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CMT > GI Pathophys (Digestive Tract) > Flashcards

GI Pathophys (Digestive Tract) Flashcards

1
Q

GI Signs & Sx

sign vs sx

A
  • sign: effect of health problem that can be observed (objective)
  • symptom: effect noticed and experienced only by person affected (subjective)
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2
Q

GI Signs & Sx

4 categories of signs & describe them

“not necessarily testing on this”

A
  1. prognostic signs: signs that point to the future or predict outcome for pt
  2. anamnestic signs that give insight to pt’s medical history (ex: acne scars on face)
  3. diagnostic signs: signs that help medical provider recognize and identify current health problems (ex: PSA antigen)
  4. pathognomonic signs: signs linked to medical condition w/ full certainty (ex: uvular deviation w/ peritonsillar abscess)
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3
Q

GI Signs & Sx

3 main types of symptoms & describe

A
  • Remitting: sx that improve or resolve completely
  • Chronic: long lasting or recurrent
  • Replasing: sx that resolve and return
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4
Q

GI Signs & Sx

dysphagia describe

A
  • oropharyngeal dysphagia: problems in transferring food bolus from oropharynx to the upper esophagus
  • esophageal dysphagia: impaired transport of food bolus through body of esophagus, may be accompanied by feeling of food getting “stuck”
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5
Q

GI Signs & Sx

Odynophagia describe/causes

A
  • sharp pain on swallowing that may limit PO intake
  • caused by Candida, herpesvirus, CMV, caustic ingestions
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6
Q

GI Signs & Sx

Pyrosis describe

A
  • heart burn
  • feeling of substernal burning (often radiates to neck)
  • caused by reflux of gastric contents into esophagus
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7
Q

GI Signs & Sx

describe dyspepsia

A
  • aka indigestion
  • persistent or recurrent pain/discomfort in upper abdomen
  • Commonly described as early satiety, postprandial fullness, gnawing or burning
  • usually indicates underlying problem
  • Types: ulcer, dysmotility, reflex
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8
Q

describe three types of dyspepsia

A
  • Ulcer: pain localized in epigastrium, frequently occurs before meals and is relieved by eating foods, antacids, or H2 blockers
  • Dysmotility: discomfort rather than pain along w/ early satiety, postprandial fullness, nausea, vomiting, bloating; worsened by food
  • Reflux: heartburn, acid regurgitation
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9
Q

GI Signs & Sx

dyspepsia contributing factors

4 components

A
  • overeating
  • eating too quickly
  • drinking too much alc/coffee
  • meds (ASA, NSAIDs, abx, DM meds, HTN meds)
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10
Q

GI Signs & Sx

alarm sx of dyspepsia

7

A
  • wt loss
  • odynophagia
  • progressive dysphagia
  • constant/severe pain
  • persistent vomiting
  • hematemesis, melena
  • failure to respond to therapy
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11
Q

GI Signs & Sx

what is manometry?

A

measurement of esophageal pressures

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12
Q

GI Signs & Sx

key hx components of dyspepsia

A
  • clarify chronicity, location, and quality of pain
  • determine relationship of pain w/ meals
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13
Q

GI Signs & Sx

key labs/dx for dyspepsia

A
  • labs: CBC w/ diff, BMP, FOBT
  • C14-urea breath test (screening for H. pylori, < 45 yrs w/ no alarm symptoms)
  • Upper endoscopy: pts > 60 or 45-59 w/ alarm sx
  • biopsy for H. pylori
  • esophageal manometry & pH studies
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14
Q

GI Signs & Sx

describe nausea

A

vague sensation of sickness or queasiness

often followed by vomiting

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15
Q

GI Signs & Sx

describe vomiting

A
  • forceful expulsion of gastric contents produced by involuntary contractions of the abd musculature when the gastric fundus and lower esophageal sphincter are relaxed
  • controlled by the brainstem (medulla)
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16
Q

GI Signs & Sx

4 causes of vomiting

w/ examples w/in each category

A
  1. visceral afferent stimulation (biliary or GI distention, irritation, dysmotility, infection, irritants)
  2. vestibular disorders (meniere syndrome, motion sickness)
  3. CNS disorders (sights, smells, emotional experiences, migraines, infections, increase ICP)
  4. Irritation of chemotherapy trigger zones (drugs, chemo, toxins, hypoxia, uremia, acidosis, rad therapy)
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17
Q

GI Signs & Sx

what is rumination

A

usually involuntary regurgitation of small amounts of food from stomach that occurs 15-30 min after eating (most common in infants)

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18
Q

GI Signs & Sx

what is obstipation?

and not just constipation spelled funny hehe

A

complete or severe constipation

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19
Q

GI Signs & Sx

Labs dx for patients w/ n/v

A
  • Urine preg in any female of child bearing age
  • UA, CBC< CMP (if severe vomiting, or for >1d, signs of dehydration)
  • Flat and upright abdomen xray if signs/sx of obstipation or perforation
  • chronic vomiting: referral to GI for upper endoscopy, small bowel xrays, assessment of gastric emptying
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20
Q

GI Signs & Sx

n/v tx

A
  • NPO for 4-6 hrs then trial clear liquids (IV hydration PRN)
  • antmiemetic meds
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21
Q

GI Signs & Sx

Anti-emetic meds

A
  • Serotonin 5-HT3-receptor antagonists (odansetron- zofran)
  • Dopamine antagonists (induce sedation- metoclopramide, promethazine)
  • Antihistamines or anticholinergics (for CNS conditions, meclizine, transdermal scoplamine)
  • Cannabinoids (marijuana)
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22
Q

GI Signs & Sx

what can cannabis use lead to?

A

prolonged use can lead to nausea, vomiting, abd pain

cannabinoid hyperemesis syndrome

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23
Q

GI Signs & Sx

Hiccups

A
  • usually benign and self limited
  • causes: gastric distention, sudden temperature changes, alcohol ingestion, emotional states
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24
Q

GI Signs & Sx

when are hiccups scary?

A
  • > 48 hrs
  • often result of irritation of vagus or phrenic nerve (ex: liver cancer, pancreatitis, disorders of stomach/esophagus, uremia, pleurisy of diaphragm)
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25
Q

GI Signs & Sx

tx for hiccups

A
  • lifting uvula, eat one tsp granulated sugar, interrupt resp cycle by holding breath, irritate diaphgram by holding knees to chest, relieve gastric distention (burping or NG tube), valsalva maneuver
  • meds: chlorpromazine 25-50mg PO or IM
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26
Q

GI Signs & Sx

describe eructation

A
  • aka belching
  • involuntary or voluntary release of gas from stomach or esophagus
  • occurs most frequently after meals when gastric distention results in transient lower esophageal sphincter relaxation
  • stomach gas commonly comes from swallowed air: rapid eating, chewing gum, smoking, carbonated beverages
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27
Q

GI Signs & Sx

describe bloating

A
  • complaint of incresed abd pressure or fullness +/- accompanied by visible distention
  • causes: dietary (eating fatty foods, too quickly, or overeating), lactose intolerance, constipation, GERD, IBS
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28
Q

GI Signs & Sx

ascites overview

A
  • accumulation of protein containing fluid w/in abdomen
  • pt may experience wt gain, increased abd distention, abd discomfort, loss of appetite, SOB
  • tends to occur in chronic disorders
  • Causes: liver disease (most common), cancer, heart failure, kidney failure, pancreatitis, TB)
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29
Q

GI Signs & Sx

dx ascites

A
  • PE: dullness to percussion, clinically detectable with 500 mL+ fluid
  • Imaging: abd US or CT
  • Paracentesis: process of obtaining a sample of ascites fluid by inserting a needle through wall of abdomen and sending fluid to lab for analysis
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30
Q

GI Signs & Sx

interpret ascites fluid:
* clear/straw colored
* cloudy
* bloody
* chylous

A
  • clear: liver cirrhosis
  • cloudy: bacterial peritonitis, perf bowel, pancreatitis
  • blood: malignancy, hemorrhagic pancreatitis
  • chylous: lymphoma, TB, malignancy
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31
Q

GI Signs & Sx

asites fluid biochemistry normals
* protein
* glucose
* amylase

Microscopy normals
* RBCs
* WBC

A
  • protein: 0.3 to 4.0 g/dL is normal; elevated is most likely SBP or TB
  • glucose: same as serum is normal; lower than serum is more likely TB or malignancy
  • Amylase: same as serum is normal; lower than serum is more likely pancreatitis
  • RBC: none is normal; >100 is malignancy or TB; >100,000 is hemorrhage/trauma
  • WBC: < 250 is normal or cirrhosis; >250 is abnormal if predominantly neutrophils (SBP) vs lymphocytes (TB)
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32
Q

GI Signs & Sx

complication of ascites

A

Spontaneous bacterial peritonitis
* infection of ascites fluid
* associated w/ CIRRHOSIS in alcoholics
* sx: abd pain/tender, fever, confusion/disorientation, drowsiness
* tx: IV abx

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33
Q

GI Signs & Sx

describe flatus

A
  • gas
  • occurs up to 20x daily in healthy adults
  • derived from: swallowed air (nitrogen) or bacterial fermentation of undigested carbs (H2, CO2, CH4 methane)
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34
Q

Esophageal Foreign Bodies

where do FB lodge?

A

spaces with luminal narrowing
* sphincters (UES, LES)
* strictures
* tumors
* previous surgeries (strictures)
* underlying disorder/disease

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35
Q

Esophageal Foreign Bodies

common causes of impaction

like specific objects

A
  • foods (steak, hot dogs, grapes, peanuts, candies)
  • bones (fish)
  • inedible objects (coins, batteries, magnets, drugs)
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36
Q

Esophageal Foreign Bodies

complications of FB

A
  • obstruction (can be partial [less emergent, UNLESS sharp objects then they have increased risk of becoming embedded in esophageal wall] or complete [emergent due to risk for pressure necrosis or perforation])
  • perforation
  • infection (can lead to infection –> retropharyngeal abscess
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37
Q

Esophageal Foreign Bodies

why should CT be non contrast

A

even small perforations can lead to contrast leaking into the body

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38
Q

Esophageal Foreign Bodies

most common anatomic location for foreign bodies

A
  • proximal esophagus at level of cricopharyngeus muscle (in line w/ clavicle on xray)
  • mid-esophagus at the level of the aortic arch –> at the carina on xray
  • lower esophageal sphincter –> 2-4 vertebra levels above gastric bubble
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39
Q

Esophageal Foreign Bodies

timing of object removal

emergent vs urgent vs non-urgent

A

Emergent Removal
* complete esophageal obstruction (can’t handle oral secretions)
* disc batteries in esophagus
* sharp pointed objects in the esophagus

Urgent Removal
* esophageal objects that are NOT sharp or objects in stomach that are sharp
* food impactions w/out complete obstruction
* objects above the duodenum that are >6cm in length
* multiple magnets, coins in esophagus

Non-Urgent Removal
* objects in stomach >2.5cm in diameter
* disc batteries in stomach up to 48 hrs if asx
* blunt objects that fall to pass stomach in 3-4wks

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40
Q

Gastrointestinal Bleeding

anatomical location of upper vs lower GI bleeds

A
  • upper: hemorrhage proximal (above) to ligament of treitz
  • lower: hemorrhage distal (below) to ligament of treitz
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41
Q

Gastrointestinal Bleeding

  • acute vs chronic bleeding
  • overt vs occult bleeding
A
  • acute: < 3d
  • chronic: > 3d
  • overt: visible blood
  • occult: only detectable w/ chemical testing
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42
Q

Gastrointestinal Bleeding

pharm MOA of NSAIDs on GI tract

A
  • COX-1 protects gastric mucosa
  • normally: PGE2 increases gastric protection by increasing mucus secretion, bicarb, mucosal blood flow
  • with COX-1 inhibition, it can cause peptic ulcers or GI bleeding
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43
Q

Gastrointestinal Bleeding

pharm MOA of NSAIDs on kidneys

A
  • COX-1 and COX-2 both protect kidneys
  • normal: PGE2 and PGI2 increase GFR (afferent arteriolar vasodilation) and increase sodium/water excretion
  • COX inhibition can cause: sodium/water retention, HTN, hemodynamic acute kidney injury
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44
Q

Gastrointestinal Bleeding

pharm MOA of NSAIDs on CV

A
  • COX-1 and COX-2 both protect kidneys
  • normal: COX-1 and TXA work on platelets –> vasoconstriction; COX-2 and PGI2 work on vascular –> vasodilation, inhibit platelet aggregation
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45
Q

Gastrointestinal Bleeding

NSAIDs and arachidonic acid

A
  • arachidonic acid is a phospholipid that constitutes the membrane of cells in the body
  • phospholipase A2 (enzyme) acts on the cell membrane to liberate arachidonic acid when physical, chemical, and hormonal stimuli are present

Arachidonic acid is further metabolized by 2 pathways to produce eicosanoids
* Cyclooxygenase pathway (COX): prostaglandins, prostacyclin, thromboxane
* 5-Lipooxyenase pathway (LOX): leukotrienes, lipoxins

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46
Q

Gastrointestinal Bleeding

differentiate volume loss & sx for fluid loss:
* mild
* moderate
* severe

A
  • mild: < 15% volume loss, sx includes resting tachy
  • moderate: 15-40% volume loss, sx include orthostatic hypotension
  • severe: > 40%, sx include hypotension
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47
Q

Gastrointestinal Bleeding

what are primary hemodynamic parameters? advanced parameters?

A
  • primary: HR, BP
  • advanced: SV, CO, TPR
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48
Q

Gastrointestinal Bleeding

what must size of bleed be to detect on CT?

A

bleeding rate of at least 0.5-1ml/min

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49
Q

Esophageal Varices

blood flow to hepatic portal system

A
  • abd aorta –> proper hepatic artery –> liver
  • splenic vein/superior mesentaric vein – hepatic portal vein –> liver
  • liver –> hepatic veins –> IVC –> RA
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50
Q

Esophageal Varices

describe portal venous system

A
  • drains blood from lower esophagus, stomach, intestines, spleen, and pancrease to the liver
  • portal vein: formed by junction of splenic vein and superior mesenteric vein; divides into L and R vein at hilum of liver
  • hepatic vein: drains blood from liver to the IVC 4cm before it enters RA
  • Obstruction: due to liver damage leads to portal hypertension and formation of collateral vessels connecting the portal vein and systemic circulation
  • portal venous pressure increases compared to systemic venous circulation causing reversal of blood flow/engorgement in collateral vessels
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51
Q

Esophageal Varices

what is a varix

A
  • abnormally dilated vessel w/ tortorous course
  • usually occurs in venous system but can occur in arterial/lymph vessels
  • most common sites: distal esophagus, proximal stomach, umbilicus, rectum, retroperitoneum
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52
Q

Mallory-Weiss Syndrome/Tear

timeline for tears to heal?

A

most tears heal within 96 hrs

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53
Q

Esophageal Perforations

how can spontaneous perforations occur

A

exposes the mediastinum to the GI contents

  • iatrogenic (85-90%)
  • penetrating injuries (gunshot/blunt force trauma)
  • FB ingestion
  • Boerhaave’s: spontaneous perforation/rupture
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54
Q

Esophageal Perforations

pathophys of Boerhaave Syndrome

A
  • sudden increase in intraluminal pressure in the esophagus, coupled w/ nega intrathoracic pressure, can lead to rupture
  • most common site of rupture of lower posterolateral third of esophagus
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55
Q

Achalasia

esophagus anatomy

A
  • outer longitudinal muscle layer and an inner circular muscle layer
  • circular muscle fibers allow peristalsis
  • upper 1/3 of esophagus: predominantly skeletal muscles
  • lower 2/3 of esophagus: smooth muscles become more dominant from the middle to distal esophagus
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56
Q

Achalasia

describe auerbach plexus (myenteric plexus) system

A
  • between circular muscle layer and the longitudinal muscle layer in the lower esophagus, stomach, and intestines
  • responsibel for peristaltic movement of the bowels
  • can act independently of nervous system
  • originates in the medulla oblongata as a collection of neurons from the ventral part of the brainstem; the vagus nerve then carries the axons to their destination in the GI tract
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57
Q

Achalasia

major and minor pathologic features

A
  • major: failed relaxation in the lower esophageal sphincter (LES) during swallowing
  • minor: impaired peristalsis in lower 2/3 of esophagus
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58
Q

Achalasia

pathophys

A
  • degeneration of myenteric plexus ganglia in lower esophagus
  • viral/autoimmune factors are suspected
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59
Q

Achalasia

secondary causes of Achalasia

A
  • malignancy
  • chagas disease (caused by protozoan parasite and seen in central/south america)
  • infiltrative disorders (amyloidosis, sarcoidosis)
  • eosinophilic esophagitis
  • MEN type 2B
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60
Q

Acute Diarrhea

define:
* diarrhea
* acute diarrhea
* chronic diarrhea
* gastroenteritis
* dysentery
* osmotic diarrhea
* secretory diarrhea

A
  • diarrhea: >3 loose stools/day
  • acute diarrhea: < 2 wks
  • chronic diarrhea: > 3 wks
  • gastroenteritis: diarrhea w/ n/v
  • dysentery: diarrhea w/ blood/mucus/pus
  • osmotic diarrhea: solutes in lumen, draws/keeps water in the lumen (ex: caused by sorbitol)
  • secretory diarrhea: intestinal secretion of solutes and water into the lumen
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61
Q

Acute Diarrhea

when to use dx tools

A

reserved for severe dehydration or illness, persistent fever, bloody stool, immunosuppression, cases of suspected nosocomial infection/outbreak

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62
Q

Acute Diarrhea

when to consider abx?

A

shigella, campy, c. diff, traveler’s (ETEC), protozoal infections

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63
Q

Acute Diarrhea

preventive measures

A
  • hand washing
  • safe food prep
  • clean water
  • vaccinations
64
Q

Acute Diarrhea

differentiate:
* noninfectious diarrhea
* infectious diarrhea
* infectious colitis

A
  • non-infection: lack of constitutional
  • infectious diarrhea: large volume (watery) stool, constitutional sx, n/v/abd cramps (gastroenteritis)
  • infectious colitis: fever, tenesmus, dysentery
65
Q

Acute Diarrhea

key findings for non-inflammatory diarrhea

A
  • usually viral
  • intestinal secretion, mucosa/cells intact
  • no fever, blood in stools, or fecal leukocytes
  • pathogens: norovirus, rotavirus, cholera, ETEC, s. aureus, giardia
66
Q

Acute Diarrhea

key findings for inflammatory diarrhea

A
  • usually invasive, toxin-producing bacteria
  • mucosa damaged
  • fever, bloody stool, fecal leukocytes
  • pathogens: shigella, campy, c. diff, salmonella, STEC
67
Q

Constipation

describe

A
  • infrequent, irregular, difficult evacuation of bowels
  • acute is < 12 wks
  • chronic > 12 wks
  • can be primary (not attributed to structural abnormalities/systemic disease) or secondary (secondary disease, meds, obstructing colonic lesions)
68
Q

Constipation

mechanism of bowel movements

A
  • colon mass movements/peristalsis move intestinal contents distally into rectum
  • rectal filling activates mechanoreceptors in the rectal wall causing awareness of the need to defecate
  • some stool then passes through anal canal by involuntary relaxation of internal anal sphincter (rectoanal inhibitory reflex) –> body then determines if rectal contents is gaseous, solid, liquid
  • abd muscles contract & valsalva is performed while relaxing external anal sphincter and puborectalis muscle (pressure graduent between rectum and anal canal expels the feces)
69
Q

Constipation

Bristol stool chart types

1-7

A
  • 1: separate hard lumps (severe constipation)
  • 2: lumpy, sausage like (mild constipation)
  • 3: sausage shape w/ cracks in surface (normal)
  • 4: smooth, soft sausage/snake (normal)
  • 5: soft blobs w/ clear cut edges (low fiber)
  • 6: mushy consistency w/ ragged edges (mild diarrhea)
  • 7: liquid consistency w/ no solid pieces (severe)
70
Q

Constipation

describe anorectual manometry w/ balloon expulsion test

A
  • measure pressures inside rectum, anus, and ability of pelvic muscles to expel stool from rectum
  • abnormal results = defecatory disorder
71
Q

Constipation

describe colonic transit studies

A
  • pts swallow radiopaque markers which are then tracked through GI tract using x-rays
  • differentiate between slow and normal transit constipation
  • if normal transit time: it’s a diosrder of gut-brain axis
72
Q

Constipation

examples of fiber, osmotic, and stimulant laxatives

A
  • fiber: metamucil, citrucel, benefiber
  • osmotic: milk of magnesia, miralax, lactulose
  • stimulant: senna
73
Q

Constipation

anal fissues as a complication

A

passage of hard/lumpy stools causes a tear in the anoderm leading to painful defecation & rectal bleeding

74
Q

Constipation

hemorrhoids as a complication

A

due to excessive straining w/ hard, lumpy stools leading to rectal pain, itching, and/or bleeding

75
Q

Constipation

fecal incontinence as a complication

A

chronic constipation leads to hard stool masses and pregressive distension of the anal sphincter complex so the patient can’t feel the urge to defecate and soft/liquid stool will lead around the constipation

76
Q

Constipation

fecal impaction as a complication

A
  • increased rectal capacity & reduced colonic motility
  • firm, putty-like mass in rectal vault on the DRE (rock like)
  • sx: rectal rain, tenesmus, overflow diarrhea, watery fecal material leaking around impacted stool
  • tx: enema, manual disimpaction
77
Q

Constipation

bowel obstruction as complication

A
  • partial or complete
  • sx: reduced appetite, n/v, abd pain, distension
  • dx: flat & upright abd xray or CT scan
78
Q

Hiatal Hernia

describe sliding hiatial hernia

A
  • most common (95%)
  • gastroesophageal junction + a portion of the stomach is above the diaphragm
79
Q

Hiatal Hernia

describe paraesophageal hiatal hernia

A
  • higher risk condition, but less common
  • gastroesophageal junction is in the normal location, but a portion of the stomach is adjacent to the esophagus in the diaphragmatic hiatus
80
Q

Hiatal Hernia

describe Nissen fundoplication

A

top of stomach is wrapped around the lower esophagus which reinforces the lower esophageal sphincter which makes it less likely that acid will back up in the esophagus

81
Q

GERD Esophagitis

normal vs GERD esophagitis

A
  • normal: LES maintains high pressure zone between esophagus and stomach; this prevents reflux of gastric contents. It will transiently relax in response to meals
  • GERD: incompetent LES has a lower baseline pressure and increased frequency of TLESRs leading to acid reflux
82
Q

GERD Esophagitis

Risk factors for GERD

6

A
  • cigarette smoking
  • obesity
  • hiatal hernias
  • food/drink (alcohol, caffeinated beverages, fried/fatty foods, citrus/spicy foods, chocolate, red sauce)
  • medicines (nitrates, Ca channel blockers)
  • lying down after meals
83
Q

GERD Esophagitis

how does barrett esophagus occur from GERD?

A

replacement of normal squamous epithelium of the distal esophagus with metaplastic columnar epithelium during the healing phase of acute esophagitis

can lead to esophageal adenocarcinoma

84
Q

GERD Esophagitis

describe esophagogastroduodenoscopy for GERD

A
  • first line endoscopic test for pts w/ alarm sx or refractory sx
  • allows for direct inspection of esophagus and gastric mucosa for objective evidence of GERD (erosive esophagitis or Barret esophagus)
  • Class A-D grading system for severity of reflux esophagitis (servere = class C/D; should trial PPIs for 2 mo and then re-do endoscopy to assess for Barrett’s Esophagus)
85
Q

GERD Esophagitis

describe ambulatory pH monitoring

A
  • allows for detection of gastroesophageal reflux
  • used to confirm the dx and check the adequacy of treatment
  • tube entered through the nose into esophagus for 24-48 hrs
  • measures the frequency of esophageal pH dropping below 4
  • use in pts w/ extraesophageal sx, GERD refractory to meds, no endoscopic findings
86
Q

GERD Esophagitis

MOA of antacids

A

balance pH in the stomach (they are basic, stomach is acidic)

87
Q

GERD Esophagitis

MOA of H2 Blockers

+ meds/doses

A
  • added at bedtime if pt is on PPI w/ noctural sx
  • decreases acid secretion by competitively blocking H2 receptors in gastric parietal cells
  • require dose adjustment in setting of renal insufficiency
  • famotidine: 20mg BID
  • cimetidine: 400mg BID
88
Q

GERD Esophagitis

MOA of PPIs

+ meds and dosing

A
  • block gastric acid secretion by irreversibly binding to and inhibiting the hydrogen potassium ATPase pump that resides on the luminal surface of the parietal cell membrane
  • take 30-60 minutes before the first meal of the day (prodrug and require activation in an acidic environment for max effect)
  • BID dosing is not FDA approved, but if used do 30-60min before brekkie and dinner
  • Omeprazole 20mg QD
  • Pantoprazole 40mg QD
  • Esomeprazole 40mg QD
  • Lansoprazole 30mg QD
89
Q
A
90
Q

Abd Wall Hernias

define:
* reducible
* incarcerated
* obstructed
* strangulated

A
  • reducible: contents of hernia which can be manipulated back into their original position through the defect from which they emerge
  • incarcerated: compressed by the defect causing it to be irreducible (cannot be pushed back into its original position)
  • obstructed: hernias containing bowel, where contents of hernia are compressed to the extent that the bowel lumen is no longer patent and causes bowel obstruction
  • strangulated: compress around the hernia prevents blood flow into the hernial contents causing ischemia of tissues & associated pain
91
Q

Abd Wall Hernias

anatomy of inguinal canal

A
  • inguinal ligament runs between ASIS and pubic tubercle (PT)
  • inguinal canal is tube like structure that runs within ligament (spermatic cord & round ligament)
  • deep inguinal ring: entry point from abd cavity into the canal; found just above midpoint of inguinal ligament
  • superficial inguinal ring: exit point from the canal; found just above and lateral to the pubic tubercle
92
Q

Abd Wall Hernias

Direct Inguinal- borders of Hesselbach

A
  • medial boundary is rectus abdominis muscle
  • lateral boundary is inferior epigastric vessels
  • inferior boundary is the inguinal ligament
93
Q

Abd Wall Hernias

indirect vs direct hernias

A
  • indirect: traverses the internal inguinal ring into the inguinal canal
  • direct: extends directly through hesselbach’s triangle and does not pass through the inguinal canal
94
Q

Intestinal Obstruction

differentiate:
* mechanical vs functional
* partial vs complete

A
  • mechanical: physical blockage
  • functional: disruption of normal motility
  • partial: some intestinal contents can pass through
  • complete: no passage of luminal contents beyond obstruction point
95
Q

Gastritis

stomach anatomy

A
  • J shaped muscle organ located in the upper left abd cavity inferior to the diaphragm
  • contributes to mechanical and chemical digestion of food and releases it into small bowel as chyme
  • greater curvature: convex lateral surface
  • lesser curvature: concave medial surface
  • held in place by the greater omentum (runs from the greater curvature to the posterior abd wall) and lesser omentum (extends from liver to lesser curvature)
96
Q

Gastritis

regions of the stomach

A
  • cardia: where food passes from esophagus into stomach
  • fundus: dome shaped region located above and to the L of the cardia
  • body: largest region
  • pylorus: funnel shaped region connects to duodenum (antrum is wider, canal is narrow, sphincter is smooth muscle which controls emptying)
97
Q

Gastritis

anatomy of stomach wall

A
  • mucosa: forms rugae (large folds in an empty stomach), contains protective alkaline mucus, gastric pits are depressions that mark entry to gastric glands
  • submucosa: contains blood vessels, lymph vessels, and nerves
  • muscularis externa: responsible for mechanically break down food into smaller particles (inner oblique, middle circular, and outer longitudinal layers)
98
Q

Gastritis

secretory cells of the gastric glands

A
  • chief cells: secrete pepsinogen which is inactive pepsin
  • parietal cells: produce HCl (high acidity w/ pH 1.5-3.5 in the stomach which denature proteins and kill ingested bacteria and activates pepsin) and intrinsic factor (helps absorb vit B12)
  • mucous neck cells: secrete alkaline mucus
  • enteroendocrine cells: D cells secrete somatostatin (inhibitory) and G cells secrete gastrin (stimulates parietal cells)
99
Q

Gastritis

describe mucosal barrier of the stomach

A
  • protects stomach from self-digestion
  • mucosal barrier: thick coating of bicarb rich mucus (acts as physical barrier & bicarb ions neutralize acid)
  • tight junctions: block gastric juice from penetrating underlying issues
  • stem cells: located at junction of gastric pits and gastric glands which replace damaged epithelial mucosal cells
  • surface epithelium is entirely replaced every 3-6 days
100
Q

Gastritis

types of chronic H. pylori gastritis

A
  • mild diffuse gastritis
  • antral-predominant gastritis: increased gastrin production (stimulates secretion of gastric acid, HCl, by pariety cells, leading to hypersecretion of acid and predisposition to peptic ulcers/gastric adenocarcinomas)
  • body-predominant gastritis: destruction of acid-secreting glands resulting in gastric atrophy and decreased acid production, predisposes pt to neuroendocrine tumors
101
Q

Gastritis

effects of H. pylori gastritis

A
  • decreases the number of delta cells which secrete somatostatin (somatostatin inhibits gastrin)
  • group 1 carcinogen
  • if chronic: at risk for gastric MALT lymphoma (B-cell NHL that begins in the stomach)
102
Q

Peptic Ulcer Disease

pathophys for smoking leading to PUD

A
  • impairs ulcer healing and increases incidence of recurrence
  • risk correlates number of cigarettes smoked daily
103
Q

Peptic Ulcer Disease

pathophys

A

Stomach & Duodenum
* normally exist in an acidic environment
* imbalance between offending agents and defense mechanisms leads to PUD

Defense Preventing Mucosal Injury
* mucus bicarbonate phospholipid layer
* epithelial layer (repair regulated by prostaglandins)

Mechanisms by Offending Agents
* H. pylori: gastritis or inflammation increases gastric acid, inhibits somatostatin, and reduces mucus
* NSAID MOA: inhibits COX1 which reduces prostaglandin (reduced mucus, mucosal blood flow, epithelial proliferation) and inhibits COX2 which delays healing

104
Q

Peptic Ulcer Disease

compare and contrast duodenal and gastric ulcers
* which is more common
* main causes
* age of onset
* impact of eating
* ulcer location
* malignancy risk

A
  • duodenal: 75% of uclers, due to H. pylori infection, peaks in the 40s, pain improves with eating and worsens 2-3 hrs later, wt gain, located inproximal duodenum, low risk for malignancy
  • gastric: 25% of ulcers, due to NSAIDs (including ASA), pain not relieved with eating (can worsen), wt loss, typically on lesser curvature of stomach, high risk of malignancy
105
Q

Gastric Cancers

3 biggest risk factors

A
  • H. pylori infection
  • smoking
  • Cadherin 1 gene mutation (CDH1- autosomal dominant)
106
Q

Gastric Cancers

describe intestinal adenocarcinomas

A
  • most common
  • caused by H. pylori which causes damage to epithelial cells (chronic gastritis)
  • cells change to resemble intestinal epithelium rather than stomach epithelium (metaplasia)
107
Q

Gastric Cancers

diffuse type of adenocarcinoma

A
  • most aggressive type
  • related to CDH-1 gene mutations (tumor suppressor gene) which codes for membrane adhesion molecule E-cadherin
  • E-cadherin, with the mutation, doesn’t work properly causing the cells to detach and uncontrollably divide
108
Q

Gastric Cancers

what are the surgical options?

2

A
  1. Distal gastrecomy w/ Bilroth II reconstruction (cancers of lower stomach)
  2. Subtotal gastrectomy w/ Roux-en-Y reconstruction (cancers of upper/middle stomach)
109
Q

Gastric Cancers

post-gastrectomy complications

A
  1. small intestinal bacterial overgrowth (SIBO)
  2. dumpin syndrome
  3. gastric stasis
  4. reduced iron/B12/calcium absorption
110
Q

Appendicitis

anatomy of peritoneum

A
  • broad serous membranous sac surrounded by connective tissue that hold digestive organs within abd cavity in place
  • composed of 2 regions (parietal which lines the abd wall; visceral which envelops the abd organs)
  • 5 major folds: greater omentum, lesser omentum, falciform ligament, mesentery, mesocolon
  • watery fluid acts as lubricant to minimize friction between surfaces
111
Q

Appendicitis

anatomy of appendix

A
  • vermiform appendix or cecal appendix
  • finger like, blind ended tube extending from cecum in RLQ
112
Q

Appendicitis

function of appendix

A
  • lymphoid tissue and is a primary site of IgA production which is vital for maintaining homeostasis of intestinal flore
  • rich in biofilms (syntrophic consortium of micro-organisms in which cells stick to each other and also to a surface) and continuously sheds healthy bacteria into the intestinal lumen
  • can be used as a replacement bladder
113
Q

Appendicitis

positioning of appendix
* pre-ileal
* post-ileal
* sub-ileal
* pelvic
* subcecal
* paracecal
* retrocecal

A
  • pre-ileal: anterior to terminal ileum (1-2 o’clock)
  • post-ileal: posterior to terminal ileum (1-2 o’clock)
  • sub-ileal: parallel w/ terminal ileum (3 o’clock)
  • pelvic: descending over pelvic brim (5 o’clock)
  • subcecal: below cecum (6 o’clock)
  • paracecal: alongside lateral border of cecum (10 o’clock)
  • retrocecal: behind cecum (11 o’clock)
114
Q

Appendicitis

describe:
* McBurney’s point
* Psoas sign
* Obturator sign
* Rovsing sign

A
  • McB: point on the LRQ of the abd at which tenderness is maximal in cases of acute appendicitis
  • Psoas: increase in pain when passively extending the R hip joint which applying counter resistance to the R hip; indicates retrocecal orientation of appedix
  • Obturator: pain caused by passive internal rotation of flexed R thigh
  • Rovsing: pain in RLQ when palpating LLQ (rebound)
115
Q

Appendicitis

pathophys

A
  • obstruction of appendiceal orifice
  • mucus accumulation and luminal distention due to : bact overgrowth (E. coli, Peptostreptococcus, pseudomonas, B. fragilis), increases in transmural pressure leading to thrombosis and occlusion of small vessels which causes necrosis and ischemia of nearby tissue
  • eventual perforation (if contained by greater omentum –> appendiceal abscess; if into abd cavity –> peritonitis)
116
Q

Appendicitis

pos CT findings

A
  • appediceal diameter >6mm w/ occluded lumen
  • appendiceal wall thickening >2mm
  • appendiceal wall enhancement
  • periappendiceal fat stranding
  • appendicolith/fecalith
117
Q

Acute Cholecystitis

pathophys

A
  • cystic duct obstruction leading to bile stasis which triggers release of inflammatory enzymes which damage the gallbladder mucosa
  • mucosal damage leads to increased fluid secretion into the gallbladder lumen (too much to be absorbed) increasing intraluminal pressure leading to distention and release of inflammatory mediators (prostaglands/lysolechithin)
  • as this worsens, there can be ischemia and bacterial infection (E. coli, Enterococcus, Klebsiella)
118
Q

Vitamins/Malabsorption

fat vs water soluble

A
  • fat: ADEK
  • water: B/C
119
Q

Vitamins/Malabsorption

causes of fat malabsorption w/ examples

A
  • low duodenal pH (< 6.5; Zollinger Ellison Syndrome)
  • low intestinal surface area (IBD, celiac, small bowel resection)
  • impaired lipid processing by bile (liver disease, cholestasis)
  • small intestinal bact. overgrowth (bile acid dysfunction)
  • pancreatic insufficiency/cancer
  • lymph disorders (whipple disease, intestinal lymphangiectasia)
120
Q

Vitamins/Malabsorption

expand on how crohn’s leads to fat malabsorption

A
  • bile acids form mixed micelles together w/ fatty acids which act as transport vehicles to deliver FA to the apical membrane of enterocytes for absorption
  • with Crohn’s, the terminal ileum is impaired leading to bile acid malabsorption causing congential diarrhea
121
Q

Vitamins/Malabsorption

describe how celiac disease leads to carb malabsorption

A
  • immune disorder triggered by gluten
  • gliadin fractions (components of gluten) promote an inflammatory reaction causing chronic inflammatory cells and villous atrophy in small intestine
122
Q

Vitamins/Malabsorption

describe how cystic fibrosis leads to protein malabsorption

A
  • in the pancreas, the thick mucus/secretions block the pancreatic duct which prevents the release of digestive enzymes which are needed to break down food and absorb nutrients from food
  • if you supplement pancreatic enzymes, you’re all good w/ digestion (not perfect tho)
123
Q

Diverticular Disease

anatomy of large intestine

A
  • terminal part of GI tract
  • primary function: completes absorption of nutrients/water, synthesize vitamins, form/eliminate feces
124
Q

Diverticular Disease

histology of large intestine

A
  • enterocytes: absorptive cells (water, salts, vitamins produced by intestinal bacteria)
  • goblet cells: secrete mucus, aids in movement of feces, protects intestine from effects of acids/gases produced by enteric bacteria
125
Q

Diverticular Disease

anatomic features

A
  • teniae coli: three bands of smooth muscle that make up longitudinal muscle layer
  • haustra: pouches that bunch up when teniae coli contract
  • epiploic appendages: small, fat filled sacs of visceral peritoneum attached to teniae coli; aids in absorption of nutrients and helps to protect blood vessels of large intestine
126
Q

Diverticular Disease

bacterial flora

A
  • 700 species that live in the intestines which are non-pathogenic if they remain
  • function: facilitate chemical digestion/absorption; syntehsize biotin, vitamin K, vitamin B5
  • deficiency of intestinal bacteria: poorly regulared immune system/gut function; associated w/ autoimmune and inflammatory conditions
127
Q

Diverticular Disease

LaPlace’s Law

A

pressure is inversely proportional to the diameter of a cylinder; sigmoid colon has the smallest lumen diameter of the colon

128
Q

Diverticular Disease

pathogenesis

A
  • intraluminal pressure causes herniation of the mucosa and submucosa through weak areas in the colon wall
  • diverticula occur in the weak spots where vasa recta or nutrient vessels penetrate the muscular layer
  • diverticulosis most commonly involves sigmoid colon (LaPlace’s law)
129
Q

Small Intestine

anatomy

A
  • primary digestive organ responsible for majority of absorption
  • 5x longer than large intestine, but diameter only 1 inch
  • duodenum, jejunum, ileum (longest, most distale; thickest, more vascular, more muscosal folds)
130
Q

Small Intestine

histology of SI

A
  • wall composed of 4 layers
  • 3 adaptations for absorption which are most abundant in proximal 2/3 (circular folds, vili, microvili)
131
Q

Small Intestine

physiology of circular folds

A
  • AKA pilcae circulares
  • deep ridges in the mucosa and submucosa from the start of the duodenum to the mid-ileum
  • help facilitate absorption by causing the chyme to spiral through SI
132
Q

Small Intestine

physiology of villi

A
  • hair-like vascularized projections found w/in circular folds
  • increase SA of mucosal epithelium
  • capillary bed composed of arteriole, venule, lacteal
  • abosrption (occurs by diffusion/active transport); carbs and proteins via venules; lipids via lacteals
133
Q

Small Intestine

physiology of microvilli

A
  • smaller villa found on villi that create brush border
  • contains enzymes which complete digestion of carbs/proteins
134
Q

Celiac Disease

describe physiology of these sx:
* dermatitis herpetiformis
* anemias
* osteoporosis/penia/malacia

A
  • derm: intensely pruritic papulovesicular rash in symmetrical distribution over extensor surfaces of elbows/knees/buttocks/scalp
  • anemia: impaired iron/folate absorption due to villi atrophy
  • osteo: defective calcium transport/vit D deficiency
135
Q

Colorectal Cancer

common metastases

A
  • Liver: 1st site of metastasis for intestinal/colonic tumors; sx include abd distention, jaundice, ascites, hepatomegaly
  • Lungs: 1st site for distal rectal tumors; sx include cough, dyspnea (+/- pleural effusion), hemoptysis
136
Q

Colorectal Cancer

describe FOBT test

A
  • high-sens guaiac based fecal occult blood test
  • identifies hemoglobin in stool
  • pos test: guaiac reagent turns paper blue (peroxidase reaction)
  • restrictions: elimate red meat 3d prior to test, limit vit C to < 250 mg QD 3d prior to test, NSAIDs can impact test
  • 3 consec pos needed
137
Q

Colorectal Cancer

describe FIT testing

A
  • fecal immunochemical test (FIT)
  • tests for hemoglobin in stool (more sensitive/specific than FOBT)
  • no med/diet restrictions
  • only 1 sample needed for pos result but can be pos from non-malignant disorders (ulcer, diverticulosis)
  • neg test cannot r/o cancer
138
Q

Colorectal Cancer

describe fecal DNA testing

A
  • detects DNA mutations and methylation markers shed from colonic tumors
  • typically combined w/ FIT tests, requires full stool sample
  • no diet/med mods
  • pos fecal DNA-FIT should have f/u colonoscpy w/in 6 mo (10% of pt will have normal colonoscopy)
139
Q

Carcinoid Tumors/Syndrome

precipitators of episodic cutaneous flushing

A
  • emotional stress
  • food, hot beverages
  • alcohol
140
Q

Inflammatory Bowel Disease

overview

A
  • describes long standing inflammationo f digestive tract caused by abnormal immune response in the bowel
  • differentiating between Crohn’s and UC requires biopsy
  • spectrum of mild sx to debilitating disease
141
Q

Crohn’s Disease

risk factors

A
  • smoking
  • HLA-B27 gene
  • NOD2 gene (affects body’s ability to recognize and attack bacterial pathogens)
  • family hx
  • sedentary lifestyle
  • reduced fiber/high fat intake
142
Q

Crohn’s Disease

pathophys

A
  • ultimately is multi-factorial
    mutations of NOD2 gene –> defects in epithelial barrier of GI tract –> more pathogens penetrate GI tract –> recruitment of cytotoxic cells –> release of proinflammatory cytokines –> intestinal inflammation –> no down-regulation of immune response –> chronic inflammation –> granulomas –> intestinal damage (edema, ulcers, perforation, fistulas) –> transmural inflammation –> intestinal perforation/fistulas –> chronic and repetitive episodes leads to scarring, fibrosis, obstruction of intestinal wall
143
Q

Ulcerative Colitis

pathophys

A

Defects in the epithelial barrier of the GI tract –> more pathogen penetration –> recruitment and activation of cytotoxic cells –> pANCA (perinuclear anti-neutrophili cytoplasmic antibodies) atttack non-pathogenic cells as pathogens –> excessive release of pro-inflammatory cytokines –> target epithelial cells –> intestinal inflammation & damage

144
Q

IBD

which IBD has high risk of colorectal cancer?

A

UC

but you screen the same way

145
Q

Ulcerative Colitis

describe complications of:
* fulminant colitis
* toxic megacolon

A
  • fulminant: colonic mucosal inflamamtion; presents w/ >10 bloody stools daily, sx of shock, abd pain/distention
  • toxic megacolon: involves inflammation extending beyond mucosal layers to muscular layers of colon
146
Q

Irritable Bowel Syndrome

pathophys

A
  • abnormal motility (increased freq of luminal contractions w/in intestines; transit time depends on IBS-C/D)
  • visceral hypersensitivity: increased sensitivity to normal abd/rectal distention; increased sensitivity to bloating/gas)
  • intestinal inflammation: dietary factors, meds, infections; increased lymphocytes/mast cells in bowel
  • psychosocial: >50% have underlying depression, anxiety, somatization disorders
147
Q

Anal Fissures

pathophys

A
  • acute longitudinal tear in anal mucosa (squamous epithelium) of anal canal distal to dentate line
  • primary causes are posterior midline (most often) or anterior
  • secondary causes are off midline
  • full thickness tear of anal mucosa
  • painful due to somatic innervation
148
Q

Anal Fissures

moa for topical vasodilators

A
  • nitroglycerin: relax anal sphincter and increase blood flow to area to allow for healing
  • nifedipine: relax anal sphincter and decrease anal resting pressure to allow for healing
149
Q

Anorectal Abscesses

what muscles compose levator ani muscle

A

three striated muscles on each side
* iliococcygeus
* pubococcygeus
* puborectalis

150
Q

Anorectal Abscesses

types of abscesses

A

BELOW LEVATOR ANI MUSCLE
* perianal
* ischiorectal
* interspincteric abscess

ABOVE LEVATOR ANI MUSCLE
* supralevator abscess

151
Q

Anorectal Abscesses

describe each abscess

A

BELOW LEVATOR ANI MUSCLE
* perianal (superficial only involves skin)
* ischiorectal (deeper, extends across sphincter into ischiorectal space, may penetrate to contralateral side, DM pts)
* interspincteric abscess (deeper, forms between int and ext anal sphincters)

ABOVE LEVATOR ANI MUSCLE
* supralevator abscess (extremely deep, can extend to peritoneum of obd organs, due to Crohn’s, diverticulitis, PID)

152
Q

Anorectal Abscesses

dentate line

A

anatomical landmark which divides upper third and lower 2/3s of anal canal

153
Q

Hirschsprung Disease

pathophys

A
  • failure of neural crest-derived ganglion cells to migrate to distal colon leading to functional obstruction due to lack of peristalsis in this area (etiehr auerbach’s or meissner’s plexus)
  • aganglionic segments also have abnormal alterations in the expression of receptors, channels, cytoskeletal proteins, neurotrophic factors
  • can be short segment disease (rectosigmoid colon, most common), long segment disease (extension proximal to sigmoid colon), and total colonic
  • muscular hypertrophy and dilatation of bowel proximal to obstruction w/ possible progression to megacolon and rupture (usually in cecum)
154
Q

Hirschsprung Disease

normal function of Auerbach’s and Meissner’s plexus

A
  • Auerbach: causes SM relaxation; muscularis
  • Meissner: controls flow, epithelial cell absorption, and secretion; submucosa
155
Q

Meckle’s Diverticulum

etiology of omphalomesenteric duct

A
  • connects midgut to the yolk sac in utero
  • normally involutes between the 5th and 6th weeks of gestation.

incomplete involution:
* meckel’s diverticulum (most common)
* omphalomesenteric cyst
* omphalomesenteric fistula (drains through umbilicus)
* fibrous bands (can lead to bowel obstruction)

156
Q

Intussusception

describe Peyer’s patches

A
  • “tonsils of intestines”
  • collection of lymphoid follicles in mucus membrane which line the small intestine
  • produce IgA (limits epithelial adherence and penetration of bacteria; ensures bacterial stay on mucosal surfaces)
157
Q

Intussusception

pathophys

A
  • idiopathic if it doesn’t involve lead point (MAJORITY)
  • Lead Point: lesion that gets trapped during peristalsis and drags a segment of intestines into a distal part of the intestine (tumor, polyp, Meckel’s, duplication cyst, vascular malformation, hematoma)
  • telescoping of bowel into itself leading to obstruction/impaired lymphatic drainage–> increasing pressure in intussusceptum bowel wall –> impairment of venous/lymph drainage –> vascular compromise –> ischemia of intussusceptum mucosa –> bowel mucosa infarcts and sloughs off –> bloody stools
  • transmural necrosis and perforation w/ prolonged ischemia

CMT (78 decks)

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