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CMPP > Intestinal Diseases 1 > Flashcards

Intestinal Diseases 1 Flashcards

1
Q

where is the ligament of treitz

A

junction of duodenum to the jejunum

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2
Q

where is the iliocecal valve?

A

junction of the ileum to the cecum

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3
Q

what are villi and what are their purpose?

A

1mm projections containing a single branch of arteriole, venous, and lymphatic circulation present in the small intestine which increase SA for absorption

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4
Q

what kind of cells line the surface of villi

A

enterocytes

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5
Q

how many microvilli do each villi have?

A

3000-5000

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6
Q

what do the microvilli contain at the tips?

A

an enzyme that aid digestion and absorption

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7
Q

what is the dense packing of microvilli called?

A

the brush border

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8
Q

where are plica circulates found?

A

the jejunum

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9
Q

how can you see the small intestines (of an adult) on xray?

A

normal adult: hardly seen
pathologic supine position: small dilated bowel loops
pathologic erect position: air fluid levels seen

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10
Q

what does a dilated jejunum look like?

A

a stack of coins

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11
Q

what does a dilated ileum look like?

A

a cylindrical tube

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12
Q

how are CHO normally broken down?

A

started by salivary and pancreatic amylase –> finished by the brush border

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13
Q

how much of dietary starch passes into the colon in an unabsorbed state?

A

10%

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14
Q

what happens when CHO are not properly broken down?

A

they transfer to the colon where bacteria degrade CHO

produces CO2, hydrogen and methane (smelly farts)

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15
Q

symptoms of CHO malabsorption

A

watery diarrhea
flatulence
acidic stool pH
milk intolerance

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16
Q

what test do we use for CHO malabsorption syndrome

A

D-xylose test

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17
Q

D-xylose test determines what?

A

if the problem with CHO malabsorption is with intestinal epithelium unable to absorb CHO
tests permeability of proximal small intestine

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18
Q

how to conduct D-xylose test

A

have pt fast overnight
give them 25g of D-xylose
urine collected for 5 hours measuring excretion of D-xylose

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19
Q

normal results of D-xylose test

A

D-xylose is absorbed in intestines, filtered by the liver, excreted in the urine unchanged

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20
Q

pathologic results of D-xylose test

A

not absorbed by intestines, substance not filtered out of kidneys, low levels of D-xylose in urine (<4.5g)

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21
Q

what does an abnormal D-xylose test suggest?

A

Celiac disease, abnormalities in intestinal epithelium

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22
Q

How will the D-xylose test read if the malabsorption syndrome is from a pancreatic abnormality?

A

normal

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23
Q

most to least common ethnicities with lactose intolerance

A

native americans
african americans
hispanics
whites

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24
Q

symptoms of lactose intolerance

A

diarrhea
abdominal pain
flatulence all after ingestion of lactose

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25
Q

cause of lactose intolerance

A

low intestinal lactase levels from mucosal injury or genetic abnormality

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26
Q

when do we do a test to determine if it’s lactose intolerance?

A

if it is not cut and dry from food diary results

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27
Q

two types of lactose intolerance testing

A

serum testing

lactose hydrogen breath testing

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28
Q

describe serum testing

A

drink 50g dose of lactose
collect serum blood glucose at 0,60,120 minutes
diagnostic: blood glucose raises by less than 20 and have symptoms of diarrhea, abdominal and, and flatulence

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29
Q

describe lactose hydrogen breath testing

A 
oral lactose (weight based) is given in a fasting state
oral hydrogen is measured every 30 minutes for 3 hours
elevated hydrogen indicates lactose intolerance
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30
Q

what gives a false positive for lactose hydrogen breath test?

A

smoking
recent use of abx
baseline drug disorder

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31
Q

when wouldn’t you use the lactose hydrogen breath test

A

in patients less than 5 years old

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32
Q

first line treatment for lactose intolerance

A

reduce lactose intake to less than 8oz milk per day

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33
Q

worst lactose offenders

A

milk, evaporated milk, condensed milk, goat milk, yogurt, ice cream

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34
Q

dairy foods with less lactose

A

mozzarella, butter, sour cream

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35
Q

enzyme replacement products

A

lactaid: reduces hydrogen breath test but not symptoms
lactrase: reduces symptoms but not breath test
dairyease

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36
Q

how to eliminate collateral damage for lactose intolerance patients?

A

make sure they’re taking calcium supplements for 1200-1500mg daily

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37
Q

what is needed to break down fat?

A

release of gastric H+ into the duodenum to release secretin

secretin enhances pancreatic bicarb secretion to raise the pH to be more basic so that fat can be absorbed

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38
Q

how does chronic pancreatitis affect fat malabsorption

A

they have chronic pancreatic enzyme insufficiency therefor they cannot secrete bicarbs, the intraluminal pH is to low and fat cannot be absorbed

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39
Q

how does ZES affect fat malabsorption

A

decreases the pH of the duodenum abnormally

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40
Q

what deficiencies do we have to be careful of in fat malabsorption syndromes?

A

vitamins A,D,E,K, and B12

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41
Q

step 1 of fat break down

A

it stays in triglyceride form until attacked by lipase secreted lingually and pancreatically.

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42
Q

what helps lipase latch onto the TG

A

colipase

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43
Q

what hang out in the intestinal lumen and follow the fat to the ileum?

A

bile salts

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44
Q

where are bile salts reabsorbed and where do they go from there?

A

absorbed at the ileum
go to the portal circulation
re-secreted into the bile

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45
Q

what is the main component of bile?

A

cholesterol

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46
Q

clinical relevance of gastric bypass surgery (roux-en-y)

A

takes out all of the duodenum, and part of the jejunum and stomach therefore the fat cannot be absorbed causing a fat malabsorption syndrome

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47
Q

how much of dietary fat is normally absorbed

A

> 94%

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48
Q

what defines a fat malabsorption syndrome

A

> 7g of fat in stool per day based on a 100g fat per day diet

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49
Q

symptoms of a fat malabsorption syndrome?

A

greasy, foul smelling diarrhea
difficult to flush
weight loss
concominant nutritional deficiencies (failure to thrive and vitamin deficiencies)

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50
Q

ileum cause of fat malabsorption

A

when 100cm of the terminal ileum is diseased or resected

results in severe impairment of absorption of bile salts

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51
Q

what happens with <100cm of the terminal ileum being diseased or resected?

A

not fat malabsorption syndrome, but chronic diarrhea because bile salts are not absorbed and their osmotic activity draws water into the colon

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52
Q

how does the pancreas contribute to fat malabsorption syndromes?

A

loss of pancreatic enzymes from chronic pancreatitis, pancreatic duct obstruction, and cystic fibrosis

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53
Q

how does the liver contribute to fat malabsorption syndromes?

A

loss of bile release die to cirrhosis or biliary tree obstruction

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54
Q

how does celiac disease contribute to fat malabsorption

A

the mucosal malformation does not allow the absorption of fat

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55
Q

describe fecal fat testing scale

A

> 7g fecal fat/day > steatorrhea
15-25g fecal fat/day > small intestine origin
32g fecal fat/day > pancreatic origin

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56
Q

how do you conduct fecal fat testing

A

make sure the pt is on a 70-120g fat/dat diet

collect 3-5/day samples

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57
Q

explain sudan III stain test

A

tests for fat malabsorption syndrome
test one stool obtained during clinical visit
detects 90% of patients with significant steatorrhea
allows for microscopic visualization of lipid globules

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58
Q

what contents in the stomach are important for protein digestion?

A

pepsinogen and pepsin

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59
Q

how does pepsin work?

A

breaks down the protein, stimulates release of CCK, stimulates release of pancreatic enzymes

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60
Q

how does the duodenum contribute to protein digestion?

A

trypsinogen is converted into trypsin which breaks down the protein

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61
Q

where does protein absorption occur?

A

proximal jejunum

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62
Q

is protein malabsorption common?

A

no

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63
Q

symptoms of protein deficiency?

A 
vague
edema
muscle atrophy (failure to thrive in children)
hypoalbuminemia
hypoproteinemia
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64
Q

what diagnostic test do we use for protein malabsorption?

A

there is no good one

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65
Q

when does protein malaborption usually develop?

A

childhood

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66
Q

where are most vitamins and minerals absorbed

A

the proximal half of the small intestines

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67
Q

where is vitamin B12 absorbed

A

in the ileum after it complexes with intrinsic factor (released by parietal cells)

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68
Q

other names for celiac disease

A

celiac sprue
gluten sensitive enteropathy
non-tropical sprue

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69
Q

celiac disease defined

A

a small bowel disorder characterized by
mucosal inflammation
villous atrophy and crypt hyperplasia
occurs upon exposure to dietary gluten

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70
Q

epidemiology of celiac disease

A

most common in white european ancestry but at ANY age

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71
Q

3 major features present in classic celiac disease

A

villous atrophy
malabsorption symptoms (nausea, bloating, gas, foul smelling stools)
resolution of mucosal lesions and symptoms with d/c of gluten foods in weeks to months

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72
Q

celiac patients usually possess Ab to which 2 substances?

A

gliadin and tissue transglutaminase

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73
Q

does severity of histologic changes correlate with severity of clinical manifestation?

A

no

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74
Q

symptoms of Atypical celiac disease

A 
minor GI complaints
anemia
unexplained elevated LFTs
neuro symptoms
arthritis
dental enamel defects
YET (severe mucosal damage and positive antibody pattern)
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75
Q

asymptomatic (silent) celiac disease why

A

no clinical symptoms

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76
Q

what portion of people with celiacs are asymptomatic?

A

40%

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77
Q

how does asymptomatic celiac disease happen?

A

the small intestine can compensate if the degree of involvement is limited

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78
Q

what do celiac pt’s have intolerance to?

A

gliadin (an alcohol soluble fraction of gluten commonly found in wheat, rye, and barley)

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79
Q

what kind of disorder is celiacs?

A

autoimmune

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80
Q

what kind of comonents contributes to development of celiacs?

A 
genetic mutation which is heritable
surgery
pregnancy
viral infection
severe illness
emotional stress
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81
Q

what happens to villi in celiacs?

A

they get atrophied and can no longer absorb as intended

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82
Q

clinical GI manifestations of celiacs

A 
diarrhea that is bulky, foul smelling, and floating
failure to thrive in children
weight loss
severe anemia
vitamin B,D, and calcium deficiency
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83
Q

neuropsychiatric disease associations in celiacs

A

peripheral neuropathy in 1/2 associated with B12, B6 (paroxidine, or E deficiency)
depression
anxiety
epilepsy

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84
Q

effects on bones from celiacs

A

increased risk of osteopenia and osteoporosis due to secondary hyperparathyroidism due to Vit D deficiency

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85
Q

effects on skin from celiacs

A

dermatitis herpetiformis
multiple intensely itchy papules and vesicles that occur in clusters around elbows, forearms, knees, scalp, back and butt

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86
Q

what complexes in dermatitis herpetiformis?

A

IgA deposits

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87
Q

how to resolve dermatitis herpetiformis?

A

gluten withdraw

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88
Q

risk of malignancy in celiacs?

A 
yes, 3-6x more likely to develop non-hodgkin's lymphoma
GI cancers (oral,esophageal, small intestine adenocarcinoma)
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89
Q

do we treat sub-clinical celiac disease?

A

yes! because of risk of malignancy

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90
Q

relate risk of malignancy in symptomatic vs asymptomatic patients?

A

risk is lower in asymptomatic, but not zero

once the disease is in remission regardless, risk approaches that of a normal person

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91
Q

how does celiacs affect pregnant women?

A

association of low-birth weight infants

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92
Q

co-occurrence of autoimmune diseases with celiacs

A

DM1 (same genetic location)
sjogren’s
scleroderma
autoimmune thyroiditis

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93
Q

who should we test for celiacs?

A 
chronic or recurrent diarrhea
malabsorption concern
unexplained weight loss
abdominal distension
DM1 patients
1st degree relatives of Celiacs
Down syndrome
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94
Q

also screen for celiacs with patients without explanation of

A 
iron deficiency anemia
folate or B12 deficiency
persistent LFT elevation
short stature
delayed puberty
recurrent fetal loss
low birth weight infants
idiopathic peripheral neuropathy
recurrent migraine headaches
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95
Q

what is important to maintain while testing for celiacs?

A

a gluten rich diet

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96
Q

step 1 celiac testing?

A

serologic tests looking for IgA anti-tissue transglutaminase antibody (IgA TTG test)

best for patients over 2y.o

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97
Q

what must you do next if serologic testing for celiacs comes back positive?

A

small bowel biopsy

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98
Q

what must you do next if serologic testing for celiacs came back negative but you suspect celiacs?

A

small bowel biopsy and genetic testing

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99
Q

what does scalloping of mucosal folds upon scoping indicate?

A

celiacs

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100
Q

first line treatment for celiacs

A

avoid wheat, rye, barley, rolled oats

creamed vegetables, dried fruits, condiments, french fries, fruit pie fillings, processed meats, salad dressings

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101
Q

how long does it typically take for antibody levels to return to normal in celiac patients?

A

3-12 months

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102
Q

what is diverticular disease?

A

presence of diverticula

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103
Q

what are diverticula?

A

outpouching of intestine

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104
Q

how many people over 60 in western countries have diverticular disease and diverticulosis?

A

50% and 20% respectively

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105
Q

average age of presentation of diverticular disease?

A

59

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106
Q

why is the diagnosis age of diverticular disease becoming younger>

A

low fiber diets?

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107
Q

gender preference of diverticular disease?

A

equal

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108
Q

where does diverticular disease occur most commonly?

A

where the vasa recta penetrate the circular muscle layer in the sigmoid colon

109
Q

most common cause of lower GI bleeding in adults

A

diverticulosis

110
Q

presentation of diverticulosis

A

abrupt painless BRBPR (left colon), maroon (right colon)
crampy pains followed by a bloody bowel movement
possible hemodynamic instability

111
Q

does bleeding usually stop on its own with diverticulosis?

A

yes

112
Q

test of choice for diverticulosis suspicion?

A

colonoscopy

113
Q

how to schedule a colonoscopy for diverticulosis

A

do within 12-48 hours of presentation

must prescribe something to clean the colon such as GoLytely etc

114
Q

what else is colonoscopy useful for in diverticulosis?

A

treat active bleeding

assess for stigmata

115
Q

what raises chances of being a stigmata in diverticulosis?

A

protuberant vessels and pigmented spots

116
Q

those at risk for poor outcomes of diverticulosis

A

comorbid disease
liver disease
poor nutrition

117
Q

describe recommendation for colonoscopies

A

no more than normal

118
Q

number one recommendation for diverticulosis treatment

A

eat 30g fiber daily

119
Q

what to do if you incedentally find diverticula upon endoscopy

A

advise pt to eat 30g fiber daily and quit smoking if they do

120
Q

what causes diverticulitis

A

food particle becomes caught in a diverticula and forms a fecalith causing erosion of the vasa recti and then causing bleeding and perforation

121
Q

what amount of diverticulitis is uncomplicated

A

75%

122
Q

how many diverticulitis cases stay unsymptomatic if treated?

A

1/3

123
Q

recurrence rate of diverticulitis?

A

20-40%

124
Q

clinical presentation of diverticulitis

A

constant abdominal pain in the LLQ present several day s prior to presentation
Nausea and Vomiting
low grade temp
tender palpable mass (20%)
change in bowel habits (diarrhea or constipation)
hematochezia
urency, dysuria, frequency due to bladder irritation mimicking an UTI

125
Q

is diverticulitis pain abrupt or insidious?

A

insidious

126
Q

when does right sided pain occur with diverticulitis?

A

with cecal diverticulitis in asian americans

127
Q

when does N/V occur with divverticulitis

A

obstructions due to inflammation or functional ileus from local peritonitis

128
Q

lab results of CBC with diverticulitis

A

mild leukocytosis in 1/2

129
Q

best diagnosing test for diverticulitis

A

CT with oral and IV contrast

130
Q

what are you looking for on a CT ordered for diverticulitis?

A

sigmoid diverticula
thickened colonic wall
inflammation within pericolic fat with or without collection of contrast material or fluid
fat stranding

131
Q

what must you do before giving IV contrast for CT scan?

A

recent kidney function test

132
Q

role of abdominal ultrasound for diverticulitis

A

rule out other pathology or alternative to CT scan

133
Q

what can an ultrasound detect in diverticulitis

A

bowel wall thickening, diverticula, some complications

134
Q

what shouldn’t we do during the acute phase of illness in diverticulitis? why?

A

colonoscopy or barium enema

risk of colonic perforation

135
Q

when should a colonoscopy be done for diverticulitis?

A

6 weeks after resolution of symptoms

136
Q

treatment for symptomatic uncomplicated diverticulitis

A

bowel rest, NPO, and antibiotics

137
Q

when to consider inpatient diverticulitis care

A

if they have toxic systemic symptoms
comorbid disease
are they reliable to pursue future appointments?

138
Q

when should diverticulitis patients be hospitalized?

A

elderly
immunosuppressed
high fever
significant leukocytosis

139
Q

duration of antibiotic course for diverticulitis

A

10-14 days depending on resoution of symptoms

140
Q

bacteria targeted in diverticulitis

A

gram - rods and anaerobes

most commonly e. coli and b. fragilis

141
Q

antibiotics of choice for diverticulitis

A

ciprofloxacin (gram -) plus metronidazole (anaerobes)

142
Q

alternative to cipro and flagyl for diverticulitis

A

augmentin (amoxicillin-clavulanate) 875mg/125mg BID

143
Q

what class is cipro part of?

A

fluoroquinolones

144
Q

moa for cipro?

A

moderate activity against gram +
excellent activity against gram -
bacteriocidal by inhibiting DNA synthesis (transcription and replication_

145
Q

what is cipro absorption impaired by?

A

antacids (take 2-4 hours after cipro)

146
Q

cannot use cipro when?

A

in patients under 18 (interferes with cartilage growth leading to arthropathy

myasthenia gravis patients (leads to worsening muscle weakness)

147
Q

side effects of cipro

A

peripheral neuropathy (pain, burning, tingling, numbness, weakness, change in sensation to light touch, pain, temp, proprioception)
IV or PO
lasts months to years, maybe irreversible

148
Q

black box warning for cipro

A

associated with risk of tendon rupture in all ages but mostly 60+ or those on corticosteroids

do not use in myasthenia gravis patients

149
Q

combo medication containing amox and beta-lactamase inhibitor

A

augmentin

150
Q

what decreases GI upset with augmentin?

A

take WF

151
Q

MOA of augmentin?

A

bacteriocidal against
+: staph aureus only
-: all
amox susciptible to degredation by beta lactamases so clavulanic acid protects it by degrading some of these enzymes found in microorganisms

152
Q

important side effects of augmentin

A

GI upset (most common)
hepatic dysfunction (elevated liver enzymes, liver failure, usually reversible)
not as common
more common in elderly or those with prolonged treatment
can occur while on treatment of weeks thereafter

153
Q

diet recommendations for diverticulitis

A

clear liquid for several days (bowel rest)

see improvement of symptoms in 2-3 days then slowly advance diet

154
Q

monitoring of the clinical course, when do see them back

A

increasing pain, fever, inability to tolerate PO after a few days
failure to improve after a few days

155
Q

what to do after resolution of diverticulitis

A

colonoscopy 6 weeks after to exclude other diagnosis of cancer and evaluate extent

156
Q

chances of recurrence of diverticulitis

A

20-40%

157
Q

elective surgery in diverticulitis

A

not necessary in patients who respond to medical therapy

158
Q

complicated diverticulitis

A

abscess on sigmoid (feel on palpation or from CT scan)
obstruction
fistula
perforation

159
Q

who is more likely to develop a complicated diverticulitis?

A

smokers

160
Q

how many patients with complicated diverticulitis will get associated abscesses?

A

1/5

161
Q

when to worry about abscesses in diverticulitis?

A

patients with uncomplicated diverticulitis with no improvement in abdominal pain or persistent fever despite three days of ABX treatment

162
Q

why do obstructions in complicated diverticulitis occur

A

occur from luminal narrowing 2ndary to inflammation or narrowed from compression of abscess

163
Q

where do obstructions usually occur in complicated diverticulitis?

A

at the flexures because it’s already narrow there

164
Q

how many patients with complicated diverticulitis get fistulas?

A

20%

165
Q

where do fistulas in complicated diverticulitis usually occur?

A

from colon to bladder causing pneumaturia, fecaluria, dysuria

or to skin: enteric cutaneous

166
Q

is perforation common with complicated diverticulitis?

A 
no, only 1-2% of the time
present with peritoneal signs, rigid abdomin, rebond tenderness
high mortality rate
cutaneous hyperesthesias
these patients look VERY sick
167
Q

antibiotics for complicated diverticulitis cover

A

gram - and anaerobic pathogens

168
Q

antibiotics for complicated diverticulitis in form of

A

IV until inflammation stabilized and pain/tenderness resolves (3-5 days or more)

169
Q

average LOS for patients with diverticulitis

A

8 days

170
Q

choice 1 of antibiotics for complicated diverticulitis

A

ceftriaxone (Rocephin) PLUS metronidazole (Flagyl)

once stable on IV go to same regimen PO

171
Q

drug class of ceftriaxone

A

Cephalosporin

172
Q

is ceftriaxone available in PO?

A

no, must transfer to cipro

173
Q

MOA of Rocephin?

A

inhibition of cell wall synthesis

high degree of stability in the presence of b-lactimase enzymes used by microorganisms

174
Q

coverage of cephtriaxone?

A

gram - and +

175
Q

exceptions of coverage of rocephin?

A

c. diff and MRSA

176
Q

side effects of ceftriaxone?

A 
biliary sludge (thick bile)- found on ultrasound
biliary colic (RUQ colicky abd pain)
discontinue rocephin with s.e.
177
Q

choice 2 antibiotic for complicated diverticulitis

A

unasyn (ampicillin/sulbactam)
zosyn (pipercillin/tazobactam)
timentin (ticarcillin/clavulanate)

178
Q

how expensive are choice 2 antibiotics for complicated diverticulitis?
(unasyn, zosyn, timentin?)

A

$1000s per dose

179
Q

what is the purpose of the second drug listed after the slash in unasyn, timentin, and zosyn?

A

it protects the first drug

180
Q

when will you prescribe unasyn, zosyn, and timentin?

A

just for a day or two to control complicated diverticulitis that switch to rosphin or flagyl

181
Q

why should you prescribe zosyn, unasyn, and timentin cautiously?

A

cross-reactivity between cephalosporins and penicillin

182
Q

how many patients with complicated diverticulitis require surgical intervention?>

A

20%

183
Q

what kind of patients get surgical intervention for diverticulitis

A

complicated diverticulitis

several episodes of recurrent uncomplicated diverticulitis

184
Q

surgical goals of diverticulitis surgery

A

remove septic focus by resecting the colon
treat obstruction or fistula (kill the blood supply to this portion of the colon > dead bowel)
restore bowel continuity

185
Q

challenges with surgery for diverticulitis

A

bowel can be very friable so difficult to resect and sew back together > may form a primary anastomosis

186
Q

how to minimizes challenges of bowel resection with diverticulitis

A

wait until symptoms resolved if possible

make a colostomy until the tissues is healthy then go back later and connect

187
Q

how are bowel resections done for diverticulitis

A

laproscopically > may need to be converted into an open procedure

188
Q

in emergent or semi-emergent settings for surgical fix of diverticulitis do a ___

A

two stage procedure

  1. hartman’s procedure (resection of diseased colon and creation of a rectal stump and colostomy
  2. reversal of colostomy about 3 months later
189
Q

most common congenital anomaly of the GI tract

A

meckel’s diverticulum

190
Q

what patholgy is associated with the rule of two’s?

A

meckel’s diverticulum

191
Q

is there familial predisposition in meckel’s?

A

no

192
Q

what is the cause of meckel’s diverticulum?

A

incomplete obliteration of the vitelline duct

193
Q

what is the vitelline duct?

A

a long narrow tube connecting the yolk sac to the midgut lumen in utero
should close at birth

194
Q

yolk sac

A

membranous sac attached to an embryo providing early nourishment to developing embryo before internal circulation takes over

195
Q

rule of two’s

A 
for meckel's diverticulum
2% of population
2:1 male to female
within 2 feet of ileocecal valve
can be 2 inches in length
2-4% of patients develop complication over the course of their lives
196
Q

is meckel’s usually symptomatic or asymptomatic?

A

asymptomatic, usually found incidentally

197
Q

who is more likely to be symptomatic for meckel’s?

A

2cm length

presence of histologically abnormal tissues increasing chance with more features

198
Q

most patients with symptoms are within what age range?

A

<10 years old!

199
Q

suspect meckel’s in patients with

A

painless lower GI bleeding <10
intussusception
features of acute appendicitis without their appendix
adults with obscure GI bleeds

200
Q

why does GI bleeding occur in Meckel’s diverticulum?

A

associated with an ulceration of the small bowel due to acid secreted by ectopic gastric mucosa residing within the diverticulum

201
Q

does the diverticulum itself bleed in meckel’s?

A

no!

202
Q

describe intensity of bleeding in meckel’s

A

chronic and insidious or acute and massive

203
Q

1st line diagnosis for meckel’s

A

meckel’s scan: 99m technetium

204
Q

how does 99m technetium work?

A

has a high affinity for gastric mucosa and should identify the diverticulum

205
Q

downside of meckel’s scan?

A

meckel’s diverticulum could have ectopic mucosa belonging to the pancreas, duodenum, or etc

206
Q

what population does meckel’s scan work best in?

A

pediatrics?

207
Q

mesenteric arteriography or abdominal exploration

A

used for adults which we suspect meckel’s in

208
Q

treatment of meckel’s

A

surgery is 1st line therapy

209
Q

what can result if surgery is not done in meckel’s?

A

compartment syndrome which can result in complete lack of use or amputation

210
Q

when should surgery/resection definitely be done with meckel’s?

A

if it’s symptomatic

211
Q

when is surgery controversial in meckel’s?

A

asymptomatic

212
Q

do we resect meckels: seen on imaging

A

no

213
Q

do we resect meckels: child up to 20

A

yes

214
Q

do we resect meckels: young and otherwise healthy <50

A

only if longer than 2cm or has a broad base >2cm

215
Q

do we resect meckels: if older than 50

A

no

216
Q

appendicitis

A

inflammation of the vestigal vermiform appendix

217
Q

where is the appendix located?

A

at the base of the cecum near the ileocecal valve where the taeniua coli converge

218
Q

what is considered a true diverticulum of the cecum?

A

the appendix

219
Q

is the appendix considered part of the cecum?

A

yes

220
Q

where does the appendix’s blood supply come from?

A

the appendiceal artery (a terminal branch of the ileocolic artery)

221
Q

what can change where the pain is in appendicitis?

A

the direction that the appendix is pointing off the cecum

222
Q

step 1 of appendicitis

A

initial inflammation of the appendiceal wall occurs as a result of
fecaliths
calculi
lymphoid hyperplasia (in teens and children)
infection
tumor (benign or malignant) > both which would be removed

223
Q

step 2 of appendicitis

A

inflammation or actual structure results in obstruction leading to local ischemia (disrupts blood supply) which leads to perforation

224
Q

after perforation of the appendix what happens?

A

a contained abscess may form in small perforations (microabscesses) and body reacts quickly

generalized peritonitis (pus spilling into general abdominal area and body can’t keep up with the flow) < quick burst

225
Q

what kind of bacterial overgrowth happens in appedicitis

A

early course: aerobic

late course: mixed infections (kitchen sink)

226
Q

when obstruction causes the appendix to burst

A

increased intraluminal pressure resulting in thrombosis and occlusion of blood supply to appendix
engorged appendiz causes visceral nerves entering spinal cord at T8-10 become stimulated > periumbilical pain

227
Q

as appendicitis progresses where does the pain migrate to

A

RLQ

228
Q

what happens when translocation of bacteria occurs in appendicitis

A

sepsis

229
Q

what increases the risk of perforation

A

the length a patient has symptoms (>48 hours greatly increases)

230
Q

when does appendicitis most commonly happen

A

ages 10-19 (2nd and 3rd decades of life)

231
Q

gender predominance in appendicitis

A

1.4: 1 (slightly more men)

232
Q

McBurney’s Point

A

1/3 of distance for ASIS to umbilicus (where migratory pain starts in 50-60% of patients with appendicitis)

233
Q

where is appendicitis pain if appendix is retrocecal

A

dull abd ache
back pain
flank pain

234
Q

other symptoms of appendicitis

A

anorexia

NV FOLLOWING onset of pain

235
Q

atypical presentations of appendicitis

A 
indigestion
flatulence
bowel irregularity
diarrhea (pelvic appedicitis)
general malaise
dysuria/frequency (mocks UTI)
236
Q

physical exam presentation of appendicitis

A

early signs subtle
low grade temp of 101F in nonperforated patients
103+ in perforated patients
McBurney’s point tenderness

237
Q

rovsing’s sign

A

appendicitis

RLQ pain upon palpation of LLQ

238
Q

psoas sign

A

pain in RLQ with passive hip extension

(retrocecal appendix)

239
Q

obturator sign

A

(pelvic appendix)

lays along right obturator internis muscle and when flex the leg and internally rotate >RLE pain

240
Q

lab findings of appendicitis

A

WBC
acute average: 14.5
gangrenous: 17.1
perforated: 17.9

241
Q

imaging of choice for appendicitis suspicion in adults

A

CT scan of abdomen and pelvis with IV and PO contrast

242
Q

what is found on CT indicating appendicitis?

A 
enlarged diameter of appendix >6mm with occluded lumen
appendiceal wall thickening >2mm
periappendiceal fat stranding
appendiceal wall enhancement (contrast)
appendicolith
no air in lumen of appendix
none in early course of progression
243
Q

is it okay to do surgery even if no CT indication of appendicitis

A

yes, have convo with pt prior to immaging

244
Q

drawback of CT for appendicitis

A

2 hours to administer oral ocntrast
difficulty keeping contrast down
radiation exposure
potential for contrast induced renal failure

245
Q

role of US for appendicitis

A 
children
can't tolerate CT or contrast
look for appendiceal diameter of >6mm
fast results
no radiation
no contrast
246
Q

disadvantages of using US for appendicitis

A

constipation or obesity can obscure view
less accurate
less likely to reveal alternative diagnosis
accuracy based on operator

247
Q

xrays for appendicitis

A

cannot diagnose appendicitis but can give alternative diagnosis

248
Q

disease severity grades

A

1: inflamed
2: gangrenous
3: perforated with localized free fluid
4: perforated with regional abscess
5: perforated with diffuse peritonitis

249
Q

goal of therap for appendicitis

A

early diagnosis and early operative intervention

250
Q

what is the gold standard of care for appendicitis

A

appendectomy

251
Q

how are appendectomies primarily done

A 
laproscopically because
lower rate of wound infection
less pain POD #1
shorter LOS
helpful if dx unsure
252
Q

what do we do prophylactically for appendectomy pre op?

A

antibiotics
prevent wound infection, intra-abdominal abscess
irrigation

253
Q

whats the target of prophylactic appendectomy abx?

A

anaerobes and gram- aerobes

254
Q

when do we give prophylactic abx for appendectomies

A

60 minutes prior to initial incision

255
Q

abx used for acute non-perforated appendicitis

A

cefoxitin (Mefoxin) IV

cefazolin (Ancef) IV plus metronidazole (flagyl)

256
Q

drug class of cefozitin

A

second generation cephalosporin

257
Q

how is mefoxin available?

A

IV or IM

258
Q

MOA of cefozitin?

A

bactericidal, inhibiting cell wall synthesis

active agains +, -, and anaerobes (broad spectrum)

259
Q

S.E. of mefoxin

A

normal, GI upset, rash, c. diff risks

260
Q

drug class of cefazolin

A

1st generation cephalosporin

261
Q

how is ancef available?

A

IV or IM

262
Q

MOA of cefazolin?

A

bactericidal, inhibiting cell wall snythesis
active against: gram - (e. coli and proteus mirabilis)
no anaerobic coverage so we add flagyl

263
Q

S.E. of ancef?

A

same as cefozitin

264
Q

most common complication post op appendectomy

A

infection
simple would infection or intrabdominal abscess
occur in patients with perforated appendicitis, not simple

265
Q

what is done during surgery to minimize infection?

A

irrigation

266
Q

is there a role for delayed closure in appendectomies>

A

no

267
Q

does illeus occur?

A

yes, could happen after any abd surgery

268
Q

what happens if surgery is initiated and appendix is fine?

A

happens in 10-15% of patients
more common in infants, elderly, and young women
look for another cause
still remove the appendix to look at histology

269
Q

elderly complications with appendicitis

A

may not mount an immune response
delay seeking care
diverticulitis and neoplasm can mimic appendicitis

CMPP (17 decks)

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