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)
2
Q
GI Signs & Sx
4 categories of signs & describe them
“not necessarily testing on this”
A
- prognostic signs: signs that point to the future or predict outcome for pt
- anamnestic signs that give insight to pt’s medical history (ex: acne scars on face)
- diagnostic signs: signs that help medical provider recognize and identify current health problems (ex: PSA antigen)
- pathognomonic signs: signs linked to medical condition w/ full certainty (ex: uvular deviation w/ peritonsillar abscess)
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
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”
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
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
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
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
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)
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
11
Q
GI Signs & Sx
what is manometry?
A
measurement of esophageal pressures
12
Q
GI Signs & Sx
key hx components of dyspepsia
A
- clarify chronicity, location, and quality of pain
- determine relationship of pain w/ meals
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
14
Q
GI Signs & Sx
describe nausea
A
vague sensation of sickness or queasiness
often followed by vomiting
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)
16
Q
GI Signs & Sx
4 causes of vomiting
w/ examples w/in each category
A
- visceral afferent stimulation (biliary or GI distention, irritation, dysmotility, infection, irritants)
- vestibular disorders (meniere syndrome, motion sickness)
- CNS disorders (sights, smells, emotional experiences, migraines, infections, increase ICP)
- Irritation of chemotherapy trigger zones (drugs, chemo, toxins, hypoxia, uremia, acidosis, rad therapy)
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)
18
Q
GI Signs & Sx
what is obstipation?
and not just constipation spelled funny hehe
A
complete or severe constipation
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
20
Q
GI Signs & Sx
n/v tx
A
- NPO for 4-6 hrs then trial clear liquids (IV hydration PRN)
- antmiemetic meds
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)
22
Q
GI Signs & Sx
what can cannabis use lead to?
A
prolonged use can lead to nausea, vomiting, abd pain
cannabinoid hyperemesis syndrome
23
Q
GI Signs & Sx
Hiccups
A
- usually benign and self limited
- causes: gastric distention, sudden temperature changes, alcohol ingestion, emotional states
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)
25
# GI Signs & Sx
tx for hiccups
* 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
26
# GI Signs & Sx
describe eructation
* 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
27
# GI Signs & Sx
describe bloating
* 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
28
# GI Signs & Sx
ascites overview
* 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)
29
# GI Signs & Sx
dx ascites
* 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
30
# GI Signs & Sx
interpret ascites fluid:
* clear/straw colored
* cloudy
* bloody
* chylous
* clear: liver cirrhosis
* cloudy: bacterial peritonitis, perf bowel, pancreatitis
* blood: malignancy, hemorrhagic pancreatitis
* chylous: lymphoma, TB, malignancy
31
# GI Signs & Sx
asites fluid biochemistry normals
* protein
* glucose
* amylase
Microscopy normals
* RBCs
* WBC
* 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)
32
# GI Signs & Sx
complication of ascites
Spontaneous bacterial peritonitis
* infection of ascites fluid
* associated w/ CIRRHOSIS in alcoholics
* sx: abd pain/tender, fever, confusion/disorientation, drowsiness
* tx: IV abx
33
# GI Signs & Sx
describe flatus
* gas
* occurs up to 20x daily in healthy adults
* derived from: swallowed air (nitrogen) or bacterial fermentation of undigested carbs (H2, CO2, CH4 methane)
34
# Esophageal Foreign Bodies
where do FB lodge?
spaces with luminal narrowing
* sphincters (UES, LES)
* strictures
* tumors
* previous surgeries (strictures)
* underlying disorder/disease
35
# Esophageal Foreign Bodies
common causes of impaction
| like specific objects
* foods (steak, hot dogs, grapes, peanuts, candies)
* bones (fish)
* inedible objects (coins, batteries, magnets, drugs)
36
# Esophageal Foreign Bodies
complications of FB
* 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
37
# Esophageal Foreign Bodies
why should CT be non contrast
even small perforations can lead to contrast leaking into the body
38
# Esophageal Foreign Bodies
most common anatomic location for foreign bodies
* 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
39
# Esophageal Foreign Bodies
timing of object removal
| emergent vs urgent vs non-urgent
**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
40
# Gastrointestinal Bleeding
anatomical location of upper vs lower GI bleeds
* upper: hemorrhage proximal (above) to ligament of treitz
* lower: hemorrhage distal (below) to ligament of treitz
41
# Gastrointestinal Bleeding
* acute vs chronic bleeding
* overt vs occult bleeding
* acute: < 3d
* chronic: > 3d
* overt: visible blood
* occult: only detectable w/ chemical testing
42
# Gastrointestinal Bleeding
pharm MOA of NSAIDs on GI tract
* 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
43
# Gastrointestinal Bleeding
pharm MOA of NSAIDs on kidneys
* 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
44
# Gastrointestinal Bleeding
pharm MOA of NSAIDs on CV
* 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
45
# Gastrointestinal Bleeding
NSAIDs and arachidonic acid
* 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
46
# Gastrointestinal Bleeding
differentiate volume loss & sx for fluid loss:
* mild
* moderate
* severe
* mild: < 15% volume loss, sx includes resting tachy
* moderate: 15-40% volume loss, sx include orthostatic hypotension
* severe: > 40%, sx include hypotension
47
# Gastrointestinal Bleeding
what are primary hemodynamic parameters? advanced parameters?
* primary: HR, BP
* advanced: SV, CO, TPR
48
# Gastrointestinal Bleeding
what must size of bleed be to detect on CT?
bleeding rate of at least 0.5-1ml/min
49
# Esophageal Varices
blood flow to hepatic portal system
* abd aorta --> proper hepatic artery --> liver
* splenic vein/superior mesentaric vein -- hepatic portal vein --> liver
* liver --> hepatic veins --> IVC --> RA
50
# Esophageal Varices
describe portal venous system
* 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
51
# Esophageal Varices
what is a varix
* 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
52
# Mallory-Weiss Syndrome/Tear
timeline for tears to heal?
most tears heal within 96 hrs
53
# Esophageal Perforations
how can spontaneous perforations occur
exposes the mediastinum to the GI contents
* iatrogenic (85-90%)
* penetrating injuries (gunshot/blunt force trauma)
* FB ingestion
* Boerhaave's: spontaneous perforation/rupture
54
# Esophageal Perforations
pathophys of Boerhaave Syndrome
* 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
55
# Achalasia
esophagus anatomy
* 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
56
# Achalasia
describe auerbach plexus (myenteric plexus) system
* 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
57
# Achalasia
major and minor pathologic features
* major: failed relaxation in the lower esophageal sphincter (LES) during swallowing
* minor: impaired peristalsis in lower 2/3 of esophagus
58
# Achalasia
pathophys
* degeneration of myenteric plexus ganglia in lower esophagus
* viral/autoimmune factors are suspected
59
# Achalasia
secondary causes of Achalasia
* malignancy
* chagas disease (caused by protozoan parasite and seen in central/south america)
* infiltrative disorders (amyloidosis, sarcoidosis)
* eosinophilic esophagitis
* MEN type 2B
60
# Acute Diarrhea
define:
* diarrhea
* acute diarrhea
* chronic diarrhea
* gastroenteritis
* dysentery
* osmotic diarrhea
* secretory diarrhea
* **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
61
# Acute Diarrhea
when to use dx tools
reserved for severe dehydration or illness, persistent fever, bloody stool, immunosuppression, cases of suspected nosocomial infection/outbreak
62
# Acute Diarrhea
when to consider abx?
shigella, campy, c. diff, traveler's (ETEC), protozoal infections
63
# Acute Diarrhea
preventive measures
* hand washing
* safe food prep
* clean water
* vaccinations
64
# Acute Diarrhea
differentiate:
* noninfectious diarrhea
* infectious diarrhea
* infectious colitis
* non-infection: lack of constitutional
* infectious diarrhea: large volume (watery) stool, constitutional sx, n/v/abd cramps (gastroenteritis)
* infectious colitis: fever, tenesmus, dysentery
65
# Acute Diarrhea
key findings for non-inflammatory diarrhea
* usually viral
* intestinal secretion, mucosa/cells intact
* no fever, blood in stools, or fecal leukocytes
* pathogens: norovirus, rotavirus, cholera, ETEC, s. aureus, giardia
66
# Acute Diarrhea
key findings for inflammatory diarrhea
* usually invasive, toxin-producing bacteria
* **mucosa damaged**
* fever, bloody stool, fecal leukocytes
* pathogens: shigella, campy, c. diff, salmonella, STEC
67
# Constipation
describe
* 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
# Constipation
mechanism of bowel movements
* **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
# Constipation
Bristol stool chart types
| 1-7
* 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
# Constipation
describe anorectual manometry w/ balloon expulsion test
* measure pressures inside rectum, anus, and ability of pelvic muscles to expel stool from rectum
* abnormal results = defecatory disorder
71
# Constipation
describe colonic transit studies
* 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
# Constipation
examples of fiber, osmotic, and stimulant laxatives
* fiber: metamucil, citrucel, benefiber
* osmotic: milk of magnesia, miralax, lactulose
* stimulant: senna
73
# Constipation
anal fissues as a complication
passage of hard/lumpy stools causes a tear in the anoderm leading to painful defecation & rectal bleeding
74
# Constipation
hemorrhoids as a complication
due to excessive straining w/ hard, lumpy stools leading to rectal pain, itching, and/or bleeding
75
# Constipation
fecal incontinence as a complication
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
# Constipation
fecal impaction as a complication
* 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
# Constipation
bowel obstruction as complication
* partial or complete
* sx: reduced appetite, n/v, abd pain, distension
* dx: flat & upright abd xray or CT scan
78
# Hiatal Hernia
describe sliding hiatial hernia
* most common (95%)
* gastroesophageal junction + a portion of the stomach is above the diaphragm
79
# Hiatal Hernia
describe paraesophageal hiatal hernia
* 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
# Hiatal Hernia
describe Nissen fundoplication
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
# GERD Esophagitis
normal vs GERD esophagitis
* 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
# GERD Esophagitis
Risk factors for GERD
| 6
* 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
# GERD Esophagitis
how does barrett esophagus occur from GERD?
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
# GERD Esophagitis
describe esophagogastroduodenoscopy for GERD
* 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
# GERD Esophagitis
describe ambulatory pH monitoring
* 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
# GERD Esophagitis
MOA of antacids
balance pH in the stomach (they are basic, stomach is acidic)
87
# GERD Esophagitis
MOA of H2 Blockers
| + meds/doses
* 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
# GERD Esophagitis
MOA of PPIs
| + meds and dosing
* 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
90
# Abd Wall Hernias
define:
* reducible
* incarcerated
* obstructed
* strangulated
* **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
# Abd Wall Hernias
anatomy of inguinal canal
* 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
# Abd Wall Hernias
Direct Inguinal- borders of Hesselbach
* medial boundary is rectus abdominis muscle
* lateral boundary is inferior epigastric vessels
* inferior boundary is the inguinal ligament
93
# Abd Wall Hernias
indirect vs direct hernias
* 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
# Intestinal Obstruction
differentiate:
* mechanical vs functional
* partial vs complete
* 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
# Gastritis
stomach anatomy
* 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
# Gastritis
regions of the stomach
* 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
# Gastritis
anatomy of stomach wall
* 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
# Gastritis
secretory cells of the gastric glands
* **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
# Gastritis
describe mucosal barrier of the stomach
* 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
# Gastritis
types of chronic *H. pylori* gastritis
* **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
# Gastritis
effects of *H. pylori* gastritis
* 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
# Peptic Ulcer Disease
pathophys for smoking leading to PUD
* impairs ulcer healing and increases incidence of recurrence
* risk correlates number of cigarettes smoked daily
103
# Peptic Ulcer Disease
pathophys
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
# 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
* 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
# Gastric Cancers
3 biggest risk factors
* *H. pylori* infection
* smoking
* Cadherin 1 gene mutation (CDH1- autosomal dominant)
106
# Gastric Cancers
describe intestinal adenocarcinomas
* 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
# Gastric Cancers
diffuse type of adenocarcinoma
* 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
# Gastric Cancers
what are the surgical options?
| 2
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
# Gastric Cancers
post-gastrectomy complications
1. small intestinal bacterial overgrowth (SIBO)
2. dumpin syndrome
3. gastric stasis
4. reduced iron/B12/calcium absorption
110
# Appendicitis
anatomy of peritoneum
* 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
# Appendicitis
anatomy of appendix
* vermiform appendix or cecal appendix
* finger like, blind ended tube extending from cecum in RLQ
112
# Appendicitis
function of appendix
* 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
# Appendicitis
positioning of appendix
* pre-ileal
* post-ileal
* sub-ileal
* pelvic
* subcecal
* paracecal
* retrocecal
* 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
# Appendicitis
describe:
* McBurney's point
* Psoas sign
* Obturator sign
* Rovsing sign
* 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
# Appendicitis
pathophys
* 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
# Appendicitis
pos CT findings
* appediceal diameter >6mm w/ occluded lumen
* appendiceal wall thickening >2mm
* appendiceal wall enhancement
* periappendiceal fat stranding
* appendicolith/fecalith
117
# Acute Cholecystitis
pathophys
* **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
# Vitamins/Malabsorption
fat vs water soluble
* fat: ADEK
* water: B/C
119
# Vitamins/Malabsorption
causes of fat malabsorption w/ examples
* 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
# Vitamins/Malabsorption
expand on how crohn's leads to fat malabsorption
* 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
# Vitamins/Malabsorption
describe how celiac disease leads to carb malabsorption
* 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
# Vitamins/Malabsorption
describe how cystic fibrosis leads to protein malabsorption
* 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
# Diverticular Disease
anatomy of large intestine
* terminal part of GI tract
* primary function: completes absorption of nutrients/water, synthesize vitamins, form/eliminate feces
124
# Diverticular Disease
histology of large intestine
* 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
# Diverticular Disease
anatomic features
* 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
# Diverticular Disease
bacterial flora
* 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
# Diverticular Disease
LaPlace's Law
pressure is inversely proportional to the diameter of a cylinder; sigmoid colon has the smallest lumen diameter of the colon
128
# Diverticular Disease
pathogenesis
* 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
# Small Intestine
anatomy
* 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
# Small Intestine
histology of SI
* wall composed of 4 layers
* 3 adaptations for absorption which are most abundant in proximal 2/3 (circular folds, vili, microvili)
131
# Small Intestine
physiology of circular folds
* 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
# Small Intestine
physiology of villi
* 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
# Small Intestine
physiology of microvilli
* smaller villa found on villi that create brush border
* contains enzymes which complete digestion of carbs/proteins
134
# Celiac Disease
describe physiology of these sx:
* dermatitis herpetiformis
* anemias
* osteoporosis/penia/malacia
* 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
# Colorectal Cancer
common metastases
* 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
# Colorectal Cancer
describe FOBT test
* 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
# Colorectal Cancer
describe FIT testing
* 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
# Colorectal Cancer
describe fecal DNA testing
* 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
# Carcinoid Tumors/Syndrome
precipitators of episodic cutaneous flushing
* emotional stress
* food, hot beverages
* alcohol
140
# Inflammatory Bowel Disease
overview
* 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
# Crohn's Disease
risk factors
* **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
# Crohn's Disease
pathophys
* 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
# Ulcerative Colitis
pathophys
**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
# IBD
which IBD has high risk of colorectal cancer?
UC
| but you screen the same way
145
# Ulcerative Colitis
describe complications of:
* fulminant colitis
* toxic megacolon
* 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
# Irritable Bowel Syndrome
pathophys
* **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
# Anal Fissures
pathophys
* 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
# Anal Fissures
moa for topical vasodilators
* 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
# Anorectal Abscesses
what muscles compose levator ani muscle
three striated muscles on each side
* iliococcygeus
* pubococcygeus
* puborectalis
150
# Anorectal Abscesses
types of abscesses
BELOW LEVATOR ANI MUSCLE
* perianal
* ischiorectal
* interspincteric abscess
ABOVE LEVATOR ANI MUSCLE
* supralevator abscess
151
# Anorectal Abscesses
describe each abscess
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
# Anorectal Abscesses
dentate line
anatomical landmark which divides upper third and lower 2/3s of anal canal
153
# Hirschsprung Disease
pathophys
* 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
# Hirschsprung Disease
normal function of Auerbach's and Meissner's plexus
* Auerbach: causes SM relaxation; muscularis
* Meissner: controls flow, epithelial cell absorption, and secretion; submucosa
155
# Meckle's Diverticulum
etiology of omphalomesenteric duct
* 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
# Intussusception
describe Peyer's patches
* "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
# Intussusception
pathophys
* 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
