Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what is the clinical term for an outpouching

A

diverticula

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

where are diverticula most common

A

sigmoid colon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

what is important to remember about GI mucosa in diverticular disease

A

it is all intact

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what is the percent incidence after age 80

A

85%

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

et/risks of diverticular disease

A

ageing
diet
poor bowel habits (all leading to constipation)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what happens to intralumanal P in diverticular disease

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

2 types of diverticular disease

A

diverticulosis

diverticulitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

diverticulosis

A

asymptomatic out pouchings of GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

diverticulitis

A

inflm that is problematic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

diverticulitis mnfts

A

dull aching pain, low grade fever, nausea, vomiting

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

why do diverticulitis pts have fevers

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

tx of diverticular disease

A

address ET/risks

sx for obstruction or perforation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

IBS

A

intestinal mobility disorder related to peristalsis with no obvious patho

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

et of IBS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

general patho of IBS

A

alterted CNS regulation of GI motor and sensory fx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

eg of fermentable cho

A

fructose

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

eg of polyol

A

sorbitol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

second speculation of patho in IBS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

what is seratonin

A

NT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

where is most seratonin produced

A

epithelial cells in the GI tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

what are the 4 normal fxs of seratonin

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

what do problems at the molecular lvl involve

A

signalling, messengers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

mnfts IBS

A

abdominal pain and discomfort
constipation/diarhea
mucoid stools
flatulence

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

what is the number one mnft/problem in ibs

A

constipation / diarhea / bowel habits

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

why may an ibs pt have mucoid stools

A

dt abn mucous sec / inc mucous sec dt seratonin dysfx

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

dx IBS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

labs done in IBS

A

cbc, lytes, parasites, stool sample, barium swallow

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

scopes done in IBS

A

endoscopy, colonoscopy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

tx IBS

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

types of drugs used to tx IBS

A

antispasmadics, antidiahreals, laxatives, abx?

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

fx of antispasmadic drug? eg

A

dec spasms and pain related to diahrea

modulon

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

peritonits

A

inflm of peritonium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

et of peritonitis

A

bacteria invading GI tract

chemical irritation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

what may cause bacterial invasion of GI tract

A

perforation of GI str

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

what may cause chemical irritation of GI

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

how do infcts enter GI

A

via perforation, ulcer, or rupture

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

PID

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

what exudate forms in peritonitis

A

thick, sticky, purulent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

fx of exude in peritonitis (2)

A

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

2) plugs perforation/seals hole in tract

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

why may mnfts of peritonitis be severe

A

systemic mnfts are occuring as a result of local infc

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

mnfts of peritonitis

A

altered perfusion
dyspnea
fluid shift

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

why is altered perfusion a result of peritonitis

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

why is fluid shift a mfnts of peritonitis

A

result of inc perm d/t vascular imflammatory response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions