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Primary Care > Outpatient GI for the PCP > Flashcards

Outpatient GI for the PCP Flashcards

1
Q

What are some common GI complaints in primary care setting?

A

Reflux/heartburn & dysphagia
Constipation
Diarrhea
Abdominal pain
Elevated LFTs/liver lesion pearls

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2
Q

Components of taking a GI history?

A

Duration/timing: acute vs chronic; time of day; triggers (eating/drinking, stress, etc)

Description of symptoms: quality, severity, location

Associated symptoms: both upper and lower GI sx (one often affects the other…); consider systemic processes (rash, joint s/s, fevers); red flag symptoms (see separate slide)

Treatments tried: historical and current

Prior evaluations: clinic visits, radiologic, procedural

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3
Q

What are some red flag symptoms in GI?

A

Dysphagia
Odynophagia
Early satiety
GI bleeding (melena/hematochezia) (upper or lower)
Unintentional weight loss
Unexplained change in symptoms (“new” IBS in a 70-year old probably isn’t a thing…)
Refractory symptoms
Unexplained iron deficiency anemia

Of note: if any red flag(s) symptoms present, refer for GI clinical visit and/or endoscopic evaluation

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4
Q

What is GERD?

A

GastroEsophageal Reflux Disease (also called heartburn)

Reflux of gastric contents into the esophagus + symptoms and/or complications

Not a single disease - multiple phenotypic presentations and different diagnostic considerations

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5
Q

How to make GERD diagnosis?

A

Suggestive symptoms

Characteristic mucosal injury seen at endoscopy and/or

Abnormal esophageal acid exposure demonstrated on pH monitoring study

Response to treatment

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6
Q

Components of a GERD-focused history?

A

Duration/timing: acute vs chronic; time of day; triggers (eating/drinking, stress, etc)

Description of symptoms: typical vs. atypical (acid reflux/heartburn, hoarse voice, cough, throat clearing, globus sensation)

Associated symptoms: dysphagia, constiption, red flag symptoms (dysphagia, odynophagia, refractory symptoms, longstanding, unevaluated sx, GI bleeding, early satiety, weight loss, night sweats, iron deficiency anemia)

Treatments tried: antacids, H2 blockers, PPIs, homeopathic/natural, lifestyle/dietary changes

Prior evaluations: prior GI clinic evals, ENT/laryngoscopy, EGD, pH testing

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7
Q

What is the first line treatment of GERD symptoms without red flag/alarm symptoms?

A

PPI trial (omeprazole MC)

Treatment takes time (70-80% relief at 4 weeks of PPI use)

Other: H2 blockers (typically less AEs than PPI but slower healing rate and slower heartburn relief than PPIs)

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8
Q

PPI pearls

A

Pre-prandial dosing is important (30-60 mins), taking with other medications is typically OK

PPIs are not necessarily forever medications (exceptions: LA grade C/D, EE (high relapse rate), Barrett’s)

Address modifiable risk factors and wean off/step-down when able/appropriate

Recommendations for medication monitoring vary (ex: AGA does not recommend monitoring Mg, creatinine, vitamin B12, vitamin D/calcium but use clinical judgement with each individual patient)

PPI tolerance

Refractory reflix

Strength varies (omeprazole as “standard” = omeprazole equivalent; pantoprazole and lansoprazole OE<1; esomeprazole and raberprazole OE >1)

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9
Q

Does taking PPIs increase the risk of GI infection?

A

Yes

“PPIs are the most effective medical treatment for GERD. Some medical studies have identified an association between the long-term use of PPIs and the development of numerous adverse conditions including intestinal infections, pneumonia, stomach cancer, osteoporosis-related bone fractures, chronic kidney disease, deficiencies of certain vitamins and minerals, heart attacks, strokes, dementia, and early death… High-quality studies have found that PPIs do not significantly increase the risk of any of these conditions except intestinal infections… the well-established benefits of PPIs far outweigh their theoretical risks.” - American College of Gastroenterology

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10
Q

What are some procedural work ups for GERD?

A

EGD, EGD WITH BRAVO capsule, pH impedence

These are typically done in GI setting, not primary care setting

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11
Q

What is EGD?

A

Direct esophageal evaluation with EGD camera

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12
Q

What are some benefits of EGD?

A

Tissue visualization (esophagitis grading, Barrett’s evaluation)

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13
Q

What are some drawbacks of EGD?

A

Invasive, requires sedation, wait time

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14
Q

What is EGD with BRAVO?

A

EGD + 72 hour acid-exposure monitoring w/ sx correlation

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15
Q

What are some benefits of EGD with BRAVO?

A

EGD pros as well as: symptom correlation, longer symptom monitoring period than pH

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16
Q

What are some drawbacks of EGD w/ BRAVO?

A

EGD cons as well as: capsule discomfort, capsule removal, monitoring device, no bile assessment

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17
Q

What is pH impedence?

A

24 hour acid/bile exposure monitoring w/ sx correlation

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18
Q

What are some benefits of pH impedence?

A

Acid + bile exposure assessment, symptom correlation

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19
Q

What are some drawbacks of pH impedence?

A

No tissue visualization, requires PO/swallow, uncomfortable, monitoring device, shorter symptom monitoring period than BRAVO

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20
Q

What is Barrett’s esophagus?

A

Damage to the lower portion of the tube that connects the mouth and stomach (esophagus)

Usually the result of repeated exposure to stomach acid (MC diagnosed in patients with long-term GERD (up to 10%))

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21
Q

How to treat Barrett’s esophagus?

A

Requires lifelong PPI (qd-BID) + surveillance EGDs

Get EGD q3-5y if no dysplasia, yearly if dysplasia (if + for dysplasia, endoscopic therapies (BARXX) available)

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22
Q

Cancer risk with Barrett’s?

A

Annual risk for esophageal adenocarcinoma is low (0.12 - 0.33% yearly)

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23
Q

How to screen for Barrett’s?

A

“Screening” should be based on risk assessment: M + chronic (>5 years) reflux and/or weekly sx + 2 risk factors

Risk factors: >5 years of symptoms, >50 yo, M, caucasian, central obesity, current/former smoker, first degree relative

Alcohol not a risk factor

Do not recommend screening in F unless multiple RFs present

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24
Q

What is a hiatal hernia?

A

A condition in which part of the stomach pushes up through the diaphragm muscle

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25
Q

How to treat hiatal hernia?

A

Lifestyle + PPI therapy first line

Surgical repair (Nissen fundoplication) - is a BIG surgery involving chest/abdominal cavities, so not an “easy fix”

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26
Q

GERD in pregnancy?

A

Common

Secondary to hormonal changes, slower GI transit time, increased intra-abdominal pressure

Most resolve post-partum; 20% have residual symptoms

Of note: do not scope during pregnancy (unless emergency) - requires anesthesia

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27
Q

GERD medications in pregnancy?

A

Antacids (need to consider composition): aluminum and Mg hydroxide are safe (class B); sodium bicarb and calcium carbonate are not safe (avoid, class C)

Alginate (Gaviscon, Maalox): generally acceptable (no FDA classification)

Sucralfate: acceptable (FDA risk category B)

H2 blockers (famotidine preferred): acceptble (FDA risk category B)

PPI: reserved for refractory symptoms; avoid omeprazole (class C), others are class B

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28
Q

What is dysphagia?

A

Difficulty initiating a swallow or sticking/choking distally

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29
Q

Is dysphagia ever normal?

A

Dysphagia is NEVER normal and ALWAYS warrants further evaluation

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30
Q

Differentiating factors of dysphagia:

A

Location: oropharyngeal and esophageal dysphagia

Type: solids and liquids (can help differentiate between underlying structural vs. functional problem)

Other types of “throat/swallowing” complaints:
odynophagia (painful swallowing), globus sensation (constant foreign body-like sensation), rumination/regurgitation (bringing things back up, voluntary vs. involuntary)

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31
Q

Components of a dysphagia-focused history?

A

Duration/timing: frequency of occurrence, how long after eating/drinking

Description of symptoms: solid food vs liquid vs pill, vomiting vs eventually goes down?

Associated symptoms: GERD sx, halitosis, food allergies, asthma, ectopic history, aspiration events, systemic dysmotility/connective tissue disease symptoms

Treatments tried: dietary modifications, elimination diets, prior dilations

Prior evaluations: prior GI clinic evals, EGD, esophageal manometry

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32
Q

Types of dysphagia?

A

Oropharyngeal, esophageal

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33
Q

Describe oropharyngeal dysphagia, causes, and testing

A

Difficulty initiating swallow, excessive chewing, “gets stuck in my throat”, coughing with eating

Structural causes: Zenker’s, cervical osteophytes/surgery, cancer

Functional causes: dementia, stroke, Parkinson’s, ALS, other neuro

Testing: modified barium swallow study/video swallow, SLP referral

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34
Q

Describe esophageal dysphagia, causes, and testing

A

Sticking in esophagus, vomiting during/after meals, “I have to push it down with water”

Structural causes: stricture/ring/web, EoE, cancer, external compression

Functional causes: esophageal spasm, dysmotility disorders (presbyesophagus, achalasia), scleroderma/CTD

Testing: esophagram, EGD, esophageal manometry

35
Q

Explain what an esophagram evaluates and the benefits/drawbacks of the test

A

Evaluate for: dysmotility, hiatal hernia, strictures, masses

Gastrografin vs. barium (gastrogafrin is toxic to lungs if aspirated so use barium in those high risk patients)

Benefits: non-invasive, no sedation, fast

Drawbacks: no mucosal evaluation, non-therapeutic, correlates poorly w/ GERD

36
Q

Explain what an EGD evaluates and the benefits/drawbacks of the test

A

Evaluate for: thickening on CT, esophagitis, strictures, masses

Benefits: direct visualization, is diagnostic and therapeutic (tissue biopsy, dilations, stent placement)

Drawbacks: invasive, requires sedation, wait time, not as helpful with motility issues

37
Q

Explain what manometry evaluates and the benefits/drawbacks of the test

A

Evaluate for: dysmotility, hiatal hernias

Benefits: no sedation, definitive diagnosis, guides treatment

Drawbacks: invasive, discomfort, requires PO and following commands

38
Q

Components of a constipation-focused history?

A

Duration/timing: bowel habit history (include childhood/teen/young adult), stools/week

Description of symptoms: size, appearance, consistency, “what does constipation mean to you?”

Associated symptoms: straining/incomplete evacuation, abdominal pain/bloating, overflow diarrhea, bleeding

Treatments tried: dietary modifications, fiber supplements, OTC/Rx laxatives, enemas/suppositories/manual disimpaction

Prior evaluations: prior GI clinic evals, imaging, sitz marker eval, pelvic floor assessment, colonoscopy

39
Q

Components of constipation work up?

A

DRE: assess for fecal impaction, distal massess

Labs: assess for causative/associated conditions (ex: CBC, BMP, TSH, celiac panel (IgA + TTG))

Abdominal XR: assess to objectively assess stool burden and rule out obstruction/ileus/etc

Sitz marker AXR: assess for dysmotility vs. pelvic floor dysfunction

CT w/ contrast: assess for large masses, other intra-abdominal abnormality/lesions, +AXR benefits

Gastrografin enema: assess for masses/strictures in the descending/sigmoid colon (of note: no longer therapeutic)

Colonoscopy: assess for masses/strictures

Pelvic floor eval: ano-rectal manometry (tone/spasm, stretch tolerance), defecography (prolapse, incomplete evacuation), EMG (sensory/motor evaluation); helps decide treatment (biofeedback, PT, surgery)

40
Q

How to interpret a sits marker test?

A

General protocol:
Day 1: patient takes 1 capsule (usually 24 markers)

NO laxatives/enemas, etc

Day 5: get abdominal XR

Assess location/number of markers:
If <20% (about 6 rings) retained: normal

If >20% of markers retained and located diffusely/colonic: slow colonic transit/dysmotility

If >20% markers retained and majority located in rectum/rectosigmoid: pelvic floor dysfunction

41
Q

How to manage constipation OTC?

A

Soluble fiber, insoluble fiber, stool softener/lubricant, osmotic, saline, stimulant

Of note: patient can become dependent on stimulant laxatives if used chronically

42
Q

Give examples of OTC constipation medications

A

Soluble fiber: psyllium, inulin, oats, fruits, barley, legumes

Insoluble fiber: wheat bran, methylcellulose, wheat, rye, grains

Stool softener/lubricant: colace (sodium docusate), mineral oil, glycerin suppository

Osmotic: MOM, Sorbitol, Miralax/PEG3350

Saline: MgCitrate

Stimulant laxative: dulcolax/Fleet (bisacodyl), senokot (senna), ex-lax (sennosides), castor oil, aloe

43
Q

Give examples of prescription medications for constipation

A

Linzess (linaclotide)
Amitiza (lubiprostone)
Trulance (plecanatide)
Motegrity (prucalopride)
Movantik (naloxegol)

Considerations: pill form, often expensive, generally requires specific diagnosis + PA, clinical monitoring/dose adjustment, no lab parameters

44
Q

Constipation pearls

A

Constipation” doesn’t mean the same thing to everyone… (are you getting out what you’re putting in?)

Dietary and lifestyle factors are important!

Consistency is key

Keep pelvic floor disorders on your radar – particularly in F w/ prior pregnancies

Unexplained changes in bowel habits and unevaluated bleeding warrant colonoscopy

45
Q

Describe acute/persistent/chronic diarrhea

A

The passage of a greater number of stools of decreased form from baseline

Some definitions additionally specify: abrupt onset, 3 or more episodes in 24 hours, loose or liquid consistency

Acute diarrhea: duration <14 days
Persistent diarrhea: duration 14-30 days
Chronic diarrhea: duration >30 days

46
Q

Components of a diarrhea-focused history?

A

Duration/timing: baseline/preceding bowel habits, triggering event (food, medication, event, travel, stress, etc), stools/day (ask about days of missed/no stools), night time stooling

Description of symptoms: appearance (oily, watery, “mush,” etc), urgency, incontinence, tenesmus

Associated symptoms: abdominal pain/bloating, bleeding, weight loss

Treatments tried: dietary modifications, fiber supplements, OTC/Rx anti-diarrheals, laxatives

Prior evaluations: prior GI clinic evals, imaging, diagnostic colonoscopy (with biopsy)

47
Q

Components of a diarrhea work up?

A

DRE: assess for fecal impaction, distal masses, prolapse

Labs: assess for causative/associated conditions (CBC, BMP, TSH, celiac panel (IgA + TTG))

Stool studies: assess for acute causes (Cdiff, enteric pathogens) or subacute/chronic causes (acute work up plus enteric parasites, O&P, fecal calprotectin, pancreatic elastase, fecal fats (qualitative vs 72h quant))

AXR: assess for overflow/constipation

CT w/ contrast: assess for enteritis/colitis and other intra-abdominal abnormality/lesions

EGD with biopsy: assess for histologic evidence of Crohn’s, celiac

Diagnostic colonoscopy: assess for endoscopic/histologic inflammation, strictures, lesions

Video capsule: assess for small bowel luminal evaluation (don’t order if prior stricture/obstruction due to high likelihood of capsule getting stuck)

Breath testing: assess for SIBO (bacterial overgrowth), fructose/lactose (intolerances)

48
Q

Acute diarrhea management?

A

Dietary/lifestyle modifications: BRAT diet + electrolyte rich fluids

Treatments: Bismuth subsalicylate 525mg, imodium/loperamide 4mg + 2mg, pre/probiotics

Medications: not required in non-severe diarrhea

49
Q

Abx regimen for diarrhea?

A

Abx only warranted for Traveler’s diarrhea

(3-day course, generally FQs (macrolide if Campylobacter risk, fevers), can combine w/ loperamide)

50
Q

Chronic diarrhea management?

A

Diarrhea + no other symptoms: Benefiber, Imodium, Lomotil

IBS-D: anti-spasmodics (dicyclomine, hyoscyamine), TCAs (amitriptyline), viberzi/eluxadoline

Celiac disease: gluten-free diet

Bile acid salt: cholestyramine/Colestid

EPI: supplemental enzymes (Creon/Viocase)

SIBO: Rifaximin/Xifaxin, other abx

Microscopic colitis: imodium, peptobismol, budesonide, biologics

IBD: 5-ASA, immunomodulators, biologics, tincture of opium

Overflow: fiber, treat as constipation; avoid combining anti-diarrheals/laxatives

51
Q

Diarrhea pearls

A

The most common cause of non-acute diarrhea in GI clinic? NOT diarrhea (consider overflow - variable consistency, missed days of stooling; convincing a patient with overflow diarrhea to take laxatives is tricky - utilize imaging and DRE)

Refer to GI AFTER appropriate ACUTE diarrhea work-up is complete

Unexplained changes in bowel habits and unevaluated bleeding warrant diagnostic colonoscopy (request biopsies!)

52
Q

Colorectal cancer screening guidelines?

A

ACG recommends screening between age 45 - 75 years old (but consider the whole patient)

Stool tests good alternative for “low risk” patients (no personal/FMHx of pre-cancerous polyps, cancer, symptoms)

Blood test, capsule not recommended

Any positive non-invasive test requires a follow-up colonoscopy

53
Q

Important history to obtain for abdominal pain

A

Duration of symptoms
Description of symptoms (location, timing, relationship to eating/stooling)
Prior surgeries
Associated symptoms (red flag features)
Current/prior treatments (and duration) (lifestyle, dietary, medications)
Prior evaluations

54
Q

Red flag features of abdominal pain

A

Hematochezia/BRBPR
Severe abdominal pain
Weight loss, sweats
Family hx

55
Q

Primary care eval of abdominal pain

A

Testing is based on suspected diagnosis (important)

Labs: CBC, BMP, CRP, LFTs, lipase, stool testing (diarrhea work up, history of pylori)

Imaging: AXR, abdominal US RUQ, CT with IV contrast, HIDA, gastric emptying study

Procedural eval: EGD referral, colonoscopy

56
Q

Abdominal pain pearls

A

Severe/acute pain = ER (GI can’t help them any faster than PCP can…)

Subacute/chronic pain without diagnosis OR known GI diagnosis = GI clinic (GERD/gastritis, PUD, gastroparesis, IBS, other functional abdominal pain, IBD)

Chronic pain with prior work-up, without organic source = pain clinic (consider complementary treatment options)

Avoid narcotics!

Strategically image and refer

57
Q

IBD patient pearls

A

All IBD patients should have a primary GI provider

What to do when you see an IBD patient with a “flare”? = get labs (CBC, BMP, CRP + fecal calprotectin, c/difficile, enteric pathogens), send to ER if concerning exam, vitals, or story
10+ stools/day, significant bleeding, obstructive signs, dehydration, sepsis; contact primary GI provider for interval recommendations and continuity of care

DON’T prescribe prednisone without 1) ruling out c/difficile + 2) contacting GI (steroid used for GI is not a burst, instead is a 6-8 week rx so important that patient follows up for monitoring - just not something PCP should be doing)

58
Q

What is LFT testing and what are its components?

A

Liver “chemistries or tests” - reflect liver injury, not “function”

ALT, AST, alkaline phosphatase, bilirubin (direct and indirect)

59
Q

What is ALT and its normal range?

A

“Transaminase”: marker of hepatocellular injury

More specific to liver than AST

Degree of elevation directly associated w/ severity of injury

Normal range (IU/L): <55

60
Q

What is AST and its normal range?

A

“Transaminase”: marker of hepatocellular injury

Also found in renal, cardiac, brain, and skeletal muscle tissues

Normal range (IU/L): 10-40

61
Q

What is alkaline phosphatase and its normal range?

A

Marker of cholestatic liver injury

Also found in bone, bowel, and renal tissues

GGT and alk phos isoenzymes can differentiate

Normal range (IU/L): 40-150

62
Q

What is direct/indirect bilirubin and its normal range?

A

Results from the breakdown of RBCs, conjugation status helps determine location/type of problem

Unconjugated (indirect): bound to albumin, can indicate a pre-hepatic or hepatic issue

Conjugated (direct): conjugation occurs in the liver, indicates hepatic dysfunction

Normal range direct (IU/L): 0-0.5
Normal range indirect (IU/L): 0.2-1.2

63
Q

Additional liver labs?

A

INR: can be HIGH in acute liver failure or chronic liver disease; reflects synthetic liver function

Albumin/total protein: part of “LFTs” - accurate in that they do reflect liver function; can be LOW due to decreased liver production or concurrent poor PO intake

Platelets: can be LOW due to
decreased thrombopoetin production in the liver AND/OR splenic sequestration in the setting of splenomegaly/portal HTN

64
Q

Signs and symptoms of liver injury/condition/disease?

A

Jaundice/icterus,
abdominal pain, distension, n/v, acholic stools, dark urine, pruritis, confusion, lethargy, peripheral edema, abnormal bleeding/bruising, fever/chills, night sweats, arthralgias, rashes, unintentional weight loss

65
Q

Important PMHx, SHx, SrgHx, FMHx to obtain when evaluating liver injury/ condition/disease?

A

Alcohol use
Illicit drug use (IV, intra-nasal, meth)
Tattoos
Sexual history
Emigration, travel history
Medications (prescriptions (esp. antibiotics, OCP, statins), OTC (Tylenol), herbal/natural supplements, mushrooms, teas, barks, etc)
Animal/insect exposure
Immunosuppression
PMHx (esp. metabolic syndrome, autoimmune)
Surgical hx (esp. CCY, liver, Roux-en-Y)
FMHx of liver disease

66
Q

Differentiating the type of liver injury helps you refine your work-up: what are the types of liver injury patterns?

A

Hepatocellular injury: disproportionate elevation in AST, ALT compared to alk phos; liver tissue issue

Cholestatic injury: disproportionate elevation in alkaline phosphatase compared to AST, ALT; “flow” issue

67
Q

Types of hepatocellular liver injuries?

A

Fatty liver disease
Hemochromatosis
Viral hepatitis
Alcoholic hepatitis
Wilson’s disease
Alpha 1-antitrypsin
Autoimmune hepatitis
Ischemic hepatitis
Drug induced liver injury (DILI)
Extrahepatic

68
Q

Types of cholestatic liver injuries?

A

Primary biliary cholangitis (PBC)
Primary sclerosing cholangitis (PSC)
Congestive hepatopathy
Biliary obstruction
Drug induced liver injury (DILI)

69
Q

What to do/order for elevated LFT work up in primary care

A

LFTs, CBC, INR, BMP

HAV/HBV/HCV/HIV

Abdominal US

70
Q

Imaging/procedural evaluations of liver injuries in primary care

A

RUQ US (liver, gallbladder, bile ducts)
US complete (includes spleen + ascites)
US w/ liver dopplers (complete + portal/hepatic vasculature)
CT abdomen with IV contrast (liver, pancreas)
MRCP (non-contrast) (bile ducts)
MRI with IV contrast (solid organs)

71
Q

Define acute liver injury

A

Acute inflammatory process – can resolve or become chronic

Not meeting criteria for liver failure (ex: DILI with otherwise functional liver)

72
Q

Define acute liver failure

A

MUST HAVE:
Acute injury (no chronic disease background)
Coagulopathy
Encephalopathy

(ex: Tylenol OD causing acute hepatitis + INR 4 + patient obtunded)

73
Q

Define chronic liver disease

A

If an acute injury persists and becomes chronic/long-standing process

Degree of active inflammation and reversibility can be variable (ex: longstanding HCV w/ mild fibrosis)

74
Q

Define cirrhosis

A

End-stage liver scarring, irreversible, with evidence of chronic liver dysfunction

Compensated or decompensated disease

75
Q

Define acute on chronic liver failure

A

Newer term

Acute decompensation of existing cirrhosis with organ failure (ex: cirrhosis with EV hemorrhage and HRS)

76
Q

Define cholelithiasis

A

Stones in the gallbladder
NOT an emergency unless causing cystic duct obstruction/cholecystitis
Can cause biliary colic
Treatment is cholecystectomy – SURGERY

77
Q

Define choledocholithiasis

A

Stones in the bile duct
Should be dealt with URGENTLY
Call/message GI clinic (don’t wait for referral)!
Risk for gallstone pancreatitis, cholangitis
Treatment is ERCP – GI

*All patients should also have surgery to prevent recurrence

78
Q

Liver take-aways

A

They’re just “liver” chemistries – but consider the whole person

Comprehensive H&P is important

Consider both acute and chronic processes + causes both inside/outside the liver

Liver disease is a spectrum – diagnose, educate, and intervene early
SEE fatty liver disease and inform your patients

Refer to your GI or Hepatology Clinic when needed

79
Q

Elevated LFT pearls

A

Concern varies by duration and degree of elevation + associated deficits

Degree of elevation:
Mild (<2x ULN): eval, trend x3 (every 2-4 weeks), and refer if does not normalize
Moderate (3-4x ULN): eval, refer
Severe (4+x ULN): eval, low-threshold for urgent referral/call to Hepatology

Duration of elevation: chronic/subacute (refer to Hepatology), acute (eval, refer based on findings (GB, acute hepatitis))

Deficits: red flags (encephalopathy, coagulopathy)

Do not order pan-serologic work-up – liver clinic will take care of this

80
Q

Hepatitis/cirrhosis pearls

A

Hepatitis B: refer to Hepatology clinic for at least 1 time visit

Hepatitis C: HCV Ab will be POSITIVE in anyone with either current or resolved hepatitis C; you CAN become reinfected with HCV if you’ve tested positive/been treated before; HCV RNA quant determines CURRENT vs PRIOR infection

All NAFLD, NASH deserve at least 1 time Hepatology visit

All cirrhosis should be managed in Hepatology clinic

81
Q

Liver lesion pearls

A

Indeterminate liver lesion on US = “MR abdomen w/wo IV contrast” + Hepatology referral (include in MR order comments “triphasic liver study to evaluate liver lesion”,
CT abdomen w/wo contrast if unable to do MRI (also “triphasic liver study” in comments))

All liver lesions should be referred to Hepatology clinic unless imaging clearly read as “benign” and “not requiring further follow-up” by radiology

82
Q

Other liver wisdom

A

If predominantly INDIRECT hyperbilirubinemia: consider Gilbert syndrome (gene mutation that decreases UGT activity;
often triggered by stress, menstruation, illness, dehydration)

RUQ pain is rarely liver-related (cirrhosis DOES NOT cause pain)

RUQ abdominal pain with normal LFTs = General GI referral (not Hepatology)

83
Q

Always refer to GI when

A

GI symptoms with red flag features or concerning labs/imaging (dysphagia, black/bloody stools, fevers/night sweats, unintentional weight loss)

New celiac disease

Unexplained pancreatitis

Concerning pancreas or liver lesions on imaging

Choledocholithiasis (call the clinic for a procedure – don’t just order referral)

Elevated liver enzymes, NOS

Chronic liver diseases, cirrhosis

Inflammatory bowel disease

GI symptoms are present, and you feel uncomfortable managing the patient

Primary Care (11 decks)

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