Cmu Clin Med Iii - Gi

Front 1

GI: ACHALASIA

Etiology

Back 1

Motor disfunction

• Absence of peristalsis
  
• Lower esophageal sphincter cannot relax
  

Degeneration of nerves

• Vagus
  
• Auerback's plexus
  

* dorsal nucleus of spinal cord

Because there is no innervation, the tone is lost

it ends up being obstructed because the sphincter cannot relax

Front 2

GI: ACHALASIA

Epidemiology

Back 2

• 1:100,000 in US
  
• most common between 20-40 y/o
  
• can be seen in childhood
  
• male = female
  

Front 3

GI: ACHALASIA

Differential

Back 3

Cancer

Metabolic disorders (hypothyroidism)

Front 4

GI: ACHALASIA

Signs/symptoms

Back 4

• Dysphagia (difficulty swallowing)
  

(always indicate if it is dysphagia with solids, liquids, or both)

• vomiting
• weight loss
• chest pain
• heart burn
• bloating (full feeling)
• inability to burp

Front 5

GI: ACHALASIA

Risks/ complications

Back 5

• aspiration pneumonia
  
• esophageal cancer
  

Front 6

GI: ACHALASIA

Diagnosis

Back 6

1. Barium swallow/ radiology (Best first test)

• will show bird's beak sign
  

2. Manometry

• measures pressures
  
• increased pressure at esophageal junction
  
• decreased pressure at ...
  

3. Endoscopy (not the best first test)

Front 7

GI: ACHALASIA

Treatment

Back 7

1. small frequent meals

2. CCB's (or long-acting nitrates)

plus tube dilation

(70-90% success with this treatment)

3. Botox

applied to sphincter

4. surgery

Front 8

GI: ACHALASIA

Prognosis

Back 8

good

Front 9

GI: ACHALASIA

Key points

Back 9

• disease of motor disfunction
  
• fibrosis and degeneration of vagus nerve and Auerbach's plexus
  
• part of differential diagnosis of chest pain
• need surveyance with routine endoscopy

(because of increased risk of CA)

Front 10

GI: ESOPHAGITIS

Etiology

Back 10

inflammation to the mucosa of the esophagus

• infection
  
• injury
  

Front 11

GI: ESOPHAGITIS: Etiology

Most common cause

Back 11

reflux

Front 12

GI: ESOPHAGITIS: Etiology

Infectious causes

Back 12

usually in compromised hosts and elderly

1. candida

• compromised hosts
• people who use inhaled steroids

2. CMV

3. HSV

Front 13

GI: ESOPHAGITIS: Epidemiology

Back 13

• 5% in US
• highest prevalence in China and Middle East
• common in pregnancy because of reflux

Front 14

GI: ESOPHAGITIS

Differential Diagnosis

Back 14

1. GERD

2. Peptic Ulcer Disease

3. Gastritis

Front 15

GI: ESOPHAGITIS

Signs/ Symptoms

Back 15

• Heartburn
• dysphagia to solids and liquids
• odynophagia (pain/ burning with swallowing)
• anemia (from bleeding)
• can be asymptomatic

Front 16

GI: ESOPHAGITIS

Diagnosis

Back 16

1. Communication

getting the right answers, the right way

establish trust with the patient

History: immunocompromised

reflux

2. Endoscopy - Best first test

-should also be done after 5 years to check for Barrett's esophagus

3. culture

may need biopsy

Front 17

Random fact:

How does herpes appear?

Back 17

cluster of vesicles on a red face

Front 18

GI: ESOPHAGITIS

Treatment

Back 18

Treat the underlying cause

• GERD
  
• CMV
  
• HSV
  
• etc.
  

Front 19

GI: ESOPHAGITIS

Prognosis

Back 19

Most do well if underlying cause if treated

Front 20

GI: ESOPHAGITIS

Risks with inadequate treatment or untreated

Back 20

Strictures

Barrett's esophagus (pre-cancerous condition) red flag -- don't miss

esophagitis --> scarring --> hypertrophy --> narrowing of the lumen --> strictures

Front 21

GI: ESOPHAGITIS

Key points

Back 21

• most commonly caused by reflux
• compromised hosed will get fungal and viral infections
• treat the underlying cause
• prognosis is good if treated adequately and quickly
• if untreated, or treated inadequately can cause: Barrett's Esophagus or strictures

Front 22

GI: ESOPHAGEAL VARICES

Etiology

Back 22

• caused by portal hypertension
  
• Varices get dilated because of pressure
  
• can rupture which causes a lot of bleeding - serious emergency
  

Front 23

GI: ESOPHAGEAL VARICES

Epidemiology

Back 23

90% caused by cirrhosis

Front 24

What are the causes of cirrhosis?

Back 24

• alcoholics
  
• non-alcoholic fatty liver disease
  
• alpha 1 antitrypsin deficiency
  

-blocks action of elastase that breaks down fibrin

(ex: 20 y/o non-smoker first presents with

emphysema then gets cirrhosis)

Front 25

Random fact:

With cirrhosis, does the liver get smaller or larger?

Back 25

The liver is small in end stage cirrhosis

(everything that fibroses gets smaller)

Front 26

GI: ESOPHAGEAL VARICES

Differential Diagnosis

Back 26

1. Upper GI bleed of any cause

2. Mallory-Weiss Syndrome

(tear in the esophageal mucosa near the stomach)

• usually a Hx of wretching (alcoholism or bulimia)
  
• usually not massive bleeding
  

Front 27

GI: ESOPHAGEAL VARICES

Signs/Symptoms

Back 27

• Vomiting massive amounts of blood that is PAINLESS (ulcers would have pain)
  
• blood is dark brown (veinous blood)
• pallor
• orthostatic
• tachycardia
• severe volume depletion

Front 28

Random fact:

What are the approximate numbers for systolic pressure and heart rate in severe volume depletion?

Back 28

Systolic BP < 100

Heart rate > 100

(these are ballpark numbers)

Front 29

GI: ESOPHAGEAL VARICES

Diagnosis

Back 29

1. Acute presentation

usually seen in emergency department

2. best first test: endoscopy

(you don't see much through the blood)

Front 30

GI: ESOPHAGEAL VARICES

Treatment

Back 30

1. establish stable vital signs

2. Oxygen

3. fluids

4. Octreotide (somatostatin)

to treat portal hypertension acutely

5. BB's (Propranolol)

for chronic portal hypertension

6. vasopressin for acute Tx

7. surgery (shunt)

Front 31

GI: ESOPHAGEAL VARICES

Prognosis

Back 31

40% mortality with first episode

50% mortality in emergency room - regardless of number of episodes

most will be dead within a year

Front 32

GI: ESOPHAGEAL VARICES

Key points

Back 32

• usually secondary to cirrhosis
  
• PAINLESS massive bleeding
• 40% die with first episode
• establish stable vital signs before any scope, test, etc.
• there are surgical Tx

Front 33

GI: GERD

Etiology

Back 33

Lower esophageal sphincter relaxes inappropriately

Triggers:

• food
  
• hormones
  
• pregnancy
  
• position
  
• smoking
  

Front 34

GI: GERD

Food triggers

Back 34

• coffee (reg or decaf)
  
• spicy foods
  
• fats
  
• too much food
  
• alcohol
  

Front 35

GI: GERD

Epidemiology

Back 35

• most people get heart burn at least 1x per mo
  

• 10-15% has some GERD
  

Front 36

GI: GERD

Differential Dx

Back 36

• Achalasia
  

• Gastritis
  

Front 37

GI: GERD

Signs and Symptoms

Back 37

• heartburn
  
• cough
  
• hoarseness
  
• hiccups
  
• asthma gets worse
  
• damages the enamel on teeth (dentists often catch asymptomatic GERD)
  

Front 38

GI: GERD

What percentage of non-cardiac CP is due to GERD?

Back 38

75%

Front 39

GI: GERD

Diagnosis

Back 39

• Therapeutic trial of PPI's or H2 blockers (Zantac)
  
• If not better in six weeks (and no red flags) then endoscopy - if > 40 scope right away
  
• manometry
  

Front 40

GI: GERD

Treatment

Back 40

• PPI's
  
• H2 blockers
  
• lifestyle changes
  
• surgery - if severe and unresponsive to TX
  

Front 41

GI: GERD

Red Flags for Esophageal CA

Back 41

• Age > 50
  
• anemia
  
• night sweats
  
• fever/chills
  
• wt loss
  

Front 42

GI: GERD

Lifestyle changes

Back 42

• avoid mints, alcohol, caffeine, etc.
  
• elevate head of bed (not just the pillow, which can make it worse)
  
• lose weight
  
• no food 3 hrs before bed
  
• avoid CCB's
  
• small Fx meals
  

Front 43

GI: GERD

Prognosis

Back 43

• Usually benign
  
• most patients do well
  
• Biggest risk is Barrett's esophagus and strictures (these two often go together)
  

Treat underlying problem

Front 44

Random facts:

Where would you find group B strep?

Back 44

only in vagina

Front 45

Radom fact:

Where would you find group A strep?

Back 45

oropharynx

Front 46

Random Fact:

What parts of the body are drained by the portal system? What does portal hypertension cause in each of these areas?

Back 46

Rectum - hemorrhoids

Umbilicus - caput medusa

Esophagus - esophageal varices

Front 47

Random Fact:

What is the drug of choice for chronic portal hypertension?

Back 47

Propanolol

Front 48

Random Fact:

What percentage of the population is taking Omeprezole?

Back 48

15%

Front 49

Random Fact:

What are the adverse effects of long-term PPI use?

Back 49

• chronic kidney disease
  
• increased dementia
  
• increased C. diff
  
• hypomagnesemia (pt on diuretics, metformin)
  
• decreased absorption
  
• increased osteoporosis
  
• rebound if stopped abruptly (pt needs to be weaned off)
  

Front 50

GI: Esophageal Cancer

Etiology

Back 50

Squamous cell cancer

Front 51

GI: Esophageal Cancer

Epidimiology

Back 51

• Men = women
  
• patient's with barrett's esophagus
  
• smokers (all head and neck CA's)
  
• alcoholics
  
• nitrates
  
• radiation
  
• higher risk in Asian countries (they eat a lot of pickles)
  
• Beatle nuts in India
  

Front 52

Random Fact:

What are do people in India eat that increased their risk of developing esophageal CA?

Back 52

Beatlenuts

Front 53

GI: Esophageal Cancer

Signs and symptoms

Back 53

• Develops anxiety
  
• insidious
  
• progressive dyspnea (patient's will often change their diet to softer foods without noticing)
  
• weight loss
  
• aspiration pneumonia (b/c of choking)
  
• vomiting
  

Front 54

GI: Esophageal Cancer

Diagnosis

Back 54

Endoscopy with biopsy is the gold standard

PET scans have a lot of false pos. & neg. and is never a 1st step in diagnosis

positron

nuclear medicine technology with CT scan (fluorine molecule and isotope is added to glucose. the resulting F18 molecule is injected - the half-life is very short) this is an $$$ treatment

Front 55

GI: Esophageal Cancer

Treatment

Back 55

• Surgery: can cut out the cancer and anastomose the two pieces together
  
• Radiation: to shrink
  
• Chemo: if it has spread, it is not taken out- just treated with chemo
  

Front 56

GI: Esophageal Cancer

Prognosis

Back 56

• Better if found early
  
• Bad if found late
  

Front 57

GI: Esophageal Cancer

Key Points

Back 57

Top three risk factors:

• smoking
  
• alcohol
  
• barrett's esophagus
  

Red Flags

• dysphagia - KEY
  
• wt. loss
  
• aspiration pneumonia
  

Front 58

GI: Gastritis

Etiology

Back 58

Damage to the mucosal surface of the stomach

Caused by:

• viral infections
  
• bacterial infections
  
• NSAIDS
  
• alcohol
  
• CA
  
• GERD
  
• food poisoning
  

Front 59

GI: Gastritis

Does smoking cause gastritis?

Back 59

not directly

Front 60

GI: Gastritis

difference b/t gastritis and gastroenteritis

Back 60

gastritis = stomach only

gastroenteritis = stomach + colon

Front 61

GI: Gastritis

Signs and symptoms

Back 61

dyspepsia

N/V

anemia - from chronic gastritis, chronic NSAID use - causes microcytic anemia (MCV would be low)

Front 62

What is dyspepsia?

Back 62

food churning

gastric pain

Front 63

GI: Gastritis

Diagnosis

Back 63

Acute: gets better on its own (usually 3 days - 2 weeks)

Chronic - not getting better

• CBC - look for microcytic anemia
  
• Endoscopy with biopsy - GOLD STANDARD
  
• Bacterial testing - test for H. pylori
  

Front 64

GI: Gastritis

Treatment: Acute

Back 64

correct underlying cause

• volume depleted (HR > 100 systolic BP < 100)
  

orthostatic hypotension

• usually viral - treat with fluids
• food poisoning - staph

(shigella, salmonella cause enteritis not gastritis)

Front 65

GI: Gastritis

Treatment: Chronic

Back 65

correct underlying cause

• NSAIDS
  
• H. pylori
  

--triple therapy - different everywhere (talk to PCP)

Front 66

GI: Gastritis

Prognosis

Back 66

Acute: Good

Chronic: Depends on etiology

• H. pylori - treatable
  
• NSAIDS - cause permanent damage
  

Front 67

GI: Peptic Ulcer Disease (Gastric ulcer/ Duodenal ulcer)

Etiology

Back 67

Ulcers

Gastron - usually steroids, NSAIDS, anything in the gut

Duodenum - 75% are H. pylori

Front 68

GI: Peptic Ulcer Disease

Signs and symptoms

Back 68

• Burning
  
• RUQ pain
  

Gastron - worse with food

Duodenal - better with food

• Microcytic anemia - low MCV
  

RED FLAGS: medical emergency

ulcer can perforate mucosa

• distended and hard abdomen
  
• air under the diaphragm on x-ray
  

Front 69

GI: Peptic Ulcer Disease

Diagnosis: Acute

Back 69

• look for hemodynamic instability/ volume depletion
  

- IV lines

- monitor

- urine output

• scope
  

Front 70

GI: Peptic Ulcer Disease

Diagnosis: Chronic

Back 70

• endoscopy
  
• urea breath test - many false pos. - not 1st choice

Front 71

GI: Peptic Ulcer

Treatment

Back 71

• Fix underlying cause
  
• can coagulate ulcers with scope
  
• NG tube
  
• H2 blockers
  
• PPI's
  
• Blood Transfusion
  
• If H. pylori - confirm, then treat with ABX
  

Front 72

GI: Peptic Ulcer

Prognosis

Back 72

• good - modern endoscopes can coagulate
  

• recurrence is rare
  

Front 73

GI: Peptic Ulcer

Key Points

Back 73

Ulcers are:

1. gastric

• worse with food
• caused by NSAIDS, steroids

2. duodenal

• better with food
• caused by H.pylori (usually not acute)

most people get scoped if not getting better

• you really need to look at it

Front 74

Random Fact:

Smoking is protective for what disease?

Back 74

ulcerative colitis

Front 75

Random Fact:

for each tablet of NSAID, how many CC's of blood do you lose in a day?

Back 75

10 cc of blood

Front 76

Random fact:

most common cause of microcytic anemia

Back 76

Iron deficiency

Front 77

Random fact

H. pylori predisposes you to what disease?

Back 77

cancer

Front 78

How do you diagnose H. pylori?

Back 78

• antibody test - too many false pos. - not used anymore

Front 79

What is a clear wave test?

Back 79

test that can be preformed without certification

• mono
  
• rapid strep
• urine

Front 80

What is a CLEA test?

Back 80

need certification to perform

• urine microscopy
  
• any blood test
  

Front 81

GI: Hepatitis

Etiology

Back 81

Inflammation of the liver that leads to necrosis

Can be infectious: Hepatitis A, B, C, D, E

Can be non-infectious:

• medications: any that are metabolized in the liver (Tylenol, anesthetics, alcohol)
  
• hematochromatosis: accumulation of extra iron in the liver
  
• Wilson's disease accumulation of copper in the liver

Can be acute or chronic

Can be autoimmune

Front 82

GI: Hepatitis

Epidemiology

Back 82

Depends on underlying cause

Front 83

GI: Hepatitis

Differential Diagnosis

Back 83

• Gallbladder disease
  
• fatty liver disease
  

Front 84

GI: Hepatitis

Signs and symptoms: Acute

Back 84

N/V

Jaundice

may have fever

RUQ pain

pale stools - like chalk

cola colored urine (bilirubin is not being reprocessed)

hepatomegaly and tenderness

Front 85

GI: Hepatitis

Signs and symptoms: Chronic

Back 85

most of the time asymptomatic

not all hepatitis has a chronic phase

Front 86

GI: Hepatitis

Which types of hepatitis have a chronic phase

Back 86

Hepatitis A - no

Hepatitis B - yes

Hepatitis C - yes

Front 87

GI: Hepatitis

Most common type of infectious Hepatitis in the US

Most common type in Asia

Back 87

US: Hep C

Asia: Hep B

Front 88

GI: Hepatitis

Diagnosis

Back 88

Increased AST, ALT, and bilirubin in different ratios depending on the disorder

Depends on etiology - whatever you suspect, order tests

• viral
  
• autoimmune
  
• drugs
  

Front 89

GI: Hepatitis

Treatment

Back 89

Best first Tx is to deal with the underlying cause

• stop ETOH
  
• stop tylenol
  
• Hep A will typically go away on its own, but there is an immunoglobulin for Hep A
  
• Hep B immunoglobulin (HBIG) if not vaccinate
  
• Hep C - Harboni - cure

- interferon - nasty side effects - not used much anymore

• Autoimmune - responds to steroids

Front 90

GI: Hepatitis

Prognosis

Back 90

• Hep A - pretty good
  
• Hep B - can lead to chronic and other issues including CA
  
• Autoimmune - common with collagen vascular disease
  
• Tylenol overdose - depends on stage - if caught early, OK
  
• Most cases of hepatitis are manageable
  

Do a good Hx so you know what you are working with

Front 91

GI: Hepatitis

Key points

Back 91

Many etiologies

fix underlying cause

Hep A - self correcting

Hep B - immunoglobulin

Hep C - Harvoni

all have similar SSx

Front 92

GI: alpha 1- antitrypsin deficiency

Etiology

Back 92

causes emphysema in the young

Trypsin is an enzyme that breaks down elastin

alpha 1 antitrypsan prevents disruption of elastin from breaking down. Elastin contributes to the elasticity of the lungs.

Front 93

GI: alpha 1- antitrypsin deficiency

Epidemiology

Back 93

• autosomal recessive
  
• manifests in early childhood
  

Front 94

GI: alpha 1- antitrypsin deficiency

Signs and symptoms

Back 94

Jaundice --> eventually leads to --> cirrhosis

--> leads to CA of the liver

Front 95

GI: alpha 1- antitrypsin deficiency

Diagnosis

Back 95

Most important:

• genetic testing
  
• biopsy of the liver
  

can get blood levels of antitripsyn

Front 96

GI: alpha 1- antitrypsin deficiency

Treatment

Back 96

• No specific Tx available
  
• don't do anything that would cause more damage to the liver
  
• Transplant - most don't get a transplant
  

- the lungs are bad

- they can't do the transplant if they have

bad lungs

- they would have to get lung and liver

transplant at the same time

Front 97

GI: alpha 1- antitrypsin deficiency

Prognosis

Back 97

• There is never a complete deficiency
  
• effects every patient differently
  
• depends on level of antitripsyn
  

Front 98

GI: alpha 1- antitrypsin deficiency

Key points

Back 98

• autosomal recessive
  
• prognosis depends on level of alpha 1 antitripsan
  
• 
  
• ultimate Tx is a liver transplant
  

Front 99

GI: Hemochromatosis

Etiology

Back 99

• disease of iron overload
  
• Fe is extremely dangerous for the heart
• defective gene prevents iron from getting reabsorbed so it gets deposited in the liver and other organs
  
• the majority of Fe you consume is excreted in feces
  
• iron goes into liver, pancreas, heart, skin, pituitary glands
  

Front 100

GI: Hemochromatosis

Epidemiology

Back 100

more severe manifestation in men

women get rid of iron via menses

Front 101

GI: Hemochromatosis

Signs and symptoms

Back 101

too much Fe leads to hepatitis and eventually cirrhosis

Fe is an irritant

most are diabetic - because of deposits in pancreas

causes cardiomyopathy

skin - bronze - tan - subtle (over years) people don't notice

arthritis - can deposit in joints

males - impotence (usually 1st manifestation on male- because of deposits in pituitary - they get small testicles

AMS - usually at late stage

Front 102

GI: Hemochromatosis

Diagnosis

Back 102

• Serum Fe increases
  
• Ferritin - SUPER HIGH 1000-2000
  
• Liver biopsy - definitive Dx
  
• MRI - will show iron deposits
  

Front 103

GI: Hemochromatosis

Treatment

Back 103

• Weekly phlebotomy until serum Fe is normal
  
• Iron chelation therapy - agent (deferoaxamine) binds to Fe and takes it out
  
• If cirrhotic, can get liver transplant
  

Front 104

GI: Hemochromatosis

Prognosis

Back 104

• Depends on which organ is damaged
  
• The earlier it is caught, the better
  
• Most die from heart disease (once it is deposited in the heart, you can't get it out)
  

Front 105

GI: Hemochromatosis

Key points

Back 105

• Difficult to diagnose
  
• SSx - very subtle
  
• men present with impotence
  
• color change happens over years
  
• ferritin - super high
  

Front 106

GI: Wilson's disease

Etiology

Back 106

• Disorder of copper metabolism
  
• deposits in liver, brain, cornea, kidney, bones, joints, etc.
  
• autosomal recessive
  

Front 107

GI: Wilson's disease

differential diagnosis

Back 107

• hemochromatosis
  
• alpha-1 antitrypsin
  

Front 108

GI: Wilson's disease

Signs and symptoms

Back 108

• patient's may be asymptomatic for a long time
  
• once it progresses can cause cirrhosis
  
• basal ganglia affected (parkinson's, psychosis, etc)
  
• deposits on skeletal muscle
  
• Kayser-Fleisher rings BOARD QUESTION
  

Front 109

What are Kayser-Fleisher rings?

Back 109

• brownish to gold colored rings that appear to encircle the iris
  

• Found in Wilson's disease
  

Front 110

GI: Wilson's disease

Diagnosis

Back 110

Lab - ceroloplasmin (protein that binds to copper) - will be low

Split lamp exam to look for Kayser - Fletcher rings - can only be seen in advanced disease

Front 111

GI: Wilson's disease

Treatment

Back 111

• medications are available
  
• liver transplant
  
• need lifelong treatment
  

Front 112

GI: Wilson's disease

prognosis

Back 112

good if treated adequately

Front 113

GI: Wilson's disease

Key points

Back 113

• accumulation of Cu
  
• genetic
  
• presentations are all different
  
• ceruloplasmin is low
  

Front 114

GI: alcoholic liver disease

Etiology

Back 114

• usually long term
  
• hepatitis
  
• fatty liver disease (CT or US will show fat)
  
• acute hepatitis
  
• cirrhosis
  
• right sided heart failure (extra fluid goes to the liver)
  
• wilson's disease
  
• hematochromatosis
  

Front 115

GI: alcoholic liver disease

Epidemiology

Back 115

10% of US abuses ETOH

100% of alcoholics get fatty liver disease

very few (10%) get hepatitis

Front 116

GI: alcoholic liver disease

signs and symptoms

Back 116

Fatty liver - usually asymptomatic

25-30% of US pop has fatty liver

cirrhosis - gynecomastia, spider angioma

Front 117

GI: alcoholic liver disease

Diagnosis

Back 117

History

PE

CAGE questionnaire

abnormal liver enzymes - not super high

biopsy - but this is not normally done

Front 118

GI: alcoholic liver disease

Treatment

Back 118

Early detection of ETOH

may have to send to detox

AA works

Front 119

GI: alcoholic liver disease

Prognosis

Back 119

Without cirrhosis: will get better once they stop ETOH - unless they have cirrhosis

With cirrhosis: 50% 10-year mortality rate

AA works

Front 120

GI: Acute pancreatitis

Etiology

Back 120

Pancreas auto- digests

Trigger causes pancreas to release enzymes

Leads to edema, necrosis, bleeding, death

Front 121

GI: Acute pancreatitis

Epidemiology

Back 121

alcoholic

gall stones

drugs (Januvia, Victosa, etc.)

high triglycerides (usually caused by accutane)

trauma (car accident)

Front 122

GI: Acute pancreatitis

Diagnosis

Back 122

ERCP - endoscopic retrograde collandial npancreotography

• difficult procedure
  
• can cause pancreatitis
  
• scope goes through ampulla of vater in second part of duodenum

Usually do a MRCP - to see if there is a stone first

Front 123

GI: Acute pancreatitis

Signs and symptoms

Back 123

1-4 hrs after eating or consuming ETOH

SERIOUS DISEASE - take it seriously

N/V

Doubled over in pain! (if there is no pain, there is no pancreatitis)

Cullen's sign

Gray turner

Tonic bowel - doesn't move - no tone

Front 124

GI: Acute pancreatitis

What is Cullen's sign?

Back 124

bluish discoloration around umbilicus

due to pancreatic hemorrhage

Front 125

GI: Acute pancreatitis

What is Gray-Turner sign?

Back 125

ecchymosis in the flank

due to pancreatic hemorrhage

Front 126

GI: Acute pancreatitis

Diagnosis

Back 126

Hx and PE

increased amylase

increased lipase

Best first test is CT

some hospitals do MRI

volume depletion because of third spacing (pancreas releases excessive fluid, and b/c of vomiting

High Ca, but sometimes can be low due to saponification (you would replace Ca, check albumin too) - measure ionized Ca (you have to ask for it)

Front 127

GI: Acute pancreatitis

Treatment

Back 127

• start 2 IV lines
  
• NG tube - suction
  
• antiemetic meds (Zofran is best)
  
• propofol - "milk of amnesia" - short duration (gone, once stopped)
  
• fentanyl
  
• atomodate???? don't know what this was
  
• demerol
  
• Patients can get septic (before sepsis, you get SIRS)

Front 128

GI: Acute pancreatitis

Prognosis

Back 128

mild - better in a week

severe - poor prognosis (40% mortality)

Complication: pseudocyst formation (shows up on CT scan)

Front 129

GI: Acute pancreatitis

Key points

Back 129

Etiology

• ETOH
  
• Stones
  
• drugs
  
• trauma
  

SSx

• Severe pain - avoid morphine (may cause spasm in the sphincter of audi
  
• super high amylase and lipase
  

Dx

• Best first - CT or MRI
  
• Volume depleted by several liters
  
• If they get septic - risk of dying is high
  
• most will have SIRS
  
• WBC's will be elevated
  

Tx

• treat aggressively
  
• can get hypocalcemia - treat with calcium gluconate
  
• may have increased sugar
  

Complications

• pseudocysts - Best first is CT scan
  
• pseudocysts give persistent amylase elevation
  

Front 130

GI: Chronic pancreatitis

Etiology

Back 130

• ETOH!!!
  
• Cystic fibrosis
  

Front 131

GI: Chronic pancreatitis

Epidemiology

Back 131

less than 5% of alcoholics get this

Front 132

GI: Chronic pancreatitis

DDx

Back 132

Many diseases can mimic it

Front 133

GI: Chronic pancreatitis

Signs and symptoms

Back 133

• Similar to acute pancreatitis but diminished
  
• Pain radiates to the back
  
• many have glucose intolerance
  
• G/I diarrhea - fatty diarrhea
  

Front 134

Why do people with chronic pancreatitis produce fatty diarrhea?

Are these people over or under weight?

Back 134

• they are no longer producing lipoprotein lipase, therefore cannot digest fat
  

• They will be underweight because they cannot digest fat
  

• We get most of our fat calories from fat
  

Front 135

GI: Chronic pancreatitis

Diagnosis

Back 135

Triad

fatty diarrhea

diabetic (usually)

chronic calcification

Labs

Hard to predict - depends on level of chronicity

amylase and lipase - typically low - pancreas is not functioning

Front 136

GI: Chronic pancreatitis

Treatment

Back 136

Best first is to fix the underlying cause

• Stop ETOH
  
• Stop fatty food
  
• replace pancreatic enzymes
  
• narcotics for pain - minimal - make a contract with patients - watch for abuse - use MAPS
  
• avoid tylenol - liver is probably shot
  
• avoid NSAIDS - alcoholics often already have gastritis
  
• Diabetes - probably need insulin
  

Front 137

GI: Chronic pancreatitis

Prognosis

Back 137

with ETOH use: poor

mortality within 10 years

without ETOH: good

stopping prevents the progression of the disease

At risk for pancreatic CA

Front 138

GI: Pancreatic CA

Etiology

Back 138

• Majority is idiopathic
  
• smoking is a risk factor
  

the majority are in the head of the pancreas

Front 139

GI: Pancreatic CA

Epidemiology

Back 139

• #5 cause of mortality in the US
  
• Men > women even if you correct for ETOH
  
• AA > caucasian
  
• usually > 50 y/o
  

Front 140

GI: Pancreatic CA

Differential diagnosis

Back 140

any GI abnormality can present as pancreatic CA

Front 141

GI: Pancreatic CA

Signs and symptoms

Back 141

• insidious - slow onset - don't notice
  
• wt. loss
  
• fatigue
  
• diabetes
  
• pain that radiates to back (most patients don't have pain)
  

Most common- painless jaundice

--if patient starts with painless jaundice, they usually die within 6 weeks

Fatty diarrhea

--If patient starts with fatty diarrhea, they usually die within 1 year

Front 142

GI: Pancreatic CA

Diagnosis

Back 142

• very difficult
  
• tumor will not show in initial stages
  
• 90% are in advanced stages when they are caught
  
• Best first is CT scan - to catch small stuff in early stages
  
• US - ok for late stages
  
• Have to have a biopsy
  

Front 143

GI: Pancreatic CA

Treatment

Back 143

• If caught early - take it out
  
• Chemo/ radiation - can give patient a year
  
• opiates
  

Front 144

GI: Pancreatic CA

Prognosis

Back 144

very poor:

majority are caught in late stage disease

10% are caught early - good prognosis

5 year survival of all stages less than 2%

majority from 6 mos to 1 year (6mos is ave)

Front 145

GI: Pancreatic CA

Key points

Back 145

• painless jaundice
  
• 6 weeks median survival
  
• difficult to Dx
  
• most patients get diagnosed in late stages
  
• unexplained diarrhea
  

Front 146

GI: Portal Hypertension

Etiology

Back 146

Problem is with the portal vein

MCC is cirrhosis

Front 147

GI: Portal Hypertension

Epidemiology

Back 147

ETOH: <10% alcoholics get it

any disease that causes cirrhosis

Front 148

Which diseases cause cirrhosis?

Back 148

• ETOH abuse
  
• Wilson's disease
  
• alpha-1 antitrypsin deficiency
  
• non-alchololic fatty liver
  

Front 149

GI: Portal Hypertension

Signs and Symptoms

Back 149

• Caput medusa
  
• fatigue
• spider angioma
• ascites
  
• gynecomastia (men)
• hemorrhoids
• esophageal varices
• asterixis (flapping tremors)
• hepatomegaly
• splenomegaly
• AMS - b/c ammonia is high
• jaundice - b/c of increased bilirubin
• lipid profile will be good - b/c they cannot digest fats
• blood sugar will be abnormal

Front 150

What are the the three sites of portal caval anastomosis (portal systemic anastomosis)?

Back 150

esophagus

umbilicus

rectum

Front 151

GI: Portal Hypertension

Diagnosis

Back 151

History

Physical Exam

Ultrasound or CT of abdomen

If ascites: can aspirate fluid and send for analysis

Front 152

GI: Portal Hypertension

Complications

Back 152

• Ascites - can lead to peritonitis
  
• shock
  
• hepato-renal syndrome
  
• esophageal varices
  

Front 153

GI: Portal Hypertension

Treatment

Back 153

Fix the underlying cause

Fix acute issues

• ascites - drain
  
• varices -
• decreased protein/albumin - increase
• increased bilirubin
• clotting issues - fresh frozen plasma

Front 154

GI: Portal Hypertension

Prognosis

Back 154

Esophageal varices: mortality > 50%

Shock

Hepato-Renal syndrome

Front 155

What is hepatic-renal syndrome?

Back 155

liver and kidneys shut down

patient gets super jaundiced

Front 156

GI: Portal Hypertension

Key

Back 156

Most common cause = cirrhosis

diagnosis is made on PE

prognosis is poor

infections: septic, SIRS, etc.

-but in the end, they die from hepatio-renal syndrome

Front 157

GI: Cirrhosis of the Liver

Etiology

Back 157

• Fibrosis/scarring of the liver
  
• irreversible destruction of the liver architecture
  

Front 158

GI: Cirrhosis of the Liver

Epidemiology

Back 158

• MCC is ETOH abuse
  
• CF
  
• Hemochromatosis
  
• Wilson's Disease
  
• Fatty Liver
  
• Alpha 1 antitrypsin deficiency
  

Front 159

GI: Cirrhosis of the Liver

Signs/ symptoms

Back 159

• decreased liver size (end stage)
  
• liver is full of nodules
  
• hepatic encephalopathy du to elevated ammonia levels (once ammonia levels rise, pt needs to stop driving)
  

Front 160

GI: Cirrhosis of the Liver

Diagnosis

Back 160

• Hx and PE
  
• US or CT
  
• Biopsy for definitive Dx
  
• decreased albumin
  
• decreased lipids
  
• increased BUN
  
• third spacing
  

Front 161

GI: Cirrhosis of the Liver

at risk for...

Back 161

hepatocellular carcinoma

Front 162

GI: Cirrhosis of the Liver

Treatment

Back 162

• will see in hospital/ ICU - not necessarily outpatient (frequent hospitalizations due to bleeding, confusion, electrolyte abnormalities)
  
• Treat underlying cause
  
• stop ETOH intake no matter cause - to reduce further damage (every drink causes liver damage)
  
• If ammonia is high - treat with meds (lactolose)
  

Front 163

GI: Cirrhosis of the Liver

Prognosis/ complications

Back 163

• 75% will get esophageal varices and hemorrhoids
  
• Once they get a complication, the prognosis is poor (they won't make it a year)
  

Complications

• Acites
  
• Varices
  
• Bleeding
  
• Encephalopathy
  

Front 164

GI: Cirrhosis of the Liver

Key points

Back 164

• Stop ETOH
  
• If ammonia level is high - no driving (you are liable if they drive and you did not warn them)
  
• with any complication, prognosis is poor (less than a year)
  

Front 165

GI: Budd-Chiari Syndrome

Etiology

Back 165

• Thrombosis of hepatic vein
  
• Acute process - not slow (1 week)
  

Front 166

GI: Budd-Chiari Syndrome

Epdimeology

Back 166

Risk Factors: (same population who get DVT's)

• post-pregnancy (hypercoaguable)
  
• oral contraceptives (OCP"S)
  
• any hypercoaguable condition
  

Front 167

GI: Budd-Chiari Syndrome

Signs/ symptoms

Back 167

100% have acites and hepatomegaly

all the symptoms of portal hypertension, but acute, not chronic

• hemorrhoids
  
• RUQ pain
  
• jaundice
  

Front 168

GI: Budd-Chiari Syndrome

Diagnosis

Back 168

• Angiography - GOLD STANDARD
  
• CT - good 1st line
  
• MRI - good but not needed
  
• increased liver enzymes
  

Front 169

GI: Budd-Chiari Syndrome

Treatment

Back 169

• Usually go to specialty clinic for this
  
• anticoagulation therapy (TPA for any condition where pt is hemodynamically unstable)
  

Front 170

GI: Budd-Chiari Syndrome

Prognosis

Back 170

Good if anticoagulation is successful

poor if not successful

Front 171

GI: Budd-Chiari Syndrome

Key points

Back 171

• usually acute presentation
  
• MCC: hypercoaguable states

--post-pregnancy
--OCP use

Front 172

GI: Liver Abcess

Etiology

Back 172

• Usually water borne illness
  
• amoebas (Amoebiasis)
  

Front 173

GI: Liver Abcess

Epidemiology

Back 173

• Rare in the US
  
• Common in parts of the world with poor water quality/ poor sanitary conditions
  

Front 174

GI: Liver Abcess

Signs and Symptoms

Back 174

• intense RUQ pain
  
• fever
  
• chills
  
• night sweats
  

Front 175

GI: Liver Abcess

Diagnosis

Back 175

increased WBC's > 15,000

blood test - antiamoebic antibodies

US - 1st best test to see access

CT

Aspirate access and culture for definitive Dx

Front 176

GI: Liver Abcess

Treatment

Back 176

metronidazole (Flagyl)

Front 177

GI: Liver Abcess

Prognosis

Back 177

• very good
  
• will respond within 72 hrs with Flagyl (2 week Tx)
  

Front 178

GI: Liver Abcess

Key points

Back 178

Rare in Us

prevalent in countries with poor sanitation

Best 1st test is US

Responds within 72 hrs of ABX (Flagyl)

Front 179

GI: Cholecystitis

Etiology

Back 179

Inflammation of the gall bladder

Stones

Front 180

GI: Cholecystitis

Epidemiology

Back 180

• Fat
  
• Female
  
• Forty
  
• Fertile (>females who have had many children, also OCP use)
  
• Rapid weight loss (predisposes them to gall stones)
  
• hyperlipidemia
• Native Americans
  
• use of Ali - blocks lipoprotein lipase
  
• Diabetics (if they have a stone, you have to take it out)
  

Front 181

GI: Cholecystitis

Signs and symptoms

Back 181

• RUQ pain - radiates to back
  
• Murphy's sign (positive if inhalation is interrupted)
  
• N/V
  
• Jaundice
  

Front 182

GI: Cholecystitis

Diagnosis

Back 182

• Hx & PE
  
• US - Best 1st test
  
• CT - less accurate, more $$, has more false pos.
  
• increased WBC's
  
• liver enzymes affected
  

Front 183

GI: Cholecystitis

Treatment

Back 183

• lap cholecystectomy
  
• ERCP (Endoscopic retrograde cholangiopancreatography) where they go in and get the stone
  

Front 184

GI: Cholecystitis

prognosis

Back 184

very good

Front 185

GI: Cholecystitis

Sludge

Back 185

• Some pts don't get stones, they get sludge
  
• Sludge can precede stones
  
• shrinks the size of the GB
  
• can lead to cholecystitis
  

Front 186

GI: Cholecystitis

Sludge : CCK

Back 186

• Cholecystic Kinase (CCK) is released when fatty foods are ingested
  
• Causes contraction of the GB to release bile
  
• Sludge prevents the contraction
  

Hida Scan- measures ejection fraction of GB

isotope is ingested and a picture is taken

Front 187

GI: Cholecystitis

Key points

Back 187

• numerous risk factors
  
• young people can get it
  
• look for it if pt has sickle cell anemia
  
• compromised hose - take stones out
  
• many pts have stones and are asymptomatic
  

Front 188

GI: Crohn's Disease

Etiology

Back 188

• Granulomatous disease (similar to TB)
  

-granuloma formation is a defense mechanism

-granulomas are formed in response to an unknown factor

• affects GI tract anywhere, but usually in the ileum
  
• Produces a skip lesion (areas where there are no granulomas)
  

Front 189

GI: Crohn's Disease

Epidemiology

Back 189

• Females > males
  
• bimodal age distribution
  

20-40

>50

Front 190

GI: Crohn's Disease

Differential Diagnosis

Back 190

Ulcerative colitis

the whole region would be affected - no skip regions as in crohn's disease

Front 191

GI: Crohn's Disease

Signs and symptoms

Back 191

• Abdominal pain
  
• fever
  
• weight loss
  
• diarrhea - bloody, but not as bad as ulcerative colitis
  
• GI - very emaciated b/c of diarrhea
  
• if they have a high BMI, it is not crohn's (b/c they have malabsorption due to diarrhea)
  
• Erythema nodosum - Rash on lower extremities (red, circular, tender) (typical of TB, sarcoidosis, crohn's)
  

Front 192

GI: Crohn's Disease

Diagnosis

Back 192

• Hx
  
• biopsy (endoscopy with biopsy)
  
• no lab test for Dx
  
• diagnose and refer to GI doc
  

Front 193

GI: Crohn's Disease

Treatment

Back 193

• Sulfasalazine (PO, rectal enema)
  
• Steroids - for acute conditions
  
• must be on an anti-inflam (sulfasalazine or others)
  
• it is a cyclic disease (has flares)
  
• in ED give IV prednisone
  
• Tumor necrosis factor (Humira)(if anti inflammatory meds fail) -risk of TB, CA, infections
  
• surgery - if bad
  
• need B12 vitamin
  

Front 194

GI: Crohn's Disease

Prognosis

Back 194

Recurrence rate is very high (3 years tops for remission)

increased risk for CA

Front 195

GI: Crohn's Disease

Key points

Back 195

usually bimodal age distribution

appears to be autoimmune disease

similar to TB

skip lesions formed

need B12

steroids for acute flare

TNF

anti-inflammatory meds

Front 196

Random fact

3 areas of hypertension

Back 196

1. portal
   
2. intracranial
   
3. systemic
   

hypertension = resistance to flow

Front 197

Random fact

Mechanism of Alli

Back 197

Blocks lipoprotein lipase (enzyme that breaks down fat)

long term use leads to colon CA

Front 198

Random fact

Drugs that reduce incidence of colon CA

Back 198

statins reduce colon CA incidence by at least 40%

baby aspirin

Front 199

Random fact

3 places medications are metabolized

Back 199

• liver
  
• kidney
  
• plasma
  

Front 200

Random fact

How much ETOH is safe?

Back 200

• each drink has 14 grams ETOH
  
• 2 drinks a day is OK
  
• excess for females is 40-60 grams
  
• excess for males is 30-40 grams
  

Front 201

Random fact

Affect of Tylenol poisoning on liver enzymes

Back 201

super high liver enzymes

Front 202

Random fact

most primitive part of brain

Back 202

Basal ganglia - responsible for habits

In a stressed situation cognitive function decreases by 50% b/c it is not in the basal ganglia

Front 203

Random fact

how does AA work to change behavior

Back 203

behavior change is a three step process

1. Que - trigger
   
2. Process - need to change this part for any addiction
   
3. Reward
   

Front 204

GI: Ischemic Bowel Disease

Etiology

Back 204

• colitis caused by lack of blood flow (ischemia) in the colon usually an arterial disease (mesenteric artery)
  
• usually due to atherosclerosis
  
• Atrial fibrillation can also throw clots to bowel and cause this
  
• ischemia = imbalance between blood supply and demand
  

Front 205

GI: Ischemic Bowel Disease

Epidemiology

Back 205

elderly patients with atherosclerosis

patients with a-fib

Front 206

GI: Ischemic Bowel Disease

Differential diagnosis

Back 206

• bowel obstruction
  
• crohn's
  
• ulcerative colitis
  
• diverticulitis
  

Front 207

GI: Ischemic Bowel Disease

Signs and symptoms

Back 207

• left lower quadrant pain
  
• diarrhea
  
• pain gets worse after eating so patients lose weight b/c they eat less to avoid pain
  
• pain is out of proportion to physical findings (PE reveals minimal findings but pain is SEVERE)
  

Front 208

GI: Ischemic Bowel Disease

Diagnosis

Back 208

• CT with contrast - best with good Hx
  
• know risk factors (elderly, a-fib, etc.)
  
• Lactate will be elevated - b/c they will go into anaerobic metabolism
  
• Amylase is elevated (any intra-abdominal process elevates amylase)
  

Front 209

GI: Ischemic Bowel Disease

Treatment

Back 209

• bowel rest (no food, etc.)
  
• IV fluids
  
• nitroglycerin helps
  
• becomes a surgical problem after acute presentation
  
• fix underlying problem (things causing their atherosclerosis, etc.)
  
• colectomy
  

If acute presentation = usually caused by embolus

If chronic presentation = usually caused by atherosclerosis

Front 210

GI: Ischemic Bowel Disease

Prognosis

Back 210

can get fibrosis and strictures leading to bowel obstruction

50% get better with treatment of underlying causes

if perforation of bowel occurs, it leads to peritonitis (presents with distended, rigid abdomen) and is life threatening

Front 211

GI: Ischemic Bowel Disease

Key points

Back 211

• same process as atherosclerosis in heart
  
• post prandial pain causes wt loss
  
• pain out of proportion to the PE
  
• LLQ pain similar to diverticulitis
  
• life threatening complication: perforation of the bowel leading to peritonitis
  

Front 212

GI: Ulcerative Colitis

Etiology

Back 212

• Chronic relapsing disease of the rectum and colon
  
• may by autoimmune
  
• has genetic and infectious components
  
• no granulomas
  
• no skip lesions present
  
• small bowel not involved (only rectum and colon)
  

Note: Crohn's can be anywhere in the GI tract, has granulomas and skip lesions

Front 213

GI: Ulcerative Colitis

Epidemiology

Back 213

• Male > Female
  
• There is a family history risk (1st deg. relative = 10x more likely to get UC)
  
• bimodal age distribution: peaks at 30-35 & 50-65
  
• Incidence is low in AA and very high in jewish populations
  

Front 214

GI: Ulcerative Colitis

Differential Diagnosis

Back 214

• Crohn's
  
• diverticulitis
  
• infectious colitis
  

Front 215

GI: Ulcerative Colitis

Signs and Symptoms

Back 215

• Bloody diarrhea
  
• lower abdominal cramping that gets better with defecation
  
• rectum is almost always involved
  

Front 216

GI: Ulcerative Colitis

Diagnosis

Back 216

need tissue biopsy via colonoscopy

(BEST 1st TEST)

Front 217

GI: Ulcerative Colitis

Treatment

Back 217

• sulfasalazine - anti-inflammatory - causes remission in 50% of patients
  
• hydrocortisone enema - steroid enema
  
• tumor necrosis factor - in some difficult to treat cases
  
• admit to hospital if bloody diarrhea is severe for bowel rest, fluids and steroids
  
• if very bad, may need colectomy (removal of part of colon) - 1/3 of patients get a colectomy
  

Front 218

GI: Ulcerative Colitis

Prognosis

Back 218

• increased risk of colon cancer
  
• need annual colonoscopies once diagnosed
  
• smokers are at decreased risk for UC (helps heal lesions)
  
• nicotine patch therapy may be useful to treat UC
  

Front 219

GI: Ulcerative Colitis

Key points

Back 219

• bimodal age distribution
  
• autoimmune, genetic, infectious etiologies
  
• bloody diarrhea
  
• 1/3 get colonectomies
  
• increased risk of colon cancer
  
• annual colonoscopy
  
• responds to sulfasalazine
  

Front 220

GI: Diverticular Disease

Etiology

Back 220

A diverticulum is an out-pouching of the intestinal wall due to weakening. (can also get it in the esophagus)

Diverticulosis:

• the process of out-pouching
  
• usually asymptomatic
  

Diverticulitis:

• inflammation of the out-pouching
  
• infection also of the diverticula
  
• causes small tears in vessels and a diverticular bleed
  
• caused by genetics or poor diet (low fiber, big fatty meals, constipation)
  

Front 221

GI: Diverticular Disease

Differential Diagnosis

Back 221

Crohn's

Ulcerative colitis

Front 222

GI: Diverticular Disease

Signs and Symptoms

Back 222

Diverticulosis

• asymptomatic
  
• alternating diarrhea and constipation
  
• feels better after a bowel movement
  

Diverticulitis

• infection and inflammation causes LLQ pain
  
• possible palpable mass in LLQ
  
• fever
  
• increased WBC's
  

Diverticular Bleed

• painless bleed
  
• can co-exist with diverticulitis and does frequently (presents together with lots of bleeding - SERIOUS!)
  

Front 223

GI: Diverticular Disease

Diagnosis

Back 223

Hx & PE

CT - 1st best imaging study

colonoscopy

• if it is only a pure diverticular bleed
  
• cannot do if they have diverticulitis with it
  
• cannot do if acutely ill (have to wait till it calms down with bowel rest, antibiotics, etc.)
  

Front 224

GI: Diverticular Disease

Treatment

Back 224

Diverticulosis

• high fiber diet (25g)
  
• Metamucil
  
• fruits and veggies
  

Diverticulitis

• bowel rest (no food)
  
• admit to hospital for this
  
• pain meds
  
• IV fluids (D5 normal saline)
  
• Antibiotics! to cover gm negatives and anaerobes (ex: copra + metronidazole or 2nd generation cephalosporin)
  

Diverticular Bleed

• stabilize patient!
  
• fluids
  
• type and crosslink blood
  
• maintain vital signs
  
• isolate source of bleed using angiography, colonoscopy or tagged RBC's