GI Block 2 Flashcards
Flexible Sigmoidoscope
Bedside transverse to descending colon and left colon.
Prep = enema (small amount)
Which is 85% of cancer
Colonoscopy
Gold standard to ID and TREAT
Prep = 8 hours prior w/ 1 gallon PEG (GOLYTE)
Virtual colonoscopy (CT colonography)
“Visual Only” - no prep
Indication for = Failed colonoscopy
Rigid sigmoidoscope
=rectum view
Anoscope
= anal view
Think hemorrhoids
Do ABX Associated Colitis patients experience diarrhea
Patients frequently experience diarrhea as a side effect of antibiotic administration
Due to alterations in colonic flora
This diarrhea is mild and self-limited
Colitis is an effect of what infection
C diff
Symptoms of ABX Associated colitis
Mild diarrhea to fulminant disease with mega colon
ABX associated colitis mode of infection
ABX disrupt normal bowel flora and allow c diff to flourish in the colon
Signs and symptoms of mild to moderate ABX Associated colitis
Mil to moderate diarrhea
- fever
- crampy abdominal pain
- decreased appetite
- malaise
Leukocytosis @ 15,000
ABX Associated colitis severe disease main signs and symptoms
- severe abdominal pain
- abdominal distention
- fever
- hypovolemia
- lactic acidosis
- hypoalbuminemia
- Leukocytosis >15,000
Criteria for ABX associated colitis Fulminant Dz
ADMIT TO ICU
- Hypotension severe
- Shock (w/ progression multi system organ failure)
- Fever greater than 101.3 F
- Ileus or significant abdominal distention/pain
- Megacolon >7cm diam (risk bowel perforation)
- WBC greater than 35,000
- Serum lactate levels > 2.2 mmol/L
ABX associated psuedomembranous colitis
Pseudo membrane on mucosal surface of bowel from severe inflammation ; raised yellow or off-white plaques up to 2 cm scattered
ABX associated colitis stool studies recommendation
hosp patients w/ ≥3 liquid stools w/in 24 hrs or outpatients w/ persistent diarrhea >1 week
ABX associated colitis tests and STUDY OF CONFIRMATION
Polymerase Chain Reaction (PCR) – study of choice = used in combo to confirm c diff
Immunoassay for glutamate dehydrogenase (GDH) = presence of C diff
Toxin Rapid Enzyme Immunoassays (EIAs) – confirmatory test to distinguish active toxin infection from colonization = detects presence of toxins [think c diff A and B test]
When is radiographic imaging warranted for ABX associated colitis
patients with clinical manifestations of severe disease or fulminant colitis
EVALS for : megacolon bowel perforation and surgical interventions
Preferred imaging for ABX associated colitis
CT of ABD and Pelvis
What is the radio sign of thickened colonic walls associated with mucosal damage from ABX associated colitis
Thumb printing
From C diff toxin
Main complication from fulminant disease
Toxic megacolon
What is treatment for nonfulimnat ABX Associated Colitis
Vancomycin PO
Fidaoxamycin
What colon diameter qualifies as a megacolon
7 cm
What symptoms do you suspect with toxic megacolon
Abdominal distention and diarrhea
Over 7cm
Is toxic colitis or acute toxic colitis obstructive
No and TOXICITY IS SYSTEMIC
What complication is most often associated with Ulcerative colitis
Toxic megacolon
IBD as well
Diagnostic criteria for toxic megacolon
Radio graph evidence
More than 7cm
[Atleast 3] Fever Pulse > 120 bpm Leukocytosis>10.5 Anemia
[Atleast 1] Dehydration Altered mental status Electrolyte Hypotension
Treatment for toxic megacolon
- Bowel rest and decompression
- IV fluids and electrolyte
- Treat toxemia and precipitating factors
- Surgical consult
Characteristics of colonic diverticula
Most ASX
LEFT QUAD pain sigmoid and descending
Constipation
Vary in size and number
Where are colonic diverticula normally
Sigmoid and descending colon
Pathogenesis related to increased intraluminal pressure in colonic diverticula
Low fiber
Insufficient water intake
Treatment recommendations for diverticulosis
Non specific treatment or further necessary
Recommend increased dietary fiber and water
Characteristics of diverticula bleeding
Painless, gross hematochezia
- bright red blood (squirts into the toilet)
- no other symptoms
Patients with active diverticula bleed get what?
Resuscitation and stabilization FIRST
Then Endoscope
Patients with non active diverticular bleed will receive referral for what?
Scope
How do patients with diverticulitis present
ABD pain and TTP @ LLQ (sometimes with a mass)
Fever
N/V
Lab findings with diverticulitis
Leukocytosis on CBC
+/- stool occult blood
What diagnostic imaging is warranted for diverticulitis?
ABD CT only
Diverticular bleeding is characterized as
Bright red blood w/ squirting after bowel movements
Typically no other symptoms
Patients present with what for diverticulitis
ABD pain and LLQ tenderness
Fever
N/V
What type of meds are indicated for mild diverticulitis
Oral broad spectrum ABX
Metronidazole + [Ciprofloxacin OR TMP/SMX DS]
Alternate = Augmentin
7-10 day course
outpatient management
What type of diet is req’d for mild diverticulitis treatment
Clear liquid diet
Treatment of severe diverticulitis
NPO
IV Broad ABX
IV Fluid and electrolyte replacement
IV Pain management
Surgical Consult
Potential complications of diverticulitis
Perforation
Abscess Forms
Fistulization
Obstruction
If your pt fails to improve on ABX regimen when treating diverticulitis what should you do
Suspect abscess Obtain CT (if complications could arise)
What is the order of acute colonic pseudo-obstruction
Hypomotility → gas accumulation → progressive dilation → possible perforation
Who is most common to be diagnosed with acute colonic pseudo obstruction
Postsurgical
Following trauma
Medical inpatients (respiratory failure, MI, CHF)
Signs and symptoms of acute colonic pseudo
Abdominal distension
Abdominal pain
Nausea & vomiting
What do plain films vs CT show for acute colonic pseudo obstruction
Plain films = colonic dilation ; usually cecum and right hemicolon
CT = rules out mechanical obstruction
Management steps in treatment for acute colonic pseudo obstruction
Consult with GI and or/ surgery
Where is volvulus most common
Sigmoid colon
Most common causes of sigmoid volvulus
Chronic constipation
Excessive use of laxatives
Excessive use of fiber
Chagas’ disease
OVER THE AGE OF 50
Presentation of sigmoid volvulus
N/V
ABD distention
Vomiting
Constipation
Physical exam of sigmoid volvulus
Distended abdomen with tympany to percussion
Tenderness to palpation
Treatment for sigmoid volvulus
Detersion via flexible sigmoidoscopy
Four major pathologic groups of colonic polyps
Mucosal Adenomatous
Mucosal Serrated
Mucosal Non-Neoplastic
Submucosal Lesions
What are the most common colonic polyps
Sporadic
Describe Adenomatous polyps
Most common 70 %
Tubular Tubulovillous Villous
Dysplastic
Hyperplastic extremely common low risk polyp
Serrated
Sessile polyps are greater risk of what
Adenomas
Juvenile polyps, hamartomas, inflammatory polyps – increased risk of cancer
Mucosal non neoplastic
Lipomas, lymphoid aggregates - no clinical significance
Pneumatosis cystoides intestinalis – air filled cysts
Carcinoid tumor - cancer
Submucosal lesions
When do polyps develop / colon cancer develop in hereditary colorectal polyposis syndrome
Polyps = 15 yrs old
Colon cancer = 40-50 yrs old
Requires genetic testing
Treatment chronologically for hereditary polyposis syndrome
Prophylactic colectomy, typically before age 20
Annual colonoscopy until colectomy
Three different hamartomatous polyposis syndromes
Peutz-Jeghers syndrome
Familial Juvenile Polyposis
Cowden disease
Common risk factors for colorectal cancer
Age [ above 45 yrs old ]
Family history
IBD
Dietary and Lifestyle Factors
Typical growth of colorectal cancer
Slow growing
What are the three types of tests for colorectal cancer screening
Stool based tests
Endoscopy tests
Radiographic tests
How does the fecal immuno chemical test and what does it detect
Uses antibodies to detect blood in stool
ANNUALLY [gFOBT is also ANNUAL]
Explain the FIT-DNA test and how often is it required
Combines the FIT with a test that detects altered DNA (cancer cells) in the stool
Every three years
What is the use of CEA antigen testing
Prognosis AFTER. Diagnosis
-marker of recurrence
Describe a colonoscopy
Visualization of entire colon
Detects cancer
Able to remove polyps
Requires full bowel prep and sedation
Describe a flexible sigmoidoscopy
Ever 5 yrs
Visualize retrosigmoid and descending colon
Laxative bowel prep
[CAN NOT REMOVE POLYPS]
CT. Colonography (visual)
Every 5 yrs
Less sensitive for polyps less than 1 cm
Light bowel prep no sedation
How often would one receive capsule colonoscopy
Every 5 yrs
Age of the average risk colorectal patient
45 and up
If pt has family members positive for colorectal cancer at what age and how often should they receive colonoscopy
Age 40
Every 5 years
Right colon symptoms of colorectal cancer
Iron deficiency anemia
Weakness or fatigue
Left colon signs and symptoms
Change in bowel habits
Stool streaked with blood
Obstructive symptoms
Constipation alternating with increased
stool frequency and loose stool
Colicky abdominal pain
Rectum signs and symptoms of colorectal cancer
Hematochezia
Tenesmus
Urgency
Decrease in caliber of stool (“ribbon stool”)
Signs of advanced or metastatic disease
Complete obstruction = ‘apple core lesion’
Weight loss
Fever, chill, night sweats
Work up for colorectal cancer
FOBT ( Guaiac or FiT)
CBC
CMP
UA
Colonoscopy
Stages of colorectal cancer
Stage I - Stage II - Stage III - Stage III - Stage IV -
Stage I - greater than 90%
Stage II – 70 - 85%
Stage III with < 4 positive lymph nodes - 67%
Stage III with > 4 positive lymph nodes - 33%
Stage IV – 5 -7%.
Hallmark symptoms of croons
ABD pain
Diarrhea with or with out blood
Fatigue
Fever
Growth failure
Terminal ileum ileitis
Small bowel Chrons disease
Ileocolitis
MOST COMMON
Small bowel + colon Crohn’s disease
What 2 classic signs do most crohns dz patients present with
Non penetrating colitis
Non-stricture disease
With further possible complications
What are the main complication risks in Crohn’s disease
May result in mucosal inflammation and ulceration, stricturing (obstruction), fistula development, and abscess formation
Symptoms from common intestinal obstruction complications of CD
Postprandial bloating
Cramping abdominal pain
Loud borborygmi
Penetrating disease and fistulization general pathology
Transmural bowel inflammation is associated with the development of sinus tracts
What does penetration of the bowel wall by sinus tract present as?
Phlegmon
Common sites for fistulas
Bladder [ENTEROVESICAL]
Skin [ENTEROCUTANEOUS]
Small bowel [ENTEROENTERIC]
Vagina [ENTEROVAGINAL]
FISTULA from recurrent UTI’s and pneumaturia
ENTEROVESICAL
Fistula that causes bowel contents to drain to the surface of the skin
ENTEROCUTANEOUS
Fistulas that may be aSX or present as a palpable mass
ENTEROENTERIC
Fistulas that pass as or feces through the vagina
ENTEROVAGINAL
What can a fistula of the retroperitoneum cause
Papas abscess or uretal obstruction
Hydronephrsosis
Perinatal disease anal fistula location
Lateral
Two extrainstestinal manifestations common in CD
Arhralgias or arthritis
Iritis or uveitis
What tests are elevated in lab testing Crohn inflammation
ESR
And
CRP
What is treatment for recurrent nonfulimnant ABX colitis disease
First = vancomycin for another 10 days
fidaxcomycin (if not used previously)
What is treatment for recurrent nonfulimnant subsequent ABX colitis disease
Vancomycin taper (2-3 months)
Vancomycin 10 days then Rifaxmin for 20 days
Fecal Transplant if more than 3 occurrences
What is treatment for fulminant ABX colitis disease
Vancomyicin PO
Metronidazole IV
Vancomycin PR
SEVERE = colectomy surgical consult*
What fecal lab tests are available in CD
Stool culture and O and P
C diff testing
Fecal lactoferrin
What establishes the diagnosis for CD
Endoscopy
What can periodic endoscopy help assess
Under or over treating with medications
What does endoscopy of CD measure
Disease and active inflammation
What is used to evaluate strictures, fistulas, and ulcerations in Cd work up?
Barium upper GI series
If small bowel involvement detected in Cd what do you use to evaluate
Capsule endoscopy
What are the 4 different callsifications of CD
ASX
Mild-moderate
Moderate-Severe
Severe/Fulminant
Key diagnosis of mild to moderate CD
Ambulatory
normal eating and drinking
ENDOSCOPE LESIONS WHICH ARE NOT SEVERE
Moderate to severe CD presents as what?
Fever
Failed mild-mod treatment
Significant anemia
N/V without obstruction
ENDOSCOPE will see mod to severe active mucosal disease
Presentation of severe/fulminant disease
Significant weight loss
Persistent symptoms
High fever
ENDOSCOPY = severe mucosal disease
Controlling inflammation (induction) helps control what?
Symptoms
What are NSAIDs associated with in CD
Flares
Causes damage to small intestinal mucosa
Symptomatic treatment for CD
Antidiarrheals
Loperamide
Bile Acid Sequestrant = if terminal ileum involved
What med is given for authors ulcers associated with CD
Oral steroid
Kenalog in orabase (triamcinolone oral prep)
Mild to mod CD treatment =
Non systemic corticosteroid = Budesonide
Systemic Corticosteroid = Prednisone FOR FLARE TREATMENT
HIGH RISK = 5 ASA (Sulfasalazine)
Moderate to Severe CD treatment
Prednisone (oral)
Until resumption of weight gain and resolution of symptoms (7-28)
LONG TERM SIDE EFFECTS
If CD patients fail to respond to oral medications what should be considered
Hospitalization
What is the best maintenance therapy for CD?
Immunomodulators
Azathioprine
6-Mercaptopurine
Methotrexate
What is the best biological therapy to induce remission in mod to severe Crohn disease
Anti tumor Necrosis Factor
Infliximab
Adalimumab
Certolizumab
What is the most common surgical indication in CD
Resection of a segment of diseased intestine
What type of symptoms would qualify as admission criteria for CD
Obstruction
Infectious complications
Severe symptoms of diarrhea, dehydration, weight loss, or abdominal pain
What kind of condition is ulcerative colitis
Idiopathic with diffuse friability, erosions, and bleeding
What is the limit of UC
Mucosal layer
What is the Montreal classification of UC
Proctitis
Left sided colitis
Extensive colitis
What are common characteristics of UC
Exacerbations with periods of remission
UC has a significant risk for what?
Toxic Megacolon
Proctitis
Proctosigmoiditis
Distal colitis
Extensive colitis
Pancolitis
Rectum Mostly
Sigmoid and Rectum (but not up to transverse
Distal to transverse
Transverse + Sigmoid
Entire Colon
Hallmark sign of UC are what 2 things?
Bloody Diarrhea
Tenesmus
What is the fever temperature for moderate UC vs Severe
99-100
Over 100
Mild to Moderate UC clinical presentation
Gradual diarrhea onset w/ BLOOD and MUCUS
Fecal urgency
Tenesmus
LLQ pain (relieved by defecation)
Sever UC Clinical presentation
More than6 bloody bowel movements
Hypovolemia
Anemia
Hypoalbuminemia
LLQ pain
TTP on exam
Describe bowel movements in UC
Frequent and small in volume as a result of rectal inflammation
Common work up exam of UC
Volume status
Nutritional status
Abdominal tenderness
DRE = evidence of BRB
What helps differentiate IBD form IBS
Fecal leukocytes
With UC lab testing also be sure to test for what?
STI’s
What type of endoscopy is best for UC
Flexible sigmoidoscopy
What are biopsy features suggest UC
Crypt abscess
Crypt branching
Shortening and disarray
Crypt atrophy
Main difference in treatment for UC
5 ASA agents as mainstay of treatment
Ulcerative Proctitis treatment
Topical mesalamine (5-ASA ) = drug of choice
4-12 weeks
Suppository or enema
Ulcerative Proctitis treatment if topical 5 ASA is contrained
Topical hydrocortisone
If can not use this use oral mesalamine
Distal colitis treatment recommendations
Topical mesalamine
Topical corticosteroids
5 ASA
Mild to moderate distal colitis refractory treatment
Co therapy with oral and topical 5 ASA
Topical corticosteroid
Add prednisone if symptoms persist
If a distal colitis patient has frequent relapse what do you give them
Topical mesalamine if tolerable then by mouth if not
Mild to moderate extensive colitis treatment
Oral and Rectal 5-ASA for 4-8 weeks
Mesalamine
Sulfasalazine w/ folic acid [highest side effect profile]
If no improvement of extensive mild to mod colitis on oral and rectal treatment what do you add?
Oral corticosteroid
Prednisone or Methylpredinsolone
Mod to severe colitis treatment
Oral corticosteroid = first line
Treat 14 days then reevaluate
If oral steroid does not improve mod to severe colitis what do you do
Give immunomodulator
Anti TNF’s = INFLIXIMAB ; ADALIMUMAB ; GOLIMUMAB
Anti-integrin therapy = VEDOLIZUMAB
SEVERE fulminant pancolitis disease treatment
Inpatient care
Surgical consultation early
NPO
Parenteral fluid/electrolyte replacement
IV corticosteroids
What is important for treatment of UC
Long term therapy to prevent relapse
Oral mesalamine = daily administration
For UC in patients with more than 2 relapses in a year what two meds are indicated
Mercaptopurine
Azathioprine
How many years after diagnosis require colonoscopy biopsy ever 1-2 years?
8 years
What are absolute surgical indications for UC
Severe hemorrhage
Perforation
Carcinoma finding
What UC patient presentation requires admission
Severe disease manifested by anemia, eight loss and fever
Fulminant disease manifested by abdominal pain, distention, fever, tachycardia
How do you diagnose microscopic colitis
Diagnosis established by histopathologic examination of biopsy specimen
Two subtypes of microscopic colitis
Lymphocytic colitis – intraepithelial lymphocytic infiltrate
Collagenous colitis – colonic subepithelial collagen band >10 micrometers in thickness
What colonic subepithelial thickness is indicative of collagenous colitis
10 micro meters
Risk factors for microscopic colitis
Female
Certain meds = NSAIDs , SSRI’S, Lansoprasole, Lisinopril, Simvastatin
Clinical presentation of micro colitis
Chronic non bloody watery diarrhea
ABD pain
Fatigue
What test is diagnostic for micro colitis
Colonoscopy with biopsy
Treatment for micro colitis
Discontinue meds if necessary
Symptomatic care = Anitdiarrheals
Persistent mico colitis treatment =
Budesonide x 4 weeks
What type of syndrome is IBS
Idiopathic altered bowel habit in the absence of any organic cause
“Functional bowel disorder”
What bio markers or confirmatory tests can diagnose IBS
NONE
based on symptom criteria
What are 5 possible etiologies of IBS
Abnormal motility Visceral hypersensitivity Intestinal inflammation Enteric infection Psychosocial abnormalities
IBS is most commonly diagnosed after an episode of what?
Bacterial gastroenteritis
IBS sings and symptoms
Crampy abdominal pain
Change in stool freq and form
Feeling of bloating
What is the name of the fecal type chart to categorize stool
Bristol Stool Chart
Classify IBS-C and IBS-D
Consitpation vs Diarrhea
Somatic / psychological complications of IBS
Dyspepsia
Heartburn
Myalgias
Gynecological symptoms
Urolological symptoms
Anxiety/Depression
What atypical symptoms (3) and lab abnormalities (3) in consistent with IBS
Rectal bleeding
Nocturnal abdominal pain
Weight loss
Anemia
Inflammation markers
Electrolyte disturbances
What type of condition is IBS
Chronic - long standing
What medical abnormalities should you ask about for a possible IBS diagnosis
GI neoplasm IBD Hyper/hypothyroidism Malabsorption syndromes Psychiatric disorders
FAMILY HISTORY
What questions should be asked about lifestyle changes when diagnosing IBS
Medication diet or exercise change
What is a lifestyle questions that should be asked to diagnose IBS
Recent travel or illness
Diagnostic criteria of IBS
More than 3 months of abdominal pain or discomfort and altered bowel habits
AND
Abdominal pain associated with 2 of the following
- Relief with defecation
- Onset associated with change in defecation frequency
- Onset associated with change in stool appearance
Additional criteria to support IBS diagnosis
Difference in stool frequency stool form stool passage Mucus Abdominal bloating Distention
Physical exam findings of IBS
+/- mild abdominal TTP
could be exaggerated if psychosomatic symptoms are present
Diagnostic testing in IBS D vs IBS C
D = test for celiac disease
C= plain abdominal films
IBS treatment strategy
Educate patient that the length of disease is a psychosomatic vicious cycle
Good diet for IBS
Regular meal pattern
Avoid large meals
Low FODMAPS
Dietary modification for IBS-D
Trial of Lactose elimination
Gluten elimination
Dietary modification of IBS-C
Increase fiber and fluid intake
IBS treatment can improve in all subtypes with what?
Increased physical activity
Adjunct pharmacological therapy for IBS
Dietary and lifestyle first
Antispasmodics Anti-constipation meds Antidiarrheals SSRA ABX Psychotropic agents
Indication for antispasmodics
Help with pain or bloating
Dicyclomine
Hyosycamine
Anti consitpation for IBS-C medications
Osmotic laxatives = TRY FIRST
Lubiprostone for women greater than 18
Linaclotide
Antidiarrheals for IBS-D
Loperamide
Bile salt sequestrants
SSRA
Alosetron Ondansetron
Rifaximin [ good for bloating]
IBS with abdominal pain or bloating receive what psychotropic agents
TCA’s
Amitriptyline
Nortriptyline
Desipramine
Imipramine
What are the steps of bilirubin synthesis and breakdown
- RBC’s are broken down to bilirubin and deposited in the bloodstream from hemoglobin
- Bilirubin binds to albumin transported to the liver
- Once in the liver it conjugates with glucuronide
- Transported into bile ducts then intestines
What are LFT’s markers of
Hepatocellualr injury
Cholestatic disease
Wha is commonly included in LFT’s
ALT
[transaminases]
AST
Alkaline phosphates
Total protein
Bilirubin
Albumin
Other markers for eval of the liver
GGT
LDH
PT/INR
Platelets
Hepatocelluar pattern of LFT’s
Elevation in the serum aminotransferases compared with the alk phosph
HIGH AST and ALT
Where is AST commonly found
Skeletal muscle and erythrocytes
Which is more specific for hepatic injustice ALT or AST
ALT
What elevation os AST and ALT is seen in transaminitis and what does it indicate
2:1 elevation
- ALCOHOL RELATED LIVER DISEASE*
- WITH LEVELS OF GGT*
Where are GGT enzymes found ( 5 )
Hepatocytes
Biliary epithelial cells
Renal tubules
Pancreas
Intestine
Cholestatic pattern of LFT’s
Disproportionate elevation in alkaline phosphatase compared with aminotrasnferases
HIGH ALK PHOS
ALP does what?
Liver and bone disease indicator enzyme that transports metabolites across cell membranes
Where is hepatic ALP present
On the surface of bile duct epithelium
Patho increase in portal pressure is due to what?
Pressure gradient between portal vein and IVC greater than 10 mmHg
When is jaundice clinically apparent
Bilirubin is greater than 2 mg/ dL
First appearing in the conjunctive(sclera icterus)
What type of bilirubin is a common jaundice characterization with increased plasma
Unconjugated (indirect)
What diseases can Casey increased bilirubin production
Hemolytic anemia
Hemolytic reactions
Hematoma
Pulmonary infarction
Impaired bilirubin uptake and storage occurs in what diseases
Posthepatitis hyperbilirubnemia
Gilbert syndrome
Crigler Najjar syndrome
Drug reactions
Conjugated hyperbilirubinemia is an Issue of what
The liver
Hepatocellular disease
Biliary obstruction
hereditary Cholestatic syndromes
What is the etiology of hemolytic unconjugated jaundice
Splenomegaly
Conjugated Cholestatic syndromes
Jaundice
Pruritus
Light colored stools
What does an ERCP work up do for Jaundice
Evaluate bile ducts if obstruction is suspected
If you suspect a jaundice patient has biliary obstruction
Endoscopic retrograde Cholangiopancreatography
ERCP
Define acute liver failure
Development of severe acute liver injury w/
Encephalopathy and impaired synthetic fx
Within 8 weeks of onset of disease
Acute liver failure is due ot what most commonly
Risks increase with what disease
Acetaminophen toxicity
Diabetes
Acute liver pain is in what general area
Right upper quadrant
Lab findings for acute liver failure
INR grater than 1.5 Elevated aminotransferases Elevated alk phos Low platelet count Elevated ammonia Alleviated amylase and lipase Elevated BUN and creatinine
What do you provide if you suspect acute liver failure in inpatient treatment
IV fluid and electrolyte replacement
Dietary monitoring
GI measures
= IV PPI or H2
What are here most common causes of hepatitis in the US
ABC
What happens during phase 1 of viral replication
ASX
Enzyme markers of hepatitis
Viral hepatitis phase 2
Prodromal phase Anorexia Athralgias Urticaria Alterations in taste
What is a phase 2 symptoms that occurs in the prodromal phase
Aversion to cigarette smoke
What is the third phase of viral hepatitis
Icteric phase
Predominant GI symptoms
Jaundice
Dark urine / Pale stools
Malaise
RUQ pain with hepatomegaly
What is phase 4 of viral hepatitis
Jaundice symptoms resolve
Liver enzymes return to normal
What type of transmission is Hep A
Fecal to oral but also contaminated food or water
Travel to endemic areas w/ poor sanitation
Signs of Hep A
ASX Fatigue Myalgia RUQ pain N/V
Distaste for cigarettes
Physical exam of hep A
Mild
Low grade fever
Scleral icterus +/- jaundice
Hepatomegaly +/- splenomegaly
Lab findings of Hep A
IGM anti HAV = acute infection , usual disappearance 3 -6 months
IgG anti-HAV may persist for years
LFT findings are ELEVATED AST and ALT
Elevation of ALK PHOS
Treatment of Acaute hepatitis A
No specific
maintain hydration
Self limited recovery with in 2-3 months in most cases
What is the mode of transmission for Hep B
Contact with body fluids sexual contact
Virus is present in saliva semen and vaginal juice
Screening is recommended in Hep B for which high risk groups
Healthcare workers
IV drug users
Prisoners
Chronic hep B patients have a substantial risk for what?
Cirrhosis and Hepatocellular carcinoma
Acute Hep B vs Chronic Hep B disease presentation
Acute
ASX
Weight loss
Chronic Fatigue Jaundice Ascites Advanced liver disease
Acute vs Chronic PE in HEP B
Acute Fever Rash Urticaria Icterus/jaundice Hepatomegaly
Chronic
Tender hepatomegaly
Signs of advanced liver disease
Wha this the ALT AST serology in Hep B with acute infx
More than 10 times
What is normally elevated in HEP B infx that indicated liver damage
Albumin
PTT/INR
CBC (platelets)
Bilirubin
What does a positive HBsAg indicate
Acute or chronic infx
What does a positive IgM anti-HBc indicate?
Acute infx
What does a positive Anti-HBs indicate
Vaccinated
Where is HBcAg
Intracellular antigen expressed in infected hepatocytes not detectable in serum
Anti-HBc appears when and what is the significance
Shortly after HBsAg
Predominantly of the IgM class Meaning ACUTE
A secretory protein that is processed from the pre core protein
Indicates viral replication and infectivity
HBeAg
increased likelihood to develop chronic HBV
What parallels the presence of HBeAg
HBV DNA
If Hep B is positive what serial testing should be done
HBsAg to condiment clearance or persistence at 6 months
Acute Hep B treatment
Antiviral therapy ONLY for mod severe liver damage patients
Liver transplant IF SEVERE liver damage
Complete recovery suspected at 16 weeks
Acute Hep B Prevention
Screening Serologic testing pregnant pts Safe sex Safe handling of blood and body fluids Vaccination
Hep B IG
[administered for known exposure followed by vaccination series]
Hep C mode of infection ; what is the high risk
Blood
50% injection drug use
HIGH RISK = conversion to chronic state
Hallmark AST and ALT of Hep C
Waxing and waning elevations
Lab findings of Hep C
Hepatic LFT’s = higher ALT than AST
+Anti-HCV EIA = requires a + HCV RNA test to confirm viral RNA
(ACTIVE INFECTION)
Serial testing = acute or chronic
Good treatment options for Hep C
Interferon == Ribavirin
Direct Acting Antivirals
Hep D requires what?
Defective RNA requires HBV for transmission and replication
What confirms diagnosis and indicates presenence of infection with Hep D
HDV-RNA
What indicates acute Hep D and may persist in pts with HBV infection
Anti HDV IgM
The most common cause of acute hepatitis world wide
Hep E
Fecal to oral transmission
Waterborne outbreaks
What is the primary diagnostic test as confirmatory test for positive hepatitis E virus IgM
+ HEV-RNA
Greater than 3 months = chronic HEV
What are makers of chronic HBV or HCV
Persistently elevated AST/ALT
Presence of HBsAg and anti-HBc
Anti-HCV
Liver biopsy findings
Chorionic HBV and HDV treatment
Antivirals
- Nucleoside or Nucleoside analog
- Entecavir
- Tenofovir
- Lamivudine
- Adefovir
- Telbivudine
Pegylated interferon
Chronic HCV treatment
Direct acting host targeting ANTIVIRAL agents
Ledipasvir
Sofosbuvir [Harvoni]
Autoimmune hepatitis is common in
Women
What extra hepatic manifestations are common in autoimmune hepatitis
Arthritis Sjogren syndrome Thyoiditis Nephritis UC Coombs-positive hemolytic anemia
Increased risk of cirrhosis and cancer
Non alcoholic fatty liver disease
Hepatic steatosis w/o significant inflammation
Can be diagnosed NONINVASIVE
Nonalcoholic steatohepatitis
Hepatic steatosis in association with INFLAMMATION, FIBROSIS, hepatocellular injury
Requires biopsy for diagnosis
Most common causes
Obesity
Diabetes
Hypertriglyceridemia (Insulin resistance)
NAFLD has an association with what organ removal
Gallbladder
Cholecystectomy
Patients with NAFLD complain of what vs NASH
NAFLD
ASX
NASH
Fatigue
Malaise
RUQ pain
What is the AST ALT ratio in NAFLD
Elevated 1:1
W/ mild elevation in ALK PHOS
MRI can do what for NAFLD
Identify fatty liver but can not distinguish from steatohepatitis
Standard approach to assessing the degree of inflammation an d fibrosis in suspected NASH generally not recommended if ASX
Percutaneous liver biopsy
Treatment of NAFLD
Lifestyle changes
Insulin sensitizing agents
Who has worse prognosis in NAFLD
Elderly
Diabetes
Higher BMI
Alcoholic steatosis Fatty liver may have what on physical exam
Hepatomegaly
Transaminase elevation in alcoholic liver disease
2:1 AST : ALT
Elevated GGT
Referral for US and biopsy
Treatment of alcoholic steatosis
Abstinence
Alcoholic steatohepatitis transaminase ratio
2:1
Other symptoms of alcoholic steatohepatitis
Muscle wasting
Abdominal distention and or ascites
Lab findings of alcoholic steatohepatitis
AST : ALT greater than or equal to 2:1 Elevated serum bilirubin Elevated GGT Elevated INR Leukocytosis
What should you obtain if you suspect alcoholic steatohepatitis
US and biopsy
Late stage progressive hepatic fibrosis
Cirrhosis
Distortion of the hepatic architecture w/ NODULES
Common cause of cirrhosis
Chronic viral hepatitis
ALD / NALD
Hemochromatosis
What classification of cirrhosis is associated with ETOH
Micronodular
What drinking habits are more at risk for cirrhosis
Chronic alcohol intake (30-50g/day) for more than 10 years
The three stages of cirrhosis correlate with what?
The thickness of fibrous septa
Clinical features of cirrhosis
Hepatocyte dysfunction
Portosystemic shunting
Portal hypertension
Compensated cirrhosis presents mostly
ASX
Non specific symptoms = anorexia, weight loss, fatigue
Deocmpensated cirrhosis symptoms
Jaundice Pruritus Upper GI bleed ABD distention = ascites Confusion = hepatic encephalopathy
The main General systemic manifestations of of cirrhosis
Decreased BP (MAP)
Hyper dynamic circulation is initiated by what
Splanchnic and peripheral vasodilation
HIGH NO
What is a put Medusae
Abdominal finding of cirrhosis
Umbilical vein opens and blood is shunted through to the abdominal veins centrally
Cruveilhier baumgarten murmur
Venous hum of Portal HTN patients
Heard with stethoscope on epigastrum
Endocrine function decreases in cirrhosis women vs men
Women
Chronic anovulation
Men
Gynecomastia
HEENT findings in systemic cirrhosis
Hepatic Fetor= sweet breathe
Parotid gland enlargement = fatty infiltration edema
2 neurological findings of systemic cirrhosis
Hepatic encephalopathy
Asterixis
Most common cbc finding of early compensated cirrhosis
Thrombocytopenia
Serum chem of cirrhosis
Hyponatremia
Hepatic panel in cirrhosis should show what
Increased AST/ALT ALK PHOS GGT Bilirubin PT
Decreased Albumin
What does an EGD help with cirrhosis confirmation
Observing esophageal varies and gastropathy
Cirrhosis treatment requires what immunizations
HAV HBV pneumoccocal vaccines
Flu shot
TIPS
Diversion of portal blood flow into hepatic vein
Reduces pressure gradient between portal and systemic circulations
Place a shunt!
Spontaneous bacterial peritonitis has what abdominal symptom
Pain without tenderness
Treatment of SBP
ADMIT
3rd gen cephalosporin
Ceftriaxone
Prophylaxis SBP
Once daily ciprofloxacin
OR
TMP-SMX DS
Azotemia in the absence of of parenchyma renal injury or disease with reduction in renal perfusion
Hepatorenal syndrome
Serum creatinine of 1.5 mg/dL or higher is common in what syndrome
Hepatomegaly syndrome
Oliguria, hyponatremia, and a low urinary sodium concentration are typical features
Hepatorenal syndrome
ADMIT TO ICU
Systemic build up of ammonia is a compilacation of cirrhosis called
Hepatic encephalopathy
Treatment of hepatic encephalopathy
LActulose = reduction in GI tract absorption
What has shown efficacy in improved hepatic encephalopathy
Pre/Probiotics
By alteration of intestinal flora
Untreated _______________ toxicity results in fulminant hepatitis and painful death syndrome
Acetaminophen
How can you treat acetaminophen toxicity
N-acetylcysteine
What can you order to observe normalization of values in toxic liver injury
Serial LFT’s
Autoimmune destruction of bile ducts and cholestasis is AKA
Primary biliary Cholangitis
What other autoimmune disorders are associated with primary biliary cholangitis
Sjogren syndrome
Autoimmune thyroid disease
Raynaud syndrome
Scleroderma
Fatigue
Xanthomas
ASX hepatomegaly
Primary biliary cholangitis
What symptoms occur later in primary biliary cholangitis
Jaundice
Steatorrhea
Portal HTN
Lab findings in PBC
Cholestatic pattern
INCREASED ALK PHOS
Bilirubin
Transaminase
HIGH LIPIDS
What markers of autoimmune diseae are present in PBC
Animitochondirla antibodies (AMA)
Antinuclear antibodies (ANA)
Treatment for PBC
Ursodeoxycholic acid
*slows progression of disease*
Treat pruritis with Bile Salt sequestrants
Diagnosis and genetic testing of hemochromatosis
Clinical aroun 50 years old
Incidental finding
Elevated AST and ALK PHOS
Elevated plasma iron and ferritin
First line treatment and subsequent for hemochromatosis
Phlebotomy
Chelation with deferoxamine
Liver transplant
Pathognomonic sign of Wilson dz
Kayser-Fleischer Rings
What copper transport protein is low in Wilson’s disease
Serum ceruplasmin
Copper Chelation Wilson disease treatment
Trientine
Penicillamine
Zinc
Test of choice for Budd-Chiari syndome
Color Doppler US
With budd-chiari syndrome you should suspect
Hepatic vein obstruction
Progenitor hepatic abscess is
Traumatic implantation of bacteria through the abdominal wall
Main clinical presentation of Phoenician hepatic abscess
Fever
Jaundice
What tests are diagnostic for US
CT guided percutaneous drainage with culture of aspirate
Benign liver neoplasm is AKA
Cavernous hemangioma
Why do hepatocellular carcinoma pts sometimes have bone pain
Metastases
What sudden sustained lab findings is indicative of hepatocellular carcinoma
Elevation of ALK PHOS
Survival rate of HC
1 an 5 year survive rates = 23% and 5%
What screening is warranted for hepatocellular carcinoma pts
Patients with :
1) Cirrhosis
2) Chronic HBV or HCV
3) Family he of HC
Hepatic US and Alpha feta protein level
Evry 6 months
Gallstones present
ASX but may cause RUQ pain
Intermittent or partial obstruction
Lead to acute cholecystitis
Acute attack preceded by a large fatty meal =
Acute cholecysitis
Clinical presentation of acute cholecystitis
Sudden onset of persistent, steady RUQ pain
May radiate to shoulder and to back
Biliary colic that has not resolved after 4-6 hours
Nausea and vomiting frequent
Fever
Physical exam findings of Acute Cholecystitis
RUQ TTP
Abdominal muscle guarding
Positive Murphy sign
CBC reveals leukocytosis
UNCOMMON to have increased serum bilirubin
Elevations of ALK PHOS and AST ALT
NO CHOLESTATIC pattern
Elevated amylase
Acute cholecystitis
First test for acute cholecystitis
RUQ US
Shows gallbladder wall thickening
Sonography Murphy sign
Complications of acute cholecystitis (4)
Gangrenous cholecystitis
Perforation
Cholecystoenteric fistula
Gallstone Ileus
Chronic cholecystitis may result in
Porcelain gallbladder
Intramural calcification of the gallbladder
Treatment of acute cholecystitis
Admission for supportive care
Laparoscopic cholecystectomy
Choledocholithiasis
Stones in the common bile duct
Obstruction in common bile duct may lead to
Cholangitis (biliary tract infx)
Severe biliary colic
RUQ epigastric pain
N/V
Jaundice
Clinical presentation of choledocholithiasis
Lab findings of choledocholithiasis
Cholestatic pattern
High ALK PHOS and bilirubin and AST ALT
Testing of choledocholithiasis
RUQ US = FIRST
ERCP = diagnosis and therapy
Severe abnormal liver fx ALT level
ALT > 15 x normal
Moderate abnormal liver fx ALT level
ALT 5-15 x higher than normal
Mild abnormal liver fx ALT level
5 x higher than normal
Treatment of choledocholithiasis
Refer to GI/Surgery
In general, bile duct stones, even small ones, should be removed, even in an asymptomatic patient
ERCP with stone extraction
Followed by laparoscopic cholecystectomy within 72 hours in patients with cholecystitis and within 2 weeks in those without cholecystitis
Complications of choledocholithiasis
Ascending cholangitis
Pancreatitis
Charcot triad of acute cholangitis symptoms
RUQ pain
Fever/Chills
Jaundice
Reynolds’s Pentad of acute cholangitis
Charcots
Altered mental status
Hypotension
- Indicates Acute Suppurative Cholangitis
Surgical emergency!*
Acute cholangitis
Bacterial infx of biliary tract as a result of obstruction invasion form duodenum
Treatment of acute cholangitis
Treatment:
Admission
For supportive care and antibiotics
ERCP
For biliary drainage and removal of obstruction
Surgery
Only if ERCP fails or is unavailable
Cholecystectomy follows once infection is cleared
To prevent recurrence
Asymptomatic Gallstone
Gallstone + Fever/Pain
Gallstone + Jaundice
Gallstone + Jaundice + Fever
Gallstone + Jaundice + Fever + AMS + Hypotension
Cholelithiasis
Cholecystitis
Choledolithiasis
Cholangitis
Supportive Cholangitis
Key features to indicate bile duct cancer
Painless obstruction
W/ Dilated biliary tree
Palpable gallbladder with painless obstructive jaundice is called what and also associated with what
Courvoiser sign
Pancreatic cancer
When should you consider carcinoma of the biliary tract
Cholestatic pattern of biliary obstruction
W/ no explanation
AND
isolated intrahepatic mass on imaging and a normal serum level of alpha-fetoprotein
What is the exocrine vs endocrine tissue of the pancreas
Acinar and duct tissue [Exocrine]
Islets of Langerhans [Endocrine]
Acute pancreatitis is most commonly due to
Gallstones and chronic alcohol abuse
Cystic fibrosis is a risk factor for what disease
Acute pancreatitis
How does hyperlipidemia induce pancreatitis
Free fatty acids are released from serum tri’s in toxic concentration by pancreatic lipase in pancreatic capillaries
Interstitial edema acute pancreatitis
Inflammation of pancreatic tissues without necrosis
Necrotizing acute pancreatitis
Inflamed pancreatic tissues with necrosis
Mild acute pancreatitis
No organ failure or systemic complications
Moderate acute pancreatitis
Transient Oran failure or local or systemic complications that revolve within 48 hours
Severe acute pancreatitis
Persistent organ failure with multiple organ involvement
Clinical presentation of acute pancreatitis
Bilateral upper quadrant pain
“Boring with radiation to the back”
N/V
Physical exam findings of acute pancreatitis (3)
Epigastric TTP
Cullens Sign
Grey Turner Sign
Cullen sign
Edema and bruising around umbilicus
Grey turner sign
Bruising of the flank with retro peritoneal or intra abdominal bleeding
Lab findings in acute pancreatitis
Increased serum amylase and lipase
CBC = leukocytosis
CMP = elevated U=BUN
hepatic panel
Elevated CRP
Diagnostic test of choose for acute pancreatitis
CT scan
More points on the ransom criteria =
Higher mortality
Treatment of acute pancreatitis
ERCP for gallstones
Conventional pain contrail of mild acute pancreatitis
Meperidine (Demerol) = less likely to induce spasm of the sphincter of oddi
Treatment of severe acute pancreatitis
Admit to ICU
Surgical consult
Chronic pancreatitis = what pts?
Chronic alcoholics
Chronic pancreatitis clinical presentation
LUQ
Anorexia
Weight loss
Constipation
Steatorrhea
Diagnostic test for chronic pancreatitis
Eval of fecal fat
Plain films or CT to eval pancreatic calcification to rule out pancreatic cancer
Secretin pancreatic function test
Stimulate the pancreas through administration of a meal or hormonal secretagogue
Normal secretory content observed
do this if you have clinical findings but not radiographic findings
Chronic pancreatitis treatment measures
Non opioid pain control
Pancreatic enzyme supplementation
Low fat diet
REFER TO GI / PANCREATOLOGY
Cant digest food , dyspepsia, cramping, bloating, watery diarrhea
Deficient exocrine pancreatic enzymes
Exocrine pancreatic insufficiency
Most common etiologies of exocrine pancreatic insufficiency
Chronic pancreatitis
Cystic fibrosis
Clinical presentation of exocrine pancreatic insufficiency
Water bulky fouls smelling diarrhea w/ steatorrhea
Weight loss
Abdominal pain bloating and flatulence
What lab can eval for exocrine pancreatic insufficiency
Fecal elastase
Mainstay of management of exocrine pancreatic insufficiency
Pancreatic enzyme replacement therapy
Clinical presentation of pancreatic cancer
Abdominal pain
Jaundice
Weight loss
Vague LUQ pain
Courvoiser sign = nontender palpable gallbladder
Lab findings on pancreatic cancer
Non specific
+/- amylase / lipase elevation or bilirubin
CA 19-9 = serum tumor marker
Imaging study to eval jaundice in pancreatic cancer
US
Imaging study to eval pain or weight loss in pancreatic cancer
Abdominal CT scan
Imaging study to eval ducts in pancreatic cancer
ERCP
Treatment of pancreatic cancer
Surgical resection
