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PAtho > Unit 1 > Flashcards

Unit 1 Flashcards

1
Q

what is diverticular disease

A

when the mucosa herniates via musclaris lt a non inflammed outpouching

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2
Q

what is the clinical term for an outpouching

A

diverticula

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3
Q

where are diverticula most common

A

sigmoid colon

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4
Q

what is important to remember about GI mucosa in diverticular disease

A

it is all intact

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5
Q

what is the percent incidence after age 80

A

85%

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6
Q

et/risks of diverticular disease

A

ageing
diet
poor bowel habits (all leading to constipation)

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7
Q

why do outpouchings occur in diverticular disease (patho)

A

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

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8
Q

what happens to intralumanal P in diverticular disease

A

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

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9
Q

2 types of diverticular disease

A

diverticulosis

diverticulitis

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10
Q

diverticulosis

A

asymptomatic out pouchings of GI tract

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11
Q

diverticulitis

A

inflm that is problematic

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12
Q

diverticulitis mnfts

A

dull aching pain, low grade fever, nausea, vomiting

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13
Q

why do diverticulitis pts have fevers

A

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

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14
Q

tx of diverticular disease

A

address ET/risks

sx for obstruction or perforation

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15
Q

IBS

A

intestinal mobility disorder related to peristalsis with no obvious patho

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16
Q

et of IBS

A

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

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17
Q

general patho of IBS

A

alterted CNS regulation of GI motor and sensory fx

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18
Q

what is the first speculation of patho in IBS

A

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

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19
Q

eg of fermentable cho

A

fructose

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20
Q

eg of polyol

A

sorbitol

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21
Q

second speculation of patho in IBS

A

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

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22
Q

what is seratonin

A

NT

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23
Q

where is most seratonin produced

A

epithelial cells in the GI tract

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24
Q

what are the 4 normal fxs of seratonin

A

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

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25
Q

what do problems at the molecular lvl involve

A

signalling, messengers

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26
Q

mnfts IBS

A

abdominal pain and discomfort
constipation/diarhea
mucoid stools
flatulence

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27
Q

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

A

its based on peristalsis and the trigger causing the problem.

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28
Q

what is the number one mnft/problem in ibs

A

constipation / diarhea / bowel habits

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29
Q

why may an ibs pt have mucoid stools

A

dt abn mucous sec / inc mucous sec dt seratonin dysfx

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30
Q

dx IBS

A

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

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31
Q

labs done in IBS

A

cbc, lytes, parasites, stool sample, barium swallow

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32
Q

scopes done in IBS

A

endoscopy, colonoscopy

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33
Q

tx IBS

A

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

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34
Q

types of drugs used to tx IBS

A

antispasmadics, antidiahreals, laxatives, abx?

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35
Q

fx of antispasmadic drug? eg

A

dec spasms and pain related to diahrea

modulon

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36
Q

fx of abx

A

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

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37
Q

peritonits

A

inflm of peritonium

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38
Q

fx peritonium

A

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

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39
Q

et of peritonitis

A

bacteria invading GI tract

chemical irritation

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40
Q

what may cause bacterial invasion of GI tract

A

perforation of GI str

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41
Q

what may cause chemical irritation of GI

A

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

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42
Q

how do infcts enter GI

A

via perforation, ulcer, or rupture

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43
Q

PID

A

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

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44
Q

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

A

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

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45
Q

what exudate forms in peritonitis

A

thick, sticky, purulent

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46
Q

fx of exude in peritonitis (2)

A

1) creates a barrier -> dec spread + localizing infc

2) plugs perforation/seals hole in tract

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47
Q

what is the compensatory response by the CNS in peritonitis

A

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

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48
Q

why may mnfts of peritonitis be severe

A

systemic mnfts are occuring as a result of local infc

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49
Q

mnfts of peritonitis

A

altered perfusion
dyspnea
fluid shift

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50
Q

why is altered perfusion a result of peritonitis

A

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

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51
Q

why is dyspnea a mfnts of peritonitis

A

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

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52
Q

why is fluid shift a mfnts of peritonitis

A

result of inc perm d/t vascular imflammatory response

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53
Q

In peritonitis, where does the fluid shift to

A

towards the site of inflm

54
Q

tx for peritonitis

A

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

55
Q

why are iv fluids given in peritonitis

A

to replace and fix fluid shift and and lyte imbalance

56
Q

what does Sx do in peritonitis

A

repairs tear or perforation causing entry of bact into peritonium

57
Q

fx of appendix

A

may have a fx in immune response

58
Q

appendicitis

A

acute inflm of appendix wall

59
Q

what ages have inc prevelenace of appendicitis + peag age

A

5-30, 20-30

60
Q

Et of appendictis

A

idiopathic with 2 theories

61
Q

what are the 2 theories of ET of appendicitis

A

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

62
Q

patho of obstruction of appendix

A

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

63
Q

what happens when lumenal P is > then venous P

A

venous statsis

64
Q

why is venous stasis bad

A

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

65
Q

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

A

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

66
Q

What happens when there is twisting or constriction of appendix bowel

A

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

67
Q

common complication of appendicitis

A

perf or ruputre of appendix -> peritonitis

68
Q

early mnft of appendicitis

A

acute gastric or periumbilical pain accompanied by nausea

69
Q

what is referred pain in appendicitis talking about

A

acute gastric or periumbilical pain that occurs at onset

70
Q

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

A

becomes colicky and spasmotic

71
Q

spasmotic pain

A

pain that is constant with periods of inc intensity

72
Q

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

A

pain migrates to LRQ and is rebound pain / gaurded pain

73
Q

gaurded pain

A

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

74
Q

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

A

mcburneys point

75
Q

mc burneys point

A

midpoint between iliac crest and umbilicus

76
Q

mnfts of appendicitis (not pain)

A

fever, inc wbc count, nausea and vomitting

77
Q

why does nausea and vomitting occur in appendicitis

A

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

78
Q

Dx of appenditis

A

patent progession of pain via Hx and Px

US, CT?

79
Q

Tx of appendicitis

A

IV fluid, abx,

appendectomy via sx

80
Q

fx of IV fluid in tx of appendicitis

A

correct fluid and lyte imbalance

81
Q

fx of sx in appendicitis

A

to remove appendix to avoid rupture/perforation

82
Q

2 chronic disorders common in IBD

A

ulcerative colitis

chrons disease

83
Q

Et of IBD

A

genetic susceptibility
environmental trigger
IR targeting against normal flora

84
Q

characteristics of genetic suscpetibility in et of ibd

A

not a monogenic issue, unclear genetic abn

85
Q

characteristic of environmental trigger in et of ibd

A

normally a bact infc “complex trait”

86
Q

what is important to note about IR targeting against normal flora

A

this is NOT autoimmunity

87
Q

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

A

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

88
Q

why does targeting of normal flora -> inflm in IBD

A

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
Q

distribution pattern of chrons

A

skip lesions thru out SI and LI

90
Q

distribution pattern of ulcerative

A

continuous lesions from distal to proximal starting at anus and rectum

91
Q

type of inflm in Chrons

A

granulomatus

92
Q

type of inflm in ulcerative

A

ulcerative and exudative (erosion of gut plus exudate formation

93
Q

level of involvment in chrons

A

primarily submucosa

94
Q

level of involvement in ulcerative

A

primarily mucosa

95
Q

what is meant my level of involvmenet

A

which part of the gut lining is affected

96
Q

areas of involvment in chrons

A

primarily terminal ilium, secondarily colon

97
Q

areas of involvement in ulcerative

A

primarily rectum and left colon

98
Q

in which IBDs is diahrea common

A

both

99
Q

incidence of rectal bleeding in chrons

A

rare

100
Q

incidence of rectal bleeding in ulcerative

A

common

101
Q

incidence of fistual in chrons

A

common

102
Q

incidence of fistula in ulcerative

A

uncommon

103
Q

incidence of stricture in chrons

A

common

104
Q

incidence of stricture in ulcerative

A

rare

105
Q

incidence of perianal abcess in chrons

A

common

106
Q

incidence of perianal abcess in ulcerative

A

uncommon

107
Q

CA dev in chrons

A

rare

108
Q

CA dev in ulcerative

A

common

109
Q

progression of chrons

A

slower and not aggressive

110
Q

mnfts of chrons

A

intermittent abdm pain
diahrea and inc BMs
wt loss

111
Q

why does intermittent abdm pain occur in chrons

A

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

112
Q

why does diahrea and inc BMs occur in chrons

A

dec absorp -> inc content being excreted

113
Q

why is there wt loss in chrons

A

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

114
Q

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

A

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

115
Q

what does the continious inflm in ulcerative colitis result in

A

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

116
Q

mnfts of colitis

A

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

117
Q

what can bloody diahrea end up resulting in

A

anemia

118
Q

what is important to remember about crampy pain in ulcerative colitis

A

it may be presistant and no different then pain in chrons

119
Q

how is dec body weight in ulcerative comparable to chrons

A

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

120
Q

how to dx chrons

A

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

121
Q

Tx for IBD

A

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

122
Q

which drugs are most common for IBD (4)

A

Sulfasalazine
Abx
Steroids
Immunomodulatory

123
Q

fx of sulfasalazine in IBD

A

anti inflm

124
Q

fx of abx in IBD

A

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

125
Q

when is abx in IBD given

A

only after immediate dx

126
Q

fx of steroids in IBD

A

given for inflm if sulfasalazine doesnt work

127
Q

which immunomodulatory drug is given in IBD

A

methotrexate

128
Q

fx of methotrexate, and its fx specific to IBD

A 
anti CA drug in inc doses,
anti folate (prevents DNA replication and cell division)
dec T cell agression in Dec doses
129
Q

why do we use immunomodulatory vs immunosurpressant

A

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

130
Q

what sx occurs if nescessary in IBD

A

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

PAtho (31 decks)

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