GI Flashcards
(116 cards)
1
Q
contents of GI
A
mouth esophagus stomach small intestine large intestine rectum anus
7-9 meters
2
Q
functions of GI
A
- digestion (break down of food for absorption)
- secretion (large volume of fluid secreted, some acidic and some basic)
- motility (coordinated movement)
- Absorption (nutrient extraction by passive active transport)
- Defense
3
Q
Mechanisms that control the GI
A
intrinsic
extrinsic
hormonal
4
Q
intrinsic control of GI
A
enteric nervous system
local control of GI
5
Q
extrinsic control of GI tract
A
via nervous system
parasympathetic via vagus nerve
sympathetic input: thoracic spinal cord
6
Q
hormonal control of GI
A
endocrine cells of stomach and intestine
paracrine control (multiple systems such as histamine and somatostatin release)
7
Q
two stages of swallowing
A
- pharyngeal
2. esophageal
8
Q
pharyngeal swallowing
A
food in pharynx stimulates closer of all openings except esophagus
food is moved to top of esophagus
UES relaxes and closes after bolus passage
9
Q
where does voluntary control of swallowing stop?
A
when food is in pharynx
10
Q
esophageal swallowing
A
begins once food bolus has passed to UES
vagus n. stimulates peristaltic contraction and LES is relaxed
11
Q
clinical importance of oropharyngeal control and esophageal motility
A
can cause aspiration (good gets into the lungs)
found following stroke and dementia or brain tumor
systemic/distal cause, not often a cause of esophagus
12
Q
cells that secrete stomach acid
A
parietal cells
13
Q
parietal cells
A
secrete H+ in exchange for a K+ via ATPase pump
14
Q
histamine
A
paracrine activator of stomach acid
binds to H2 receptors on parietal cells
15
Q
gastric glands
A
secrete mucins that produce the gel layer
16
Q
mucins
A
competent of mucus gel layer that adheres to the gastric epithelium
17
Q
mucus gel layer
A
composed of mucins and small amounts of HCO3 to this layer
allows for pH to be around 7.0
irritation can cause gasatritis
18
Q
irritation of mucus layer
A
stimulates additional mucin secretion
gastric juices are able to upset the stomach layer
19
Q
which part of the stomach is a reservoir
A
corpus
20
Q
antrum
A
part of the stomach that exerts powerful muscular contractions to break off food
21
Q
what controls gastric emptying
A
stomach contraction
duodenal pyloric relaxation via the vagus nerve
chemical composition of the chyme
22
Q
composition of chyme
A
acid, fat, hyperosmolar solutions will empty more slowly
23
Q
major site of absorption
A
small intestine
24
Q
part of the small intestine that gives it high absorption rates
A
brush border
carbohydrates, proteins, lipids, H2O, and electrolytes
25
if you can't absorb something
increase in osmolarity within small bowel lumen
will cause diarrhea, cramps
GI moves it along quickly
26
slowing down of peristaltic contractions causes?
more complete absorption
constipation
27
most of GI microbes are found
in the colon
28
colon absorbs
most of the fluids and electrolytes
esp. water and potassium
29
common signs and symptoms of GI Dz
abdominal or chest pain
altered ingestion of food
altered bowel movements
GI tract bleeding
course of sepsis
30
complications of GI disease
dehydration
sepsis
bleeding
31
evaluation of GI symptoms
```
labs
imaging (plain films, CT scan, ultrasound, EGD, sigmoidoscopy, colonscopy)
```
32
labs for GI symptoms
chemistry panel and CBC
LFTs or amylase/lipase levels to eval liver of pancreatic pathology
33
imaging done for GI
plain films
CT scan
ultrasound
EgD
flexible sigmoidoscopy
colonoscopy
34
plain films
KUB/upright
useful ut limited
used for bowel obstruction, ileus, or constipation
35
usually diagnostic study of choice
CT scan
36
ultrasound
increasingly used for appendicitis, kids, and decrease radiation exposure
37
EDG
evaluates esophagus, stomach, duodenum
direct visualisation
can biopsy specimens, pics, dilate, or inject substances
38
flexible sigmoidoscopy
evaluation of left colon
preform biopsy and removal of masses
39
colonoscopy
evaluation of colon
under direct visualization
can preform biopsy, pictures, and removal of masses
40
etiologies of esophageal achalasia
unknown
41
esophageal achalasia
loss of lower esophageal neurons and defective innervation
42
consequences of esophageal achalasia
lower sphincter fails to relax properly
tonic contraction of the LES is unusually harsh
causes defective peristalsis in esophagus eventually a dilated distal esophagus
43
symptoms of esophageal achalasia
vomiting (bc throat is full)
chest pain/discomfort
cough
aspiration
poor breath/foul breath
symptoms worsen when lighting down
44
treatment of esophageal achalasia
botulinum toxin
can rip esophagus, or stent it (both risk reflux) so both are secondary until Botox
45
how does Botox fix esophageal achalasia
relaxes the LES
paralyzes it slightly to let food pass
46
normal function to prevent acid reflux
gastric acid kept awn from esophagus by tonically contracted LES and peristalsis of esophagus
47
reflux
barrier is breached
reflex of caustic gastric acid
relatively unprotected esophagus results in burning substernal pain
48
recurrent reflux
causes scarring and inflammation of esophagus
LES is is less competent
49
causes of GERD
facilitated by weak LES or herniation of stomach thru diaphragm hiatus
50
causes of hiatal hernia
obesity
overeating
pregnancy
ascites
anything that increases abdominal pressure
51
mechanisms of GERD
1. loss of LES tone or esophageal peristalsis (pregnancy, alcohol, overeating)
2. increased stomach volume or pressure
3. increased gastric acid production
52
consequences of GERD
recurrent esophageal mucosa
1. friable, bleeding ulcers/esophagitis
2. hemorrhage and perforation
3. fistula formaiton
4. esophageal strictures
5. replacement of normal squamous epithelium with columnar epithelium
53
Barrett's esophagus
when columnar epithelium of esophagus (caused by GERD) cause esophageal adenoCA
54
processes of peptic and duodenal ulcer disease
1. excessive acid secretion (acid not proper buffer)
| 2. inadequate mucosal defense (gel layer decreases)
55
etiologies of peptic and duodenal ulcer disease
```
H. pylori infection
NSAID use
smoking
alcohol
stress
reflux of bile into stomach
```
56
H. Pylori infection
colonizes more than 50% of people
spread is fecal oral
most show gastritis but only some develop clinical ulcer disease
57
H. pylori pathology
increases gastric acid production
weakens mucosal defenses
if treated for ulcer but not H. Pylori dz will rapidly recur
58
urease
H. pylori
neutralizes gastric acid
gastric mucosal injury via ammonia
ammonia creates a nest/protection of the bacteria from H. pylori
59
pathophysiology of NSAID induced dz
inhibition of prostaglandin synthesis by NSAIDs causing diminished vasodilation and local relative ischemia of gastric mucosa
mucosa can not repair itself or produce mucus/bicarbonate = inadequate mucosal defense
makes ulcers and worsen if NSAID use continues
60
spectrum of acid DX
first comes erosive gastritis followed by ulceration
61
erosive gastritis
first manifesto of acid induce Dz
gastric mucosa is irritated up to shallowly ulcerated
maybe ne acute or chronic
62
acute erosive gastritis
follows an episode of insult to the gastric mucosa
heavy EtOH and heavy NSAID use
63
chronic erosive gastritis
caused by the same mechanisms
just not severe enough to cause more than shallow mucosal ulceration
64
ulceration
eaten away top layer of exposed skin
surrounding rim of inflammation with yellow scar tissue in middle
can be duodenal or gastric
65
gastric ulcer
ulceration penetrating through the mucosa to the submucosa and muscularis mucosa
surrounded by erosive gastritis
most common site is the lesser curvature of stomach
66
duodenal ulcers
same thickness of penetration
more likely to be associated with H pylori infection and genetics
67
signs of ulcers
gnawing pain in epigastrium or sub sternal chest pain
may radiate to back
relieved by food and antacids
can present atypical, painlessly (elderly)
68
complications of an ulcer
bleeding
perforation
obstruction (due to scaring)
69
treatment of acid disorders
antacids/Tums
H2 blocks (Famotidine/Pepcid)
Proton pump inhibitors (Lansoprazole/Prevacid)
70
antacids
Tums
contains ions that soak up the acid within the stomach, rendering it neutral (decreases the amount of acid that is there)
meant to be PRN
excessive use can cause metabolic acidosis
71
H2 Blockers
Famotidine/Pepcid
blocks effects of histamine in gastric mucosa -- no H+ activation over time
72
Proton pump inhibitors
Lansoprazole/Prevacid
block the H+/K pump that creates the acidic environment
strongest acid treatment
need a bit of acid to work, so can't be taken with food or concurrent with H2 blockers
73
ligament of Treitz
separates upper and lower GI
74
upper GI bleed
melena
black tarry and smelly stools
consequence of blood digestion in GI tract
coffee ground emesis or hemetemasis (vomiting red blood)
75
Lower GI bleed
hematochezia
maroon BM to bright red bleeding BM
76
why is the GI tract so prone to bleeding?
lots of vasculature on surface
if you have a platelet disorder this is particularly problematic bc GI tract can be easily damaged
77
dumping sundrome
too rapid transit of chime to small intestine
causes cramping, diarrhea, and light headedness
osmotic load induced fluid shifts from vasculature to intestine (not going slowly instead taking a big load and pulling water in)
MC cause surgical alteration, neurologic issues, diabetes
78
gastroparesis
prolonged transit of chyme to intestine
causes bloating, nausea, bacterial overgrowth, erratic blood glucose and bezoars
MC cause: autonomic neuropathy
79
2 pathophysiological mechanisms of diarrhea
osmotic diarrhea
| secretory diarrhea
80
osmotic diarrhea
failure to absorb osmotically active substance from the intestine
causes water retention by intentional contents
takes water with it
deficient absorption, pancreatic deficiency
81
secretory diarrhea
secreted hormones by untested cause water secretion form intestinal epithelial cells
pushes water out of cell into stool
enterotoxins, tumor products, lacatives
82
gateroenteritis
stomach flu
acute inflammation of stomach and intestines
typically caused by virus
s/s: N/V/D, cramps
disease is self limiting and treatment is supportive
norovirus is likely cause, typically don't give anti diarrheal bc they need to get it out
83
autoimmune reaction to normal bowel flora
Inflammatory bowel dz
causes collateral damage to GI
results in cramping, abdominal pain, weight loos, irregular bowels
infection response
84
two types of IBD
churn's
| ulcerative colitics
85
Crohn's Disease
Full thickness bowel wall involvement from mouth to anus with skip lesions (random spots of inflammation)
-impacts muscularis, cirrosal outer layer
often causes perirectal abscess snd fistula formation
commonly found in distal illeum
slightly higher CA chances
86
ulcerative colitis
found in colon and rectum only
often causing proctitis with bloody stools with tenesmus (fee like you have to poop but don't)
affects ONLY mucusoal layer
higher potential for CA due to higher cell turnover
87
Crohn's disease causes
transmural inflammation causes lympatic obstruction and eventually edema, mucosal ulceration, and fissures
88
pathophysiologic consequences of Crohn's
1. inflammation that interferes with nutrient absorption
2. bowel wall thickens decreasing lumen diameter (prone to blockage)
3. inflammation promotes adhesion formation (scar tissue connecting tissue)
4. inflammation causes abscess and fistula formation
89
UC most commonly begins
at rectum and spreads proximally to colon
UC is mild dz with few exacerbations
bc this only effects MUCOSA it is not quite as severe
90
s/s of IBD flare
sharp, cramping abdominal pain
bloody diarrhea (frankly blood)
break down of mucosa
infection symptoms (Fever, cills)
toxic megacolon
91
toxic megacolon
colon gets so infected it dilates and moves air thru
increases in size then it gets thinner so it might perforate
92
IBD flare ups outside bowels
10-20% of pts
arthritis or uveitisi
93
arthritis and IBD
begins with LBP and morning stiffness
more common in crohn's
best treated by treating IBD (manifestation)
94
uveitis
painful inflammation of middle eye wall causing blurred vision, redness and sensitivity to light
95
treatment for IBD
5-Asa derivatives
prednisone/solumedrol
azathioprine/imuran
inflizamab/remicade
96
5- ASA Derivatives
aminosalicylates
mesalamine (Asacol)
initial treatment for IBD (non flare)
multiple, some enema, some oral and suppository
more helpful in UC than Crohn's
mainstay of treatment for both (esp. mild)
97
steroids
work really well but don't want to have them on it for life
Prednisone/Solumedrol
treat acute flare of IBD
given IV at high dose for a dew days
de-escalated to oral for a taper
98
azathioprine (Imuran)
immunomodulary agent that is used to tread IBD
refractory to 5ASA
2-3 months to begin working so CI for flares
SE: cytopenias, hepatitis, fever can occur so you need CBC and LFT often
increase risk of developing lymphoma and non melanoma skin CA
99
inflixamab (remade)
immunomodulary agent that is used to tread IBD
more effective in Crohn's can be used to induce remission in acute flare or maintenance
increases risk for infection
100
most common cause of small bowel obstruction
adhesions
iatrogenic cause via surgery or inflammation
causes finding of small intestine
101
SBO can also be caused by
tumor or hernia that is incarcerated
102
treatment of partial SBO
watchful waiting
don't want surgery bc it can lead to more adhesions
partial SBO is painful but not obstipation or distention
103
treatment of complete SBO
surgery to remove obstruction
104
SBO s/s
```
constipation/obstipatoin
cramping (due to peristaltic rushes)
infection symptoms (Fever chills, elevated WBC, hypotension)
```
distal SBO= distention of abdomen
proximal SBO = vomiting
105
MC cause for LBO
most common cause is colon CA
could be a volvulus, adhesions (rare)
106
Volvulus
bowel twisting
107
LBO
```
increased distention
feculant vomiting (vomiting actual shit)
```
108
treatment of LBO
surgical treatment
109
diverticulum
def. + caused by
herniation of mucosa and submucosal layers of the colon thru the muscularis layer
caused by low fiber, highly refined diet, chronic constipation/squeezing
110
most common spot of diverticulum
L side of bowel
111
complications of diverticulosis
diverticulitis
diverticular bleeding
112
diverticulitis
blockage of the entrance of pouch by swelling or fecal matter
causes bacterial overgrowth, distention, and venous congestion
local infection, perforation, and abscesses may occur within 3-5 days
113
diverticulitis s's
slowly progressive abdominal pain
fevers (infection rxn)
BM changes
114
diverticulitis outpatient treatment
oral antibiotics covering GRAM NEGATIVES and anaerobes (i.e. augmentin) and clear liquid diet
115
diverticulitis hospital treatment
IV abx to cover GRAM NEGATIVES and ANAEROBES (i.e. metronidazole)
patients are NPO
116
diverticular bleeding
thin walls of diverticular sac and stretching to blood vessel occasionally rupture and painless bleeding occurs
hematochezia
