Chapter 14 Flashcards
May appear after broad spectrum anitbiotics
Oral Candidiasis
Pseudomembranous candidiasis
thrush
risk of oral candidiasis
lowered immunity, diabetics
oral lesion—reactive mass to chronic irritation—fibrosis
fibroma MC along bite line
benign vascular mass [red/purple] on gingiva, fast growth
Pyogenic Granuloma—-bad name
who gets pyogenic granuloma
pregnant women, children—-pregnancy tumor
why do women get pyogenic granuloma
hormonal factors, irritation
reactive fibromas and pyogenic granulomas are what?
oral proliferative lesions
raised white patch inside oral cavity, cannot be scraped off
leukoplakia
what causes leukoplakia?
cellular irregularity, cigs, alochol, irritants
leukoplakia is an ex of dysfunctional cells how?
epithelial hyperplasia and Keratosis
Risk of leukoplakia
inflammation: cigs, alchohol, candidiasis..males 40-70
Diagnosis of leukoplakia
biopsy to rule out CA. 25% pre-cancerous»squamous cell carcinoma
Erythroplakia is important why?
Over 50% transition into oral CA
Hairy Leukoplakia is linked with what?
EBV virus, and immunosuppression
Verrucous Leukoplakia would be what
Oral HPV, hyperkeratosis, warty appearance
what does verrucous mean
wart, warty. yum
Oral CA develops from
Dysplasia, TP53 mutations
95 % of all cases of oral CA are this type
squamous cell carcinoma, multple primary tumors common
symptoms of oral CA
oropharyngeal pain/dysfunctiong
Prognosis of oral CA
less than 50% long term, early detection!
Risks of oral CA
alcohol, cigs, >30 years old, HPV-16
Lesions: raised plaque, firm–need biopsy
squamous cell carcinoma
irregular borders, maybe leukoplakia-like, whitish gray or erythematous—red types of changes
squamous cell carcinoma
locations of squamous cell carcinoma
- ventral tongue 2. floor of mouth 3. lower lip 4. soft palate 5. gingiva
better prognosis of squamous cell carcinoma–usually develops at back of mouth
following HPV infxn =]
salivary gland diseases affect
- parotid mc 2. sublingual 3. submandibular 4. minor
xerostomia is what
dry mouth—decrease saliva
who gets xerostomia–
old ppl, ADRs [adverse drug rxn], irradition, Sjogren
what is sjogren, for good measure
autoimmune, exocrine destruction
IgA and enzymes would be present in what
salivary gland pathologies
tongue fissuring, ulcerations, increased risk of candida
xerostomia
femal, less that 20 years old , painful sore in mouth
aphthous ulcer
risks of aphthous ulcer —what brings them on, actually
smoke, stress, trauma, fever, certain foods
Tx of a canker sore
b12, nsaids, corticosteroids
young children, 80% aysmptomatic, 10 to 20% acute herpetic gingivostomatitis
the initial HSV infxn
generally, what/where is hsv 1 and hsv 2
orofacial and genital, but location does not indicate type
ithching, burning, tingling, small vesicles 1-3 mm…HA, sore throat, malaise, fever
HSV
what provokes HSV
UV, fever, cold, trauma, URTI, pregnancy
cure for HSV
no cure, antivirals slow replication though
Why is HSV studied here, can it be bad?
It can spread to the brain, which is life-threatening
HSV-1, acute CNS inflammation/swelling
Herpesviral encephalitis
What are the risks for oral candidiasis?
decreased immune, broad-spectrum antibiotics, diabetics—something about milk and infants….ask jesse
DDx along oral candidiasis
leukoplakia, oral CA
pain when swallowing is referred to as
odynophagia
mc cause of esophagitis, 25-40% of adults
reflux esophagitis
idiopoathic, LES dys, inc gastric volume, obesity, hiatal hernia, pregnancy, smoke, booze
reflux esophagitis
esophageal inflamm secondary to injury of mucosa
esophagitis
MC outpatient GI complaint
GERD—type of esopagitis
over 40, dysphagia, heartburn, “sour brash”
esophagitis
treatment if GERD
antacids, PPIs (omeprazole)—poroton pump inhibitor
esophagitis due to chemical would be acute, self-limited due to
smoke, booze, pills, hot, acid/base, irradiation, chemo
secodnary to ulcer, immunosuppressed–could be fungal
infectious esophagitis due to candidiasis, HSV CMV
MC laceration of esopohageal lining
Mallory Weiss tear
what causes a mallor-weiss tear
forceful vomiting, acute illness/intoxication. INadequate LES relax leads to longitudibal esophageal tears. leaceration to gastroesophageal jxn
TX to mallory-weiss tear. what was the Dx
balloon tamponade..endoscopy
widening of the diaphragm, stomach protrudes into thorax
hiatal hernia
causes of hiatal hernia
congenital, aqcuired, idiopathic
MC type of hiatal hernia—bell shaped dilation
Axial, 95%
Non-axial hernia, tell me about it
more likely to cause problem, like strangulation. asymmetrical
hiatal hernia occurs in who
20& of adults 70% over 70
90% of hiatal hernias are asymptomatic, no question here, bro
okie dokie
a complication of having GERD, metaplasia of distal esophagus
Barrett Esophagus
Preneoplastic lesion. Stratified sdquamous into columnar epithelia, contain goblet cells
Barrett Esophagus—stomach cells into esophagus
10% of symptomatic GERD will become
Barrett esophagus
Risks for Barrett Esophagus
males 4x, caucasians 30-100x, obese, 40-60, family Hx
endoscopy of barrett esophagusd
red velvety mucosa, bands “tongues” extend supoeriorly
super bad complications of barrett esophagus
esophageal adenocarcinoma, ulcerations, strictures.
Tx of Barrett
STOP irritants: smoke, irritating foods, eating late
Meds, omeprazole, laser ablation,
benign esophageal tunor is technically what
leiomyoma–benign, smooth muscle tumor
the naughty esophageal tumor
adenocarcinoma or squamous cell carcinoma9/10 worldwide
50% of US esophageal cancers, risks
adenocarcinoma, Barrett, GERD, living in US lol
9 out of 10 esophageal cancers, worldwide
squamous cell carcinoma
cancer with features that develop late, with early lymphatic invasion, with is very bad
adenocarcinoma, poor prognosis of 25% for 5 years
featues of adenocarcinoma of esophagus
odynophagia, vomiting, cachexia, fatigue, weakness
cancer more common through irriation, greater than 45, more in african americans, rural, underdeveloped
achalasia–lower esophagus fails to relax
squamous cell carcinoma. very poor prognosis less than 10%
the stomach is a common cause of morbidity
but, benign gastritis can turn into agressive gastric CA
features of gastritis
epigastric pain, nausea, vomiting, could be specific, pinpoint—mucosal ulceration–hemorrhage.
vomiting hematemesis is what
melena is what
blood contact with stomach—coffee ground appearance
black, tarry feces
MC infxn of gastritis
h. pylori
risks of gaastritis
alcohol, nsaids, ibuprofen, naproxen—aleve, aspirin. AGE
how to NSAIDs cause gastritis
decrease bicarbonate, i guess
acute gastritis—acute erosive hemorrhagic gastritis
aucte onset, usually a trauma to the mucosa, most likely from the risks, like nsaids. pathogenesis tends to be multifactorial—
epigastric pain (gnawing, burning) nauseam vomit, anorexia, hematamesis–maybe
acute gastritis, dependent association with NSAIDs
tx of acute gastritis
PPIs, H2 receptor antagonists…decrease gastric acidity
multiple, small, shallow ulcers in the stomach or duodenum…what causes this
Acute Peptic Ulceration—-following severe physiological stress. or huge NSAIDs: drop bicarb/prostaglandins
examples of what traumas can cause Acute peptic ulcerations
shock, sepsis, trauma, burns—–ichemia ofthe area
could also be intracranial disease—(vagal nerve hypothesis)
nausea, upper abdominal “discomfort”—no hematemesis, or rare
chronic gastritis
what can be associated with chronic gastritis
Helicobacter pylori infxn., peptic ulcers, combined with other stressors
Risks and more about H pylori
poor childhood sanitation, MC asymptomatic, 70-90%of chronic gastritis ppl have h pylori
effects of Hy. pylori
increase acid prod., epithelia metaplaisa—risk for gastric CA
Autoimmune gastritis–
MC elderly, antibodies against parietal cell, pernicous anemia
Sites of Peptic Ulcer diesase
Duodeum 4x, gastric antrum—solitary, punched out lesion
5 to 10 % with H pylori within the stomach will develop
peptic ulcer disease
what is peptic ulcer disease
chronic, recurrent gastritis
pain of peptic ulcer diease
gnawing burning, MC at night and 1-3 hrs postprandial
relieved by alkaline stuff
Hemorrhage would be medical emergency
Tx of PUD
antibiotics, antacids, PPIs H2 antagonists
pain relief immeidately postprandial
pain returns a couple of hours later–might get worse
duodenal ulcer
pain of gastric ulcer
worse on an empty stomach or postprandial
BOTH are worse at night
narrowing of pyloric sphincter, MC Dx shortly after birth
projectile vomit looks like milk, hyperperistalsis
pyloric stenosis 1/400 births. tuner syndrome increased(also aortic coarctation)
Tx. pyloromyotomy
general inflammation and enlargement of glands(salivary)from infxn, traum or autoimmune
sialadenitis
MC (viral) of sialadenitis and what does it cause in adults….pediatrics?
Mumps from paramyxovirus of the parotids
how does mumps effect pediatrics….adults?
self limiting of parotid, pancreatitis and orchitis in adults in addition to parotids
What, besides mumps, can cause sialadenitis, presents how?
S. aureus. dehydration and obstruction
a salivary gland pathology where the glands are blacked or ruptured
mucocele, or mucous cyst, ranula
where will mucocele production edema
lower lip in children & elderly
salivary gland neoplasms, are rare, what is effected most often?
parotid glands 65-80% and 15-30% are malignant
less common location of salivary neoplasms happen where and how malignant is it
submandibular gland -10%. 40% are malignant
sublingual & minor salivary glands (10-25%) and 50-90% malignant
pleomorphic adenoma
benign, painless, slow growing but MOBILEneoplasm of the parotid gland. 60% of parotid gland tumors
how can pleomorphic adenomas cause naughty trouble
may recur following excision, 2-10% transition into CA
Carcinoma ex pleomorphic adenoma
invasive, less mobile 50% 5 year
details of pleomorphic adenomas—made of what and one more special thing
cartilage & bone
encapsulated
Regurgitaion, Dx. just after birth
atresia of esophagus, tracheal fistula, stenosis(fibrosis)
Mechcanical esophageal lesion/obstruction
achalasia, what is it and what type of obstruction is it?
failure of esophagus to relax, it is a functional obstruction
what is aperistalsis?
uncoordinated peristalsis, it is a functional obstruction
what is ectopia?
ectopic gastric mucosa (inlet patch), upper 1/3 of esophagus and asymptomatic (MC) irritation that is a risk of CA
irritaion of upper esophagus that is MC asyptomatic, but can lead to cancer
ectopi, ectopic gastric mucosa
triad of achalasia
- Incomplete LES relaxation
- Increased LES tone
- Esophageal aperistalsis
symnptoms of achalasia
dysphagia, regurgitation, chest pain(heartburn), weight loss
signs of achalasia
proiximal esophageal dilation
Tx. of achalasia
botulism toxin, pneumatic dilatation
primary achalasia is due to what
loss of inhibitory innervation to LES—idiopathic
what is secondary achalasia secondary to?
Chagas disease, irradiation, diabetes, polio
Inflamm near Auerbachs plexus—pathognomonic
pyloric stenosis
really? go to bed.
MC dx shortly after birth, projectile milk like looking vomit
pyloric stenosis
reactive of neoplastic mass projecting from mucosa—of stomach
gastric polyp—common in 5% endoscopies
—-associated with chronic gastritis
MC form of gastric polyps
inflamm & hyperplastic polyp 75%. no way to turn into cancer
2 other types of gastric polyps
fundic gland polyp 15% PPI
Gastric adenomas 10%
30% of what transition into adenocarcinomas of the stomach
gastric adenoma, which is 10% of gastric polyps
will have dysplasia
—biopsy is only way to tell type
> 90% of all gastric cancers
gastric adenocarcinomas
5% and 3% of gastric cancers, respectively
lymphomas, carcinoids…
where and what are risks for stomach cancer
country of Japan 20x.
Risks, chronic inflam: H. pylori, EBV 10%
—dysplastic adenomas
symptoms: gastritic, altered bowels, nausea/anorexia
Weight loss, hemorrhage, anemia
gastric cancer—MC develop late, Dx. late :(
5 yr survival: 90% is early, but most late–20% MC
disorders of small and large intestines simply involve what
malabsorption or diarrhea
pain, distention, constipation, vomit
intestinal obstructions—MC small intestine
80% of all mechanical obstructions
abdonimal wall defect–intestinal protrusion (inguinal/umbilical), edema, infarct?
herniation—mechanical obstruction
inflam, fibrosis, adeherent intestinal segments
Adhesions–mechanical obstruction
intussusception
telescoping of the proximal bowel into the distal segment
congenital outpounching located on the small intestine
meckel diverticulitum
2 inches
2% of pop. 2% symptomatic, males have 2x risk
congenital aganglionic megacolon
Hirschsprung Disease
lacks neruologic ganglia in rectum and sigmoid colon
result of defective neural crest cell migration…1 in 5000
hirschsprung disease
Dx. failure to pass meconium–
obstructs proximal bowel
sever dilation of proximal bowel
hirschsprung disease
MC in males, but more sever in femals, Tx surgical excision of area without ganglia
hirshcsprung
prob with arteries—superior mesenteric, inf mesenteric, celiac….
ischemic colitis, Ischemic Bowel Disease
a drop in BP or occlusion—-old ppl
if bad enough, could result in mucosal infarction
occlusion of arteries—ischemic colitis
causes o thrombosis for ischemic bowel
atherosclerosis, vasculitis, hypercoagulability
inflam, stati—cirrhosis
a myocardial infarction, angioplasty, and endarterectomy causes what in regards to ischemic bowel
aterial, embolism
non-occlusive ischemia is due what
drop in BP, heart failure, hemorrhage, shock, dehydration
weight loss and muscle wasting, abbdominal distension
malabsoroption
borborygmus, flatulence
malabsorpsotion do more and look at tslide syou missed
non-infectious malabsorption
immune-mediated, reaction to gliandin—not glutenin, the 2 breakdown components of gluten
celiac disease
gluten-sensitive enteropathy
celiac sprue
what has gluten
wheat, barley, rye.
what kind of hypersensitivity is gluten disease
Type IV
B & T cells damage S.I.—villous atrophy in the duodenum and jejunum
Crypt hyperplasia
celiac—many cases are familial!!! (HLA-DQ2 or DQ8)
how is celiac disease formally diagnosed
IgA/IgG antibody / biopsy
people usually just kinda figured it out thru diet
1% of US and Europe,
Caucasians
MC Dx age 30-60
Rarely, pediatric: 6-24 months
Celiac Disease
possible iron deficiency anemia: fatigue, pallor
usually bloating, diarrhea
risk of intestinal adenocarcinoma!!!
celiac
1 in 10 ppl with celiac may have immune probs other places…most notably
on the skin
Dermatitis Herpetiformis :)
arms, elbows, legs, buttocks, itchy—neutrophils
tropical sprue
Cycles of: mucosal injury, malnutrition, inflammation
environmental enteropathy
MC affects children, age 2-3years
living in or recentyl visted tropical areas
150 mil worldwide
environmental enteropathy
seems to be autoimmune: villus flatting—like celiac
Infectious: responds to antibodies
environmental enteropathy
decrease of lactase at SI brush border
cant digest lactose
lactase deficiency
bloating, cramps, gas, diarrhea, MC 30 mins postprandial
lactose intolerance
Acquired (MC): lactose intolerance
congenital:
young adulthood
auto. recessive, rare, life-threatening
Dx of lactose intolerance?
breath hydrogen test
12,000 children die each day of this disease of the small intestine
500 infants each year in US
infectious enterocolitis
Microbial infxn: abdominal pain, urgency/incontinence, perianal discomfort, hemorrage
Infectious enterocolitis
Agents of infectious enterocolitis can include
Bacteria, Virus, Protozoa
Gram (-), comma shaped bacteria that will cause enterocolitis MC in India/Africa
1-5 day incubation
Vibrio cholerae
Noninvasive: minimal tissue damage
So why does it cause bad times?
Secretes cholera toxin (remember it is gram -)
what does cholera toxin do?
Opens CFTR—-chloride ion secretion
Vomiting and watery diarrhea, cramping early from electrolyte imbalances….hypotension bc fluid loss
1 L of H20 per hour
cholera
Tx of cholera
fluids, electrolytes, antibiotics, zinc
no Tx: 50-70% death
Traveler’s Diarrhea
enterotoxigenic E. coli is MC :)))
Defined by 3 or more unformed loose stools within 24 hours
travelers diarrhea
MC bacterial enteric pathogen in the U.S.
contaminated chicken etc
Campylobacter enterocolitis
Campylobacter enterocolitis can kind of kick start a couple of things
well, dysentery and fever, but reactive arthritis—HLA-B27 or Guillian Barre
Last for less than 1 month, no Tx. needed
C. jejuni, Shigella, E. coli, Salmonella
Acute self-limited colitis
Pseudomembranous Colitis
Clostridium difficile overgrowth, colon—-enterotoxins
fever, watery diarrhea, pain
risks for pseudomembranous
Tx?
hospitalization, old age, down immunity
vancomycin or metronidazole
MC gastroenteritis—-1/2 of all
children. ..
adults. …
viral!
Rotavirus
Norovirus
MC parasitic infxn
Giardia lamblia-resists cold and chlorine
“Beaver Fever”
Fecal comtaminated water
Giardia lamblia is non-invasive, so it does what?
alters, S.I. enzymes
blind ended outpouching of the colon
sigmoid diverticulitis
95% of the time it will be sigmoid colon
complications of diverticulitis
infxn, abscess, maybe hemorrhage
risks of diverticulitis
age, refined foods, constipation—high intraabdominal pressure. 50% over age 60. 20% symptomatic
presentation of diverticulitis
cramping, left lower abdominal pain, tenesmus (sensation of inadequate BM), diarrhea
diverticulitis is progressive, they become larger and more numerous aaand Tx.???????????????????
They need to change their diet
Super general term—–altered bowel habits
bloating, diarrhea OR constipation—speeding up or slowing down
chronic and relapsing abdominal pain
IBS
MC peeps for IBS
20-40 MC
females, with psychological stress
what defines IBS….is what it isn’t—-
No cellular abnormalities (gross, histologic)
Commins, 5-10% of US adults
Tx. of IBS
fiberrr, lower carbs, stress management
Abnormal loca immune response of da tummy
Idiopathic/hypersensitivity rxn
Crohn’s or ulcerative colitis
Inflammatory Bowel Disease
who gets IBD
females, adolescence, Caucasians, hygiene hypothesis?
MC in ileum, but can go eintre GI tract
transmural—throughtout the wall of GI–
Crohn disease (regional enteritis)
rectum, distal colon
mucosal and maybe submucosal
ulcerative colitis
hypothesis for crohn disease
t cell autoimmune rxn
no known cure
presentation of crohn disease
melena 50%, mild diarrhea, fever, abdonal pain
“skip lesions”, granulomas, ulcerations, strictures
skin rxn, arthritis, AS ankylosing spondylitis, eye irritation, fatigue
ok, Crohn is 1 in 500, what is Tx?
Risk for what
probiotics, immunosupressive meds,
GI adenocarcinoma
Tx of Crohn?
probiotics, immunosuppressive meds
having crohn is risk for
G.I. adenocarcinoma
8-10 years, after Dx.
area of narrowing in the G.I. tract is called what
—transmural in crohns
stricture
“skip lesions” are common with Crohn’s
‘cobble sttone appearance
what condition has a cobble stone appearance?
Crohn’!
again, what is the MC location for Crohn’s
terminal ileum, ileocecal area
superficial mucosa ulcerations are in what condition
MC begin in rectum—will have ‘pseudopolyps’
ulcerative colitis
Crohns lesions are “transmural”
what should you be associated with ulcerative colitis?
toxic megacolon, polyarthritis, sacroiliitis, AS, eye irritation
what gets this bad stuff (ulcerative colitis)
20-25 years old, 1 in 5,000.
smoking is inhibitory–opposite of crohn’s
increasing incidence!
onset of ulcerative colitis
tenesmus–feeling of still have to pass poops
fever, abdominal pain, lower ab cramping
Relapsing episodes: “attacks”
stool: grossly bloody & mucoid “stringy”
Dx of ulcerative colitis
coloscopy and biopsy
dysplasia of UC increases what huu huh huh?
risk for adeno carcinoma
Crohns---IBD malabsorptive fissures, strictures, granulomas entire GI tract, fibrosis, skip lesions
UC---IBD not malabsorptive pseudopolyps, non granulomatous rectume/distal colon, little to no fibrosis diffuse ulcerations
what is a polyp
a mass, protrduiong into lumen
epithelial/mucosal proliferation
inflammatory polyps follow inflammation so
what is a hamartoma?
mature cell types, minimal risk
a polyp that resembles dysplasia
hyperplastic, well-differentiated, pilled-up epithelia, multiple
MC Dx. in elderly: 50- 60 years
what is the bad polyp
Def is dysplastic
Adenomatous: neoplastic mass
“pre-malignant”—-adenocarcinomas
adenomas of the GI tract aaaarrree
benign mass-but considered malignant until proven otherwise–sessile or pedunculated
can be a risk for adenocarcinoma is dysplasia happens
occult bleeding—-anemia
what is familial adenomatous polyposis
a bunch of polyps MC 500-2500 whoa
rare, autosomal dominatnt, aggressive situation of numerous adenomas, teenaged onset
almost 100% chance for colon CA by age 30
familial adenomatous polyposis
how to find FAP
occult blood in stool, probably anemic
Fx Hx
5% of US develops colorectal CA wow
40% of cases are lethal…so 1/10 CA deaths
types of colorectal CA
adenocarcinomas
carcinoid tumors
MC calignancy of the GI tract
130,00 new cases each year
55,000 deaths
colorectal adenocarcinoma
80% of Dx are age 50-70
risks: males, IBD, developed nations
US diet, 30x the risk
inccreased retention time because of low fiber diet alters the microbiota
increases risk for bad stuff
Insidious onset!
usre diarrhea and constipation
occult blood in stool, iron-deficiency—must rule out CA in elderly
small intestine tumors
vague symptoms
mc in duodenum
1% of all gi malignancies
50% adenocarcinomas 50% carcinoid
MC acute abdominal condition
7% of all population
acute appendicitis
onset is
early: periumbilical/epigastric discomfort
late: RLQ tenderness—-deep/constant pain
- —progresses into sharp pain
appendicitis
obstruction is common cause 50-80%
ischemia—inflammation
appendicitis
