasm
parotid gland, which can also be a site of extra-pulmonary sarcoidosis
57
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
58
odynophagia
pain with swallowing
59
Plummer Vinson triad
iron def dysphagia esoph web
60
feeling of food stuck in throat with swallowing (immediate discomfort) cough choking
Oropharyngeal dysfuntion
61
delayed discomfort dysphagia
esophageal dysfunction
62
dysphagia characterized by difficulty with solids
obstructive pathology
63
dysphagia characterized by difficulty with solids and liquids
neuromuscular dysmotility
64
diagnostic testing for dysphagia
BARIUM SWALLOW esophagogastroduodenoscopy (EGD) manometry
65
What anatomical structures in the GI tract are evaluated by the barium swallow?
esophagus, LES, stomach
66
What anatomical structures in the GI tract are evaluated by the gastric emptying study?
stomach, pyloric sphincter, duodenum
67
What anatomical structures in the GI tract are evaluated by the small bowel follow through (SBFT)
stomach to terminal ileum
68
What anatomical structures in the GI tract are evaluated by the barium enema?
appendix to rectum
69
complications of NG tube
esophageal reflux | pressure necrosis
70
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
71
complications of gastrostomy tube
patient may yank the tube
72
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 ```
73
laparascopy
visualization of the peritoneal cavity using a laparoscope
74
laparotomy or celiotomy
surgical incision into the abdominal cavity
75
ectomy
surgical removal or something
76
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
77
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
78
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
79
Traction diverticulum- where in the esophagus is it found?
between UES and LES
80
Where is the epiphrenic diverticulum found
above the LES
81
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
82
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
83
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 ```
84
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) ```
85
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
86
Promotility agents in GERD
metoclopramide is an example, no longer recommended for GERD
87
GERD treatments that are safe in pregnancy
antacids, PPIs, H2 blockers
88
How do we treat refractory GERD?
Nissen fundoplification
89
GERD complications
``` Esophageal ulceration Esophageal stricture Barrett esophagus Adenocarcinoma Reflux- induced asthma Laryngeal disorders ```
90
Esophageal cancer: 2 major types
Squamous cell carcinoma (more common worldwide) | Adenocarcinoma (more common in the US, less common worldwide)
91
Barrett's esophagus
intestinal metaplasia of the distal esophagus secondary to chronic GERD increases risk of adenocarcinoma
92
Risk factors for esophageal cancer
``` alcohol tobacco chronic GERD obesity (adenocarcinoma) nitrates preserved meats ```
93
H and P for esophageal cancer
``` progressive dysphagia weight loss odynophagia reflux GI bleeding vomiting weakness cough, hoarseness ```
94
Esophageal cancer diagnostic studies
barium swallow EGD (biopsy is what makes the diagnosis) MRI, CT, PET scan
95
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
96
Mallory- Weiss syndrome
longitudinal mucosal laceration in the distal esophagus and proximal stomach, minor injury
97
Boerhaave syndrome
perforation or rupture in the distal esophagus, tears all layers of the esophagus; life-threatening
98
chest pains, uncoordinated contractions, corkscrew pattern on barium swallow
diffuse esophageal spasm
99
inability to relax the LES; bird's beak on barium swallow
achalasia
100
bad breath, regurgitation of food eaten days ago
Zenker diverticulum
101
Common symptoms of GERD
persistent cough | heartburn
102
Which is associated with ischemia- sliding hiatal hernia or paraesophageal hiatal hernia?
paraesophageal hiatal hernia
103
What is gastritis
inflammation of the gastric mucosa, acute (erosive) or chronic (non-erosive), related to NSAIDs, alcohol, corrosive materials, h. pylori, stress
104
Where is B12 absorbed?
terminal ileum
105
How do we diagnose H. Pylori?
urea breath test antral biopsy serum h.pylori antibodies
106
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
107
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
108
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
109
Ulcer associated with severe burn
Curling's ulcer
110
Ulcer associated with intracranial injuries
Cushing's ulcers
111
Zollinger- Ellison syndrome
increased gastrin
112
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
113
Treat a peptic ulcer
1. rule out active bleeding: CBC, EGD, Stool guiac 2. decrease gastric acid levels PPI H2 antagonist 3. protect mucosa Sucralfate Bismuth subsalicylate Misoprostol 4. Treat H. Pylori: PPI, Amoxicilin or metronidazole, clarithromycin 5. Surgery -perforation repair -parietal cell vagotomy -antrectomy 6. COX2 inhibitors (still have some gastric side effects)
114
complications of peptic ulcer
hemorrhage perforation lymphoproliferative disease
115
Zollinger-Ellison syndrome
gastrin- producing tumor in the duodenum or pancreas ``` refractory PUD abdominal pain n/v indigestion diarrhea steatorrhea other endocrine abnormalities ``` 1. Labs: fasting gastrin level (>1000) secretin stimulation test (secretin induces a steep rise in gastrin levels in patients who do have ZE) 2. 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 3. 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
116
Gastric cancer subtypes
1. ulcerating (this is why we biopsy the area around all gastric ulcers) 2. polypoid 3. superficial spreading 4. linitis plastica, involving all layers of the stomach
117
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 ```
118
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
119
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
120
complications of surgical therapy for obesity
``` nutritional deficiencies iron b12 folate thiamine vit D GERD Dumping syndrome: bloating, swelling, steatorrhea, diarrhea ```
121
Most effective treatment of a duodenal ulcer not due to cancer?
H. Pylori triple therapy PPI Amoxicillin Clarithromycin (metronidazole if pt allergic to clarithromycin)
122
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
123
Branching rods, oral infection, what bacteria is this?
actinomyces israelii
124
How does malabsorption present?
weight loss, bloating, diarrhea, steatorrhea, glossitis, dermatitis (zinc deficiency), edema (protein malabsorption)
125
Where is ethanol absorbed?
stomach
126
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
127
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
128
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
129
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
130
Sudan stain
if you suspect fat malabsorption bacterial overgrowth pancreatic insufficiency
131
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
132
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
133
Acute diarrhea
134
chronic diarrhea
1. inflammatory - autoimmune disorders - Crohn disease - Ulcerative colitis - Chronic infection 2. fatty - pancreatic insufficiency - Whipple disease 3. 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?)
135
The formula for stool osmotic gap
290-2(Na+K)= stool osmotic gap
136
Pediatric diarrhea
infection - rotavirus (winter) - adenovirus (plus conjunctivitis) antibiotic use -macrolides immunosuppression
137
What is the cut-off in osmotic gap for secretory diarrhea
138
What is the cut-off in osmotic gap for osmotic diarrhea
>125
139
Which tumors can cause diarrhea due to hormone excess
carcinoid tumor VIPoma gastrinoma medullary thyroid cancer
140
most common food-borne bacterial GI infections in the US
campylobacter | salmonella
141
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 ```
142
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
143
What are the subtypes of IBS?
IBS with diarrhea IBS with constipation Mixed IBS IBS unsubtyped
144
What symptoms are NOT c/w IBS alone?
``` anorexia weight loss malnutrition progressively worsening pain pain that prevents sleep rectal bleeding ```
145
What lab findings are NOT consistent with IBS alone?
electrolyte disturbances anemia increased inflammatory markers
146
What imaging is helpful in ruling out other diagnoses when you are considering IBS?
abdominal x-ray abdominal CT barium studies
147
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
148
IBD
inflammatory disease Crohn Ulcerative colitis
149
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 1. Barium study with small bowel follow-through 2. Colonoscopy: granulomas, colonic ulcers ``` Complications: malabsorption fissures fistulas strictures obstruction abscess formation ``` Treatment for Crohn disease: 1. steroids +/- abx for acute exacerbations 2. azathioprine or mercaptopurine> methotrexate 3. 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
150
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 ```
151
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
152
Extraintestinal manifestations of IBD
``` arthritis ankylosing spondylitis erythema nodosum pyoderma gangernosum uveitis primary sclerosing cholangitis ```
153
Serologic markers for IBD
ASCA:anti-saccharomyces cerevisiae abs often positive in Crohn pANCA- perinuclear anti-neutrophil cytoplasmic antibodies, often positive with UC
154
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
155
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
156
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
157
What is the most common benign small bowel tumor?
leiomyoma
158
WHat is the most common malignant small bowel tumor?
carcinoid
159
Large bowel obstruction common causes:
neoplasm adhesions volvulus diverticulitis radiology: bowel distention proximal to the obstruction treatment: NPO, maintain hydration, colonoscopy, surgery if necessary
160
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
161
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
162
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
163
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)
164
Ileus
paralytic obstruction of small bowel secondary to decreased peristalsis infection, ischemia, recent surgery, DM typically less than 5 days. small bowel recovers first (
165
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
166
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)
167
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
168
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
169
When is inpatient admission for diverticulitis treatment indicated?
``` elderly immunocompromised significant comorbidities high fever with significant leukocytosis unable to tolerate oral intake ```
170
What are the steps in inpatient management of diverticulitis
1. IV fluids 2. broad- spectrum empiric antibiotics (similar to appendicitis) 3. If there are signs of peritonitis (guarding, tenderness), then sent the patient for emergency exploration through midline incision
171
What are the complications of diverticulitis?
Colonic abscesses fistulas sepsis
172
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
173
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
174
Anorectal abscess
infection of anal crypts, hair follicles H and P: throbbing rectal pain, fever, tenderness on DRE Treatment: Antibiotics I and D
175
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
176
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
177
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
178
The biggest risk factor for colon cancer
presence of colon polyps, especially the adenomatous ones
179
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 ```
180
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
181
Gardner syndrome
APC mutation colon polyps osteomas soft tissue tumors
182
Turcot syndrome
APC gene mutation colonic adenomas CNS tumors
183
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)
184
Peutz-Jeghers syndrome
Hamartomas in the GI tract | pigmented lesions on lips and oral mucosa
185
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)
186
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
187
How do we stage colon cancer? what characterizes stages 3 and 4?
node involvement: stage III, involves chemotherapy met's beyond nodes: stage IV
188
Colon cancer post- treatment surveillance
CEA every 3 months for 3 years CT chest/abdomen/pelvis every year Colonoscpoy at 1, 3, 5, years
189
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
190
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
191
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
192
Melena- dark blood
upper GI or proximal small bowel blood
193
Coffee ground emesis
blood that has been sitting in the stomach for some time
194
Causes of upper GI bleed
``` peptic ulcer disease Mallory- Weiss tears esophagitis esophageal varices gastritis ```
195
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)
196
imaging of choice for lower GI bleed
colonoscopy
197
imaging of choice for upper GI bleed
EGD
198
Where does the EGD end
duodenum
199
Where does a colonoscopy stop?
terminal ileum
200
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
201
Tagged RBC scan
tagged technetium helps localize bowel bleed to quadrant, helpful for intermittent bleeds
202
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
203
Management steps for GI bleed
1. H and P 2. Continuous monitoring of vital signs 3. 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 5. type and cross 2 U PRBC 6. Labs:CBC, coags (guaiac stool if necessary, to confirm blood) Treat and determine the cause 7. NG tube to rule out massive upper GI bleed 8. If colonoscopy is nondiagnostic and not feasible (too much active bleeding may obscure visualization), and bleeding persists, then radionucleotide scan and/or angiogram
204
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
205
The 3 most common causes of acute pancreatitis
gallstones chronic alcohol use idiopathic
206
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
207
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
208
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
209
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)
210
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
211
Chronic pancreatitis causes
almost always due to alcoholism | recurrent
212
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 ```
213
Chronic pancreatitis treatment
``` stop alcohol use stop smoking opioids pancreatic enzymes vitamin supplements small, low-fat meals surgical repair of ductal damage ```
214
Complications of chronic pancreatitis
``` ductal obstruction pseudocyst malnutrition glucose intolerance pancreatic cancer ```
215
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
216
Treatment of pancreatic pseudocyst
often resolves on its own drain for diagnosis debridement or percutaneous drainage if the cyst persists over 4 weeks
217
Pancreatic pseudocyst complications
rupture abscess hemorrhage pseudoaneurysm (digests vessels so that they bleed into the cyst)
218
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: 1. resection (whipple procedure) 2. adjuvant chemotherapy 3. pancreatic enzymes 4. 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
219
Trousseau syndrome
migratory thrombophlebitis classically associated with pancreatic adenocarcinoma
220
Gastrinoma- stomach tumor
Gastrin- secreting glandular tumors that cause Zollinger- Ellison syndrome
221
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
222
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
223
Necrolytic migratory erythema
uncommon presentation of glucagonoma | rash, erythematous plaques on the face, perineum, extremities
224
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 ```
225
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
226
acute cholycystitis
inflammation of the gallbladder | Usually, a gallstone obstructs the cystic duct, leading to infection and inflammation behind the obstruction
227
Acalculous choecystitis
patients on TPN critically ill patients inflammation, without obstruction
228
Murphy sign
inspiration stopped by pain when you put your hand over the RUQ positive test consistent with cholecystitis
229
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)
230
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
231
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
232
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 ```
233
Charcot triad- cholangitis
RUQ pain jaundice fever cholangitis until proven otherwise
234
Reynolds pentad, cholangitis
Charcot triad (RUQ pain, fever, jaundice) + AMS and hypotension or shock
235
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 ```
236
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.
237
Primary biliary cirrhosis
- autoimmune disease that destroys the intrahepatic bile ducts (cholesterol, bile acids) - more common in women - associated with autoimmune diseases
238
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
239
What laboratory finding is a hallmark of primary biliary cirrhosis?
Elevated serum antimitochondrial antibodies (AMA)
240
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
241
What condition is associated with cholangiocarcinoma?
primary sclerosing cholangitis is associated with cholangiocarcinoma, which is cancer of the bile duct
242
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
243
Gilbert disease
- mild deficiency of UDPGT - mild jaundice following fasting, exercise, stress - increased indirect bilirubin (
244
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
245
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
246
Deep palpation of RUQ leads to arrest of inspiration due to pain
Murphy sign | Cholecystitis
247
Charcot triad (fever, jaundice, RUQ pain), hypotension, AMS
Reynold's pentad | Cholangitis
248
RLQ pain on passive extension of the hip
psoas sign | appendicitis
249
RLQ pain on passive internal rotation of the flexed hip
obturator sign | appendicitis
250
LUQ pain and referred left shoulder pain
Kehr's sign splenic rupture
251
Ecchymosis of skin overlying the flank
acute pancreatitis
252
Ecchymosis of the skin overlying the periumbilical area
Cullen sign | acute pancreaitis
253
What are the major stages of liver change due to chronic alcohol use
1. hepatic steatosis (Reversible early on) 2. steatohepatitis (fat and inflammation) 3. cirrhosis
254
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: 1. avoid all alcohol 2. weight loss: most likely beneficial, but no proven benefit 3. Control any diabetes aggressively to keep HbA1C
255
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
256
Treat alcoholic liver disease
``` stop alcohol use thiamine folate high caloric intake liver transplant (eligible after sober 6 months) ```
257
Cirrhosis
``` alcohol Hep B and C bile duct obstruction, chronic cholestasis- PBC, PSC hemochromatosis Wilson disease A1AT deficiency Non-alcoholic steatohepatitis autoimmune hepatitis ```
258
What do hepatocytes do?
conjugate bilirubin synthesize proteins metabolize toxins
259
What hand finding is associated with alcoholic cirrhosis?
Dupuytren contracture
260
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
261
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
262
How do you diagnose Budd- Chiari?
Best initial diagnostic test: US Gold standard test: hepatic venography
263
How do we treat Budd-Chiari syndrome?
``` Thrombolytics to dissolve the clot) Diuretics Anticoagulation Angioplasty Shunting ```
264
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) 1. esophageal varices 2. hemorrhoids 3. caput medusae 4. renal varices 5. paravertebral varices
265
Serum- ascites albumin gradient (SAAG) subtract!
measure albumin in the ascites measure the albumin in the serum SAAG= serum alb- ascites albumin
266
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 ```
267
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
268
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
269
What if you have elevated WBC on paracentesis? high WBC high protein low glucose LDH higher in ascites than serum
consider spontaneous bacterial peritonitis
270
What is the treatment for spontaneous bacterial peritonitis (SBP)?
1. 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 2. Give IV albumin because it maintains plasma volume, preserves renal function, and reduces renal impairment and mortality
271
How do we treat portal hypertension?
1. salt restriction and diuretics (spironolactone and furosemide combined each morning) 2. beta blockers to reduce risk of bleeding (propanolol, nadolol) 3. vasopressin or sclerotherapy 4. hepatic shunting 5. 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
272
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
273
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
274
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
275
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)
276
+ANA and anti-smooth muscle antibodies (ASMA)
Type 1 autoimmune hepatitis
277
anti- liver- kidney- microsomal (LKM) antibodies or liver cytosol antigens
type 2 autoimmune hepatitis
278
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
279
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)
280
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
281
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: 1. hypoglycemia 2. excessive RBC production -increased erythropoietin 3. refractory watery diarrhea 4. hypercalcemia 5. various skin lesions
282
Erythropoietin increase may be explained by... Potentially Really High Hematocrit
Pheochromocytoma Renal Cell Carcinoma Hemangioblastoma HCC
283
What's the most widely-used screening test for hemochromotosis?
Ferritin (high)
284
What lab value do you look for with WIlson disease?
serum ceruloplasmin (low)