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Mar: Sem 2 - Health Assessment > Exam 4 GI Assessment Part 2 [Ashley] > Flashcards

Exam 4 GI Assessment Part 2 [Ashley] Flashcards

1
Q

Gastric outlet ____ onset may be ____ or ____

Slide 26

A

obstruction
acute
slow

Slide 26

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2
Q

acute gastric outlet obstructions are caused by what?

A

edema & inflammation in pyloric channel at the beginning of duodenum

Slide 26

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3
Q

What are the symptoms of a pyloric obstruction? treatment?

A

recurrent vomiting, dehydration, and hyperchloremic alkalosis
Tx: NGT, IV hydration; normally resolves in 72hrs

Slide 26

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4
Q

Repetitive ulceration and scarring may lead to ____ & ____

A

Fixed-stenosis & Chronic obstruction

Slide 26

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5
Q

How many types of gastric ulcers are there? and what are they caused by?

A

5
Caused by NSAIDs, H. Pylori, and ETOH

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6
Q

what is the treatment for gastric ulcers?
What is the specific treatment for H. pylori?

A

antacids, H2 blockers, PPIs, prostaglandin analogues, cytoprotective agents
H Pylori ts: triple therapy (2 abx and PPI) X 14d

Slide 27

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7
Q

Classifications of gastric ulcers

A

Slide 27 picture

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8
Q

Describe Zollinger Ellison syndrome

A

Non B cell islet tumor of the pancreas, causing gastrin hypersecretion
Gastrin stimulates gastric acid secretion. Gastric acid normally inhibits further gastrin release (neg feedback)
This feedback loop is absent in ZE syndrome

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9
Q

What are the symptoms associated with ZE syndrome?

A

peptic ulcer dz, erosive esophagitis, diarrhea
pts have increased gastric fluid vol, possible e-lytes imbalances, and endocrine abnormalities

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10
Q

What types of patients experience ZE syndrome?

A

0.1-1% of PUD pts
M>F; most commonly b/w ages 30-50
up to 50% of pts with gastrinomas are metastatic at time of diagonsis

Slide 28

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11
Q

Tx indicated for ZE syndrome

A

PPI and surgical resection of gastrinoma

slide 28

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12
Q

Pre-operative considerations for ZE syndrome

A

Correct e-lytes, increased gastric pH w/meds, RSI

Slide 28

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13
Q

What is the function of the small intestines?

A

Small intestinal motility mixes the contents of the stomach w/ digestive enzymes, further reducing particle size and increasing solubility
The major function of the small intestine is to circulate the contents & expose them to the mucosal wall to maximize absorption of water, nutrients, and vitamins before entering the large intestine
The circular and longitudinal muscle layers coordinate to achieve segmentation
Segmentation: two nearby areas contract and thereby isolate a segment of intestine
Segmentation allows the contents to remain in the intestine long enough for the essential substances to be absorbed into the circulation
It is controlled mainly by the enteric nervous system with modulation of motility by the extrinsic nervous system

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14
Q

when considering sm bowel dysmotility, it is helpful to distinguish eteliogies based on what?

A

Reversible and nonreversible causes

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15
Q

What are the reversible causes of sm intestines?

A

mechanical obstruction such as hernias, malignancy, adhesions, and volvuluses
bacterial overgrowth leading to alterations in absorptive function
ileus, electrolyte abnormalities, and critical illness

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16
Q

How is nonreversible sm bowel dysmotillity classified?
What are they?

A

structural or neuropathic
Structural: scleroderma, connective tissue disorders, IBD
Neuropathic:pseudo-obstruction in which the intrinsic and extrinsic nervous systems are altered and the intestines can only produce weak, uncoordinated contractions
–>This leads to bloating, nausea, vomiting, and abdominal pain

Slide 30

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17
Q

How does the large intestine function?

A

Large intestine acts as reservoir for waste & indigestible material before elimination, & it extracts remaining electrolytes & water
Distention of the ileum will relax the ileocecal valve to allow intestinal contents to enter the colon
Subsequent cecal distention will contract the ileocecal valve
The colon also exhibits giant migrating complexes
Giant migrating complexes serve to produce mass movements across the large intestine
In the healthy state, these complexes occur approximately 6-10x a day

Slide 31

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18
Q

What 2 primary symptoms manifest with colonic dysmotility?

A

altered bowel habits and/or intermittent cramping

Slide 32

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19
Q

Most common diseases assd w/ colonic dysmotility

A

IBS and IBD

Slide 32

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20
Q

Rome II criteria define IBS as having what?

A

abdominal discomfort along with 2 of the following features:
-defecation relieves discomfort
-pain is assoc w/abnormal frequency (> 3x per day or < 3xper week)
-pain is associated with a change in the form of the stool

Slide 32

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21
Q

In ____ contractions are ____ d/t colonic wall ____ by the inflamed gastric mucosa, but the ____ remain

A

IBD
suppressed
compression
giant migrating complexes

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22
Q

If there is an increased frequency of giant migrating complexes, what happens?

A

their pressure-effect further compresses the inflamed mucosa, which can lead to hemorrhage, thick mucus secretion, and significant erosions

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23
Q

What are the common inflammatory bowel diseases?
What is their incidence?

A

IBD is the 2nd most common inflammatory disorder (RA is 1st)
UC
Chrones
18:100,000

Slide 33

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24
Q

what is ulcerative colitis?
what happens in severe cases?
Normal symptoms?

A

Mucosal dz of rectum and part or all of the colon
In severe cases, the mucosa is hemorrhagic, edematous, ulcerated
Sx: diarrhea, rectal bleeding, crampy abdominal pain, N/V, fever, weight loss

Slide 33

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25
Q

What labs might be seen in UC?

A

↑plts,↑erythrocyte sedimentation rate,↓H&H,↓albumin

Slide 33

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26
Q

What warrants surgical colectomy with UC?

A

Hemorrhage requiring 6+ units blood in 24-48hrs

Slide 33

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27
Q

Toxic megacolon is a complication of ____ triggered by ____
what percentage of cases resolve? require colectomy?
what is the most dangerous complication of toxic megacolon?

A

UC, e-lyte distrubances
1/2 and 1/2
colon perforation: mortality rate 15%

Slide 33

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28
Q

what is Crohn’s disease?
Where is the most common site?

A

Acute or chronic inflammatory process that may affect any/all of the bowel
Most common site is the terminal ilium, usually presenting w/ileocolitis, RLQ pain & diarrhea

Slide 34

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29
Q

What are the 2 patterns of disease seen in Crohn’s disease?

A

penetrating-fistulous, or obstructing

Slide 34

30
Q

symptoms of Crohn’s? how does it progress?

A

weight loss, fear of eating, anorexia, diarrhea

Persistent inflammation gradually progresses to fibrous narrowing & stricture formation
Diarrhea decreases and is replaced by chronic bowel obstruction

Slide 34

31
Q

Extensive inflammation in Chron’s leads to what?

A

Loss of absorptive surfaces, resulting in malabsorption & steatorrhea

Slide 34

32
Q

Colonic disease may ____ in ____ causing ____

A

fistulize, stomach/duodenum, fecal vomitus

Slide 34

33
Q

1/3 of Chron’s pts have additional symptoms such as

A

Arthritis, dermatitis, kidney stones

Slide 34

34
Q

What is the medical treatment for IBD?

A

5-Acetylsalicylic acid (5-ASA)- mainstay for IBD *antibacterial & anti-inflammatory
PO/IV Glucorticoids during flares
Antibiotics: Rifaximin, Flagyl, Cipro
Purine analogues

Slide 35

35
Q

What is the surgical treatment for IBD

A

Last resort. Resected segment should be as conservative as possible.
Small intestine resection should be limited to <1/2 length
>2/3 SI resection leads to “short bowel syndrome”, requiring TPN

Slide 35

36
Q

Most carcinoid tumors originate from ____
May occur where?
What happens with carcinoid tumors?

A

GI tract
any GI tissue/segment
Secrete peptides & vasoactive substances: gastrin, insulin, somatostatin, motilin, neurotensin, tachykinins, glucagon, serotonin, other biological actives

Slide 36

37
Q

____% of pts with carcinoid tumors experience ____

A

ten
carcinoid syndrome

Slide 36

38
Q

What is Carcinoid syndrome?
symptoms?

A

Lg amts of serotonin & vasoactive substances reach systemic circulation
Sx: flushing, diarrhea, HTN/HoTN, bronchoconstriction
May acquire right heart endocardial fibrosis
Left heart generally more protected as the lungs clear some of the vasoactive substances

Slide 36

39
Q

How are carcinoid tumors diagnosed?
Treatment?
pre-op considerations?

A

Dx: urinary or plasma serotonin levels, CT/MRI
Tx: avoid serotonin-triggers, control diarrhea, serotonin antagonists & somatostatin analogues
Preop: Octreotide before surgery and prior to tumor manipulation to attenuate volatile hemodynamic changes

Slide 36

40
Q

What are the secretory characterisitcs of carcinoid tumors?
Location and presentation of carcinoid tumors?

this is a graph from the textbook

A
41
Q

What is acute pancreatitis?
How mcuh has incidence increased and why?
What does the pancreas contain?

A

inflammatory disorder of pancreas
10 fold, likely d/t increased alcoholism along w/ better diagnostics
numerous digestive enzymes

Slide 39

42
Q

How is autodigestion of the pancreas normally prevented?

A

Proteases packaged in precursor form
Protease inhibitors
Low intra-pancreatic calcium, which decreases trypsin activity
Failure of any of these mechanisms can trigger pancreatitis

Slide 39

43
Q

What are the most common causes of pancreatitis and how do they result in pancreatitis?

A

Gallstones and alcohol abuse are most common causes (60-80% cases)
Gallstones obstruct ampulla of vater, causing pancreatic ductal HTN
Pancreatitis is also seen in immunodeficiency syndrome, hyperparathyroidism/↑Ca²

Slide 39

44
Q

What are the symtpoms seen in acute pancreatitis?
complications?

A

excruciating epigastric pain that radiates to back, N/V, abd distention, steatorrhea, ileus, fever, tachycardia, HoTN
25% experience serious complications s/a shock, ARDS, renal failure, necrotic pancreatic abscess

Slide 40

45
Q

Hallmark labs of acute pancreatitis?
what imaging can be used to diagnose?

A

increased serum amylase & lipase
contrast CT or MRI, endoscopic US (EUS)

Slide 40

46
Q

What is the treatment for pancreatitis?
what is associated with greater risk of infectious complications?

A

Aggressive IVF, NPO to rest pancreas, enteral feeding (preferred over TPN), opioids
TPN associated w/greater risk of infectious complications

Slide 40

47
Q

What is Endoscopic-retrograde cholangiopancreatography (ERCP)

A

Fluoroscopic examination of biliary & pancreatic ducts
Interventions include stone removal, stent placement, sphincterotomy, hemostasis

Slide 40

48
Q

Are upper or lower GI bleeds more common?

A

upper

49
Q

in upper GI bleeds > ____% blood loss will cause ____ & ____

A

25%
hypotension and tachycardia

50
Q

in upper GI blled, orthostatic hypotension normally indicates what hct?

A

<30%

Slide 41

51
Q

In GI bleed, melena indicates what?

A

bleed is above the cecume (Where Sm intestine meets colon

Slide 41

52
Q

What labs are seen in GI bleed? Why?

A

BUN >40mg/dL dt absorbed nitrogen into bloodstream

Slide 41

53
Q

What is the therapeutic procedure of choice for GI bleed? what are other choices? Last choice?

A

EGD is dx/therapeutic procedure of choice
endoscopic ulcer ligation (perforation rx 0.5%)
ligation of bleeding varices
Mechanical balloon tamponade is last resort for uncontrolled variceal bleeding

Slide 41

54
Q

Lower GI bleed generally occurs in which population?

A

elderly

Slide 42

55
Q

Causes of Lower GI bleed

A

diverticulosis, tumors, colitis

Slide 42

56
Q

lower GI bleed treatments?
persistent bleeding warrants what?

A

Unprepped sigmoidoscopy performed as soon as Hemodynamically stable
Colonoscopy performed if pt can tolerate prep
Persistent bleeding warrants angiography and embolic therapy

Slide 42

57
Q

what is an adynamic ileus?

A

Colonic ileus characterized by massive dilation of the colon without mechanical obstruction
Loss of peristalsis leads to distention of the colon

Slide 43

58
Q

What are causes of adynamic ileus?

A

May be c/b e-lyte disorders, immobility, excessive narcotics, anticholinergics
Also thought to be due to neural-input imbalance of excessive sympathetic stimulation along with inadequate parasympathetic input to the colon

Slide 43

59
Q

Tx for ileus?
What happens if left untreated?

A

Restore e-lyte balance, hydrate, mobilize, NG suction, enemas
Neostigmine 2-2.5mg over 5 min produces immediate results in 80-90%
Cardiac monitoring required
If left untreated, ischemia and perforation may occur

Slide 43

60
Q

what are the anesthesia effects on the GI system?

A

In the preop, pts are often nervous and sympathetically charged
Inhibition of GI activity is directly proportional to the amount of norepinephrine secreted from SNS stimulation, so the higher anxiety = higherinhibition
Volatile anesthetics depress the spontaneous, electrical, contractile, and propulsive activity in the stomach, small intestine, and colon

Slide 44

61
Q

How does the GI system recover from anesthesia? What inhibits GI function and motility?

A

The small intestine is the first part of the GI tract to recover, followed by the stomach in approximately 24 hours and then the colon 30 to 40 hours postoperatively
Volatile agents, coupled with sympathetic nervous system hyperactivity associated withsurgery can inhibit GI function and motility

Slide 44

62
Q

Nitrous oxide is ____X more soluble than nitrogen in the blood so it will ____ into ____-containingt cavities from the blood faster than ____ can diffuse out

A

30
diffuse
gas
nitrogen

Slide 45

63
Q

What is gut distention correlated with?

A

pre-existingamount of gas in the bowel, as well as the duration of nitrous oxide administration, and the concentration of nitrous oxideadministered

Slide 45

64
Q

what medication should be avoided in lenghty abdominal surgeries or when the bowel is already distended?

A

Nitrous

65
Q

NMB only affect ____ muscle, so ____ remains intact

A

skeletal
GI motility

Slide 45

66
Q

What medications will help wake the GI system up after anesthesia? How?
which reversal agent does not have any effect on motility?

A

Neostigmine (AchE-I) will increase PNS activity and bowel peristalsis by increasing the frequency & intensity of contractions
This cholinergic activity is partially offset by concurrent administration of the anticholinergic medications (glycopyrrolate or atropine) which counteractthe bradycardia associated with neostigmine
The alternate reversal agent, Sugammadex, does not appear to have any effect on motility

Slide 46

67
Q

What is a common medication known to cause reduced GI motility and constipation?
Where do they work?

A

opioids
Opioids exert their function on both central & peripheralmu, delta, and kappa receptors

Slide 47

68
Q

where in the GI tract has a high density of peripheral mu-opioid receptors?

A

myenteric and submucosal plexuses

Slide 47

69
Q

Activation of the mu-opioid receptors causes what?
What other adverse events are assoicated with opioids?

A

delayed gastric emptying and slowertransit through the intestine
Other adverse events include nausea, anorexia, delayed digestion, abdominal pain, excessive straining during bowel movements, and incomplete evacuation

Slide 47

70
Q

____ and ____ movements are the two primary movements within and along the GI tract

A

Mixing and propulsive

Slide 49

71
Q

____, ____, ____ can induce ileus, inflammatory states, mesenteric ischemia, and partial or total disruption of myogenic continuity

A

hemodynamic changes, bowel manipulation, and open abdominal surgeries

Slide 49

Mar: Sem 2 - Health Assessment (32 decks)

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