Unit 1 Flashcards
1
Q
what is diverticular disease
A
when the mucosa herniates via musclaris lt a non inflammed outpouching
2
Q
what is the clinical term for an outpouching
A
diverticula
3
Q
where are diverticula most common
A
sigmoid colon
4
Q
what is important to remember about GI mucosa in diverticular disease
A
it is all intact
5
Q
what is the percent incidence after age 80
A
85%
6
Q
et/risks of diverticular disease
A
ageing
diet
poor bowel habits (all leading to constipation)
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
8
Q
what happens to intralumanal P in diverticular disease
A
increased, lt inc strain on GI wall lt mucosia herniating thru muscularis externa
9
Q
2 types of diverticular disease
A
diverticulosis
diverticulitis
10
Q
diverticulosis
A
asymptomatic out pouchings of GI tract
11
Q
diverticulitis
A
inflm that is problematic
12
Q
diverticulitis mnfts
A
dull aching pain, low grade fever, nausea, vomiting
13
Q
why do diverticulitis pts have fevers
A
endogenous pyrogens (cytokines -> interlukin 1 and 6) are released into blood stream resulting in fever
14
Q
tx of diverticular disease
A
address ET/risks
sx for obstruction or perforation
15
Q
IBS
A
intestinal mobility disorder related to peristalsis with no obvious patho
16
Q
et of IBS
A
unclear, but risks and triggers are related to diet, followed y smoking, stress, lactose intolerance
17
Q
general patho of IBS
A
alterted CNS regulation of GI motor and sensory fx
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
19
Q
eg of fermentable cho
A
fructose
20
Q
eg of polyol
A
sorbitol
21
Q
second speculation of patho in IBS
A
molecular signalling defect via seratonin, resulting in dysfx at the molecular lvl regarding seratonin
22
Q
what is seratonin
A
NT
23
Q
where is most seratonin produced
A
epithelial cells in the GI tract
24
Q
what are the 4 normal fxs of seratonin
A
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
