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GI Flashcards

1
Q

What causes sugar into acid?

A

oral bact.

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2
Q

Name a oral bact. that will incre. acid

A

S. Mutans formation plaque

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3
Q

Acid does to teeth

A

Destroy teeth enamel and denten
-Solubilized hydroxyapatite crystals
-Flouride introduce in enamel=Fluorapatite crystals
:Incr. R to acid solubility

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4
Q

plaque on teeth

A

Biofilm protecting bact on teeth

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5
Q

dental cavity is also known as

A

dental caries

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6
Q

Clinical aspect for dental cavities

A

Cell making enamel r lost

Surpass denten=expose pulp/N. to hot/cold=incre. sent.

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7
Q

which cell can regen if destroyed in teeth

A

denten can regenate

NOT enamel

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8
Q

Tx for dental cavities

A

Fill

Prevent=clean (brush/floss)

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9
Q

Gingivitis

A

inflamed gingivitis

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10
Q

Inflamed gingiva

A

Oral mucosa that para/kertinized

Next to teeth

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11
Q

Whole oral keratinized

A

no only gingiva

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12
Q

Gingivitis caused by

A

oral bact. Forming biofilm (plaque) on teeth

plaque beneath gum line–>gingiva infection=gingivits

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13
Q

Consequence of gingivitis

A 
gingival erythema and edema 
Bleed
Change contour
Loss of soft tissue around teeth 
Peridontitis=lost teeth
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14
Q

Define Xerostomia

A

dry mouth b/c dysfunctional salivary gland

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15
Q

What causes a decre. of salivary production in salvary glands

A

Medication side effect
Autoimmune dis. =Sjogern synd. (attack glands)
Radiation complication (oral cancer)

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16
Q

S/S of Xerostomia

A

Dry mouth
Tongue papilla atrophy w/ fissure and uleraction
-no trauma but epith. damage b/c of tissue sep.

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17
Q

Xerostomia complication

A

Incr. risk of oral thrush(candidas)/dental caries

Dysphagia and Dysarthia

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18
Q

define dysphagia and dysarthia

A

no Swallow and speaking

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19
Q

Types of Salivary glands

A 
Parotid=serous(behind ears)
Submandibular(mixed)
-serous(MC) and mucus
-mouth floor/near jaw
Sublingual (mixed) 
-mucus(MC) and serous
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20
Q

What in saliva

A 
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
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21
Q

Tx Xerostomia

A

change medication
tx sjogern synd.
drug=incre. production w/in muscarine cholinergic Recep.

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22
Q

develop. of esophagus

A 
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
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23
Q

Congential esophageal disorder-caused by

A

Heart defects
Genitinuranry malformation
N. Dis.

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24
Q

Esophageal disorder=atresia

A 
Blind end 
Def.=decre. lumen space 
-developmental issue 
-result=mechanical destruction 
Esomagus is asoc. w/ fisutal
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25
S/S atresia
throw-up food while feeding | no good for life
26
Tx of atresia
sugery but need to find a new opening for feeding
27
Congential esophageal disorder=fistula
Extra opening/lumen | Abnormal open
28
S/S of fistual
Aspiration, Suffocation, Pneumonia
29
Tx fistula
surgery and feeding tub to stomach but might need imaging
30
cardiac esophageal dis.
Esophageal varices
31
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
32
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
33
Esophageal varices=can blood vs. rupture
Yes Vomit blood Survive=loster liver perfusion -damage/compormise function
34
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
35
Reflux esophagitis
Stomach/pancreatic content into esophagus | Esophageal mucosa producing inflammation damage
36
S/S of reflux esophagitis
Heart burn=recurrent burning sensation in the chest b/c of mucosal injury Food=decre. LES tone
37
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.
38
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 ```
39
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 ```
40
Reflux esophagitis-Dis. progression
Stricter, Pain, Obstruction, Perfuration, Barret's esophagus Initial lesion=scarring=incre. additional reflux b/c of damaged LES
41
Barret's Esophagus
Pre Cancerous lesion | Metaplasia of St. sq.-->columnar w/ incre. goblet cells
42
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 ```
43
define Gastritis and acute or chronic
inflamed stomach w/ mucosal injurt Both -acute=PMN lesion -chronic=other immune cells
44
Gastritis=gastropathy
Decre. immune response and visible injury repair
45
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 ```
46
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 ```
47
Gastritis-etiology ulcers
``` Chemical -Gastric Acid -duodenal reflux Drug -Asprin -NSAIDS Infection=H. pylori Lifestyle=alcohol and cig. smoking ```
48
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
49
Gastritis=Non-steriodal Anti-inflam. drug. (NSAIDS)
Decre. prostaglandins Incre. and gastritis Ej of drug=IBPROPHIN
50
define prostaglandins
Incre. BF +bicarb./mucus secretion +mucosal repair/renew
51
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
52
Gastritis=stress
Ulcer=2ndry to stress Shallow ulcer=alcohol, drug and stress -trauma, surgery and medical disorder
53
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
54
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
55
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
56
Chronic Gastritis-Princious anemia
attacking parietal cells=inhib. intrinsic factor =anemia
57
Duodenal ulcer stomach or an issue in the intestine that affect stomach
issue in the intestine that affect stomach
58
Duodenal ulcer or stomach ulcer more common
duodenal ulcer
59
duodenal ulcer-risk factor
Diet Smoking Excess Alcohol consumption
60
Duodenal ulcer-H. pylori
Change mucosal immune response | Increase excess acid
61
Types of intestinal obstruction
Volvulus and intussusception
62
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 ```
63
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
64
Malabsorption issues
``` MC systemic cause=chronic diarrhea Defective absorp. of food contents -Macromolec.=fat, prot. carb -Vitamins -Electrolytes, minerals and H2O ```
65
Malabsoption-common cause
Pancreatitis and cystic fibrosis | Celiac dis.
66
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 ```
67
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 ```
68
Inflam. Bowel dis. (IBD) Types
``` Infection=acute - no antBT response -no infectious organisms Chronic -non infectous w/ flare-up -not autoimmune -spon. remissions ```
69
acute IBD AKA
infectious enterocolitis
70
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 ```
71
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
72
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
73
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
74
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 ```
75
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)
76
Chronic IBD-types
chrons dis. and ulcerative colitis
77
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 ```
78
chronic IBD-ulcerative colitis
Superficial Limited to colon mucosa Begins @ analrectal junction and proximal extend Charct. -necrotic lesion in crypts of crypts of lieberkuhn
79
Sim. of chrons and ulcerative choliitis
10% of pts=lesions | Bloddy diarrhea and malabsopr.
80
diff. b/w chrons and ulcerative colitis
ulcerative coliits dnt have obstruction, peroration or fistural
81
Tx for chronic IBD
Chrons=remove and reconnect | UC=surgers
82
hemorrhoids AKA
anal varieces
83
hemorroids-cuased by
``` Straining during defecation b/c constipation Venous stasis b/c prego. Portal hypertension (~ esophageal varieces) ```
84
Hemorrhoids-Tx
Anti-inflam. to decre. swelling (thrombosis) Stool softener to prevent constipation Surgically remove
85
Hemorrhoids-pathology
Thin wall, dilated, submucosal vessels protrude beneath mucosa Inflamation and develop thromboses lead to superficial ulceration
86
hemorroid-s/s
pain and rectal bleeding
87
Hemorrhoids-tx
anti-inflam Stool soften Remove by surgery

Mech. 2 (8 decks)

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