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GI Flashcards

1
Q

hydrochloric acid

A
  • secreted by parietal cells
  • dissolves food
  • activates pepsin (for protein digestion)
  • stimulates duodenal release of other digestive enzymes
  • kills bacteria
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2
Q

pepsin

A

digests proteins into small absorbable peptides

-prehormone pepsinogen secreted by CHIEF CELLS (to prevent autodigest) –> converted to pepsin by HCl in gastric lumen

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3
Q

parietal cells (make HCl) stim by 3 hormones

A

GASTRIN - stim stomach acid secretion and motility
-secreted by G cells –> enterochromaffin-like cells (ECL) secrete histamine –> parietal cells secrete HCl

HISTAMINE - produced by ECL cells in response to gastrin

  • stim parietal cells to secrete HCL
  • H2 blockers reduce acid secretion

ACETYLCHOLINE - directly stim parietal cells to secrete HCl
-parasympathetic (via vagus) inc GI activity “rest + digest”

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4
Q

somatostatin

A

produced by pancreatic delta (D-cells) acts as negative feedback –> INHIBITS SECRETION OF GASTRIN, insulin, glucagon, pancreatic enzymes and inhibits gallbladder contraction

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5
Q

mucus layer protection x2

A

mucus production

bicarbonate production

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6
Q

fx of large intestine (3)

A
  1. absorb remaining water from undigested food
  2. transport undigested food for removal via feces
  3. absorb certain vitamins produced by bacteria (K, biotin)
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7
Q

doudenum

A

responsible for most small int absorption, analyzes chyme and releases approp hormones:

SECRETIN - released by duodenum, inhibits parietal cell gastric acid production + causes pancreas to release bicarbonate (to buffer)

CHOLECYSTOKININ (CCK) - aids in breakdown of fats/proteins by stimulating pancreatic release of digestive enzymes

  • increases bicarb release (pancreatic enzymes work maximally in basic environment)
  • stimulates GB contraction + bile release (emulsify fats into smaller micelles)
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8
Q

pancreas (exocrine)

A

ACINAR CELLS - produce substances that drain into duodenum:

BICARBONATE: neutralizes gastric acid and activates the other enzymes below

PROTEASES (trypsinogen, chymotrypsinogen) - precursors to enzymes that breakdown protein

AMYLASE: breaks down starches into simple sugars

LIPASE: breaks down fats into fatty acids (w/ help of bile salts that inc surface area)

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9
Q

pancreas (endocrine)

A

ISLETS OF LANGERHANS:

  • INSULIN - produced by beta cells
  • GLUCAGON - produced by alpha cells
  • SOMATOSTATIN - produced by delta cells
  • suppresses release of GI hormones (CCK, gastrin, secretin, insulin, glucagon, panc enzymes)
  • in CNS, inhibits growth hormone production
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10
Q

esophagitis**

A

GERD MC cause, INFECTION IN IMMUNOCOMPROMISED (CANDIDA, CMV, HSV)

  • RF: pregnancy, smoking, obesity, ETOH use, chocolate, spicy foods, caustic
  • med causes: NSAIDs, BB, CCB, BISPHOSPHONATES, vitamins

-sx- ODYNOPHAGIA (painful swallow), DYSPHAGIA (difficult swallow), retrosternal chest pain

  • dx- upper endoscopy
  • candida - linear lesions (fluconazole)
  • CMV - large, shallow ulcers (gancyclovir)
  • HSV - small deep ulcers (acylcovir)
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11
Q

infectious esophagitis*

A

MC in immunocompromised pt
-CANDIDA, CMV, HSV

  • sx- ODYNOPHAGIA (PAINFUL SWALLOW), dysphagia, retrosternal chest pain
  • CANDIDA - LINEAR YELLOW-WHITE PLAQUES –> PO FLUCONAZOLE
  • CMV - LARGE SUPERFICIAL SHALLOW ULCERS –> GANCICLOVIR
  • HSV - SMALL, DEEP ULCERS –> ACYCLOVIR
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12
Q

eosinophilic esophagitis

A

allergic, inflammatory eosinophilic infiltration of esophageal epithelium

  • MC in children
  • MC assoc w/ ATOPIC DZ (food allergy, non food allergy, asthma, eczema, etc)
  • sx- dysphagia +/- reflux or feeding difficulties
  • dx- endoscopy - normal +/- MULTIPLE CORRUGATED RINGS, +/- white exudates
  • tx- remove foods w/ allergic response; inhaled topical corticosteroids (w/out spacer)
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13
Q

pill-induced esophagitis

A

MC w/ NSAIDs, BISPHOSPHONATES, potassium chloride, iron pills, vit C, BB, CCB

  • sx- odynophagia, dysphagia
  • dx- endoscopy - small, well-defined ulcers of various depths
  • tx- take pills w/ at least 4 oz water, avoid recumbency for 30-60 min
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14
Q

caustic (corrosive) esophagitis

A

ingestion of corrosive substances: alkali (drain cleaner, lye, bleach) or acids

  • sx- odynophagia, dysphagia, hematemesis, dyspnea
  • dx- endoscopy to see extent of damage or complications (perforation, stricture, fistula)
  • tx- supportive, pain med, IV fluids
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15
Q

GERD

A

transient relaxation of LES / INCOMPETENT LOWER ESOPHAGEAL SPHINCTER, esophageal motility disorders, delayed gastric emptying +/- hiatal hernia

-complications: esophagitis, stricture, Barrett’s, adenocarcinoma

  • sx- HEARTBURN (PYROSIS), often retrosternal and post-prandial (30-60 min), increased in supine position, relieved w/ antacids; REGURGITATION, DYSPHAGIA, cough at night (acid aspiration into lungs)
  • atypical sx: hoarseness, aspiration pneumonia, “asthma” broncospasm from acid, NON-CARDIAC CHEST PAIN (mc cause), weight loss
  • ALARM SX: DYSPHAGIA, ODYNOPHAGIA, WL, BLEEDING (suspect malignancy or cx)
  • dx- clinical
    1. ENDOSCOPY - often used 1st if persisetent sx or complications of gerd
    2. ESOPHAGEAL MANOMETRY - dec LES PRESSURE
    3. 24 AMBULATORY PH MONITORING GOLD STD

-tx-
Stage 1: lifestyle modification
Stage 2: “as needed” pharmacotherapy - antacids, OTC H2 receptor antagonists (famotidine, ranitidine)
Stage 3: scheduled therapy - H2RA, PPI, prokinetic agents
PPI DRUG OF CHOICE IN MOD-SEV DZ; NISSEN FUNDO IF REFRACTORY

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16
Q

BARRET’S*

A

esophageal ADENOCARCINOMA
-RELATED TO GERD
epithelium replaced by precancerous metaplastic columnar cells from cardia of the stomach (more used to acidic enviro but don’t belong there)

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17
Q

achalasia*

A

idiopathic proximal loss of GANGLION CELLS IN AUERBACH’S PLEXUS –> INC LES PRESSURE –> obstx + lack of peristalsis
(esophageal wall ganglion cells in auerbach’s plexus normal produce nitric oxide –> relaxes smooth muscle)
-MC in 50s

  • sx-
  • DYSPHAGIA TO BOTH SOLIDS + LIQUIDS, malnutrition, WL, dehydration, REGURGE, chest pain, cough (btw 25-60yo)
  • esophageal dilation may occur if left untreated
  • dx-
  • ESOPHAGEAL MANOMETRY - GOLD STD, shows inc LES pressure >40mmHg, dec peristalsis
  • DOUBLE-CONTRAST ESOPHAGRAM “BIRD’S BEAK APPEARANCE OF LES” (narrowing)
  • ENDOSCOPY may be needed to r/o carcinoma or other etiologies
  • tx- decrease pressure –> botox injection (6-12 mo), nitrates, CCBs, pneumatic dilation of LES, esophagomyomectomy
  • ddx- diffuse esophageal spasm or zenker’s diverticulum
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18
Q

diffuse esophageal spasm*

A

strong non-peristaltic esophageal contractions

  • sx- stabbing, chest pain worse w/ HOT OR COLD liquids/foods
  • dx- esophagram shows “corkscrew” esophagus
  • tx- nitrates, CCBs
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19
Q

zenker’s diverticulum

A

pharyngoesophageal diverticulum/pouch (false diverticulum - only involves mucosa)

  • sx- dysphagia, globus sensation, neck mass, regurge of foods, cough, halitosis (old trapped food in pouch)
  • dx- BARIUM ESOPHAGRAM
  • tx- diverticulectomy, cricopharyngeal myotomy; observe if small + asymptomatic
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20
Q

nutcracker esophagus

A

etio unknown; may be assoc w/ GERD
-EXCESSIVE CONTRACTIONS DURING PERISTALSIS

-sx- dysphagia (liq/solids), chest pain, asymtomatic

-dx- MANOMETRY - INC PRESSURE DURING PERISTALSIS
normal EGD/esophagram

-tx- lower esophageal pressure w/ CCB, nitrates, botox, sildenafil

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21
Q

boerhaave syndrome

A

FULL THICKNESS RUPTURE OF DISTAL ESOPHAGUS, assoc w/ REPEATED, FORCEFUL VOMITING or perf during endoscopy

  • sx-RETROSTERNAL CHEST PAIN WORSE W/ DEEP BREATHING OR SWALLOWING, hematemesis
  • CREPITUS ON CHEST AUSCULTATION due to PNEUMOMEDIASTINUM
  • dx-
  • CHEST CT/XRAY - pneumomediastinum, eso thickening
  • CONTRAST ESOPHAGRAM - DEFINITIVE + leakage,
  • tx-
  • small/stable: IV fluids, NPO, abx, H2 blockers
  • large/severe: surgical repair

Patient will be complaining of severe chest pain
PE will show Hamman crunch (mediastinal crackling with each heartbeat)
Chest X-ray will show pneumomediastinum
Diagnosis is made by esophogram with water-soluble oral contrast
Most commonly caused by a full-thickness esophageal rupture due to IATROGENIC> forceful vomiting
Most common location is left posterolateral distal esophagus
Treatment is emergent surgical consult and broad-spectrum antibiotics

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22
Q

mallory-weiss syndrome (tears)*

A

UGI bleeding from longitudinal mucosal lacerations @ gastroesophageal junction or the gastric cardia
-sudden rise in intragastric pressure or gastric prolapse into esophagus (excessive vomitting or bulimic)

  • sx- PERSISTENT RETCHING/VOMIT –> HEMATEMESIS AFTER ETOH BINGE, melena, hematochezia, syncope, abdominal pain, hydrophobia
  • dx- UPPER ENDOSCOPY –> SUPERFICIAL LONGITUDINAL MUCOSAL EROSIONS
  • tx- SUPPORTIVE, acid suppression promotes healing
  • severe bleeding –> epinephrine injection, sclerosing agent, band ligation, hemoclipping or balloon tamponade
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23
Q

esophageal webs + rings

A

web: thin membranes in mid-upper esophagaus
- may be congenital or acquired (ex complication of eosinophilic esophagitis)

  • PLUMMER-VINSON SYNDROME: dysphagia, esophageal webs, iron def anemia, atrophic glossitis
  • MC cauc F 20-60y
  • SCHATZKI RING: lower esophageal web - MC assoc w/ sliding hiatal hernias
  • sx- dysphagia esp to solids
  • dx- BARIUM ESOPHAGRAM (SWALLOW)
  • tx- ENDOSCOPIC DILATION IF SX BUT W/OUT REFLUX (antireflux surgery if not)
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24
Q

esophageal varices*

A

dilation of collateral submucosal veins as complication of PORTAL VEIN HTN

  • RF: CIRRHOSIS MC CAUSE ADULTS (portal vein thrombosis mc in children)
  • 90% w/ cirrhosis devo varices, 30% bleed (mortality rate 30-50% w/ 1st bleed) 70% rebleed w/in 1st year (1/3 rebleeds are fatal)
  • sx- UPPER GI BLEED, may devo s/s hypovolemia
  • dx- UPPER ENDOSCOPY + “red wale” markings + cherry red spots –> inc risk of bleed
  • TYPE/SCREEN, FLUIDS + NG TO EMPTY CONTENTS BEFORE ENDOSCOPY
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25
Q

HIATAL HERNIA TYPES

A

Type I: “SLIDING HERNIA” MC TYPE - 95%

  • GE jx and stomach slide into mediastinum (inc reflux)
  • tx- like GERD

Type 2: “rolling hernia” (paraesophageal)

  • fundus of stomach protrudes through diaphragm w/ GE jx remaining in anatomic location - may lead to strangulation
  • tx- surgical repair to avoid complications
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26
Q

esophageal neoplasms*

A

SQUAMOUS CELL - MC CAUSE ESOPHAGEAL CANCER WORLDWIDE (90%)

  • MC upper 1/3; peaks 50-70yo
  • RF: TOBACCO/ALCOHOL USE, decreased fruits/veg, achalasia, hot beverages, exposure to noxious stimuli, men, nitrates, inc incidence AA; dec incidence w/ NSAIDs + coffee

ADENOCARCINOMA - MC CAUSE IN UNITED STATES

  • MC younger pt, obese, caucasians, MC lower 1/3
  • ADENOCARCINOMA IS USUALLY COMPLICATION OF GERD leading to Barrett’s
  • sx-
  • DYSPHAGIA TO SOLID FOOD –> FLUIDS, odynophagia
  • WL, chest pain, anorexia, cough, hoarse, reflux, hematemesis +/- virchow’s node
  • hyperCa in pt w/ squamous cell (due to PTH)
  • dx- UPPER ENDOSCOPY W/ BX TEST OF CHOICE, double contrast barium esophagram
  • tx- resection, radiation, chemo (5-FU), depending on stg
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27
Q

gastritis*

A

superficial inflam/irritate of mucosa w/ mucosal injury

  • inbalance btw aggressive and protective measures
  • -> H. PYLORI MC
  • -> NSAIDs/ASA 2nd mc
  • -> acute stress (critically ill)
  • -> others: heavy ETOH, bile salt reflux, meds, radiation, trauma, ischemia, pernicious anemia, portal HTN
  • sx- MC ASYMPTOMATIC
  • epigastric pain, N/V, anorexia +/- upper bleed (minimal)

-dx- ENDOSCOPY GOLD STD = thick, edmatous erosions <0.5cm –> h.pylori testing

-tx-
-H.pylori positive –> “CAP” = clarithromycin + amox + PPI
alt metronidazole
-H.pylori negative –> acid suppresion: PPI, H2 block, antacids
-pharm prohylaxis for pt at high risk for stress-related: IV PPI or H2

Acute: NSAIDs > alcohol
Type A chronic: pernicious anemia
Type B chronic : H. pylori

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28
Q

gastropathy

A

mucosal injury w/out evid of inflammation

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29
Q

peptic ulcer disease*

A
  • DEC PROTECTIVE FACTORS IN GASTRIC ULCER
  • dec mucus, bicarb, prostaglandins; NSAIDs
  • mc in antrum of stomach; older pt 55-70y
  • worse w/ meals
  • INC DAMAGING FACTORS (ACID/PEPSIN) IN DUODENAL ULCER
  • acid, pepsin, h.pylori
  • 4x MC; younger pt 30-55yo
  • better w/ meals
  • H.PYLOR MC CAUSE
  • NSAIDS 2ND MC - inhibit prostaglandin-mediated synthesis of protective mucus
  • Zollinger-Ellison syndrome: gastrin-producing tumor
  • etoh, smoking, stress (sev medical), M, elderly, steroids, malignancy
  • SUSPECT GI MALIG (ZES, GASTRIC CANCER) IN NONHEALING GU
  • sx- DYSPEPSIA = EPIGASTRIC PAIN, WORSE AT NIGHT
  • ulcer-like or acid dyspepsia - relief w/ food, antacids, nocturnal sx –> assoc w/ DU
  • food-provoked dyspepsia - pain 1-2 hrs after meals + weight loss –> assoc w/ GU
  • PUD IS MC CAUSE OF UPPER GI BLEED
  • complications: bleeding, perforation (esp anterior DU), penetration (esp posterior DU), obstruction
  • dx- ENDOSCOPY GOLD STD + bx to rule out malignancy
  • upper GI series - used w/ pt unable/willing to do endoscopy
  • all GU seen must f/u w/ endoscopy to r/o malignancy and document healing (8-12 wks later)
  • tx-
  • H.pylori –> “CAP” clarithromycin + amox + PPI

-H.pylori neg –> PPI; H2 blocker, misoprostol, antacids, pepto, sucralfate

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30
Q

zollinger ellison syndrome

A

gastrinomas: gastrin-secreting neuroendocrine tumors –> gastric acid hypersecrete –> PUD

-MC in duodenal wall (45%), pancreas (25%)
>66% malignant

-sx- ABDOMINAL PAIN AND DIARRHEA, multiple peptic ulcers, refractory “kissing” ulcers
diarrhea

-dx- fasting gastrin level (best screening) = >1000pg/mL and gastric pH <2
+ SECRETIN TEST: inc gastrin release w/ secretin (normally inhibits)

  • tx- local: surgical resection
  • metastatic: PPIs, surgical resection if liver involved
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31
Q

gastric carcinoma

A

Patient will be a man
With a history of H. pylori infection
Complaining of loss of appetite, unintentional weight loss
PE will show left supraclavicular node (Virchow’s node), left axillary node (Irish node), periumbilical node (Sister Mary Joseph’s node)
Comments: Adenocarcinoma is most common

  • MC males >40yo, presents late
  • RF: H.PYLORI, salted, cured, smoked, pickled foods w/ nitrates/nitrites (converted by h.pylori?)
  • dx- upper endoscopy w/ biopsy
  • tx- gastrectomy, rad/chemo; poor prognosis
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32
Q

bilirubin metabolism

A

prehepatic:

  • bilirubin produced from heme metabolism (80% old RBC, 20% turnover immature RBC, myoglobin)
  • heme degraded by macrophages in liver + spleen
  • heme –> biliverdin (green) –> bilirubin (red-orange) –> sent to liver for conjugation and excretion
  • unconjugated (indirect) bilirubin isn’t soluble in water

intrahepatic phase:

  • unconjugated/indirect bilirubin is conjugated w/ a sugar in hepatocytes via enzyme GLUCURONOSYLTRANSFERASE (UGT)
  • conjugated (direct) bilirubin is now water-soluble (for bile excretion)

posthepatic phase:

  • once soluble in bile, transported and stored in GB
  • in intestine, conj bili is converted to urobilinogen which can go through 3 main pathways:
    1. oxidized by intestinal bacteria into stercobilin (gives stool brown color)
    2. small amount converted in kidney to urobilin and excreted (gives urine yellow color)
    3. some recycled back to liver & bile for reuse
  • in dz where excess direct bilirubin –> excreted into urine (why dark urine and light stools are seen in elevated direct/conj bilirubin)
  • in hemolysis (inc unconj/indirect bilirubin,) urine may be dark due to hemoglobinuria not bilirubinemia
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33
Q

jaundice

A

yellowing of skin, nail beds + sclera by tissue bilirubin deposition as a consequence of hyperbilirubinemia
-occurs when levels >2.5mg/dL

etiologies:

  • inc bilirubin overproduction (hemolysis), dec hepatic bilirubin uptake, impaired conjugation, biliary obstruction, hepatitis
  • inc bilirubin w/out inc LFTs –> suspect familial bilirubin disorders (dubin-johnson synd, gilbert synd) + hemolysis
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34
Q

dubin-johnson syndrome

A 
"Dubin", "Direct bilirubinemia" "Dark liver"
hereditary conjugaed (direct) hyperbilirubinemia due to dec hepatocyte excretion

-sx- consititutional sx, mild icterus

  • dx- mild isolated conjugated (direct) hyperbilirubinemia (btw 2-5) but can increase w/ concurrent illness, pregnancy or OCPs
  • grossly black liver on biopsy

-tx- none

ROTOR’S SYND - simlar but milder in nature; assoc w/ conj and unconj hyperbili and not assoc w/ grossly black liver on bx

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35
Q

crigler-najjar syndrome

A

hereditary unconjugated hyperbilirubinemia (0.6-1.0/million)

  • glucuronosyltransferase (UGT) is enzyme needed to convert indrect to direct
  • Type I: no UGT activity (auto recessive)
  • Type II: very little UGT activity <10% normal
  • sx- neonatal jaundice w/ severe progression in the 2nd week leading to kernicterus (bili-induced encephalopathy) –> hypotonia, deafness, oculomotor palsy + death by 15 mo
  • dx- isolated indirect (unconj) hyperbilirubineia w/ normal LFTs; liver normal on bx
  • tx-
  • Type I: PHOTOTHERAPY plasmapheresis in crisis, liver transplant definitive
  • Type II: not usually necessary, PHENOBARBITAL shown to inc UGT (but not in type I)
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36
Q

gilbert’s syndrome

A

hereditary unconjugated hyperbilirubinemia (relatively common 5-10% pop)
-reduced UGT activity –> dec bili uptake –> inc indirect bili

  • sx- TRANSIENT EPISODES OF JAUNDICE DURING STRESS, FASTING, ETOH OR ILLNESS
  • dx- slightly inc isolated indirect bili w/ normal LFT (often incidental finding)
  • tx- none needed
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37
Q

patterns of liver injury

A

hepatocellular damage: inc ALT + AST
-ALT more sensitive for liver dz

cholestasis: inc levels of alk phos w/ inc GGT
- inc bilirubin greater than inc ALT/AST

liver “synthetic” fx

  • PT depends on synthesis of coag factors (vit K dependant): 2,7,9,10
  • PT is an earlier indicator of severe liver injury/prognosis than albumin (prolonged PT when 80% of protein synthesizing ability lost)
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38
Q

liver lab patterns: AST:ALT > 2

A

alcohol hepatitis
“S” in AST for “Scotch”
AST levels usually <500, AST found in mitochondria, ETOH causes direct mitochondrial injury = inc AST

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39
Q

liver lab patterns: ALT>AST

A

viral/toxic/inflam process (usually)
AST + ALT > 1000 –> usually acute viral hepatitis (A, B and rarely C)
-chronic hep b/c/d –> mildly inc ALT + AST (usually <400)

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40
Q

liver lab patterns: inc alk phos –> inc alk phos + GGT

A

biliary obstx or intrahepatic cholestasis

  • GGT most sensitive indicatory of biliary injury
  • if ALP inc w/out GGT, look for other sources (bone, gut)
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41
Q

liver lab patterns: inc ALT > 1000, + ANA, + smooth muscle AB, inc IgG

A

autoimmune hepatitis

-responds to corticosteroids, azathioprine

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42
Q

cholelithiasis

A

cholesterol 90%, pigmented 10%
black stones: hemolysis or etoh cirrhosis
brown stones: inc in asian pop, parasites/bacterial infx

RF: 5F’s, OCPs, natives, cirrhosis, infx, rapid WL, IBBD, fibrates, inc trigs

  • sx- mc asymptomatic
  • biliary “colic” = episode of abrupt RUQ/epigastric pain

-dx- US

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43
Q

choledocholithiasis*

A

gallstones in common bile duct

  • primary: stones form in duct
  • secondary: mc, stones pass from GB into duct
  • sx- asymptomatic, or biliary colic w/ RUQ tender, +/- jaundice
  • complications: acute pancreatitis, acute cholangitis
  • dx-
  • transabdominal US often initially
  • ERCP DIAGNOSTIC TEST OF CHOICE (and treatment)
  • magnetic resonance cholangiopancreatography (MRCP) and endoscopic US w/ pt w/ intermediate risk

-tx- ERCP extraction preferred over lapo choledocholithotomy

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44
Q

acute cholangitis*

A

Patient will be complaining of right upper quadrant pain, jaundice, fever (Charcot triad)

Diagnosis is made by RUQ ultrasound, CT scan, or ERCP (gold standard)

Most commonly caused by choledocholithiasis leading to bacterial infection, E. coli

Treatment is antibiotics, definitive treatment is ERCP with antibiotics typically an adjunct
(amp/sulbactam, pip/tazo OR ceftriaxone + metronidazole OR FQ + metronidazole)

Comments: Charcot triad + hypotension and AMS = Reynolds pentad, acute obstruction

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45
Q

acute cholecystitis*

A

gall bladder/duct obstx by stone –> inflam/infx
-MC e.coli, klebsiella, entercocci, b.fragilis

  • sx- RUQ pain continuous, N, precipitated by fatty meals
  • F, + murphy’s sign, palpable GB (30%), + boas sign - referred pain to right shoulder subscapular area (phrenic nerve irritation)
  • dx-
  • US initial test of choice
  • HIDA SCAN GOLD STANDARD (pos = no visualization of GB)
  • tx- NPO, IV fluids, Abx (ceftriaxone + metronidazole) –> cholecystectomy
  • if non-operative –> cholecystostomy
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46
Q

chronic cholecystitis

A

assoc w/ gallstones
-strawberry GB: interior resembles strawberry 2ry to cholesterol submucosal aggregation –> porcelain GB (premalignant condition)

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47
Q

fulminant hepatitis (acute hepatic failure)

A

rapid liver failure + hepatic encephalopathy (often w/ coagulopathy)
-acute = w/in 8 wks after onset of liver injury in pt that was healthy prior

  • ACETAMINOPHEN MC CAUSE, drug rx, viral hepatitis (A-E), Reye syndrome
  • sx- ENCEPHALOPATHY (+asterixis), COAGULOPATHY
  • dx- INC AMMONIA in serum, INC PT/INR (>1.5), HYPOGLYCEMIA
  • tx-
  • encephalopathy: LACTULOSE (converts to lactic acid by bacteria, neutralizes ammonia), RIFAXIMIN, NEOMYCIN (abx that decrease bacteria producing ammonia), PROTEIN RESTRICTION (reduces breakdown of protein into ammonia)
  • LIVER TRANSPLANT only definitive tx
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48
Q

reye’s syndrome

A

fulminant hepatitis mc seen in children assoc w/ ASA use during viral infx (can occur w/out ASA)

-sx- rash (hands/feet), intractable vomiting, liver damage, encephalopathy, dilated pupils, multi-organ failure

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49
Q

viral hepatitis

A

prodromal phase: constitutional, N/V, loss of appetite, DECREASED SMOKING
-hep A assoc w/ spiking a fever

icteric phase: jaundice (most don’t devo this phase)

chronic hepatitis: >6 mo duration, only B, C, D assoc w/ type; may lead to end stage liver dz (ESLD) or hepatocellular carcinoma (HCC)

-labs: inc ALT > inc AST, both >500 if acute (<500 chron) +/- inc bilirubinemia

  • prognosis: clinical recovery 3-16 wks
  • 10% HBV and 80% HCV become chronic
50
Q

Hep A

A
  • fecal-oral; contaminated food, day care, m w/ m, shellfish
  • outbreaks during international travel 40%
  • asymptomatic children <6yo MC source adults

-prodromal: constitutional sx, DECREASED SMOKING;
ONLY VIRAL HEP ASSOCIATED W/ SPIKING A FEVER

  • icteric phase: JAUNDICE (most don’t devo), presents when fever breaks
  • dx- ACUTE: +IGM HAV AB
  • tx- self-limiting
  • post-exposure prophylaxis (close contacts): HAV immune globulin
51
Q

Hep E

A
  • fecal-oral; assoc w/ waterborne outbreaks
  • dx- IgM anti-HEV
  • tx- self-limiting
  • highest mortality during pregnancy (esp 3rd tri) –> inc risk fulminant hep
52
Q

Hep C

A
  • parenteral transmission (IV drug used, blood transfuse before 1992); sex, perinatal, breastfeeding uncommon
  • 80% pt devo chronic infx
Often asymptomatic 
Screen individuals born between 1945 and 1965
Transmission via blood
Screen with anti-HCV
Confirm with HCV RNA 
HCV genotype prior to treatment

HCV-RNA: + in acute, neg in resolved, pos in chronic

  • tx- PEGYLATED INTERFERON ALPHA-2B AND RIBAVIRIN
  • SCREEN FOR HCC VIA SERUM ALPHA-FETOPROTEIN + ULTRASOUND
53
Q

acute hepatitis summary*

A

HAV: fecal-oral, shellfish, alone (no carrier), asymptomatic, acute

HBV:
HBsAg: active infection
Anti-HBs: recovered or immunized
Anti-HBc IgM: early marker of infection, positive in window period
Anti-HBc IgG: best marker for prior HBV
HBeAg: high infectivity
Anti-HBeAb: low infectivity

HCV: IVDA, chronic, cirrhosis, carcinoma, carrier

HDV: dependent on HBV coinfection

HEV: fecal-oral (enteric) high mortality rate among pregnant (expectant) patients, epidemics,

HAV and HEV are fecal-oral: “The vowels hit your bowels”
HAV and HBV have preventative vaccine available

Autoimmune hepatitis: young females
Alcoholic hepatitis: moderate transaminase elevation, AST > ALT (2:1)
Supportive rx

54
Q

Hep B**

A
  • transmission: parenteral, sexual, perinatal, percutaneous
  • acute: 70% subclinical, 30% jaundice
  • chronic: about 10% adult acquired, 90% perinatal acq
  • chronic asymptomatic carrier: +HBsAg +HBe-AB, normal LFTs, low HBV-DNA
  • although asymptomatic, can still transmit
  • chronic infection: +HBsAg, with inc AST & ALT

serological tests
+HBsAg (surface antigen) - 1st evidence of infx, establishes infection and infectivity (pos >6 mo = chronic)
+HBsAb (surface ab) - distant resolved infx (recovery) or vaccination marker, (if none after 6 mo = chronic)
+HBcAb (core antibody) - IgM indicates acute (1st to appear), IgG indicates chronic or distant resolved infx
+HBeAg (envelope antigen) - inc viral replication & inc infectivity
+HBeAb (envelope antibody) - indicates waning viral replication, dec infectivity
+HBV-DNA - presence in serum correlates w/ active replication in liver

  • tx-
  • acute - supportive
  • chronic - if inc ALT, inflam on bx or +HBeAg
  • alpha-interferon 2b, lamivudine, adefovir (interferon c/i in decompensated liver dz)
55
Q

hepatic vein obstruction / budd-chiari syndrome

A

hepatic venous outflow obstx (thrombosis or occlusion) –> dec liver drainage –> portal HTN + cirrhosis

  • mc women 20-30s
  • RF: idiopathic, hypercoaguable states

primary: hepatic vein thrombosis MC
secondary: hep vein or IVC occlusion (tumor compress)

-sx-
Triad: ACITES, HEPATOMEGALY, RUQ ABDOMINAL PAIN

  • dx- US SCREENING OF CHOICE
  • VENOGRAPHY GOLD STD
  • tx- SHUNTS, BALLOON ANGIOPLASTY W/ STENT
  • anticoag + thrombolysis (if <3-4 wks and not IVC)
  • acities: diuretics, low sodium, paracentesis
56
Q

hepatocellular carcinoma HCC

A

primary liver neoplasm = HCC
-hepatic malig more commonly 2ry to mets (lung, breast)

-RF: chronic viral hep B, C, D, cirrhosis

  • dx- ULTRASOUND, ct scan, mri, angiogram
  • INC ALPHA-FETOPROTEIN

-tx-surgical resection if confined to lobe and not assoc w/ cirrhosis

57
Q

cirrhosis

A

PE will show gynecomastia, palmar erythema, ↑ bleeding
Hepatic encephalopathy: asterixis, confusion
Portal hypertension: caput medusae, splenomegaly, ascites
Most commonly caused by alcohol > hepatitis, autoimmune
Comments: ↑ risk for HCC

irreversible liver fibrosis w/ nodular regeneration 2ry to chronic liver disease
-ETOH MC in US, chronic viral hep (C*, B, D), nonalcoholic fatty liver disease, hemochromatosis

  • sx- fatigue, WL, cramps, anorexia
  • ASCITES, GYNECOMASTIA (liver can’t metabolize estrogen), spider angioma, caput medusa, bleeding (dec coag factors), palmar erythema, jaundice, dupuytren’s contractures
  • HEPATIC ENCEPHALOPATHY - confusion, lethargy (accumulated ammonia from protein breakdown), ASTERIXIS, FETOR HEPATICUS, INC AMMONIA
  • ESOPHAGEAL VARICES - due to portal HTN
  • spontaneous bacterial peritonitis

-dx- ULTRASOUND

  • tx-
  • encephalopathy: LACTULOSE OR RIFAXIMIN (neomycin 2nd line)
  • ascites: Na+ restrict –> diuretics (lasix, spiro), paracentesis
  • pruritus: CHOLESTYRAMINE (questran) - bile acid sequestrant
  • liver transplant definititive
58
Q

primary biliary cirrhosis

A

idiopathic autoimmune d/o INTRAHEPATIC SMALL BILE DUCTS –> dec bile salt excretion, cirrhosis + ESLD
-MC MIDDLE-AGED WOMEN (40-60) ONLY ADULTS!

-sx- FATIGUE, PRURITUS, RUQ PAIN, HEPATOMEGALY, JAUNDICE

-dx- cholestatic pattern: inc Alk Phos, inc GGT
+ANTI-MITOCHONDRIAL AB HALLMARK
-LIVER BX DEFINITIVE

  • tx- URSODEOXYCHOLIC ACID 1ST LINE (protects cholangiocytes from toxic effect of bile acids)
  • cholestyramine + UV light for pruritus
59
Q

primary sclerosing cholangitis*

A

autoimmune, progressive cholestasis, DIFFUSE FIBROSIS OF INTRAHEPATIC AND EXTRAHEPATIC DUCTS

  • MC assoc w/ IBD, 90% have UC +/-crohn’s
  • mc men 20-40yo, rare

-sx- jaundice, pruritus, fatigue, ruq pain, hepato + splenomegaly

-dx- cholestatic pattern: inc Alk Phos, inc GGT
-inc ALT/AST, inc bilirubin, inc IgM
+P-ANCA
-ERCP GOLD STD

-tx- transplant definitive, stricture dilate to relieve sx

60
Q

wilson’s disease (hepatolenticular degeneration)

A

FREE COPPER ACCUMULATION IN BRAIN, LIVER, KIDNEY, CORNEA - rare autosomal recessive

  • sx- CNS –> basal ganglia (parkinson-like sx)
  • personality + bx changes, arthralgias from jt deposits
  • LIVER: HEPATITIS, HEPATOSPLENOMEGALY, CIRRHOSIS, HEMOLYTIC ANEMIA

-dx- DEC CERULOPLASMIN (serum carrier mol for Cu)
INC URINARY COPPER EXCRETION

  • tx- D-PENCILLAMINE 1st line- chelates copper
  • zinc: enhances fecal copper excretion + blocks absorption
61
Q

acute pancreatitis*

A

Patient will be complaining of epigastric pain radiating to the back, nausea, and vomiting
PE will show ecchymosis of left flank (Grey-Turner sign), umbilical ecchymosis (Cullen sign)
Labs will show elevated lipase (best) and amylase
Ranson criteria and APACHE are used to predict the severity (Note: they are difficult to apply and have not been found to be that good)
Most commonly caused by gallstones > alcohol
Treatment is IV fluids
Comments: Pancreatic pseudocyst complication in adults

GALLSTONES + ETOH MC CAUSE
-meds, malignancy, scorpion bite, CF, mumps in children

-acinar cell injury –> intracellular activation of pancreatic enzymes –> autodigestion of pancreas

  • sx- constant, boring epigastric pain (radiate to back) relieved w/ leaning forward, sitting, fetal position
  • tachy, decreased bowel sounds
  • necrotizing/hemorrhagic: CULLEN’S, GREY TURNER SIGN
  • labs: leukocytosis, inc glucose, inc bili, inc trigs
  • LIPASE: MORE SPECIFIC THAN AMYLASE inc 7-10d
  • AMYLASE >3x ULN suggestive
  • ALT inc 3-fold suggests gallstone pancreatitis
  • HYPOCALCEMIA bc nectrotic fat binds Ca
  • CT DIAGNOSTIC TEST OF CHOICE (Ranson’s Criteria)
  • abdominal US, xray –> “sentinel loop” = loalized ileus; colon cut-off sign –> abrupt colapse of colon near pancreas
  • tx-
  • supportive: NPO, IV FLUID, ANALGESIA w/ meperidine
  • ABX NOT USED ROUTINELY –> if severe/necrotizing –> BROAD SPECTRUM
  • ERCP only useful in obstructive jaundice
62
Q

chronic pancreatitis

A

chronic inflam causing parenchymal destruction, fibrosis + calcification –> loss of exocrine and sometimes endocrine fx

  • ETOH ABUSE (70%) IDOPATHIC
  • CYSTIC FIBROSIS MC CAUSE IN CHILDREN
  • TRIAD: CALCIFICATIONS, STEATORRHEA, DIABETES MELLITUS
  • dx- XRAY: CALCIFIED PANCREAS; amylase/lipase not usually elevated
  • tx- ORAL PANCREATIC ENZYME REPLACEMENT, etoh abstinence
63
Q

pancreatic carcinoma

A

RF: SMOKING, >60YO, chronic pancreatitis, ETOH, DM, M, obesity, AA

  • ADENOCARCINOMA: DUCTAL MC (90%)
  • 70% FOUND IN HEAD OF PANCREAS
  • 5 year survival rate <5%; (average 6 months)
  • sx- usually have mets at time presenting - regional lymph nodes and liver
  • abdominal pain radiates to back, relieved w/ sitting up and leaning forward, painless jaundice, WL, pruritus, acholic stools/dark urine (bile duct obstx)
  • COURVOISIER’S SIGN = PALPABLE, NONTENDER, DISTENDED GB ASSOC W/ JAUNDICE
  • CT SCAN - INITIAL DX TEST OF CHOICE; ERCP most sensitive
  • labs: inc tumor markers CEA, CA 19-9
  • tx- WHIPPLE PROCEDURE
  • advanced/inoperative - ERCP w/ stent place to reduce itch
64
Q

meckel’s (ileal) diverticulum

A

persistent portion of embryonic vitteline duct (yolk stalk)
-rule of 2’s: 2% of pop, 2 feet from ileocecal valve, 2% symptomatic, 2” length, 2 ypes of ectopic tissue, 2 years MC age at presentation, 2x mc boys

  • ectopic pancreatic or gastric tissue may secrete digestive hormones –> bleeding
  • usually asymptomatic; PAINLESS RECTAL BLEED OR ULCERATION; may cause intussusception, volvulus or obst
  • dx- Meckel’s scan looks for ectopic gastric tissue in ileal area
  • tx- surgical excision if symptomatic
65
Q

small bowel obstruction*

A

POST-SURGICAL ADHESIONS MC (60%)
-malignancy mc cause of large bowel obstx

  • sx- “CAVO”
  • CRAMPING, ABD PAIN
  • ABDOMINAL DISTENTION (distal = more prominent)
  • VOMITING - bilious if proximal
  • OBSTIPATION - abscence of stool/flatus
  • high-pitched tinkles on auscultation + visible peristalsis –> hypoactive bowel sounds late in obstx

-dx- abd xray –> AIR-FLUID LEVELS IN STEP LADDER PATTERN, DILATED BOWEL LOOPS, stack of coins or string of pearls sign

  • tx- non-strangulated –> NPO, IV fluids +/-bowel decompress via NG suction
  • strangulated –> sx
66
Q

paralytic (adynamic) ileus

A

decreased peristalsis w/out structural obstx
-POST-OP, OPIATES, HYPOKALEMIA, hyperCa, metabolic

  • sx-similar to obstx, decreased/no bowel sounds
  • dx- XRAY - FIRST LINE
  • tx- NPO (or restrict to sips/liquid), NG suction if V, electrolyte repletion, tx underlying cause
67
Q

ogilvie’s syndrome

A

colonic pseudo-obstruction (acute dilation)

  • mc involves cecum + right hemicolon
  • post-op, elderly, ill, metabolic, trauma, meds
  • sx-ABDOMINAL DISTENTION, pain, N/V/C
  • dx- XRAY - dilated right colon from cecum w/ cutoff at splenic flexure
  • tx- conservative in absence of severe sx
  • neostigmine if risk for perforation (>12cm dilated) or if failed conservative tx for >48hrs
  • decompression w/ NG or enemas if fail other tx; surgery
68
Q

celiac disease (sprue)

A

small bowel autoimmune inflammation 2ry to a-gliadin in gluten –> loss of villi and absorptive area –> impaired fat absorption

Patient will be complaining of diarrhea, steatorrhea, flatulence, weight loss, weakness and abdominal distension

Labs will show IgA anti-endomysial (EMA) and anti-tissue transglutaminase (anti-tTG) antibodies

Definitive Diagnosis is made by small bowel biopsy

Treatment is gluten free diet

Comments: Associated with dermatitis herpetiformis (chronic, very itchy skin rash made up of bumps and blisters)

69
Q

volvulus

A

twisting of any part of bowel @ mesenteric attachment site
-mc sigmoid colon and cecum

  • sx- obstx sx
  • tx- endoscopic decompression intial tx of choice; surgical 2nd line
70
Q

irritable bowel syndrome

A

abdominal pain associated w/ altered defecation/bowel habits (D/C or alternate) - no organic cause

  • pain often relieved w/ defecation
  • onset mc teens, early 20s, mc women

-pathophys- abnormal motility (chem imbalance or gut microbes), visceral hypersensitivity (low pain thresholds), psychosocial interaction

  • ROME IV CRITERIA (dx): RECURRENT ABD PAIN (ave 1 day/week last 3 mo) assoc w/ at least 2 OF FOLLOWING:
  • RELATED TO DEFECATION
  • onset assoc w/ CHANGE IN STOOL FREQ
  • onset assoc w/ CHANGE IN STOOL FORM

-alarm sx: blood, anorexia or WL, F, nocturnal sx, family hx GI cancer, persistent D causing dehydration, severe C

  • tx- SMOKING CESSATION, LOW FAT/UNPROCESSED FOOD DIET, avoid bev w/ sorbitol or fructose (apples, raisins), avoid cruciferous veg, sleep, exercise
  • diarrhea –> anticholinergics or antidiarrheal
  • constipation –> prokinetics, laxatives
71
Q

chronic mesenteric ischemia

A

Patient with a history of atherosclerotic disease
Complaining of acute onset of crampy abdominal pain

CT imaging will show bowel wall edema

Most commonly caused by inadequate blood flow through the mesenteric vessels

especially @ splenic flexure after meals (some collateral flow) DULL ABD PAIN WORSE AFTER MEALS “intestinal angina”; WL

  • dx- ANGIOGRAM confirms dx; colonoscopy - muscle atrophy w/ loss of villi
  • tx- bowel rest, surgical revascularization
72
Q

acute mesenteric ischemia

A

sudden decrease of mesenteric blood supply to the bowel –> inadequate perfusion especially @ splenic flexure

  • MC DUE TO OCCLUSION: EMOBOLUS/THROMBUS, non-occlusive causes: shock, cocaine
  • sx- SEVERE ABD PAIN OUT OF PROPORTION TO EXAM, N/V/D, peritonitis/shock in advanced disease
  • dx- ANGIOGRAM DEFINITIVE, colonoscopy: patchy, necrtotic areas
  • tx- surgical revascularization (angioplasty w/ stent or bypass), sx resection if not salvageable
73
Q

ischemic colitis

A
  • mc due to systemic HypoTN or atherosclerosis involving superior and mesenteric arteries
  • mc at areas w/ decreased collaterals (splenic flexure + rectosigmoid jx)

-sx- LLQ PAIN W/ TENDER, BLOODY DIARRHEA

  • dx- COLONOSCOPY
  • tx- restore perfusion + observe for signs of perforation
74
Q

toxic megacolon

A

EXTREME COLON DILATION >6CM + SIGNS OF SYSTEMIC TOXICITY

  • sx- F, abd pain, D/N/V, rectal bleed, tenesmus, electrolyte disorders
  • abd tender, rigid, tachycardia, dehydration, HypoTN, AMS

-dx- XRAY - DILATED COLON >6CM

  • tx- BOWEL DECOMPRESSION, rest, NG tube, broad abx
  • colostomy for refractory cases
75
Q

ulcerative colitis

A

limited to colon (begins in rectum w/ contiguous spread proximally - RECTUM ALWAYS INVOLVED

  • mucosa and submucosa layers involved
  • smoking decreases risk
  • sx- abd pain LLQ mc, collicky, tenesmus, urgency, BLOODY DIARRHEA HALLMARK, stools w/ mucus/pus, hematochezia mc, arthritis (seronegative)
  • complications: primary sclerosing cholangitis, colon ca, toxic megacolon

-dx- flex sig in acute disease
-COLONOSCOPY C/I IN ACUTE COLITIS –> RISK OF PERFORATION
-BARIUM ENEMA C/I IN ACUTE –> MAY CAUSE TOXIC MEGA COLON
-colonoscopy - uniform inflammation +/- ulceration in rectum or colon “PSEUDOPOLYPS”
-barium enema - “STOVE PIPE” sign (loss of haustra)
+P-ANCA

  • tx- surgery curative
  • acute: AMINOSALICYLATES (sulfasalazine, mesalamine) –> CORTICOSTEROIDS –> IMMUNE MOD AGENTS
76
Q

crohn’s disease

A

any segment of GI tract - mouth to anus

  • mc in terminal ileum –> RLQ pain
  • transmural depth
  • sx- abd pain, RLQ mc (crampy), WL more common, diarrhea w/ no visible blood
  • complications: perianal dz (fistulas, strictures, abscesses, granulomas), malabsorption Fe/B12 deficiency

-dx- upper GI seriew w/ small bowel follow through test of choice in acute dz
-colonoscopy: “SKIP LESIONS” AND “COBBLESTONE APPEARANCE”
-barium enema: “STRING SIGN” narrowed/scarred area
+ASCA

-tx- +/-aminosalicylates, CORTICOSTEROIDS, IMMUNE MOD AGENTS OR ANTI-TNF

77
Q

colon polyps

A
  1. pseudopolyps/inflammatory - due to IBD (not cancer)
  2. hyperplastic: low risk for malignancy
  3. adenomatous polyps - ave 10-20y before becoming cancerous (esp >1cm)
    - tubular adenoma - nonpedunculated (mc and least risk)
    - tubulovillous (mix) - intermediate-risk
    - villous adenoma - highest risk of cancer
78
Q

colorectal cancer

A

Second leading cancer cause of death
Third most common cancer in men and women

(ADENOCARCINOMA)

Risk factors: age, IBD, adenomatous polyps, FAP, HNPCC
Rectosigmoid > ascending > descending

Left-sided cancer: tends to obstruct
Right-sided cancer: tends to bleed

Iron deficiency anemia

Colonoscopy
CEA

CRC MC CAUSE OF LARGE BOWEL OBSTX IN ADULTS
-barium enema - APPLE CORE LESIONS

  • local stage 1-3: surgical resection
  • stage 3 + metastatic: chemo mainstay of tx (5FU)
79
Q

colon cancer screening

A

average risk

  • fecal occult blood test: annually @50
  • colonoscopy: q 10y (or flex sig q 5y)

1st degree relative >60 risk

  • fecal occult blood test: annually @40
  • colonoscopy: q 10y

1st degree relative <60 risk

  • fecal occult blood test: annually @ 40 (or 10 yrs before)
  • colonoscopy: q 5y
  • lynch: screen @20-25y, colonoscopy q 1-2y
  • FAP: screen @10-12y w/ flex sig
80
Q

inguinal hernias

A

INDIRECT: @ internal inguinal ring, LAT to. inferior epigastric artery; often congenital due to persistent patent process vaginalis
-MC young children + young adults; MC overall type for men + women, right-sided more common

DIRECT: protrudes MEDIAL to inferior epigastric vessels
-does not reach scrotum

  • sx- MAY DEVO SCROTAL SWELLING W/ INDIRECT
  • incarcerated: painful, enlargement of an irreducible hernia
  • strangulated: ischemic incarcerated hernias w/ systemic toxicity
81
Q

femoral hernias

A

protrusion of contents through femoral canal below inguinal ligament - often incarcerated/strangulated
-MC in WOMEN

82
Q

umbilical hernias

A

through umbilical fibromuscular ring

  • congenital - failure of umbilical ring closure
  • usually resolves by 2yrs; sx repair if persistent >5yo to avoid incarceration/strangulation

-adults - due to loosening of tissue around ring

83
Q

incisional (ventral) hernias

A

mc w/ vertical incisions and obese patients

84
Q

obturator hernias

A

rare hernia through pelvic floor

  • contents protrude through obturator foramen
  • mc women (esp multiparous) or women w/ sig WL
85
Q

hemorrhoids*

A

-RF: inc venous pressure, straining, pregnancy, obesity, prolonged sitting, cirrhosis w/ portal hypoTN

Internal - superior hem vein, proximal to dentate line
-INTERMITTENT RECTAL BLEEDING MC; BRIGHT RED BLOOD PER RECTUM

External - inferior hem vein, distal to dentate line
-PERIANAL PAIN, AGGRAVATED W/ DEFECATION

  • dx- visual inspection, DRE, FOBT
  • proctotsigmoidoscopy, colonoscopy
  • tx- conservative: inc fiber, fluids; sitz baths, topical cortico for pruritus/discomfort/thrombosis
  • failed conservative, debilitating pain, strangulation –> rubber band ligation, sclerotherapy or infrared coag
  • hemorrhoidectomy for stage IV or not responsive
86
Q

anorectal abscess + fistulas

A

abscess - often from bacterial infx of anal ducts/glands
MC staph, e.coli - MC IN POSTERIOR RECTAL WALL
-sx- swelling, pain worse w/ sitting, coughing, pooping

fistula - open tract btw 2 epithelium lined areas
-sx- +/-anal discharge and pain

-tx- I+D followed by WASH: warm-water cleanse, analgesics, sitz baths, high fiber diet

87
Q

anal fissures*

A

Patient will be complaining of rectal pain and bleeding which occurs with or shortly after defecation, MC POSTERIOR MIDLINE

PE will show fissure located in the posterior midline
Diagnosis is made by visual inspection

Treatment is sitz baths, analgesics, high fiber, inc water, stool softners/lax
-2nd line: topical vasodilators (nitroglycerine or nifedipine)

Comments: If fissures are located laterally, search for pathologic etiologies

88
Q

pilonidal cyst/abscess

A

near gluteal cleft near midline of coccyx or sacrum w/ small, midline pits
-mc white M, obese, hirsute pt, prolonged sitting, local trauma; rare >40yo

-tx- I+D - excision of sinus/tracts if recurrent

89
Q

phenylketonuria

A

autosomal recessive disorder of a.acid metabolism

  • dec ability to metabolize phenylalanine into tyrosine due to deficiency of enzyme PAH –> accumulate phenylalanine in body fluids –> neurotoxic
  • normally screen at 24wks gestation, irreversible if not detected by 3 yo
  • sx- VOMITING, MENTAL DELAYS, convulsions, inc DTR, children often BLONDE, BLUE EYES, FAIR SKIN
  • dx- URINE W/ MUSTY/MOUSY ODOR

-tx- LIFETIME DIET RESTRICTION OF PHENYLALANINE + inc tyrosine supplementation
(foods high in phenylalaine: milk, cheese, nuts, fish, chicken, meats, eggs, legumes, aspartame)

90
Q

vitamin a

A

fx: vision, immune fx, embryo devo, hematopoiesis, skin health and cellular health
- sources: kidney, liver, egg yolk, butter, green leafy veg
- deficiency RF: pt w/ liver dz, ETOHics, fat-free diets

  • sx of deficiency: VISION CHANGES (ESP NIGHT-BLINDNESS), impaired immunity (poor wound heal), taste loss, SQUAMOUS METAPLASIA (conjuctiva, resp epithelium, urinary tract)
  • BITOT’S SPOTS: white spots on conjunctiva due to squamous metaplasia of corneal epithelium

-excess: teratogenicity, alopecia, ataxia, vision changes, skin disorders, hepatoxicity

91
Q

vitamin c (ascorbic acid) deficiency

A

RF: diet lacking raw citrus, green veg (heat denatures vit c), smoking, alcoholism, elderly, malnourished

  • SCURVY: 3 “H”s
  • Hyperkeratosis: hyperkeratotic follicular papules
  • Hemorrhage: vascular fragility (abn collagen) w/ recurrent hemorrhages in gums, skin (perifollicular) and joints; impaired wound healing
  • Hematologic: anemia, inc bleeding time
92
Q

vitamin D deficiency

A
  • RICKETS (children): SOFTENING OF BONES leads to bowing deformities, frx, dental problems, devo delays
  • OSTEOMALACIA (adults): body pains, muscle weakness, frx, LOOSER LINES (radiolucencies on xray)
93
Q

vitamin B1 (THIAMINE) deficiency

A

ETOH MC cause in US

  • BERIBERI:
  • “dry”: nervous system changes, paresthesias, demyelination –> peripheral neuropathy
  • “wet”: high output HF, dilated cardiomyopathy

-WERNICKE’S ENCEPHALOPATHY TRIAD: “AGO”
Ataxia, Global confusion, Ophthalmoplegia

-KORSAKOFF’S DEMENTIA: memory loss (esp short term), confabulation. IRREVERSIBLE

94
Q

vitamin B2 (RIBOFLAVIN) deficiency

A

ORAL-OCULAR-GENITAL SYNDROME

  • oral: lesions, MAGENTA COLORED TONGUE, ANGULAR CHEILITIS
  • ocular: photophobia, corneal lesions
  • genital: scrotal dermatitis
95
Q

vitamin B3 (NIACIN/NICOTINIC ACID) deficiency

A

Patient will be complaining of Dermatitis, Dementia, and Diarrhea

  • chronic alcoholism, ISONIAZID, oral contraceptives
  • NEUROLOGIC: PERIPHERAL NEUROPATHY, seizures, HA
  • stomatitis, cheilosis, glossitis, flaky skin, anemia
96
Q

vitamin B12 (COBALAMIN) deficiency

A

animal foods primary source; binds to IF in stomach for later absorption in terminal ileum

  • PERNICIOUS ANEMIA: AUTOIMMUNE DESTRUCTION OF GASTRIC PARIETAL CELLS that secrete IF = B12 def
  • STRICT VEGANS (B12 must be supplemented)
  • MALABSORPTION: ETOH-ISM, CELIACS, CROHN’S
  • dec IF production: acid-reducing drugs, bypass
  • sx- NEURO: PARESTHESIAS, GAIT ABNORMAL, MEMORY LOSS, DEMENTIA, GI SX
  • tx- IM B12 for pernicious (won’t absorb oral)
97
Q

NONINVASIVE (ENTEROTOXIN) INFECTIOUS DIARRHEA

A 
-vomiting, watery, voluminous, no fecal WBC/blood
STAPH AUREUS
BACILLUS CEREUS
VIBRIO CHOLERAE + VIBRIO PARAHEMOLYTICUS
ENEROTOXIGENIC E.COLI
CLOSTRIDIUM DIFFICILE
  • enterotoxins increase GI secretion of electrolytes –> SECRETORY DIARRHEA
  • NO CELL DESTRUCTION OR MUCOSAL INVASION
  • SMALL BOWEL AFFECTED –> LARGE VOLUME STOOLS
  • VOMITING PREDOMINANT SYMPTOM
  • ABSENT FECAL BLOOD/WBC/MUCUS
98
Q

INVASIVE INFECTIOUS DIARRHEA

A
  • high fever, +blood/WBC, not as voluminous (noninvasive), mucus
  • DONT GIVE ANTI-MOTILITY DRUGS! (may cause toxicity)
CAMPYLOBACTER ENTERITIS
SHIGELLA
SALMONELLA
ENTEROHEMORRHAGIC E.COLI 0157:H7
YERSINIA ENTEROCOLITICA
  • CYTOTOXINS CAUSE MUCOSAL INVASION + CELL DAMAGE
  • LARGE BOWEL AFFECTED –> MANY SMALL VOL STOOLS, HIGH FEVER
  • vomiting not as common
  • POS FECAL BLOOD/WBC + MUCUS
99
Q

PROTOZOAN INFECTIONS

A

GIARDIA LAMBLIA
AMEBIASIS
CRYPTOSPORIDIUM
ISOSPORA BELLI

100
Q

giardia lamblia

A
  • contaminated water from remote streams/wells aka Beaver’s fever or “backpacker’s diarrhea”
  • boil H20 x 1 minute to kill cysts
  • sx- FROTHY, GREASY, FOUL DIARRHEA (no blood or pus)
  • dx- STOOL OVA + PARASITES: trophozoites /cysts in stool
  • tx- FLUIDS + METRONIDAZOLE, FURAZOLIDONE IN KIDS
101
Q

amebiasis

A

sources: entamoeba histolytica transmitted by fecally contaminated soil/water
- mc seen in travelers to developing nations

  • sx- GI colitis, dysentery, AMEBIC LIVER ABSCESSES
  • dx- STOOL OVA + PARASITES
  • tx- FLUIDS
  • colitis: METRONIDAZOLE + intraluminal antiparastic (paromomycin, diloxanide furoate, diiodohydroxyquin)
  • abscess: metronidazole or tinidazole + intraluminal antiparastic
102
Q

osmotic diarrhea

A

MALABSORPTION of nonabsorbable substances (inc solutes in GI tract promotes D by pulling water into gut)
-DECREASED DIARRHEA W/ FASTING, INCREASED OSMOTIC GAP, inc fecal fat

  • rapid transit of GI contents: LACTULOSE, SORBITOL, ANTACIDS
  • bacterial overgrowth: WHIPPLE’S DZ (tropheryma whippelii), TROPICAL SPRUE
  • malabsorption abnormalities: CELIAC, pancreatic or bile salt insufficiency, LACTOSE INTOLERANCE
103
Q

secretory diarrhea

A

NORMAL OSMOTIC GAP, large volume, NO CHANGE IN DIARRHEA WHEN FASTING

  • hormonal: serotonin (carcinoid syndrome), calcitonin (medullary cancer of thyroid), gastrin (zollinger-ellison syndrome)
  • laxative abuse
104
Q

whipple’s disease

A

TROPHERYMA WHIPPELII
-mc farmers around contaminated soil

  • sx- MALABSORPTION - WL, steatorrhea, nutrition deficient, F, RHYTHMIC MOTION OF EYE MUSCLES WHILE CHEWING
  • dx- DUODENAL BX: PERIODIC ACID-SHIFF - POSITIVE MACROPHAGES, non acid-fast bacilli, DILATION OF LACTEALS
  • tx- PCN or tetracycline for 1-2 years
105
Q

constipation

A

<2x/wk, staining, hard stools, feeling incomplete empty

  • disordered mvmt through colon/anus/rectum (usually proximal tract is fine)
  • slow colonic transit - idiopathic, motor disorder (colorectal ca, DM, hypothyroid
  • drugs: VERAPAMIL, OPIOIDS
  • tx-
  • fiber
  • bulk-forming laxatives: psyllium methylcellulose (citrucuel), polycarbophil (fibercon), wheat dextran (benefiber)
  • osmotic laxatives: polyethylene glycol (Golytely, Miralax), lactulose, sorbitol, saline laxatives (milk of mag, magcitrate)
  • stimulate laxatives: bisacodyl (Dulcolax), senna
106
Q

YERSINIA ENTEROCOLITICA

A

DIARRHEA
-source: contaminated pork, milk, water, tofu

  • sx- F, abd pain, MIMIC ACUTE APPENDICITIS (can cause MESENTERIC ADENITIS)
  • tx- FLUIDS, if severe –> FQ, bactrim
107
Q

ENTEROHEMORRHAGIC E.COLI 0157:H7

A

DIARRHEA

  • sources: undercooked beef, unpasteurized milk/cider, day centers, contaminated water
  • produces cytotoxin
  • IP: 4-9 days

-sx- watery diarrhea –> bloody, crampy abd pain, V
+/- low grade fever

-tx- FLUIDS; ABX CONTROVERSIAL (inc incidence of hemolytic uremic syndrome in children)

108
Q

SALMONELLA

A

DIARRHEA

  • mc source: poultry products, exotic pets (turtles)
  • hi risk groups: sickle cell (inc risk osteo)
  • SALMONELLA GASTROENTERITIS: s. typhimurium
  • 5-14d IP; abd pain, F, cramps, MUCUS + BLOODY DIARRHEA
  • TYPHOID (ENTERIC) FEVER: s. typhi
  • > 1-2 wks IP
  • CEPHALIC PHASE: HA, constipation, pharyngitis, cough –> crampy abd pain PEA SOUP STOOLS, INTRACTABLE FEVER, RELATIVE BRADYCARDIA
  • blanching “ROSE SPOTS” appear in wk 2

-tx- FLUIDS +/- FLUOROQUINOLONES, ceftriaxone, bactrim

109
Q

SHIGELLA

A
  • GRAM NEG
  • highly virulent; IP 1-7days
  • sx- LOWER ABD PAIN, EXPLOSIVE WATERY D –> BLOODY/MUCUS
  • may lead to toxic megacolon, complications include reactive arthritis +/- FEBRILE SEIZURES IN CHILDREN
  • dx- stool cultures; +/- LEUKEMOID RX (WBC>50K)
  • SIGMOIDOSCOPY - PUNCTATE AREAS ULCERATION

-tx- FLUIDS; severe –> BACTRIM 1ST LINE, FQ

110
Q

CAMPYLOBACTER ENTERITIS

A

MC cause of BACTERIAL ENTERITIS in US
MC ANTECEDENT EVENT IN POST-INFX GUILLAIN-BARRE SYNDROME
-contaminated food (undercooked poultry), raw milk, water, dairy cattle

  • sx- F, HA, abd pain (MIMICS ACUTE APPENDICITIS)
  • diarrhea watery –> bloody

-dx- stool culture: gram neg, “S, COMMA, OR SEAGULL SHAPED” organisms

  • tx- fluids
    severe: ERYTHROMYCIN 1ST LINE, fq, doxy
111
Q

C.DIFF

A

Patient with a history of recent ABX use (clinda most common)
Complaining of frequent watery stools, abdominal pain
Diagnosis is made by nucleic acid amplification test (NAAT)
Treatment is:
Adults Nonsevere or severe - oral vancomycin or oral fidaxomicin
Fulminant - oral vancomycin with parenteral metronidazole
Children Nonsevere - oral vancomycin or oral metronidazole
Severe or fulminant - oral vancomycin
Comments: Patients with at least two Clostridioides difficile infection recurrences treated with appropriate antibiotic therapy, the guidelines recommend use of fecal microbiota transplantation

diarrhea: org overgrowth 2ry to alteration of normal flora (mc after abx –> CLINDAMYCIN or chemo)
- strikingly inc WBC, PSEUDOMEMBRANOUS COLITIS, may cause perf or toxic megacolon

  • tx- METRONIDAZOLE 1ST LINE MILD
  • PO VANCO 2ND LINE (1ST LINE IF SEVERE)
112
Q

ENTEROTOXIGENIC E.COLI

A

MC cause TRAVELER’S DIARRHEA –> unsanitary drinking water/ice, unpeeled fruits

  • IP 24-72 hrs
  • diarrhea, cramp, vomit

-tx- FLUIDS, +/-BISMUTHS; severe –> FQ

113
Q

VIBRIO CHOLERAE + PARAHEMOLYTICUS

A

diarrhea: contaminated food and water; outbreaks during poor sanitation & overcrowding conditions (esp abroad)
- RICE WATER STOOLS

VIBRIO CHOLERAE (or vibrio parahemolyticus)

  • gray, no fecal odor or pus
  • may rapidly produce dehydration (up to 15L/day)

VIBRIO PARAHEMOLYTICUS & V. VULNIFICUS
diarrhea: assoc w/ raw shellfish, esp Gulf of Mexico

-tx- fluid replacement +/- TETRACYCLINES, FQ

114
Q

intussusception**

A

Patient will be a child six months - three-years-old
Complaining of colicky abdominal pain, vomiting and bloody stools (currant jelly)
Diagnosis is made by ultrasound (“target sign”)
Treatment is air/contrast enema

Intussusception is the most common cause of intestinal obstruction in children under two years of age

Under five years of age, enlarged Peyer’s patches secondary to recent viral illness are the most common lead point. In kids over age five, an underlying lesion, such as Meckel’s diverticulum or HSP vasculitis, is found in up to 75% of cases.

In patients with high suspicion for intussusception air-contrast enema is both diagnostic and therapeutic. Contraindications to the use of air-contrast enema include hemodynamic instability with shock, free air under the diaphragm, and peritonitis. Children with these features need emergent surgical intervention.

Intussusception in adults is rare but when present, involves the small bowel in 80% of cases.

115
Q

G6PD deficiency*

A

Patient with a history of taking antimalarials, sulfonamides, nitrofurantoin, fava beans.
Infection is also a cause for the hemolysis
Labs will show HEINZ BODIES, presence of bite cells on the smear
Consider testing patients prior to starting potential agents in at risk patients
Comments: X-linked recessive

116
Q

diverticulitis*

A

Patient will be complaining of abdominal pain that is localized to the left lower quadrant, fever, nausea, vomiting, and a change in bowel habits
PE will show localized guarding, rigidity, and rebound tenderness
Diagnosis is made by CT scan
Treatment is abx

117
Q

ileus

A

Postoperative, electrolyte abnormalities (hypoK)
Nausea/vomiting, constant pain
Distension + ↓ bowel sounds

118
Q

pyloric stenosis*

A

Patient will be 2–8 weeks of age
Complaining of nonbilious projectile vomiting after feeding and early satiety
PE will show RUQ olive-like mass (hypertrophied pylorus)
Labs will show hypochloremic hypokalemic metabolic alkalosis
Diagnosis is made by ultrasound or UGI series (string sign)
Treatment is surgical

119
Q

refeeding syndrome

A

Refeeding syndrome is a complication that occurs during nutritional therapy of malnourished patients. It is marked by hypophosphatemia, hypokalemia, thiamine deficiency, congestive heart failure and peripheral edema.

Alcoholism, eating disorder, malnourished, malignancy
Electrolyte abnormalities. Check labs often, replenish carefully
Monitor patient when resuming feeds
Evaluate for heart failure and dysrhythmias

120
Q

Wernicke Encephalopathy

A

WERNICKE’S ENCEPHALOPATHY TRIAD: “AGO”
Ataxia, Global confusion, Ophthalmoplegia

Patient will be a chronic alcoholic
Complaining of ataxia and confusion
PE will show nystagmus
Most commonly caused by thiamine (B1) deficiency
Treatment is aggressive thiamine repletion
Comments: replace thiamine BEFORE glucose
Korsakoff (irreversible memory loss)

121
Q

metabolic syndrome

A

Metabolic syndrome refers to a group of findings that increase the chance of developing both type 2 diabetes and atherosclerotic cardiovascular disease, which in turn increases an individual’s cardiovascular risk.

ATP III criteria (2001), need at least three of the following five traits:

  • Abdominal obesity >102 cm Men, >88 cm Women
  • Serum triglycerides ≥ 150 mg/dL or drug treatment for elevated triglycerides
  • Serum high-density lipoprotein (HDL) cholesterol < 40 mg/dL in men and < 50 mg/dL in women or drug treatment for low HDL cholesterol
  • Blood pressure ≥ 130/85 mmHg or drug tx for HTN
  • Fasting glucose ≥ 100 mg/dL (5.6 mmol/L) or drug treatment for elevated blood glucose
122
Q

PYROSIS

A

HEARTBURN

Concepts / Lists (16 decks)

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