GI Flashcards
What causes sugar into acid?
oral bact.
Name a oral bact. that will incre. acid
S. Mutans formation plaque
Acid does to teeth
Destroy teeth enamel and denten
-Solubilized hydroxyapatite crystals
-Flouride introduce in enamel=Fluorapatite crystals
:Incr. R to acid solubility
plaque on teeth
Biofilm protecting bact on teeth
dental cavity is also known as
dental caries
Clinical aspect for dental cavities
Cell making enamel r lost
Surpass denten=expose pulp/N. to hot/cold=incre. sent.
which cell can regen if destroyed in teeth
denten can regenate
NOT enamel
Tx for dental cavities
Fill
Prevent=clean (brush/floss)
Gingivitis
inflamed gingivitis
Inflamed gingiva
Oral mucosa that para/kertinized
Next to teeth
Whole oral keratinized
no only gingiva
Gingivitis caused by
oral bact. Forming biofilm (plaque) on teeth
plaque beneath gum line–>gingiva infection=gingivits
Consequence of gingivitis
gingival erythema and edema Bleed Change contour Loss of soft tissue around teeth Peridontitis=lost teeth
Define Xerostomia
dry mouth b/c dysfunctional salivary gland
What causes a decre. of salivary production in salvary glands
Medication side effect
Autoimmune dis. =Sjogern synd. (attack glands)
Radiation complication (oral cancer)
S/S of Xerostomia
Dry mouth
Tongue papilla atrophy w/ fissure and uleraction
-no trauma but epith. damage b/c of tissue sep.
Xerostomia complication
Incr. risk of oral thrush(candidas)/dental caries
Dysphagia and Dysarthia
define dysphagia and dysarthia
no Swallow and speaking
Types of Salivary glands
Parotid=serous(behind ears) Submandibular(mixed) -serous(MC) and mucus -mouth floor/near jaw Sublingual (mixed) -mucus(MC) and serous
What in saliva
Protein -alpha amylase to brkdwn carb. -lysozyme to attack bact. w/in mouth Glycoprot.(mucus cells) -mucin=lub/move food -->esophagus -conc. antBD Ion/H2O=Bicarb(buffering acid in mouth) IgA=plasma around acini andpolymerized
Tx Xerostomia
change medication
tx sjogern synd.
drug=incre. production w/in muscarine cholinergic Recep.
develop. of esophagus
Trachea and esophagus is one tube Trachea buds off of forgus (lung buds) -dnt sep.=fistual Esophagus gills in and reacnulized for an open tube -dnt occur=atresia
Congential esophageal disorder-caused by
Heart defects
Genitinuranry malformation
N. Dis.
Esophageal disorder=atresia
Blind end Def.=decre. lumen space -developmental issue -result=mechanical destruction Esomagus is asoc. w/ fisutal
S/S atresia
throw-up food while feeding
no good for life
Tx of atresia
sugery but need to find a new opening for feeding
Congential esophageal disorder=fistula
Extra opening/lumen
Abnormal open
S/S of fistual
Aspiration, Suffocation, Pneumonia
Tx fistula
surgery and feeding tub to stomach but might need imaging
cardiac esophageal dis.
Esophageal varices
how are the blood vs. in esophageal varieces and what does the incre. p. do to the walls
Distention and cn rupture
Incre. P.=thin wall, incre. wrinkles and polyps
can esophageal varies cause portal HTN
Yes b/c decre./block BF in liver=incre. P in protal vn
Portal vn drain from GIT=incre. P GIT
-incre. p=blood vs. destention
-channels are formed to decre. P.
-esophageal 1st location=potential connection
Esophageal varices=can blood vs. rupture
Yes
Vomit blood
Survive=loster liver perfusion
-damage/compormise function
Tx for esophageal varices
tx liver disorder=surgery remove varices to decre. blood vol.
-recurrent dis.=incre. damage and scarring affecting LES tonicity and incre. heart burn
Reflux esophagitis
Stomach/pancreatic content into esophagus
Esophageal mucosa producing inflammation damage
S/S of reflux esophagitis
Heart burn=recurrent burning sensation in the chest b/c of mucosal injury
Food=decre. LES tone
LES tone
Tonically contracted sm. muscle ring
-prevent backflow (especailly acid)
-relax during swallowing to allow food into stomach
Respond to NT=NO and vasoactive intestinal peptide(VIP)
Swallow by Vagus N.
Reflux Esophagitis-caused by
Food=pepermint, coffee, chocolate -even lying dwn after eating Impair contraction reflux esophageal contraction after LES relax -decre. P. in Esophagus and incre. gastric acid=back flow in esophagus Incre. gastric vol/P. -incre. acid production -gastric production Akaline Injury Hiatal Hernia
Reflux esophagitis-mucosal inflam.
Acid damage Epith. and underlying tissue -Esophagus not R to acid only abrasion :St. sq. epith. is NOT keratinzied Infiltration of granulocytes -Intraepith. Eosinophils -PMN=advanced ids. Erosion=bleeding ulcer and exudate
Reflux esophagitis-Dis. progression
Stricter, Pain, Obstruction, Perfuration, Barret’s esophagus
Initial lesion=scarring=incre. additional reflux b/c of damaged LES
Barret’s Esophagus
Pre Cancerous lesion
Metaplasia of St. sq.–>columnar w/ incre. goblet cells
Reflux Esophagitis-tx
Decre. Food causing heart burn Take drugs to decre. acid production surgery to stop gastric obstruction Collapse Ballon/surgical repair hernia -decre. P or LES and decre. esophageal reflux
define Gastritis and acute or chronic
inflamed stomach w/ mucosal injurt
Both
-acute=PMN lesion
-chronic=other immune cells
Gastritis=gastropathy
Decre. immune response and visible injury repair
Gastritis-compromised mucosal defense
Damaged cells -Directly ingestion of A/B -toxicity=NSAIDS, alcohol, radiation, chemo. -decre. mucus production (incr. age) Decre. Bicarb secretion -affected by NSAIDS uremia and H. Pylori
Gastritis-mucosal compromised pathology
Necrotic Damaged to mucosa Create gap in protective Barriers -lost tissue and form ulcer Lamina Propria and submucosal=mucosal inflammation Perforated muscularis mucosae (damaged) Shallow ulcer=muscularis
Gastritis-etiology ulcers
Chemical -Gastric Acid -duodenal reflux Drug -Asprin -NSAIDS Infection=H. pylori Lifestyle=alcohol and cig. smoking
Gastritis-duodena reflux
2ndry to motility defect ulcer
Pyloric sphincter allows duodenal content–>stomach
-Duodenalcontents=bile acids/other pancreatic secretion
Decre. in stomach motility=delays emptying gastric contents
-incre. stomach acid exposure
Food retnetion=incre. gastric Acid production/presence
Gastritis=Non-steriodal Anti-inflam. drug. (NSAIDS)
Decre. prostaglandins
Incre. and gastritis
Ej of drug=IBPROPHIN
define prostaglandins
Incre. BF
+bicarb./mucus secretion
+mucosal repair/renew
Gastritis-H. Pylori
Gram - Spiral/bacilli
From Camylobacter fam.
Chronic Gastritis pts.
Indirectly infect mucosal
-H. Pylori w/in mucosa
-incre. PMN
-lumphatic nodules w/in MALT
-mucus immune cells tries to - bact. =incre. epith. damage
Effect
-incre. release of gastrin and somatostatin=incre. gastric acid
-compromise defense
:mucosal damage 2dry to immune response
:release urease and cleave urea=incre. ammonia
-inhib. and decre. bicarb transporter
Gastritis=stress
Ulcer=2ndry to stress
Shallow ulcer=alcohol, drug and stress
-trauma, surgery and medical disorder
Stress Gastritis=damage
Ischemia
Trama=hypotension
Decre. gastric perfusion b/c stress response
-b/c cortisol=decre. BF to GIT and incre. brain
Syst. acidosisi 2dry to dis.
-decre. mucosal intracellulary pH and decre. brain
Chronic gastritis-3 outcomes
Inflam. infiltrates
-gastric mucosal Atrophy=parietal cells
Glands lost=decre. gastric acid and gastrin secretion
Autoimmune=autoantiBD for parietal cells/IF and gastrin
Chronic Gastritis-caused by
H. Pylori (MC)=superficial plasma cell respond to bact. presence
Autoimmune dis.
-pernicious anemia
-Gastric adenocarcionma (goblet cel metaplasia w/in mucosa epith.)
-GI endocrine hyperplasia
Chronic Gastritis-Princious anemia
attacking parietal cells=inhib. intrinsic factor =anemia
Duodenal ulcer stomach or an issue in the intestine that affect stomach
issue in the intestine that affect stomach
Duodenal ulcer or stomach ulcer more common
duodenal ulcer
duodenal ulcer-risk factor
Diet
Smoking
Excess Alcohol consumption
Duodenal ulcer-H. pylori
Change mucosal immune response
Increase excess acid
Types of intestinal obstruction
Volvulus and intussusception
Intestinal Obstruction-Volvulus
Def:=bowel twisting by rotating mesenteric contact is obstructed W/in sm. and lrg. intestine Cause vascular blockage S/S -obstruction :abdo distention b/c upstream accum :Vomit(block)/constipation(nothing is getting out) -Infarct :abdo pain/tenderness :Nausa, vomit, blood diarrhea (hemorrhage) :melanotic stool b/c blood Tx=surgery
Intestinal obstruction-Intussuception
Def.=peristalsis/contraction cuase intestine seg. slide to the next seg.
Traped seg. drag mesentary=block occur
-obstruct, constrict mesenteric constriction
Tx=contrast/air enema to reverse blockage fold OR sugery
Malabsorption issues
MC systemic cause=chronic diarrhea Defective absorp. of food contents -Macromolec.=fat, prot. carb -Vitamins -Electrolytes, minerals and H2O
Malabsoption-common cause
Pancreatitis and cystic fibrosis
Celiac dis.
Malabsorption-Ciliac dis.
NOT autoimmune BUT gluten senstivity Immune med. enteropathy -ingestion certain grains :Gluten brkdwn and body response NOT autoantiBD just antiBD -damage from immne response=decrease surface of absorb. cuasing malab. :lost BB=microvili enterocyte :lost villi -Immune cell :NK cell (CD8 T lympho.) :APC for CD4 :others
malabsorption-celiac dis. pathogen
Immune dis. Gluten-->gliadin-->Gliadin deaminated-->APC w/ T/B cell(antBD) Vilus atrophy w/ gland and decre. BB Histology/microscopic evidence -villus atrophy w/ glands -decre. BB -immune infiltrates
Inflam. Bowel dis. (IBD) Types
Infection=acute - no antBT response -no infectious organisms Chronic -non infectous w/ flare-up -not autoimmune -spon. remissions
acute IBD AKA
infectious enterocolitis
acute IBD-infecteous agents
Vibrio cholera (bact.) Campylobacter jejuni(travlers diarrhea-bact.) Salmonella enteritidis (nontyphoid-bacilli) Salmonella enterica (Typhoid fever-bacilli) Clostridium difficile=pseudomembranous colitis(bact.) Escherichia coli-bacilli
acute IBD-vibrio cholera
produce toxin
-cell influx–>unfold–>transport to intracell sig. and affecting cystic fibrosis transmemb. reg. prot.
-Incre. Cl in lumen w/ Na following=incre. H2O in lumen w/ H2O diarrhea
Tx=supportive until bact. /toxin is clear
not invasive but colonize in epith.
Limited hist. changes
acute IBD-travelers diarrhea
PPl from country is R
Caused by
-campylo bact. jejuni
:assoc. w/ ingestion of undercooked chicken, unpast. milk and contaminated H2O
:colonize mucosa
-Salmonella enterica (typhi and pratyphi)
-ETEC
-Others
Pathology
-Campylobact. jejuni=mucosal and intraepith. PMN invasive w/ crypts
-Crypts abscesses=PMN accum.
:maintenance of crypts architecture ~ to EIEC
Acute IBD-Escherichia coli (E. coli)
Enterotoxigenic E. coli (ETEC)
-Travelers diarrhea (~C. jijuni)
-2 toxin
:heat labile=~ cholera and heat kill bact./toxin
:Heat stable=only cGMP and suruvie heat
Enterohemorrhagic E. coli (EHEC)
-Cows reservoir (assoc. w/ cont. bact.)
-Toxin=dysentery like dis. (~ shigella/salmonella)
:indre. fluid efflux and blood (bloody diarrhea)
Enteroinvasive E. coli(EIEC)
-~shigella and R to acid
-prolif. intracell in M cell on Payers patches
Acute IBD-Typhoid fever
Caused by salmonella Enterica -2 subtypes=typhi and paratyphi -Nontyphoid salmonella bact. Payers patches in ileum -incre. size -enlarged mesenteric lymph node -PMN accum in superficial muccosa -Debris filled w/in lamina propri: MAC, lymphocyte and plasma cell -ulceration ion/perferation of ileum -damage organ :splenomegaly and hypertrophy of phagocytic cells :liver=focal necrosis w/ MAC aggrogets and typhoid nodules
Acute IBD-pseudomemb. colitis
AKA antiBT assoc. colitis and C. Diff.
Clostridium difficile(C. diff.) overgrowth
-Norm. componenet of intestinal microbiota
:But antBT cn kill off microbiota that usually kill C.Diff.
-Also by immunosup.
C. diff. release toxin
-binds small GTPase like rho
-disrupt epith. cytok. (tight junction) and diarrhea b/c H2O absorb
-also induce cytokine(PMN pseudomemb.) release and apoptosis (damage mucosa)
Chronic IBD-types
chrons dis. and ulcerative colitis
chronic IBD-chrons dis.
Anywhere along GIT Transmural (enter wall) ulcer or granuomatous Discont./entire wall thickness of inflam ulcers Charact. -involve. adj. mesentery and lymph node -def. nutrient b/c colon damage Initial clinic presentation -mild diarrhea, fever, abdo pain -intermittent attack w/ wall damage
chronic IBD-ulcerative colitis
Superficial
Limited to colon mucosa
Begins @ analrectal junction and proximal extend
Charct.
-necrotic lesion in crypts of crypts of lieberkuhn
Sim. of chrons and ulcerative choliitis
10% of pts=lesions
Bloddy diarrhea and malabsopr.
diff. b/w chrons and ulcerative colitis
ulcerative coliits dnt have obstruction, peroration or fistural
Tx for chronic IBD
Chrons=remove and reconnect
UC=surgers
hemorrhoids AKA
anal varieces
hemorroids-cuased by
Straining during defecation b/c constipation Venous stasis b/c prego. Portal hypertension (~ esophageal varieces)
Hemorrhoids-Tx
Anti-inflam. to decre. swelling (thrombosis)
Stool softener to prevent constipation
Surgically remove
Hemorrhoids-pathology
Thin wall, dilated, submucosal vessels protrude beneath mucosa
Inflamation and develop thromboses
lead to superficial ulceration
hemorroid-s/s
pain and rectal bleeding
Hemorrhoids-tx
anti-inflam
Stool soften
Remove by surgery
