Week 8 GI Flashcards

1
Q

GI red flags in adult/children

A
  • Rectal bleeding
  • Weight loss
  • Unexplained fever
  • Anemia
  • GI malignancy
  • Nocturnal diarrhea (ulcerative colitis)
  • Acute bowel changes in > 50 yrs old
    • Bowel shape, freq, caliber of movement
  • Abdominal mass
  • Persistent vomiting
  • Jaundice
  • Dysphagia
  • Ordynophagia - ongoing GERD sx or GI malignancy
  • Perianal disease
    • Perianal abscess or fistula
  • Arthritis
    • Inflammatory bowel disease
  • Bilious emesis
  • Jaundice
  • Hematemesis
  • Family hx of colon cancer
  • Poor weight gain / linear growth
  • Absent pubertal changes
  • mass, blood in stool
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2
Q

Crohns disease

A
  • Chronic inflammation of GI tract with extraintestinal sx’s
  • environmental trigger
  • mouth to the anus (primarily in ileocolon)
  • skipped lesions, cobblestone with granulomas, fissured lesions
  • “Transmural” = involves the WHOLE thickness of the colon; all layers
  • Cron skipped on the cobblestone”
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3
Q

Crohns on exam

A
  • Cardinal sxs: abdominal pain, diarrhea (bleeding), fatigue, and SIGNIFICANT weight loss
  • Growth failure
  • Vague cramping
  • Erythema nodosum, psoriasis
  • Uveitis, episcleritis
  • Oral ulcers/canker sore
  • Decreased ROM, polyarthritis, sacrolitlits
  • Rectal fissures, fistulas
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4
Q

crohns treatment

A
  • mild/remission: mesalamine (aminosalicylates)
  • mod-severe: corticosteroids
  • immunosupppresants
  • immunomodulators: infiximab (induction/maintenance)
  • antibiotics: fistulas or C diff
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5
Q

Crohns diagnostics

A
  • CBC, CRP, ESR, CMP (kidney function, electrolytes, glucose), vitamin b12, folate, iron
  • calprotectin (confirms bowel inflammation)
  • Albumin for blood loss
  • Stool for ova and parasites, fecal leukocytes, C. Diff.
  • Abdominal CT or MRI to monitor
  • Endoscopy (cobblestone)
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6
Q

Ulcerative colitis

A
  • chronic inflammation of colonic mucosa or submucosal layer in colon and rectum only
  • _Co_litis _Co_ntinuous” lesions
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7
Q

ulcerative colitis systemic sx’s

A
  • fatigue, sometimes weight loss
  • hematochezia (massive hemorrhage)
  • stool blood/mucus
  • Arthritis
  • Erythema nodosum, pyoderma gangrenosum, oral ulcers
  • Clubbing
  • uveitis, scleritis
  • Sclerosing cholangitis
  • Autoimmune hemolytic anemia
  • Venous and arterial thromboembolism
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8
Q

risk factors for colon cancer

A
  • Age > 50
  • longer duration of disease
  • younger onset
  • severity of inflammation
  • primary sclerosis cholangitits
  • Family history of colorectal cancer
  • Inflammatory bowel dz
  • Smoking
  • Familial polyposis syndrome
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9
Q

if patient has 1st degree relative with colon cancer, when to start screening?

A

10 years prior to 1st degree relative’s diagnosis, then every 5 years thereafter

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10
Q

when does risk for colon cancer increase? when to screen?

A
  • age > 50 yrs
  • prior colorectal cancer
  • ulcerative coliitis
  • genetics
  • familial polyposis syndrome
  • long term cigarette smoking
  • high fat high caloric diet

risk can increase 7-8 yrs after disease onset w/ risk of 0.5% per year after

  • after diagnosis, screen 7-8 years post diagnosis then next 2-3 years
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11
Q

once in remission for IBD, more likely to relapse but also want to evaluate for

A

infectious causes Salmonella

  • Shigella
  • Campylobacter
  • Clostridium difficile
  • Yersinia
  • Amebiasis
  • Escherichia coli 0:157:H7
  • STIs including Neisseria gonorrhoeae and Chlamydia trachomatis
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12
Q

risk factors for UC

A
  • History of Campylobacter infection
  • A first-degree relative with ulcerative colitis
  • History of nontyphoid Salmonella infection

SMOKING is NOT a risk factor but it is for Crohn’s disease

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13
Q

Irritable bowel syndrome (IBS) diagnosis: Rome IV

A

Rome IV

  • recurrent abdominal pain at least 1x/week x 3 months, with 2 or more of:
    • with defecation
    • Change in freq of stools
    • change in form/look of stool (Bristol stool scale)
  • symptom onset at least 6 months before diagnosis
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14
Q

Irritable bowel syndrome (IBS) diagnosis: Manning criteria

A

3 or more:

  • feeling of incomplete evacuation;
  • passage of mucus;
  • visible abdominal distention;
  • pain relief with defecation;
  • looser stool at pain onset;
  • more frequent stools at pain onset.
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15
Q

diagnosing functional bowel disorder always assumes there are NO

A

structural, biochemical, organic explanation for the symptoms

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16
Q

IBS patho

A
  • altered gut reactivity (motility, secretion)
  • hypersensitive gut with enhanced visceral perception and pain
  • disordered gut-brain interaction
  • other:
    • altered inflammatory mediators
    • altered gut serotonin regulation
    • bacterial overgrowth
    • genetic predisposition
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17
Q

IBS workup

A
  • assess for any alarm/red flags
  • if none, get stool hemoccult & CBC
  • ESR, CMP, stool studies depend on clinical pic
  • lactose free diet (r/o lactose intolerance)
  • if > 50 & didn’t get routine colon cancer screening OR have red flags = get colonoscopy
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18
Q

if have IBS-C (constipation), what workup?

A
  • therapeutic trial of fiber
  • consider partial colonic obstruction or non IBS causes of dysmotility too
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19
Q

if have IBS-D (diarrhea), what workup?

A
  • get stool culture, ova and parasites, celiac sprue/dz workup, or bowel biopsy (depending on clinical picture).
  • If new symptom onset 45 years or older = colonoscopy to rule out microscopic colitis
    • if negative, consider therapeutic trial of loperamide
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20
Q

if have IBS pain predominant, what workup?

A
  • get abdominal x-ray
    • if negative for small bowel obstruction (SBO), consider therapeutic trial of an antispasmodic medication
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21
Q

IBS treatment for mild sx’s

A
  • Symptom diary
    • food triggers (sorbitol, lactose, caffeine, eating in excess, beans, raw vegetables)
    • psychosocial triggers
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22
Q

IBS med treatment for moderate to severe sx’s for IBS-C:

A
  • increased dietary fiber (25g/day) – soluble fiber > insoluble
  • polyethylene glycol (MiraLAX) – osmotic laxative
  • lubiprostone – chloride channel activator that increases intestinal fluid secretion to improve intestinal transit5
  • linaclotide– guanylate cyclase c agonist; increased intestinal chloride and bicarbonate secretion leads to acceleration of intestinal transit, may also have analgesic effect
  • plecanatide – guanylate cyclase c agonist
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23
Q

IBS med treatment for moderate to severe sx’s for IBS-D:

A
  • loperamide – antidiarrheal, inhibits peristalsis; PRN
  • alosetron – 5-HT receptor antagonist, decreases colonic motility. Approved for use in women with severe IBS-D who have failed conservative treatment for greater than 6 months. Adverse events include ischemic colitis and severe constipation.
  • eluxadoline – mu-opioid receptor agonist + delta opioid receptor antagonist + kappa opioid receptor agonist; reduces visceral pain and diarrhea with constipation side effect. Avoid use in patients who do not have a gallbladder, carries FDA warning for risk of pancreatitis.
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24
Q

IBS med treatment for moderate to severe sx’s for IBS pain predominant

A
  • hyoscyamine, dicyclomine, peppermint oil – antispasmodics that reduce smooth muscle contractions and visceral hypersensitivity
  • antidepressants (TCAs, SSRIs )
  • antibiotic (Rifaximin) – alters gut microbiota; given as 2-week course
  • probiotics
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25
Q

IBS psychological treatment (when sx severe enough to impair QOL)

A
  • Cognitive behavioral therapy, dynamic psychotherapy, hypnosis and stress management, and relaxation
    • effective in reducing abdominal pain and diarrhea (but not constipation) and anxiety
  • Tricyclic antidepressants
    • alters GI physiology, has neuromodulatory effects and analgesic properties
    • if abdominal pain is frequent or severe
    • most commonly used is amitriptyline, desipramine
  • Selective serotonin reuptake inhibitors
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26
Q

if no GI red flags, and have abdominal pain with defecation,

A

don’t need routine testing for IBS

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27
Q

in pediatric, constipation presents as

A
  • hard or pebble like stools
  • parental reports of excessive straining or pain during efforts to pass stool
  • infants may also have a very wide range of normal stool frequency, including only 1 stool a week
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28
Q

< 4 month infants can use what as an osmotic agent?

A
  • corn syrup
  • fructose and sorbital = harder to digest, osmotic laxative in fruit juice, prune juice
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29
Q

Hirschsprung disease aka aganglionosis

A
  • extreme form of slow-transit constipation
  • bowel narrows at the areas that lack of slow transit
  • seen on contrast studies.
  • can see at birth if meconium is not passed in the first 48 hours of life but 60% with Hirschsprung will be dx’ed OUT of neonatal period.
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30
Q

Hirschsprung disease sx’s

A
  • recurrent abdominal distention
  • emesis
  • failure to thrive
  • acute enterocolitis
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31
Q

Hirschsprung disease diagnosis & treatment

A
  • rectal biopsy & histologic exam via suction technique
  • treatment: surgical removal of affected portion of intestine
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32
Q

causes/types of chronic constipation

A
  • Normal-transit (functional) constipation
  • Slow-transit constipation
  • Rectal evacuation (defecatory) disorders
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33
Q

Normal-transit (functional) constipation

A
  • a normal system that may have transient alterations leading to constipation (majority of pt)
  • tx: increasing fiber or osmotic laxative
    • if fails, indication of altered transit times, further management
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34
Q

Slow-transit constipation

A
  • reduced motility due to individual differences in bowel function
  • young females after puberty
  • diet can cause low stool volumes
  • tx: stimulant laxatives
    • increase intestinal motility and secretions BUT cramp/dependence long term
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35
Q

Rectal evacuation (defecatory) disorders

A

variations that limit or inhibit normal passage of stool out of the body

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36
Q

would you recommend diet and exercise for chronic constipation?

A

NO! is NOT effective with chronic constipation unless dehydration is the source of sx’s

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37
Q

Osmotic laxatives and poorly absorbed sugars (polyethylene glycol or lactulose) MOA

A
  • drawing water into the intestines along an osmotic gradient
  • take several days to work; less likely to cause the bloating and flatus of fiber, or the cramping
  • caution with sensitive electrolyte or volume status (renal or heart failure) as absorption of sodium, magnesium, or phosphorus is possible.
  • Dehydration!
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38
Q

stimulant laxatives (Senna) MOA

A
  • promote intestinal motility and secretions
  • work quickly, hours, but abdominal cramping
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39
Q

Stool softeners (eg, docusate sodium) MOA

A
  • detergents that allow water to more effectively interact with solid stool
  • preventative/adjunct to other methods or for prevention, rather than treatment, of constipation
    • give post op pt’s
40
Q

Enemas and suppositories MOA

A
  • distending the rectum, promoting increased peristalsis and relaxation of the internal sphincter
  • soften the stool directly (tap water, molasses), provide lubrication (soap suds, mineral oil), provide an osmotic load for increased water secretion by the intestine (phosphate), or topically stimulate colonic muscle contraction (bisacodyl suppositories).
41
Q

what meds decrease colonic motility?

A
  • opioids and tricyclic antidepressants (TCAs)
  • stimulant laxatives also effective when don’t know cause
  • if chronic opioid use, want to improve bowel motility
    • use peripherally acting mu-opioid receptor antagonist (PAMORAs) when Senna doesn’t work
42
Q

complication if kids hold in their poop

A

develop constipation because holding it stretches the rectum and lower colon, which decreases the tone, retention, and causes impaction leading to defamatory disorder

43
Q

encopresis

A

fecal incontinence or soiling, is the repeated passing of stool (usually involuntarily) into clothing.

44
Q

secondary encopresis

A

liquid stool leaks around impaction stool and we THINK it’s diarrhea when it’s not

45
Q

if child has pain/discomfort with stooling, they hold it in and this can cause

A

perianal fissures, mild infections (strep), perianal abscess

46
Q

treatment for child with impaction

A
  • laxative/enemas over 2-5 days since manual is traumatizing
  • afterwards, continue laxatives and maintain consistent daily evacuation so colon can return to normal tone.
  • then wean off stimulant laxative WHILE increasing soluble fiber
47
Q

when to do abdominal xray for impaction?

A
  • compliance
  • hard to assess for completeness of evacuation
48
Q

treatment for adult with impaction

A
  • manual disimipaction
  • once removed, biofeedback used to retrain evacuation process and help relax pelvic floor with laxatives as needed
49
Q

constipation physical examination includes

A
  • Evaluation perineum for scarring, fistulas, fissures, or external hemorrhoids which may lead to painful stooling.
  • Visualization of the perineum during a Valsalva maneuver shows perineal descent of 1-3 cm
    • Failure of the pelvic floor to move significantly = failure to relax the pelvic floor muscles during defecation.
50
Q

In adults or children who have failed to respond to initial therapies to constipation

A
  • digital rectal examination to assess for retention or impaction of stool, rectal masses, or anal strictures
  • in children, monitoring abdominal girth can also provide an indication of progressive constipation.
51
Q

if suspect defecatory or anatomic issue, what work up?

A

physiological testing: colonic transit testing (swallows a radiopaque marker in a capsule and gets serial X-rays)

anorectal manometry (feels pressure during poop contraction/relaxation of sphincters & sensation)

52
Q

laboratory testing indicated in cases with constipation when

A

larger collection of symptoms

get thyroid function, calcium, electrolytes, CBC, urinalysis based on history

53
Q

reasons for a colonoscopy?

A
  • young/healthy with acute bowel change
  • >50 years old
  • red flags
54
Q

primary (idiopathic) constipation

A
  • irritable bowel syndrome (constipation predominant)
  • disordered colonic transit (normal or slow transit)
  • evacuation disorders (a failure to adequately empty the rectal contents)
55
Q

secondary constipation

A
  • related to medical and psychogenic conditions, medications, structural anomalies, and lifestyle
  • ignoring the urge to defecate; inadequate fiber or fluid intake; medications; pregnancy; hypothyroidism; hypoparathyroidism; diabetes; hypokalemia; hypercalcemia; motility disorders; psychological disturbances; and neurologic disorders.
56
Q

celiac disease is immune mediated and triggered by ______.. it usually ____

A

exposure and coexists with other autoimmune disorders like women with history of hypothyroidism

57
Q

methylcellulose

A

bulk laxative, absorbs water to soften stool consistency and increase mass

58
Q

Docusate

A

detergent; stool softener

59
Q

first step in evaluating ASYMPTOMATIC person with elevated liver transaminases:

A
  • repeat tests to confirm abnormality
  • look for patterns in liver tests
60
Q

Predominant elevations of the transaminases (AST and ALT) are indicative of

A

hepatocellular injury

61
Q

ALT vs AST

A

ALT more specific to liver

AST more specific to cardiac muscle, skeletal muscle, kidneys, brain, pancreas, lungs, leukocytes, and erythrocytes

62
Q

predominantly elevated alkaline phosphatase liver enzyme compared to all

A

think cholestatic injury (form abnormal or absent bile flow)

cholestasis can happen without jaundice bc liver maintains capacity to secrete bile until severe

63
Q

if bilirubin is elevated, want to determine if

A

hyperbilirubinemia is unconjugated (from increased hemolysis or impaired bilirubin conjugation (Gilbert’s or Crigler Najjar type 1 or 2) or conjugated

64
Q

conjugated hyperbilirubinemia can occur with

A

cholestasis, impaired hepatic release of conjugated bilirubin (eg, Dubin-Johnson or Rotor syndromes), extrahepatic obstruction (eg, stones, strictures, or tumors), or hepatocellular injury

65
Q

to diagnose unconjugated hyperbilirubinemia

A

look for signs of hemolysis on a peripheral smear

additional labs that shows hemolysis is high lactate dehydrogenase (LDH) and low serum haptoglobin

66
Q

with a conjugated hyperbilirubinemia, need to determine if

A

there is a extra hepatic obstruction using imaging ( if yes, requires surgery)

67
Q

what liver panel/function test consists of?

A
  • Albumin, a protein made in the liver
  • Total protein. This test measures the total amount of protein in the blood.
  • ALP (alkaline phosphatase), ALT (alanine transaminase), AST (aspartate aminotransferase), and gamma-glutamyl tansferase (GGT). These are different enzymes made by the liver.
  • Bilirubin, a waste product made by the liver.
  • Lactate dehydrogenase (LD), an enzyme found in most of the body’s cells. LD is released into the blood when cells have been damaged by disease or injury.
  • ProthrombIn time
68
Q

lab values that tell you hepatocellular injury

A

elevated AST, ALT

69
Q

8 main hepatic causes of chronically elevated aminotransferase levels

A
  • Alcohol abuse
  • Medications
  • Chronic hepatitis B and C infection
  • Steatosis and nonalcoholic steatohepatitis (aka nonalcoholic fatty liver disease or NAFLD)
  • Autoimmune hepatitis
  • Hemochromatosis
  • Wilson disease (in < 40 years old pts esp if have psychiatric illness)
  • Alpha1-antitrypsin deficiency
70
Q

Nonhepatic causes of chronically elevated aminotransferase levels

A
  • Celiac sprue
  • Inherited disorders of muscle metabolism
  • Acquired muscle diseases
  • Strenuous exercise
71
Q

any liver abnormalities, you want to ask about….

A

alcohol use history!

inquire about drug use, OTC meds (NSAIDs, antibiotics, statins, antiepileptic meds), herbs

72
Q

if there is AST/ALT split (ratio of AST to ALT is elevated at least 2:1)…

A
  • SUSPICIOUS OF ALCOHOL ABUSE/alcohol liver disease
  • 2x level of Gamma-glutamyl transferase (GGT) also sus
73
Q

Drug-induced liver injury (DILI)

A
  • dose related
  • acetaminophen most common cause
  • antiobitcs, antiepileptics, NSAIDs, antituberculosis drugs
74
Q

What meds can cause Hepatocellular Injury Pattern (elevated aminotransferases)?

A
  • allopurinol
  • diclofenac
  • isoniazid
  • phenytoin
  • valproic acid
75
Q

risk factors for hepatitis C infection

A
  • blood transfusions, intravenous [IV] drug use, occupational exposures, tattoos, and body piercing)
  • higher in men sex men
  • ALWAYS ASSESS risk factors!
76
Q

hepatitis B and A transmission

A
  • Hepatitis B:
    • injectables
    • sexual transmission
  • Hepatitis A::
    • POOR sanitation
77
Q

if they have/or had signs of insulin resistance, hypertension, and/or hyperlipidemia, be concerned about

A

non alcoholic fatty liver disease

78
Q

treatment for physiologic GER

A
  • offer non pharm & reassurance, explaining patho to parents
  • don’t over feed
  • no supine for 20-30 mins after feeds
  • flat prone/L side lying only when infant awake.
  • THICKENING feeds with rice cereal
79
Q

GERD sx’s in peds

A
  • GER with complication
  • Regurgitation w/ or w/o vomiting
  • Irritability, excessive crying, not sleeping well
  • Wheezing or cough, poor weight gain, stridor
  • back arching
80
Q

pediatric gerd red flags

A
  • Onset after six months
  • Neurological signs
  • Bilious or projectile vomiting
    • Think pyloric stenosis
  • Bloody emesis
  • Bloody stool
  • Nocturnal vomiting
  • Abdominal distention
  • Diarrhea or constipation
  • Lethargy
81
Q

GERD treatment peds

A
  • 1st line: lifestyle modifications
  • Sx’s mild to moderate:
    • Trial of hydrolyzed formula,
    • no dairy for mom
    • small freq feeds for 2-4 weeks FIRST.
    • If fails…try famotidine for 4 weeks
      • if fails, try omeprazole or lansoprazole x 3-4 weeks MINIMUM
  • Refer if don’t work
82
Q

GERD sx’s in adults

A
  • heart burn/discomfort or burning behind the sternum, may radiate to neck
  • Worse after eating and lying supine
  • Better after antacids
  • Regurgitation
  • chronic cough
  • globus
  • hoarseness
  • postnasal drip
  • dysphagia
  • worsening asthma/wheezing
83
Q

non pharm GERD tx in adults

A
  • lifestyle / diet
  • avoid caffeine, carbonated beverages, alcohol, chocolate, fatty and spicy foods
  • weight loss in overweight pt
  • no large meals for 3 hrs before bed
  • don’t overeat
  • prop HOB when laying
84
Q

GERD pharm tx in adults

A
  • want to reduce acid secretion
  • PPIs (83% effective) TWICE DAILY for severe sx’s x 2-4 months
    • dexlansoprazole, esomeprazole, lansoprazole, omeprazole, pantoprazole
  • H2 blockers 52%
    • cimetidine, famotidine, nizatidine, ranitidine
  • SE: h/a diarrea, constipation, abd pain, hip fracture, 2x C diff risk
  • OTC antacids 20% for breakthrough sx’s

either step up with H2 blocker, inc dose until PPI or step down with PPI BID dec dose

85
Q

cirrhosis clinical presentations early vs late

A
  • Weakness, malaise, dark urine, pale stool, hematemesis, abdominal pain
  • Derm changes : skin pruritis, spider angiomata, palmer erythema, nail bed changes
  • jaundice, clubbing, portal HTN, epigastrium venous hum, gynecomastia, ascites, peripheral edema, neuro symptoms (encephalopathy)
86
Q

cirrhosis diagnostics

A
  • LOW albumin, platelets, anemia, pancytopenia
  • HIGH PT/PTT, bilirubin
  • normal/high AST/ALT
87
Q

gold standard for cirrhosis diagnosis & other imaging

A
  • Gold Dx: liver biopsy & find cause (invasive)
  • dx too: fibroscan (liver stiffness, non invasive) & fibrotest
  • ultrasound (liver size, portal circulation, ascites, tumor)
88
Q

MELD classification tool

A

predicts 3 month survival with cirrhosis regardless of cause

89
Q

treatment for hep B vs Hep C

A

hep B: antiviral

hep C: antiviral + polymerase inhibitors

90
Q

If have esophageal varies give

A
  • non selective BB (propranolol/nadolol)
  • EGD to see varicies and ligation if can’t tolerate BB
  • Na restriction 1-2g/day
91
Q

ascites and hepatic encephalopathy treatment

A

ascites: lasix, Na restriction, antibiotics

hepatic encephalopathy: lactulose or neomycin (decreases ammonia levels)

92
Q

cirrhosis non pharm

A
  • high fiber diet
  • 1.2g protein/day
  • dietician (high fiber/protein, low Na)
  • no ETOH, NSAIDs, illicit drugs
  • vaccinations
93
Q

celiac patho

A

gluten sensitivity to wheat, barley, rye proteins

changes in surface of small intestine tract/damage to villi = can’t absorb nutrients

94
Q

biggest complication of celiac disease

A

growth failure and fractures

95
Q

celiac risk factors

A

DM, thyroid dz, IgA deficiency, family hx, Down syndrome, Turner syndrome

Clinical Presentation: may be asymptomatic

96
Q

consider EGD if

A
  • failed empirical trial (4-8 wks PPI BID)
  • sudden onset of sx’s 50 yrs+
  • alarm sx’s (anemia, dysphagia, weightloss,, bleeding, odynophagia)
  • sx’s of stricture, ulceration
  • malignancy
97
Q

celiac sx’s

A
  • diarrhea, bloating, cramping, constipation
  • steatorrhea
  • weight loss
  • growth failure
  • FTT, prolonged fatigue
  • dermatitis herpetiformis (pic) - intense itchy rash w/ papules on extensors (elbows/knees)