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
Q

S/S atresia

A

throw-up food while feeding

no good for life

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26
Q

Tx of atresia

A

sugery but need to find a new opening for feeding

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27
Q

Congential esophageal disorder=fistula

A

Extra opening/lumen

Abnormal open

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28
Q

S/S of fistual

A

Aspiration, Suffocation, Pneumonia

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29
Q

Tx fistula

A

surgery and feeding tub to stomach but might need imaging

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30
Q

cardiac esophageal dis.

A

Esophageal varices

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31
Q

how are the blood vs. in esophageal varieces and what does the incre. p. do to the walls

A

Distention and cn rupture

Incre. P.=thin wall, incre. wrinkles and polyps

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32
Q

can esophageal varies cause portal HTN

A

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

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33
Q

Esophageal varices=can blood vs. rupture

A

Yes
Vomit blood
Survive=loster liver perfusion
-damage/compormise function

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34
Q

Tx for esophageal varices

A

tx liver disorder=surgery remove varices to decre. blood vol.
-recurrent dis.=incre. damage and scarring affecting LES tonicity and incre. heart burn

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35
Q

Reflux esophagitis

A

Stomach/pancreatic content into esophagus

Esophageal mucosa producing inflammation damage

36
Q

S/S of reflux esophagitis

A

Heart burn=recurrent burning sensation in the chest b/c of mucosal injury
Food=decre. LES tone

37
Q

LES tone

A

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
Q

Reflux Esophagitis-caused by

A
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
Q

Reflux esophagitis-mucosal inflam.

A
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
Q

Reflux esophagitis-Dis. progression

A

Stricter, Pain, Obstruction, Perfuration, Barret’s esophagus
Initial lesion=scarring=incre. additional reflux b/c of damaged LES

41
Q

Barret’s Esophagus

A

Pre Cancerous lesion

Metaplasia of St. sq.–>columnar w/ incre. goblet cells

42
Q

Reflux Esophagitis-tx

A
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
Q

define Gastritis and acute or chronic

A

inflamed stomach w/ mucosal injurt
Both
-acute=PMN lesion
-chronic=other immune cells

44
Q

Gastritis=gastropathy

A

Decre. immune response and visible injury repair

45
Q

Gastritis-compromised mucosal defense

A
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
Q

Gastritis-mucosal compromised pathology

A
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
Q

Gastritis-etiology ulcers

A
Chemical 
-Gastric Acid 
-duodenal reflux 
Drug 
-Asprin 
-NSAIDS
Infection=H. pylori
Lifestyle=alcohol and cig. smoking
48
Q

Gastritis-duodena reflux

A

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
Q

Gastritis=Non-steriodal Anti-inflam. drug. (NSAIDS)

A

Decre. prostaglandins
Incre. and gastritis
Ej of drug=IBPROPHIN

50
Q

define prostaglandins

A

Incre. BF
+bicarb./mucus secretion
+mucosal repair/renew

51
Q

Gastritis-H. Pylori

A

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
Q

Gastritis=stress

A

Ulcer=2ndry to stress
Shallow ulcer=alcohol, drug and stress
-trauma, surgery and medical disorder

53
Q

Stress Gastritis=damage

A

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
Q

Chronic gastritis-3 outcomes

A

Inflam. infiltrates
-gastric mucosal Atrophy=parietal cells
Glands lost=decre. gastric acid and gastrin secretion
Autoimmune=autoantiBD for parietal cells/IF and gastrin

55
Q

Chronic Gastritis-caused by

A

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
Q

Chronic Gastritis-Princious anemia

A

attacking parietal cells=inhib. intrinsic factor =anemia

57
Q

Duodenal ulcer stomach or an issue in the intestine that affect stomach

A

issue in the intestine that affect stomach

58
Q

Duodenal ulcer or stomach ulcer more common

A

duodenal ulcer

59
Q

duodenal ulcer-risk factor

A

Diet
Smoking
Excess Alcohol consumption

60
Q

Duodenal ulcer-H. pylori

A

Change mucosal immune response

Increase excess acid

61
Q

Types of intestinal obstruction

A

Volvulus and intussusception

62
Q

Intestinal Obstruction-Volvulus

A
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
Q

Intestinal obstruction-Intussuception

A

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
Q

Malabsorption issues

A
MC systemic cause=chronic diarrhea
Defective absorp. of food contents 
-Macromolec.=fat, prot. carb 
-Vitamins 
-Electrolytes, minerals and H2O
65
Q

Malabsoption-common cause

A

Pancreatitis and cystic fibrosis

Celiac dis.

66
Q

Malabsorption-Ciliac dis.

A
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
Q

malabsorption-celiac dis. pathogen

A
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
Q

Inflam. Bowel dis. (IBD) Types

A
Infection=acute 
- no antBT response 
-no infectious organisms 
Chronic 
-non infectous w/ flare-up 
-not autoimmune 
-spon. remissions
69
Q

acute IBD AKA

A

infectious enterocolitis

70
Q

acute IBD-infecteous agents

A
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
Q

acute IBD-vibrio cholera

A

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
Q

acute IBD-travelers diarrhea

A

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
Q

Acute IBD-Escherichia coli (E. coli)

A

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
Q

Acute IBD-Typhoid fever

A
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
Q

Acute IBD-pseudomemb. colitis

A

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
Q

Chronic IBD-types

A

chrons dis. and ulcerative colitis

77
Q

chronic IBD-chrons dis.

A
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
Q

chronic IBD-ulcerative colitis

A

Superficial
Limited to colon mucosa
Begins @ analrectal junction and proximal extend
Charct.
-necrotic lesion in crypts of crypts of lieberkuhn

79
Q

Sim. of chrons and ulcerative choliitis

A

10% of pts=lesions

Bloddy diarrhea and malabsopr.

80
Q

diff. b/w chrons and ulcerative colitis

A

ulcerative coliits dnt have obstruction, peroration or fistural

81
Q

Tx for chronic IBD

A

Chrons=remove and reconnect

UC=surgers

82
Q

hemorrhoids AKA

A

anal varieces

83
Q

hemorroids-cuased by

A
Straining during defecation b/c constipation 
Venous stasis b/c prego. 
Portal hypertension (~ esophageal varieces)
84
Q

Hemorrhoids-Tx

A

Anti-inflam. to decre. swelling (thrombosis)
Stool softener to prevent constipation
Surgically remove

85
Q

Hemorrhoids-pathology

A

Thin wall, dilated, submucosal vessels protrude beneath mucosa
Inflamation and develop thromboses
lead to superficial ulceration

86
Q

hemorroid-s/s

A

pain and rectal bleeding

87
Q

Hemorrhoids-tx

A

anti-inflam
Stool soften
Remove by surgery