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Flashcards in Unit 1 Deck (130):
1

what is diverticular disease

when the mucosa herniates via musclaris lt a non inflammed outpouching

2

what is the clinical term for an outpouching

diverticula

3

where are diverticula most common

sigmoid colon

4

what is important to remember about GI mucosa in diverticular disease

it is all intact

5

what is the percent incidence after age 80

85%

6

et/risks of diverticular disease

ageing
diet
poor bowel habits (all leading to constipation)

7

why do outpouchings occur in diverticular disease (patho)

weak points in wall where blood vessels enter that are normally tight, loosen with age

8

what happens to intralumanal P in diverticular disease

increased, lt inc strain on GI wall lt mucosia herniating thru muscularis externa

9

2 types of diverticular disease

diverticulosis
diverticulitis

10

diverticulosis

asymptomatic out pouchings of GI tract

11

diverticulitis

inflm that is problematic

12

diverticulitis mnfts

dull aching pain, low grade fever, nausea, vomiting

13

why do diverticulitis pts have fevers

endogenous pyrogens (cytokines -> interlukin 1 and 6) are released into blood stream resulting in fever

14

tx of diverticular disease

address ET/risks
sx for obstruction or perforation

15

IBS

intestinal mobility disorder related to peristalsis with no obvious patho

16

et of IBS

unclear, but risks and triggers are related to diet, followed y smoking, stress, lactose intolerance

17

general patho of IBS

alterted CNS regulation of GI motor and sensory fx

18

what is the first speculation of patho in IBS

ingestion of fermentable cho's and polyols results in inability to digest by stomach -> content moving to LI causing normal flora to digest and create gas as a by product -> pain

19

eg of fermentable cho

fructose

20

eg of polyol

sorbitol

21

second speculation of patho in IBS

molecular signalling defect via seratonin, resulting in dysfx at the molecular lvl regarding seratonin

22

what is seratonin

NT

23

where is most seratonin produced

epithelial cells in the GI tract

24

what are the 4 normal fxs of seratonin

Motility - peristalsis
sensation - pain
secretion - mucous, H , enzymes
perfusion - dilation/constriction of vessels

25

what do problems at the molecular lvl involve

signalling, messengers

26

mnfts IBS

abdominal pain and discomfort
constipation/diarhea
mucoid stools
flatulence

27

can a pt have both constipation and diahrhea (not simultaneously)? how so?

its based on peristalsis and the trigger causing the problem.

28

what is the number one mnft/problem in ibs

constipation / diarhea / bowel habits

29

why may an ibs pt have mucoid stools

dt abn mucous sec / inc mucous sec dt seratonin dysfx

30

dx IBS

difficult to dx, work by exclusion to ensure its not an organic disease, Labs, scopes, presentation

31

labs done in IBS

cbc, lytes, parasites, stool sample, barium swallow

32

scopes done in IBS

endoscopy, colonoscopy

33

tx IBS

based on mnfts and sev, avoid offending foods, dec stress, drugs

34

types of drugs used to tx IBS

antispasmadics, antidiahreals, laxatives, abx?

35

fx of antispasmadic drug? eg

dec spasms and pain related to diahrea
modulon

36

fx of abx

may be used if normal gut flora is prolifferating too quicky dt inc synth of polyols and fremented chos by them

37

peritonits

inflm of peritonium

38

fx peritonium

serous memb that forms lining of abdominal cavity, composed of mesothelium and CT, keeps organs in place and attatches them to abdm strs

39

et of peritonitis

bacteria invading GI tract
chemical irritation

40

what may cause bacterial invasion of GI tract

perforation of GI str

41

what may cause chemical irritation of GI

peptic ulcer, HCl, bile, PID, ruptured appendix, colonoscopy, sx

42

how do infcts enter GI

via perforation, ulcer, or rupture

43

PID

infc that ascends up female reproductive system via infundibulum -> inc risk for peritonitis

44

How does the large str of the peritonium affect patho (2)

badly. 1) inc prolif of bact d/t its easy spread 2) richly vascularised area -> potential CVS absorption of toxins -> systemic infc

45

what exudate forms in peritonitis

thick, sticky, purulent

46

fx of exude in peritonitis (2)

1) creates a barrier -> dec spread + localizing infc
2) plugs perforation/seals hole in tract

47

what is the compensatory response by the CNS in peritonitis

causes SNS to limit peristalsis in attempt to dec amount of content which passes by the perforation in attempt to dec amount of content lost into peritonium

48

why may mnfts of peritonitis be severe

systemic mnfts are occuring as a result of local infc

49

mnfts of peritonitis

altered perfusion
dyspnea
fluid shift

50

why is altered perfusion a result of peritonitis

dt inc inflm + inflm vascular response -> blood shunting dt hyperemia and vasodilation

51

why is dyspnea a mfnts of peritonitis

inc pain on breathing dt inflamed peritonium placing pressure on diaphragm -> results in inc discomfort when diaphragm moves

52

why is fluid shift a mfnts of peritonitis

result of inc perm d/t vascular imflammatory response

53

In peritonitis, where does the fluid shift to

towards the site of inflm

54

tx for peritonitis

IV abx, anti imflm med, IV fluids, Sx, Pain med

55

why are iv fluids given in peritonitis

to replace and fix fluid shift and and lyte imbalance

56

what does Sx do in peritonitis

repairs tear or perforation causing entry of bact into peritonium

57

fx of appendix

may have a fx in immune response

58

appendicitis

acute inflm of appendix wall

59

what ages have inc prevelenace of appendicitis + peag age

5-30, 20-30

60

Et of appendictis

idiopathic with 2 theories

61

what are the 2 theories of ET of appendicitis

1) fecalith obstructs cecum or anywhere in appendix -> blockage
2) twisting of bowel or appendix -> constriction of appendix lumen

62

patho of obstruction of appendix

obstruction -> inc intralumenal P dt blocked mucous drainage -> pressure pressing outwards on appendix wall -> lumneal P > venous P

63

what happens when lumenal P is > then venous P

venous statsis

64

why is venous stasis bad

venous stasis -> no drainage of appendix wall -> no influx of arterial blood -> ischemia

65

what happens when there is ischemia in the appendix wall dt obstr

necrosis, wall is compromised and normal flora is allowed to invade -> inflm

66

What happens when there is twisting or constriction of appendix bowel

localized accumulation of appendix content -> increase in intralumanl P etc..

67

common complication of appendicitis

perf or ruputre of appendix -> peritonitis

68

early mnft of appendicitis

acute gastric or periumbilical pain accompanied by nausea

69

what is referred pain in appendicitis talking about

acute gastric or periumbilical pain that occurs at onset

70

how does pain change over the course of 12h in appendicitis

becomes colicky and spasmotic

71

spasmotic pain

pain that is constant with periods of inc intensity

72

After the pain is spasmotic, what term is used to describe the pain /what happens (appendicitis)

pain migrates to LRQ and is rebound pain / gaurded pain

73

gaurded pain

pt assumes fetal position in attempt to relax abdm m. and dec pain

74

where does the pain eventually localize in appendicitis (late stage)

mcburneys point

75

mc burneys point

midpoint between iliac crest and umbilicus

76

mnfts of appendicitis (not pain)

fever, inc wbc count, nausea and vomitting

77

why does nausea and vomitting occur in appendicitis

dt proximity of neural pathways to pain center in brain PLUS GI mnfts

78

Dx of appenditis

patent progession of pain via Hx and Px
US, CT?

79

Tx of appendicitis

IV fluid, abx,
appendectomy via sx

80

fx of IV fluid in tx of appendicitis

correct fluid and lyte imbalance

81

fx of sx in appendicitis

to remove appendix to avoid rupture/perforation

82

2 chronic disorders common in IBD

ulcerative colitis
chrons disease

83

Et of IBD

genetic susceptibility
environmental trigger
IR targeting against normal flora

84

characteristics of genetic suscpetibility in et of ibd

not a monogenic issue, unclear genetic abn

85

characteristic of environmental trigger in et of ibd

normally a bact infc "complex trait"

86

what is important to note about IR targeting against normal flora

this is NOT autoimmunity

87

why is targeting of normal flora by IR in IBD not autoimmunity

Bacteria are not considered self components, so their targeting is not autoimmunity. there is no change in MHC to target this

88

why does targeting of normal flora -> inflm in IBD

flora has developed symbyiotic relationship with cells in GI tract and flora may be attatched to these cells -> when IR kills flora, it also damages host cell -> inflm in GI

89

distribution pattern of chrons

skip lesions thru out SI and LI

90

distribution pattern of ulcerative

continuous lesions from distal to proximal starting at anus and rectum

91

type of inflm in Chrons

granulomatus

92

type of inflm in ulcerative

ulcerative and exudative (erosion of gut plus exudate formation

93

level of involvment in chrons

primarily submucosa

94

level of involvement in ulcerative

primarily mucosa

95

what is meant my level of involvmenet

which part of the gut lining is affected

96

areas of involvment in chrons

primarily terminal ilium, secondarily colon

97

areas of involvement in ulcerative

primarily rectum and left colon

98

in which IBDs is diahrea common

both

99

incidence of rectal bleeding in chrons

rare

100

incidence of rectal bleeding in ulcerative

common

101

incidence of fistual in chrons

common

102

incidence of fistula in ulcerative

uncommon

103

incidence of stricture in chrons

common

104

incidence of stricture in ulcerative

rare

105

incidence of perianal abcess in chrons

common

106

incidence of perianal abcess in ulcerative

uncommon

107

CA dev in chrons

rare

108

CA dev in ulcerative

common

109

progression of chrons

slower and not aggressive

110

mnfts of chrons

intermittent abdm pain
diahrea and inc BMs
wt loss

111

why does intermittent abdm pain occur in chrons

dt eating and peristalsis causing content to move past lesions -> pain

112

why does diahrea and inc BMs occur in chrons

dec absorp -> inc content being excreted

113

why is there wt loss in chrons

dt l/o SA in SI -> dec area for absorption dt inc amount of scar itssue-> dec absorption of nutrients -> nutrient def

114

visually, what does chrons disease look like or is described as

"cobblestone" apperance dt presence of linear ulcerations, edema, surrounded by inflm

115

what does the continious inflm in ulcerative colitis result in

thickening tissue -> inc exudate prod moving into gut lumen -> edema and congestion

116

mnfts of colitis

bleeding
frank blood in stool/bloody diarrhea
crampy pain + abdmn cramping
dec body weight

117

what can bloody diahrea end up resulting in

anemia

118

what is important to remember about crampy pain in ulcerative colitis

it may be presistant and no different then pain in chrons

119

how is dec body weight in ulcerative comparable to chrons

less weight is lost in ulcerative dt no lesions in SI occuring -> not as much SA for absorption is lost

120

how to dx chrons

hx and px, differential dx. sigmoidoscopy, colonoscopy, biopsy too look for IBD

121

Tx for IBD

depnds on severity,
nutrition (dietary mods to remove offendting foods)
drugs
sx

122

which drugs are most common for IBD (4)

Sulfasalazine
Abx
Steroids
Immunomodulatory

123

fx of sulfasalazine in IBD

anti inflm

124

fx of abx in IBD

leads to decreasing amount of normal flora to aid in dec inflm + prophylaxis, to prevent normal flora from entering GI wall.

125

when is abx in IBD given

only after immediate dx

126

fx of steroids in IBD

given for inflm if sulfasalazine doesnt work

127

which immunomodulatory drug is given in IBD

methotrexate

128

fx of methotrexate, and its fx specific to IBD

anti CA drug in inc doses,
anti folate (prevents DNA replication and cell division)
dec T cell agression in Dec doses

129

why do we use immunomodulatory vs immunosurpressant

immunosupressants cause too much T cell damage which is not the goal

130

what sx occurs if nescessary in IBD

in attempt to repair fistulas, constriction, drain ulcers, resection parts of bowel