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AGPCNP Board Prep > Ch9: GI & Hepatology > Flashcards

Ch9: GI & Hepatology Flashcards

1
Q

what causes almost all duodenal ulcers?

A

h. pylori

> 95%

its not too much acid, its not too much stress - its a bacterial infection

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2
Q

(2) typical symptoms of GERD

A
  1. heartburn
  2. regurgitation

a CLINICAL diagnossi

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3
Q

how do you diagnose GERD

A

clinically, based on symptoms

upper endoscopy, barium radiograph, H. pylori testing are NOT needed routinely, only if refractory to standard care or alarm symptoms

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4
Q

ALARMS findings in GERD that warrant upper endoscopy

A

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)

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5
Q

dysphagia

A

difficulty swallowing

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6
Q

odynophagia

A

painful swallowing

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7
Q

first line pharm therapy for GERD

A

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)

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8
Q

when should you refer a patient with GERD for GI evaluation with upper endoscopy?

A
  • failing PPI BID at maximum recommended dose

- protracted PPI use with adverse effects (e.g., nutrient malabsorption, bone loss, pneumonia, C. diff)

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9
Q

once someone has been on a PPI for at least _____, they will have rebound hyperacidity when coming off of them

A

8 weeks

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10
Q

Possible adverse effects from protracted PPI use (4)

A
  • micronutrient malabsorption (vitamin B12, calcium, magnesium, iron)
  • increased fracture risk, decreased bone density
  • pneumonia
  • C. diff infection risk
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11
Q

Lifestyle modifications for GERD

A
  • weight loss PRN
  • elevate the head of the bed
  • avoid meals 2-3 hours before bedtime
  • avoid trigger foods (chocolate, caffeine, alcohol, acidic foods)
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12
Q

common GERD triggers

A
  • chocolate
  • caffeine
  • alcohol
  • acidic foods (tomatoes, lemonade, etc.)
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13
Q

clinical presentation of GERD

A
  • heartburn
  • regurgitation
  • recurrent cough
  • chronic pharyngitis
  • hoarseness

often exacerbated by obesity

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14
Q

one of the most common reasons for adults to have hoarseness and recurrent cough

A

GERD

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15
Q

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

A
  • esophageal cancer
  • esophageal strictures
  • esophagitis
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16
Q

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?

A

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

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17
Q

pt is diagnosed with a duodenal ulcer. which medication will you prescribe to specifically prevent recurrence of the ulcer?

A
  • 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

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18
Q

when is leukocytosis (elevated WBC >10,000) an anticipated finding?

A

significant bacterial infection, such as appendicitis, pyelonephritis, bacterial pneumonia, pelvic inflammatory disease, etc.

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19
Q

leukocytosis

A

WBCs >10,000 mm3

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20
Q

normal range WBC count

A

6,000 - 10,000 mm3

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21
Q

normal % of neutrophils on a CBC with diff

A

60%

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22
Q

normal % of lymphocytes on a CBC with diff

A

30%

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23
Q

normal % of monocytes on a CBC with diff

A

6%

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24
Q

normal % of eosinophils on a CBC with diff

A

3%

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25
Q

normal % of basophil on a CBC with diff

A

1%

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26
Q

Nobody Likes My Educational Background: mnemonic for order of differential cells on WBC

A 
N - neutrophil
L - lymphocytes
M - monocyte
E - eosinophil
B - basophil
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27
Q

“polys” or “segs’ refers to

A

neutrophils

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28
Q

what are “bands”

A

immature (young) neutrophils

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29
Q

point of action for neutrophils

A

bacterial infection

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30
Q

point of action for lymphocytes

A

viral infection

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31
Q

point of action for monocytes

A

debris (recovering from illness)

naturally go up when the body is tidying up after infection

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32
Q

point of action for esosinophils

A

allergens, parasites (3 WERIDS: worms, wheezes, weird diseases)

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33
Q

point of action for basophils

A

anaphylaxis, not fully understood

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34
Q

what does a WBC with a left shift mean

A

leukocytosis with neutrophilia (high neutrophils) and elevated bands (immature neutrophils)

suggests bacterial infection

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35
Q

normal range for “bands”

A

<3%

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36
Q

classic presentation of appendicitis

A
  • 12-hr history of epigastric discomfort and anorexia that gradually shifts to nausea and RLQ abdominal pain
  • positive peritoneal irritation signs (obturator, psoas, rovsing)
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37
Q

most helpful imaging in suspected appendicitis

A

abdominal CT with contrast

abdominal US is okay to use in slender folks

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38
Q

(2) most common causes of acute pancreatitis

A
  • alcohol abuse

- untreated gallstones

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39
Q

what is “Blumberg’s sign”

A

sign for rebound tenderness

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40
Q

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?

A

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

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41
Q

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?

A

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)

42
Q

imaging test most helpful for diagnosis of diverticulitis

A

abdominal CT with contrast

AVOID COLONOSCOPY with acute diverticulitis disease

43
Q

how do you diagnose a suspected duodenal ulcer

A

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

44
Q

why is serum testing for h. pylori not recommended?

A

remains positive decades after active infection has resolved

45
Q

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

A

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

46
Q

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?

A

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)

47
Q

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?

A

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

48
Q

alk phos when elevated means….

A

bile flow through the liver is not working

commonly elevated in acute cholecystitis

49
Q

which hepatitis is MOST likely caused by fecal-contaminated food or water

A

hepatitis A

50
Q

which hepatitis is MOST likely caused by sexual-contact

A

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)

51
Q

which hepatitis is MOST likely caused by injection drug use

A

hepatitis C

52
Q

what does positive HBsAg indicate?

A

acute or chronic hepatitis B infection

53
Q

what does positive anti-HAV indicate?

A

hepatitis A immunity

54
Q

what does positive Anti-HCV indicate?

A

hepatitis C immunity

55
Q

adults born between ______ should be screened for HCV, regardless of other risk factors

A

1945-1965

5x more likely to have hepatitis C than other adults

56
Q

route of transmission: hepatitis A

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
57
Q

is vaccination/ immune globulin post-exposure prophylaxis available: hepatitis A

A

yes, both

post-exposure prophylaxis with immune globulin (Gammagard) and/or immunization for close contacts who are not immune to HAV

58
Q

long-term sequelae of hepatitis A infection

A

none really - it is an acute infection only, chronic hepatitis A does not exist

low mortality rate

59
Q

lab results indicative of active hepatitis A infection

A

HAV IgM positive

elevated LFTs >10x upper limit normal (marked elevation)

60
Q

lab results indicative of past infection with hepatitis A

A

anti-HAV positive (positive antibodies)

LFTs should be normal

61
Q

interpret: anti-HAV negative

A

non-immune to hepatitis A

62
Q

pt is found to have active hepatitis A infection. next steps?

A
  • 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)
63
Q

route of transmission: hepatitis B

A

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
64
Q

is vaccination/ immune globulin post-exposure prophylaxis available: hepatitis B

A

yes, both

post-exposure prophylaxis with Hepatitis B immune globulin (HBIG) and HBV immunization for blood/body fluid contacts in nonimmune folks

65
Q

long term possible sequelae of hepatitis B infection (4)

A
  • chronic hepatitis B
  • cirrhosis
  • hepatocellular carcinoma
  • liver failure
66
Q

lab results indicative of acute hepatitis B infection

A

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

67
Q

earliest lab result to become positive after an exposure to hepatitis B

A

HBV core IgM antibodies

68
Q

lab result that indicates an individual is super contagious with hepatitis B

A

HBeAg

69
Q

lab results indicative of chronic hepatitis B infection

A

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

70
Q

lab result indicative of hepatitis B immunity

A

HBsAb (aka, anti-HBs)

71
Q

lab result indicative of not immune to hepatitis B

A

HBsAg negative
anti-HBc negative
anti-HBs (HBsAb) negative

72
Q

pt is found to have active hepatitis B infection. next steps?

A
  • 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
73
Q

route of transmission: Hepatitis C

A

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
74
Q

is vaccination/ immune globulin post-exposure prophylaxis available: hepatitis C

A

no, neither

75
Q

possible long-term sequelae of hepatitis C infection

A
  • chronic hepatitis C
  • cirrhosis
  • hepatocellular carcinoma
  • liver failure
76
Q

lab results indicative of active acute hepatitis C infection

A

anti-HCV positive
HCV viral RNA positive via NAT
elevated LFTs

** however, cannot definitively differentiate acute from chronic

77
Q

lab results indicative of chronic hepatitis C infection

A

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

78
Q

lab results indicative of hepatitis C in the past

A

anti-HCV positive (non-protective antibodies)
HCV viral RNA negative/absent
LFTs are normal

79
Q

do antibodies to hepatitis C indicate immunity?

A

no, anti-HCV antibodies are not protective they only indicate a past infection

80
Q

route of transmission: hepatitis D

A

blood, body fluids

can only be transmitted in the presence of hepatitis B disease

81
Q

is vaccination/ immune globulin post-exposure prophylaxis available: hepatitis D

A

no, neither

however, if you prevent Hepatitis B (vaccine or IG), then you can prevent hepatitis D! requires co-infection

82
Q

possible sequelae of hepatitis D infection

A
  • severe infection
  • liver failure
  • death
83
Q

lab results indicative of acute hepatitis D infection

A

HBsAg positive (requires hep B coinfection)
hepatitis D IgM positive
markedly elevated LFTs

84
Q

who is at risk for hepatitis A

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
85
Q

symptoms of all types of viral hepatitis

A
  • fever
  • fatigue
  • loss of appetite/anorexia
  • nausea/vomiting
  • abdominal pain
  • gray-colored bowel movements
  • joint pain
  • jaundice
86
Q

is there a potential for chronic infection from hepatitis A?

A

no

most people with acute disease recover with no lasting liver damage

87
Q

% of adults >14yo with acute hepatitis A infection who will have jaundice

A

70-80%

88
Q

who is at risk for hepatitis B

A
  • 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%)
89
Q

incubation periods for folks with Hepatitis A, B, or C

A 
SHORTEST >>
hepatitis A (15-50 days; av 28)

hepatitis C (14-180 days; av 45)

hepatitis B (45-160 days; av 120)
>> LONGEST
90
Q

% of adults with hepatitis B who will have symptoms?

A

30-50% will develop symptoms

otherwise, asymptomatic
more likely to be asymptomatic if immunosuppressed (5-15% will show symptoms)

91
Q

how likely is chronic infection after hepatitis B infection?

A

if unimmunized,

> 90% of infants
6-10% of adults

92
Q

who is at risk for hepatitis C infection

A
  • 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
93
Q

% of adults with hepatitis C who will have symptoms?

A

20-30% develop symptoms of acute disease

94
Q

how likely is chronic infection after hepatitis C infection?

A

75-85% chance of becoming chronic

15-25% chance of clearing the virus

95
Q

severity of hepatitis A infection?

A

most people with acute disease will recover with no lasting liver damage! rarely fatal. never becomes chronic

96
Q

severity of hepatitis B infection?

A

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

97
Q

severity of hepatitis C infection?

A

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

98
Q

who is recommended to have Hepatitis B Screening for chronic infection?

A
  • 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
99
Q

who is recommended to have Hepatitis C screening for chronic infection?

A
  • 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
100
Q

treatment for hepatitis A, generally

A

no medication is available

supportive measures only

101
Q

treatment for hepatitis B, generally

A

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

102
Q

treatment for hepatitis C, generally

A

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

AGPCNP Board Prep (21 decks)

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