Outpatient GI for the PCP Flashcards

Question

How to treat hiatal hernia?

Answer 1

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

Answer 2

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

Answer 3

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

Answer 4

Difficulty initiating a swallow or sticking/choking distally

Answer 5

Dysphagia is NEVER normal and ALWAYS warrants further evaluation

Answer 6

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)

Answer 7

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

Answer 8

Oropharyngeal, esophageal

Answer 9

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

Answer 10

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

Answer 11

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

Answer 12

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

Answer 13

Evaluate for: dysmotility, hiatal hernias Benefits: no sedation, definitive diagnosis, guides treatment Drawbacks: invasive, discomfort, requires PO and following commands

Answer 14

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

Answer 15

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)

Answer 16

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

Answer 17

Soluble fiber, insoluble fiber, stool softener/lubricant, osmotic, saline, stimulant Of note: patient can become dependent on stimulant laxatives if used chronically

Answer 18

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

Answer 19

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

Answer 20

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

Answer 21

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

Answer 22

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)

Answer 23

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)

Answer 24

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

Answer 25

Abx only warranted for Traveler's diarrhea (3-day course, generally FQs (macrolide if Campylobacter risk, fevers), can combine w/ loperamide)

Answer 26

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

Answer 27

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!)

Answer 28

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

Answer 29

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

Answer 30

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

Answer 31

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

Answer 32

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

Answer 33

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)

Answer 34

Liver “chemistries or tests” - reflect liver injury, not “function” ALT, AST, alkaline phosphatase, bilirubin (direct and indirect)

Answer 35

“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

Answer 36

"Transaminase”: marker of hepatocellular injury Also found in renal, cardiac, brain, and skeletal muscle tissues Normal range (IU/L): 10-40

Answer 37

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

Answer 38

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

Answer 39

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

Answer 40

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

Answer 41

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

Answer 42

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

Answer 43

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

Answer 44

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

Answer 45

LFTs, CBC, INR, BMP HAV/HBV/HCV/HIV Abdominal US

Answer 46

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)

Answer 47

Acute inflammatory process – can resolve or become chronic Not meeting criteria for liver failure (ex: DILI with otherwise functional liver)

Answer 48

MUST HAVE: Acute injury (no chronic disease background) Coagulopathy Encephalopathy (ex: Tylenol OD causing acute hepatitis + INR 4 + patient obtunded)

Answer 49

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)

Answer 50

End-stage liver scarring, irreversible, with evidence of chronic liver dysfunction Compensated or decompensated disease

Answer 51

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

Answer 52

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

Answer 53

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

Answer 54

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

Answer 55

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

Answer 56

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

Answer 57

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

Answer 58

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)

Answer 59

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