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Pathophysiology Ch. 36 Cheat Sheet by

gastrointestinal disroders

Dysphagia: difficulty swallowing

Dysphagia Type 1
Problem with delivering food or fluid to the esophagus
decreased ability to initiate the swallowing sequence*
person may cough to dislodge the solid/­liquid or may aspirate when attempting to swallow
symptoms tend to worsen with liquid rather than solid
Dysphagia Type 2
Problem with transp­orting the bolus (food piece) down the throat
result of a disorder (struc­tural or neurom­usc­ular)) in which the perist­altic movement of the throat is altered
persons may feel as though the food is stuck behind the sternum and if underlying pathology is not resolved can worsen to include liquids
disorders include esophageal divert­icula: outpou­chings of one or more layers of the esophagus | achalasia: in which the smooth muscle is altered | neoplasms or strictures
Dysphagia Type 3
Problem with bolus entering the stomach
Secondary to lower esophageal dysfun­ction or lesions that obstruct the pathway
catego­rized as a tightness or pain in the substernal area when swallowing
tumors in the medias­tinum or below may reduce LES function and chronic inflam­mation of the lower esophagus can lead to further inability

Esophageal Pain

Heartb­urn­/Py­rosis
caused by a reflux of the gastric fluids
a substernal burning sensation that radiates up to the neck
the acid irritates the esophageal mucosa and can also cause spasm of the throat muscles
Chest pain
esophageal distention (enlar­ging) or powerful muscle contra­ctions
pain radiates to neck, jaw, shoulder and arm (similar to angina pectoris) and odynop­hagia
esophageal obstru­ction ir diffuse esophageal spasm where there is a high magnitude spasm between normal perist­alsis
infection chest pain
infections in the esophagus in immuno­com­pro­mised indivi­duals
dull, aching chest pain
can worsen heartburn and regular chest pain

Abdominal pain: first sign of GI tract disroder

visceral pain
due to stretching or inflam­mation
diffuse, poorly localized pain which can be knawing, burning or cramping
somatic pain
injury to abdominal pain, parietal perito­neum, mesentery or diaphragm
sharp intense pain at the area of injury, well localized
referred pain
pain in the same neuros­egment felt in other part
sharp well localized pain that may be felt deep and at a location away from the injury
acute
instan­taneous onset
chronic
gradual onset
usually accomp­anied by other signs/­sym­ptoms such as vomiti­ng/­emesis or bowel alteration

Diarrhea

acute diarrhea
due to acute infection, emotional stress, leakage of liquid stool around impacted stool
chronic
symptoms last longer than 4 weeks, due to chronic GI tract infection, altera­tions in motility or integrity, malabs­orp­tion, endocrine disorders
episodic diarrhea
probably related to food allergy or ingestion of irritants such as caffeine
osmotic
increased amount of poorly soluble nutrient intake such as carbs which pull water into the bowel lumen
secretory
caused by toxins that stimulate intestinal fluid secretion and lower absorp­tion, ~ 1L of diarrhea
exudative (mucus, blood or protein)
blood, protein and mucus getting into the bowel lumen from the site of inflam­mation
motility distru­bances
decreased time and contact of chyme with the absorptive enzymes
increase in fluidity and frequency of the stool, may be very liquidy

Disorders of the mouth

Stomatitis
ulcerative inflam­mation of the mouth oral mucosa
causes:
viral or bacterial infect­ions, mechanical trauma, irritant exposure (alcoh­ol/­tab­acco), medica­tion, radiation therapy, autoimmune disorders and nutrient deficiency
most common type: herpetic gingiv­ost­oma­titis
HSV acquired most by children which causes tingling and itching and leave behind painful ulcers that have ruptures and HSV stays dormant in the dorsal ganglia reacti­vating years later
treate­ment:
antivi­ral­/bi­otics for infect­ions, topical or systemic steroids for autoimmune causes, general treatment in oral hygiene and topical barriers or steroids

Hiatal hernia

the stomach pushes up into the chest cavity through the diaphragm
-
risk increases with age, women more than men
-
2 types: siding hernia (most common), paraes­oph­ageal hernia or mixed
sliding herniais when a portion of the stomach and gastro­eso­phageal junction move up the diaphragm
-
paraes­oph­ageal hernia is when the greater curvature of the stomach pushes up
risk factor
anything that increase intraa­bdo­minal pressure such as pregnancy, obesity and chronic straining or coughing
treatment
similar to GERD with surgery fro acute manife­sta­tions
life threatning in a large proion of the stomach becomes incarc­erated which is rare

GERD

pathoe­genesis
any agent that alters the strength of the LES or increases intraa­bdo­minal pressure
risk factor
ingesting fatty foods, smoking, alcohol, pregnancy, caffeine, anatomical features such as a hiatal hernia
clinical manifests: attributed to esopha­gitis (infla­mma­tion)
heartburn, regurg­ita­tion, chest pain, dysphagia (diffi­culty swallo­wing))
treatment
increase LES strength, esophageal clearance, imprvoe gastric emptying, suppress acidity, avoid dietary risk factors
treatment (cont.)
antacids, histamine blockers (sporadic GERDS), proton pump inhibitors have been known to reverse changes from chronic GERD, surgical interv­ention
Barrett esophagus
compli­cation of GERDS where the epithelium of the esophagus changes to another
leads to a higher risk of cancer
progre­ssion can lead to ulcera­tion, fibrotic scarring, esophageal strictures
LES: lower esophageal sphincter
GERDS: backflow of gastric contents into the esophagus

peptic ulcer disease

etiology
disorder of the upper GI tract caused by acids and pepsin which causes injury to the mucosa of the throat, stomach or duodenum
-
an increase in the factors that cause ulcers than those that do not
cause
NSAIDS, smoking, genetics, h. pyelori which is crucial to the formation of ulcers and thrives in acidic conditions
H. pyelori
lowers healing and has a high rate of recurrence
gastric cause
breakdown of the mucosal barrier that usually prevents the acid from diffusing to the rest of the body (aspirin, NSAIDS, alcohol and bile)
duodenal cause
excess acid secretion and increased activity of the vagus nerve which stimultes the cells to release gastrin which targets cells to release HCl leading to high HCl
clinical manifests
epigastric burning pain relived by food or dairy or antacids | life threat­ening compli­cation such as GI bleeding
diagnosis
Upper GI barium contrast radiog­raphy, endoscopy to visualize ulcers, testing for h. pyelori
treatment
encourage healing of mucosa by reducing acid, prevent recurr­ence, h. pyelori antibi­otics, proton pump inhibitors and sucralfate which forms a protective barrier, no smoking, reduce stress

ulcerative colitis

etio
chronic inflam­mation of rectal and colon mucus, large ulcers forming
clinical manifest and comlic­ation
increased risk of cancer after 7 - 10 years, exaceb­ations and remission, bloody diarrhea and lower abdominal pain
treatment
cortic­ost­eroid, broad spectrum antibi­otics, salicylate analog, immuno­mod­ulating drugs, IV followed by oral cyclos­porine for refractory
inflam­mation - abscess formation - abscesses begin to combine - large ulcers form

Colon cancer

risk factor
age 40+, high fiber and fat diet, polyps, chronic irrita­tio­n/i­nfl­amm­ation, hereditary
diagnosis
recommend colono­scopy every 10 years after reaching risk age
familial adenom­atous polypsis:
where three or more family members have colorectal cancer, two genera­tions of colorectal cancer or one or more cases of colorectal cancer before age 50
clinical manifest based on location
right: tarry, black stool | left side: interm­ittent cramping with stringy stool with mucus or blood | rectum: change in bowel habits, urgent need to defecate upon waking, rectal fullness, altern­ating diarrh­ea/­con­sti­pation, rectal ache
prognosis
the earlier the prognosis the better, based on tumor size, location, invasion, if it metast­asized, and uses the TMN classi­fic­ation
treatment
colostomy (opening colon via abdomen), surgical removal, chemo or radiation
second only to lung cancer in the US

Intestinal obstru­ction

partial or complete blockage of samll/­large bowel
mechan­ical: tumors, hernia, volvolus
functi­onal: inhibition of perist­alsis
ogilvie: recurrent bout of ileus
clinical manifest
increase bowel sound, pain, nausea, vomit
absence of bowel sounds
upper jejunal area: vomit, dehydr­ation and electr­olyte depletion
risk factors
surgery for adhesions
congenital abnorm­alities of the bowel
metastatic cancer esp from female reprod­uctive or intestinal tract
treatment
remove mechanical block
surgical interv­ention or decomp­ression with tube
fluid/­ele­ctr­olyte replac­ement
other info
if left untreated can lead to perfor­ati­on/­isc­hemia, and necrosis
necrosis leads to bowel gangrene, sepsis and perito­nitis
fluid, gas, water, electr­olyte accumulate in bowel

Intestinal gas

altered motility or lack of digestive enzyme
caused by swallowing air, normal bacter­ial­/enzyme activity, or neutra­liz­ation of bicarb in the upper GI
belching
normal expelling of swallowed air
abdominal distention
failure to digest nutrients or defect in intestinal motility
excessive flatus
bacterial digestion of certain foods that are gas causing (legumes, vegeta­bles)

MOTILITY DISORDERS

 

Irritable Bowel Syndrome IBS

altern­ating diarrhea and consti­pation accomp­anied by cramping with no pathology of the GI tract
etiology also unclear
clinical manifest
diarrhea, consti­pation, cramping, mucus in stool, nausea
treatment
antidi­arrheal agents, antisp­asmodic agents, high fiber diet

Volvulus

- twisting of the bowel itself resulting in bowel obstru­ction and blood vessel constr­iction
- results from 180 twist, ingested foreign body, or adhesion and cannot always be determined
- usually in cecum or sigmoid colon

Intuss­usc­eption

etiology
telesc­oping of a portion of the bowel into adjacent portion resulting in obstru­ction (bowel pushes itself into the other.)
risk factors
infants and males
treatment
surgical

Intuss­usc­eption

Megacolon

■ Congenital or acquired
■ Massive dilation of colon
■ Cause: prolonged consti­pation
■ Pseudo­mem­branous colitis may result in acute megacolon: surgical emergency.

Hirsch­sprung Disease

a congenital disease in which the autonomic ganglia are reduced or absent. more common in males than females and in children. Causes difficulty in passing of stool 48 hours after birth in children
■ Clinical manife­sta­tions
– Profuse diarrhea, hypovo­lemic shock, intestinal perfor­ation
– Stasis of stool and megacolon may occur.
– Fecal stagna­tion; entero­colitis with bacterial overgrowth
■ Treatment
– Colonic lavage, surgical interv­ention

NEOPLASM OF GI TRACT

 

Esophageal cancer: 1-2% of all

risk factor
men are more likely than women, genetic, diet high in nitros­amine, smoking, barrett esophagus, alcohol
progno­sis­/di­agnosis
poor prognosis, can quickly metast­asize
treatment
stent placement, tumor ablati­on/­removal via heat and laser, surgery, radiation and chemot­herapy

small intestinal neoplasms

benign or malignant, accounts for less than 5 %
-
clinical manifest
depends on the type and extent of obstru­ction, can lead to biliary stasis (stopping of bile) jaundice, bleeding and ulcers
treatment
surgical removal of tumor and parts of the intestine - chemot­herapy

Gastric carcinoma

risk factor
more prevalent in Japan, men older than 30 years, h. pylori infection, epsetein barr, geneti­c/d­ietary factors, smoking
stages
are determined by penetr­ation into a major muscle of the stomach and looking at the lymphatic system
treatment
aspirin has protective benefits, surgical removal
clinical manifest
early - asympt­omatic | advanced: anorexia, weight loss and bleeding

Colonic polyps

clinical manifest
usually none, but may cause gross bleeding and abdominal pain
treatment
varies in size, type and location and removed using a scope

Colonic polyps image

Colon cancer staging

  

Consti­pation

small, infrequent or difficult bowel movement
fewer than 3 stools per week
low fiber, low exercise, slower perstalsis due to aging or pathol­ogical disorders
fecal impaction can occur where the stool starts blocking the GI tract

MALABS­ORPTION DISORDERS

DISORDERS REGARDING THE SMALL INTESTINE AND INTAKE OF NUTRIENTS

Celiac disease

a familial intole­rance to gluten
will lead to inflam­mation and atrophy of intestinal vili
causes:
impaired nutrient absorption due to reduced surface area
diagnosis
intestinal biopsy, anti tissue transg­lut­aminase anitbody and imunog­lobulin A endomysial antibody
treatment
gluten free diet, cortic­ost­eroids, supple­mental folate, b12, and fat soluble vitamin

Tropical sprue/­ent­ero­pathy

etiology
of unknown cause but usually causes bacterial overgrowth in the large intestine where the mucus membrane is damaged due to fermen­tation
samll intestine
the mucus lining atrophies leading to malabs­orption and folate and b12 acid deficiency
risk factor
those who live or visit countries along the equator and in adults more than children
clinical manife­staion
bloody diarrhea, abdominal distention and fat in stool steato­rrhea
treatment
antimi­cro­bials, antidi­arr­heals and vitami­n/e­lec­trolyte supplement

Dumping syndrome

dumping of stomach contents into the small intestine after a short amount of time
most likely due to pyloric sphincter regulation loss - the sphincter is what allows chyme movement from stomach to intestine
risk factor­/cause
common after gastre­ctomy, gastric surgery for obesity, cancer or ulcers
due to the large amount of partially digested food entering the intestine it can cause a shift in osmotic causing diarrhea
there is also rapid absorption of glucose in the blood leading to very high plasma insulin but results in low energy a few hours later due to no food storage in the stomach
clinical manife­station
diarrhea, abdominal pain, rapid fall in blood glucos­e/h­ypo­gly­cemia
treatment
eating small but more meals about 6 -8 thoughtout the day

Dumping syndrome image

Short bowel syndrome

due to removal of majority of the intestines
causes severe diarrhea and malabs­orption
reduced ability to absorb due to short area to allow for absorption
(esp if ileocecal valve is removed)
clinical manifest
diarrhea
treatment
supportive to nutrient intake

INFLAM­MATORY BOWEL DISEASE

 

Crohn disease

regional enteritis or granul­omatous
affects proximal portion of the colon or terminal ileum
etio
chronic inflam­mation of all layers of the intestinal wall due to obstru­ction and inflam­mation of the lymph vessels
diagnostic findings
ulcera­tions, strict­ures, fibrosis, fistulas
clinical manifest
fever, diarrhea, right lower quad pain, RLQ mass, tenderness
treatment
alleve­iating and reduce inflam­mation, stop smoking, drugs similar to ulcerative colitis, no definitive care mostly supportive

Crohns v. ulcerative

ESOPHAGEAL DISORDERS

 

Mallor­y-Weiss Syndrome

etiology
bleeding caused by tear in the mucosa due to excessive vomiting
clinical manifest
vomiting of blood (hemat­emesis) and passing or large amounts of blood rectally
diagnosis
endoscopic examin­ation
treatment
blood transf­usion thought bleeding may stop on its own, contro­lling active bleeding with coagul­ation techni­ques, epinep­hrine injection etc.

esophageal varices

etiology
portal hypert­ension from alcoholism or viral hepatitis
causes
in tropical areas a species of liver fluke
a high mortality rate and it affects more than half of patients with cirrhosis

Portal hypert­ension

  

Vomiti­ng/­emesis

forceful expulsion of the gastric contents through the mouth
coordi­nated sequence of abdominal muscles and reverse esophageal perstalsis
also caused by altera­tions in the integrity of the GI tract wall and motility (obstr­uct­ion))

ENTERO­COLITIS

 

Antibiotic associated colitis

etiology
inflam­mation and necrosis of th large intestine due to clostr­idium difficile or antibi­otics and mediated by bacterial toxins
clinical manifests
diarrhea, abdominal pain, leukoc­ytosis, sepsis or perfor­ation
treatment
stop antibi­otics if possible, treat ischemia or any contri­buting factors, fecal transplant if severe

Necrot­izing entero­colitis

occurs in infants <34 week or low weight infants <5 lbs
diffuse or patch necrosis
etiology
bowel ischemia, perinatal oxygen defici­ency, use of hypertonic formula
clinical manifest
distended abdomen and stomach and perfor­ation (hole in stomach)
treatment
fluids, antibi­otics, surgery for ischemia or perfor­ation
typhlitis
specia­lized necrosis in adult cancer patient with poor prognosis

Apendi­citis

etiology
inflam­mation of the appendix due to fecalith or stone made of feces
clinical manifest
perium­bilical pain, RLQ pain, nausea, vomit, fever, diarrhea and systemic inflam­mation
treatment
immediate surgical removal, antibi­otics, fluids, any localized abscesses may be drained with a tube
untreated append­icitis can lead to rupture and perito­nitis

Divert­icular disease

etiology
presence of divert­icula or hernia­tions on the colon - divert­icu­losis
cause
low intake of dietary fiber causing high intral­uminal pressure
clinical manifest
divert­icu­losis - asympt­omatic | divert­icu­litis: inflam­mation of the divert­icula has fever, acute lower abdomen pain and leukoc­ytosis
treatment
antibi­otics and surgery for abscesses

INFLAM­MATORY STOMACH DISORDERS

 

Gastritis: stomach lining

acute
precip­itated by ingestion of irritating substances such as alcohol, aspirin, non-st­eroidal anti-i­nfl­amm­atory drugs (NSAIDS), viral bacteria
clinical manifest
maybe asympt­omatic, anorexia, postpr­andial discom­fort, hemate­mesis
treatment
remove the cause
chronic
helico­bacter pylori which is transm­itted person to person, fecal to oral route or water borne
compli­cation
peptic ulcer, atrophic gastritis (thinning of the lining), gastric adenoc­arc­inoma, mucos associated lymphoid tissue and decreased acid + intrinsic factor

Gaster­oen­teritis

etiology
inflam­mation of stomach and small intestine
chronic
secondary to another GI disorder
acute
direct infection by pathogenic bacteria or toxin
-
may be cause by imbalance in the normal flora
clinical manifests
diarrhea secere­tory, abdominal discom­fort, nausea, vomit, fever and malaise
treatment
replace fluids and electr­olytes
 

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  • Published: 31st July, 2024

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