Ch9: GI & Hepatology Flashcards
what causes almost all duodenal ulcers?
h. pylori
> 95%
its not too much acid, its not too much stress - its a bacterial infection
(2) typical symptoms of GERD
- heartburn
- regurgitation
a CLINICAL diagnossi
how do you diagnose GERD
clinically, based on symptoms
upper endoscopy, barium radiograph, H. pylori testing are NOT needed routinely, only if refractory to standard care or alarm symptoms
ALARMS findings in GERD that warrant upper endoscopy
A - anemia (iron deficiency, signals GI bleeding)
L - loss of weight (involuntary)
A - anorexia (persistent)
R - recent onset of progressive symptoms
M - melena (tarry or bloody stools) or hematemesis (vomiting, bright red blood)
S - swallowing difficulty (dysphagia, odynophagia)
dysphagia
difficulty swallowing
odynophagia
painful swallowing
first line pharm therapy for GERD
PPIs (proton pump inhibitors)
usually taken QD prior to the first meal of the day for maximum effect
Can use lowest effective dose as daily, on demand, or intermittent therapy
acceptable alternative: H2 receptor antagonist therapy (e.g., ranitidine)
when should you refer a patient with GERD for GI evaluation with upper endoscopy?
- failing PPI BID at maximum recommended dose
- protracted PPI use with adverse effects (e.g., nutrient malabsorption, bone loss, pneumonia, C. diff)
once someone has been on a PPI for at least _____, they will have rebound hyperacidity when coming off of them
8 weeks
Possible adverse effects from protracted PPI use (4)
- micronutrient malabsorption (vitamin B12, calcium, magnesium, iron)
- increased fracture risk, decreased bone density
- pneumonia
- C. diff infection risk
Lifestyle modifications for GERD
- weight loss PRN
- elevate the head of the bed
- avoid meals 2-3 hours before bedtime
- avoid trigger foods (chocolate, caffeine, alcohol, acidic foods)
common GERD triggers
- chocolate
- caffeine
- alcohol
- acidic foods (tomatoes, lemonade, etc.)
clinical presentation of GERD
- heartburn
- regurgitation
- recurrent cough
- chronic pharyngitis
- hoarseness
often exacerbated by obesity
one of the most common reasons for adults to have hoarseness and recurrent cough
GERD
78yo M with PMH of longstanding GERD presents with 1-mo history of dysphagia, “feeling like the food gets stuck in my throat.” Physical exam unremarkable. Labs return an iron deficiency anemia
top (3) differential dx
- esophageal cancer
- esophageal strictures
- esophagitis
78yo M with PMH of longstanding GERD presents with 1-mo history of dysphagia, “feeling like the food gets stuck in my throat.” Physical exam unremarkable. Labs return an iron deficiency anemia. You suspect esophagitis, esophageal strictures, or esophageal cancer. Next diagnostic step?
upper endoscopy with biopsy
barium swallow would outline the lesion, but would still need an upper endoscopy with biopsy were a lesion to be found
pt is diagnosed with a duodenal ulcer. which medication will you prescribe to specifically prevent recurrence of the ulcer?
- antibiotics (since duodenal ulcers are caused by h.pylori bacteria)
you will also prescribe PPI and recommend antacid to help heal the ulcer, but the antibiotics are what will prevent it from coming back by eradicating the underlying cause
when is leukocytosis (elevated WBC >10,000) an anticipated finding?
significant bacterial infection, such as appendicitis, pyelonephritis, bacterial pneumonia, pelvic inflammatory disease, etc.
leukocytosis
WBCs >10,000 mm3
normal range WBC count
6,000 - 10,000 mm3
normal % of neutrophils on a CBC with diff
60%
normal % of lymphocytes on a CBC with diff
30%
normal % of monocytes on a CBC with diff
6%
normal % of eosinophils on a CBC with diff
3%
normal % of basophil on a CBC with diff
1%
Nobody Likes My Educational Background: mnemonic for order of differential cells on WBC
N - neutrophil L - lymphocytes M - monocyte E - eosinophil B - basophil
“polys” or “segs’ refers to
neutrophils
what are “bands”
immature (young) neutrophils
point of action for neutrophils
bacterial infection
point of action for lymphocytes
viral infection
point of action for monocytes
debris (recovering from illness)
naturally go up when the body is tidying up after infection
point of action for esosinophils
allergens, parasites (3 WERIDS: worms, wheezes, weird diseases)
point of action for basophils
anaphylaxis, not fully understood
what does a WBC with a left shift mean
leukocytosis with neutrophilia (high neutrophils) and elevated bands (immature neutrophils)
suggests bacterial infection
normal range for “bands”
<3%
classic presentation of appendicitis
- 12-hr history of epigastric discomfort and anorexia that gradually shifts to nausea and RLQ abdominal pain
- positive peritoneal irritation signs (obturator, psoas, rovsing)
most helpful imaging in suspected appendicitis
abdominal CT with contrast
abdominal US is okay to use in slender folks
(2) most common causes of acute pancreatitis
- alcohol abuse
- untreated gallstones
what is “Blumberg’s sign”
sign for rebound tenderness
45yo M with PMH alcohol abuse presents with 12-hr history of acute-onset epigastric pain radiating to the back with bloating, nausea, and vomiting
on physical exam, has epigastric tenderness, hypoactive bowel sounds, distended abdomen that is hypertympanic.
what do you suspect? next steps?
suspect acute pancreatitis
order CBC with diff, amylase/lipase
send to ER because vomiting with hypertympanic abdomen = likely paralytic ileus
also because needs pain management and likely wont be able to keep down PO meds
64yo F presents with 3-day history of intermittent LLQ pain accompanied by fever, cramping, nausea, and 4-5 loose stools/day.
On physical exam, abdomen is soft, NABS, tenderness to palpation over LLQ. negative rebound tenderness.
what do you suspect? next steps?
suspect diverticulitis
CBC with diff will expect left shift (neutrophilia), CRP, fOBT,
abdominal CT with contrast to confirm
can be managed outpatient with oral antibiotics (usually ciprofloxacin and metronidazole)
imaging test most helpful for diagnosis of diverticulitis
abdominal CT with contrast
AVOID COLONOSCOPY with acute diverticulitis disease
how do you diagnose a suspected duodenal ulcer
H. pylori stool antigen or urea breath test
do NOT order h. pylori serology …. people can pick up H. pylori infection and rid themselves of it but decades later still be serologically positive. very common for this to be positive in the absence of active infection
why is serum testing for h. pylori not recommended?
remains positive decades after active infection has resolved
34yo M presents with 3-mo h/o intermittent upper abdominal pain described as epigastric burning, gnawing pain about 2-3 hours after eating. Relieved by foods and antacids. Awakening at 1-2am with these symptoms.
on physical exam, tenderness to palpation at the epigastrum and LUQ. hyperactive bowel sounds
what do you suspect? next steps
classic presentation for a duodenal ulcer
confirm with h. pylori stool antigen or urea breath test
treat with triple or quadruple therapy including an antibiotic and PPI
52yo F who was recently laid off from her job, taking 3-4 doses of NSAIDs/day for the last 2-3 months to help with headaches and a 1-month history of intermittent nausea, burning, and pain limited to the upper abdomen, often worse with eating.
On physical exam, she is tender to the epigastrium, LUQ. slightly hyperactive bowel sounds
what do you suspect? next steps?
Per Fitzgerald, we suspect erosive gastritis
I also suspect IBS and duodenal ulcer
next steps to stop the NSAIDs, consider short-term PPI therapy –> if not improved, consider H. pylori testing (urea breath or stool antigen test)
54yo F presents with 24-hr history of significant epigastric and RUQ abdominal pain that is constant, with 2-3 minute periods of worsening accompanied by nausea, 2 episodes of vomiting, and intermittent fever.
On physical exam, there is tenderness at the epigastrum and abdominal RUQ, positive Murphy’s sign.
what do you suspect? next steps?
suspected acute cholecystitis (gallstones)
CBC with diff, AST, ALT, alk phos (ALP)
order abdominal US of RUQ
recommend gut rest and referral to a surgeon
alk phos when elevated means….
bile flow through the liver is not working
commonly elevated in acute cholecystitis
which hepatitis is MOST likely caused by fecal-contaminated food or water
hepatitis A
which hepatitis is MOST likely caused by sexual-contact
hepatitis B
(best concentrated in sexual fluids. hepatitis C is poorly concentrated in sex fluids. is possible to get hepatitis C this way, but unlikely)
which hepatitis is MOST likely caused by injection drug use
hepatitis C
what does positive HBsAg indicate?
acute or chronic hepatitis B infection
what does positive anti-HAV indicate?
hepatitis A immunity
what does positive Anti-HCV indicate?
hepatitis C immunity
adults born between ______ should be screened for HCV, regardless of other risk factors
1945-1965
5x more likely to have hepatitis C than other adults
route of transmission: hepatitis A
fecal-oral
ingestion of fecal matter, even in microscopic amounts, can occur from:
- close person-to-person contact with an infected person
- sexual contact with an infected person
- ingestion of contaminated food and drinks
is vaccination/ immune globulin post-exposure prophylaxis available: hepatitis A
yes, both
post-exposure prophylaxis with immune globulin (Gammagard) and/or immunization for close contacts who are not immune to HAV
long-term sequelae of hepatitis A infection
none really - it is an acute infection only, chronic hepatitis A does not exist
low mortality rate
lab results indicative of active hepatitis A infection
HAV IgM positive
elevated LFTs >10x upper limit normal (marked elevation)
lab results indicative of past infection with hepatitis A
anti-HAV positive (positive antibodies)
LFTs should be normal
interpret: anti-HAV negative
non-immune to hepatitis A
pt is found to have active hepatitis A infection. next steps?
- LFTs (ALT/AST, bilirubin) for liver status
- notify public health officials
- supportive care for treatment
- liver transplant is only an option in rare, select, severe cases that develop fulminant hepatic failure (typically only happens when HAV is contracted in the context of pre-existing liver disease)
route of transmission: hepatitis B
blood, body fluids (sexually transmitted)
contact with infectious blood, semen, and other body fluids occurs primarily through:
- birth to an infected mother
- sexual contact with an infected person
- sharing of contaminated needles, syringes, or other injection drug equipment
- needlesticks or other sharp instrument injuries
is vaccination/ immune globulin post-exposure prophylaxis available: hepatitis B
yes, both
post-exposure prophylaxis with Hepatitis B immune globulin (HBIG) and HBV immunization for blood/body fluid contacts in nonimmune folks
long term possible sequelae of hepatitis B infection (4)
- chronic hepatitis B
- cirrhosis
- hepatocellular carcinoma
- liver failure
lab results indicative of acute hepatitis B infection
HBV core IgM antibodies (IgM anti-HBc) positive (will be positive in acute infection only)
HBsAg positive (in acute and chronic)
HBeAg positive
markedly elevated LFTs >10x upper limit of normal
earliest lab result to become positive after an exposure to hepatitis B
HBV core IgM antibodies
lab result that indicates an individual is super contagious with hepatitis B
HBeAg
lab results indicative of chronic hepatitis B infection
HBsAg
LFTs will be normal or slightly elevated
IgM anti-HBc will be negative! Antibodies to Hepatitis B CORE are only positive in acute infection
lab result indicative of hepatitis B immunity
HBsAb (aka, anti-HBs)
lab result indicative of not immune to hepatitis B
HBsAg negative
anti-HBc negative
anti-HBs (HBsAb) negative
pt is found to have active hepatitis B infection. next steps?
- LFTs for baseline function
- screen for coinfection with Hepatitis A, Hepatitis C, HIV, other STIs
- immunize against HAV if not immune
- refer for specialist consultation for antiviral therapy consideration
route of transmission: Hepatitis C
blood, body fluids
primarily through contact with BLOOD of an infected person (rare through body fluids), usually through:
- sharing of contaminated needles, syringes, or other injection drug equipment
- less commonly through sexual contact with an infected person, birth to an infection mother, or needlestick/sharps injury
is vaccination/ immune globulin post-exposure prophylaxis available: hepatitis C
no, neither
possible long-term sequelae of hepatitis C infection
- chronic hepatitis C
- cirrhosis
- hepatocellular carcinoma
- liver failure
lab results indicative of active acute hepatitis C infection
anti-HCV positive
HCV viral RNA positive via NAT
elevated LFTs
** however, cannot definitively differentiate acute from chronic
lab results indicative of chronic hepatitis C infection
anti-HCV positive
HCV viral RNA positive via NAT
LFTs are normal or slightly elevated
** however, cannot definitively differentiate acute from chronic, only difference here was LFTs being more normal in chronic
lab results indicative of hepatitis C in the past
anti-HCV positive (non-protective antibodies)
HCV viral RNA negative/absent
LFTs are normal
do antibodies to hepatitis C indicate immunity?
no, anti-HCV antibodies are not protective they only indicate a past infection
route of transmission: hepatitis D
blood, body fluids
can only be transmitted in the presence of hepatitis B disease
is vaccination/ immune globulin post-exposure prophylaxis available: hepatitis D
no, neither
however, if you prevent Hepatitis B (vaccine or IG), then you can prevent hepatitis D! requires co-infection
possible sequelae of hepatitis D infection
- severe infection
- liver failure
- death
lab results indicative of acute hepatitis D infection
HBsAg positive (requires hep B coinfection)
hepatitis D IgM positive
markedly elevated LFTs
who is at risk for hepatitis A
- travelers to regions with intermediate or high rates of Hepatitis A
- sex contacts of infected persons
- household members or caregivers of infected persons
- men who have sex with men
- users of certain illegal drugs
- persons with clotting-factor disorders
symptoms of all types of viral hepatitis
- fever
- fatigue
- loss of appetite/anorexia
- nausea/vomiting
- abdominal pain
- gray-colored bowel movements
- joint pain
- jaundice
is there a potential for chronic infection from hepatitis A?
no
most people with acute disease recover with no lasting liver damage
% of adults >14yo with acute hepatitis A infection who will have jaundice
70-80%
who is at risk for hepatitis B
- infants born to infected mothers
- sex partners of infected persons
- persons with multiple sex partners
- persons with STDs
- MSM
- people who use injection drugs
- household contacts of infected persons
- healthcare and public safety workers exposed to blood in their work
- hemodialysis patients
- residents and staff of facilities for developmentally disabled persons
- travelers to regions with intermediate or high rates of hepatitis B (HBsAg prevalence >2%)
incubation periods for folks with Hepatitis A, B, or C
SHORTEST >> hepatitis A (15-50 days; av 28)
hepatitis C (14-180 days; av 45)
hepatitis B (45-160 days; av 120) >> LONGEST
% of adults with hepatitis B who will have symptoms?
30-50% will develop symptoms
otherwise, asymptomatic
more likely to be asymptomatic if immunosuppressed (5-15% will show symptoms)
how likely is chronic infection after hepatitis B infection?
if unimmunized,
> 90% of infants
6-10% of adults
who is at risk for hepatitis C infection
- current or former injection drug use
- recipients of blood products before 1992
- long-term hemodialysis
- known exposures to HCV (healthcare worker after needlestick, organ recipients)
- HIV
- infants born to HCV infected mothers
% of adults with hepatitis C who will have symptoms?
20-30% develop symptoms of acute disease
how likely is chronic infection after hepatitis C infection?
75-85% chance of becoming chronic
15-25% chance of clearing the virus
severity of hepatitis A infection?
most people with acute disease will recover with no lasting liver damage! rarely fatal. never becomes chronic
severity of hepatitis B infection?
most folks with acute disease will recover with no lasting liver damage, and acute illness is rarely fatal
only 10% of adults will develop chronic hep B
of those with chronic hep B, 15-25% will develop cirrhosis, liver failure, or liver cancer
severity of hepatitis C infection?
acute illness is uncommon - most folks who do have acute symptoms will recover with no lasting liver damage
however, 75-85% of folks with acute infection will develop chronic hepatitis C
of those with chronic hep C, 5-20% will develop cirrhosis over the next 20-30 years, and 1-5% will die from cirrhosis or liver cancer
who is recommended to have Hepatitis B Screening for chronic infection?
- all pregnant folks
- people born in regions with intermediate to high rates of hepatitis B (HBsAg prevalence >2%)
- US-born persons who were not vaccinated as infants whose parents were born in regions with high rates of Hepatitis B (HBsAg prevalence >8%)
- infants born to Hepatitis B positive mothers
- household, needle-sharing, and sex contacts of HBsAg-positive persons
- men who have sex with men
- injection drug use
- elevated LFTs of unknown etiology
- hemodialysis patients
- people on immunosuppressive or cytotoxic therapies
- HIV-infection
- blood, plasma, organ, semen, or other tissue donors
who is recommended to have Hepatitis C screening for chronic infection?
- persons born between 1945-1965
- persons who have ever injected drugs
- recipients of blood products before 1992
- long-term hemodialysis
- known exposure to HCV
- HIV infection
- children born to infection mothers (cannot test before 18 months)
- folks with s/s of liver disease (e.g., elevated LFTs)
- blood, plasma, organ, semen, or other tissue donors
treatment for hepatitis A, generally
no medication is available
supportive measures only
treatment for hepatitis B, generally
no medications available for acute infection, supportive measures only
with development of chronic infection, will regularly monitor for signs of liver disease progression and some patients may be candidates for antiviral therapy
treatment for hepatitis C, generally
antivirals and supportive therapy in acute infection
with development of chronic infection, will regularly monitor for signs of liver disease progression and some patients will be candidates for antivirla therapy
