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issues and policy > GI > Flashcards

GI Flashcards

1
Q

LLQ pain most likely DX

A

diverticulitis

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2
Q

PUD men vs women

A

3 to one in favor of men

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3
Q

PUD hpylori

A

90% of duodenal ulcers and >75% of gastric ulcers

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4
Q

PUD caused by meds

A

NSAIDS, ASA and glucocorticoids

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5
Q

Duodonal ulcer main age range

A

30-55

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6
Q

gastric ulcers main age range

A

55-65

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7
Q

PUD alcohol and diet

A

not really associated, role of stress is uncertain, more commin in greater than 1/2 ppd smokers

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8
Q

PUD S and S

A

GNAWING epigastric pain
releife when eating- duodenal
pain worse when eating - gastric

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9
Q

PUD physical findings

A

often unremarkable, maybe some mild epigastric tenderness
gi bleed in 20%
5-10%perf

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10
Q

PUD lab

A

maybe anemia, consider endoscopy after 8-12 weeks of treatment
consider H pylori testing

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11
Q

PUD H2 receptor antagonists

A

ines- cimetidine 800mg, rinatidine300mg, famatidine40mg, nizanidine300mg, before bed

QD
then BID
then PPI in am

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12
Q

PPI 30 minutes before meals

A

azoles- 30 min before meals

lansoprazole
reberprazole etc

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13
Q

Mucosal protective agents when to give

A

2 hours apart from other agents

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14
Q

sucralfate 1g qid (carafate) dosing pearl

A

requies an acidic environment, avoid antacids and H@ blockers they are associated with a DECREASE IN nosocomial pneumonia

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15
Q

bismuth sulfate (pepto)

A

has direct antibacterial action against HPylori

promotes prostaglandin productiona and natural bicarb

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16
Q

Misoprostol (Cytotec) four times daily with meals

A

profolaxyis against NSAID ulcers
stims mucus and bicarb produciton
MAY STIM UTERINE CONTRACTION AND INDUCE ABORTION
discontinue offending agent first if possible
this is the PPI in pts who cannot stop NSAIDS

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17
Q

NSAIDS and h2 blockers (zoles) caraate adn antacids

A

do not prevent nsaid induced ulcers,

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18
Q

antacids (mylanta, maalox, MOM etc)

A

do not reduce the amount of gastric acidity or secretions-

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19
Q

H. Pylori Eradication therapy pearls

resistant quickly to

A

Must be combo

quickly resistant to - Metonidaole (flagyl) and clarithromycin- (biaxin)

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20
Q

H.Pyori eradication therapy no quick resistance to

A

amoxicillin or tetracycline

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21
Q

Hpylori combo therapy

A

2 abx + a ppi (zole) or bismuth QID (has direct anti H pylori action)

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22
Q

H pylori combo therapy MOC

A

MOC
Metro-flagyl 500 bid
prilosec (zole) 20mg bid premeal
clarithromycin (Biaxin) 500mg BID with meals for 7 days

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23
Q

H Pylori combo therapy AOC

A

AOC
ammox- 1g bid with meals
prilosec (zole) 20mg BID beofre mieals
clarithromycin(biaxin) 500 bid before meals for 7 days

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24
Q

Hpylori combo therapy MOA

A

metrinodizole -flagyl, 500bid with mealls

prilosec 20mg and amoxicillin 1g bid with meals for 7 dyas

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25
Q

Hpylori has bismuth regimin but has more side effects

A

bsmuth sunsalicylate 2 tabs fur times a day
flagyl 250 four times a day
tetracyn 500mg foru times a day
all with meals and then at bedtime

can add prilosec to this as well am and qhs for 7 days

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26
Q

antiulcer regimine is reccomended post h pylori eradication for 3-7weeks to ensure ulcer healing

A

for duodonal- omeprazole priolsec PPI 40mg qday or lansoprazle prevacid 30mg per day for 7 weeks

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27
Q

antiulcer regimine post H pylori H2 (dines)

A

H2 like famantodine Pepcid of sucarafate for 6-8 weeks

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28
Q

PUD in hospital management

A 
IV access and fluids
cbc,ptt,BMP
02
endoscopy, gi angioagraphy (sx consult)
urinary cath
NPO with ng tube for lavage - bleeding stops sopontaneously in 80 percent of cases
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29
Q

PUD in hospital upright films

A 
show free air in 70% of the cases
monitor ab 
IV H2 blockers- the dines famtadine
ffp for coagulopathy
transfuse with plat if below 50K
H2 or sucarlfate fro 6-8 weeks
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30
Q

perf bowl sounds

A

quiet

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31
Q

normal plt

A

150-400k

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32
Q

HEP ABC

A

viral

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33
Q

HEP A

A

fecal oral,

common from food or water (huricane busted pipes)

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34
Q

Hep A blood and stool

A

infectious during the 2-6 week incubation period

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35
Q

HEP A mortality

A

rate is low, fulmination hep A is rare

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36
Q

Hep B where is it

A

blood born DNA virus present in the serum, saliva, senem and vag secretions

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37
Q

Hep B transmission

A

via blood to blood, sex, mother fetus

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38
Q

Hep C what is it

A

blood born RNA virus where source is often uncertain

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39
Q

Hep C transmission

A

associated with blood, think drug needles (50%)

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40
Q

Hep C signs and symptoms pre icteric

A

per-icteric- fatigue, malaise, NV HA, aversion to smoking and ETOH

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41
Q

Hep C icteric

A

weight loss, jaundice, pruritius , RUQ pain, CLAY COLORED STOOL, dark urine
may have low grade fever or hepatosplenomegaly

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42
Q

Hep C labs

A

WBC low to normal
UA- protein and bili
Elevted AST and ALT (500-2000IU/L
LDH, Bili,Alk phos, and PT are normal to slightly elevated

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43
Q

Serology testing for Hep A-

A

look for antibody (anti-HAV) and IGM-which would imply recent infection
these peak during first 6 weeks then disappear in 3-6 months these are diagnostic of acute hep A

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44
Q

diagnostic of acute hep A

A

ANTI-HAV AND IGM ANTIBODY

IGG antibody to hep A implies previous exposure and on its own is not diagnostic of acute HAV infection -could be previous exposure, noninfectivity or immunity to recurring HAV infeciton

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45
Q

serology of active HEP A

A

anti-hav and IGM

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46
Q

serology of recovered hep A

A

anti HAV and IGG

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47
Q

Hep B serology first

A

first is HBSAG- will remain positive in asymptomatc carriers and chronic hep B patients

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48
Q

Hep B serology second

A

second is antibody to HBcAG or ANTI-HBC and IGM shortly after HBSAG goes away but before anti HB (antibody to HB appears)

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49
Q

Hep B serology third

A

HBeAG - protein derived from HBV core and indicates circulating HBV and HIGHLY INFECTIOUS SERA only in HBsAG+ sera presence indicates infectivity

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50
Q

anti hep B

A

often apears when HBeAG dissapers and signals diminished viral replication and infectivity

51
Q

serology summary

active hep B

A

HBSAG, HBEGA, ANTI-HBC, IGM ie the hep B surface antigen, the protine derived from the core and the antibody plus IGM

52
Q

serology

chronic Hep B

A

hep B surface antigen, anti Hep B, anti, HBE, IGM and IGG

53
Q

serology

recovered Hep B

A

anti HBc, Anti HBsAG

54
Q

hep B actute vs chronic

A

acute has HBeAG and anti HBC plus only IGM

chronic has anti HBE, and IGG

55
Q

Hep c how to find

A

enzyme immunoassay detects presence of antibodies to Hep C
sens and specificity are low- when suspected RIBA assy detects antibodies to HCV antigens
PCR used to differentiate between prior exposure and current viremia

56
Q

Hep C acute

A

Anti HCV-HCV, RNA

57
Q

Hep management

A 
supportive, rest during the acute phase
increase fluids 3-4L per day
avoid alcohol, detox the liver
no or low protein diet
serax if sedation is necessary 
vitamin K for prolonged PT (>15sec) 
Lactulose 30ml oray or rectally for elevated ammonia. or hepatic encephalopathy
58
Q

BS with obstruction

A

high pitched tinkling

59
Q

normal ast alt

A

less than 35-40

60
Q

IgM vs IGG for hep A

A

IGM immediate

IGG gone

61
Q

HBS AG is the tip off for B

A

HBE-AG is high virl load
anti HBE-ag is diminished load
IGM is immediate

IGM and IGG equals chronic

62
Q

recoverd hep B

A

just anti anti

63
Q

hep C needs PCR to tell

A

acute vs chronic

64
Q

Diverticulitis

A

LLQ disease more common in women

low fiber diet

65
Q

diverticulitis

A

infammation or localized perf of one or more diverticula with abcess formation

66
Q

diverticulitis causes and incidence

A

more common in women, low fiber diet

67
Q

diverticulitis s and s

A

mild to moderate aching LLQ pain
constipation vs loose stool vs both
nausea and emisis

68
Q

physical findings diverticulitis

A

low grade fever
LLQ tenderness and pain on palpation
free perf features more dramatic presentaiton

69
Q

Diverticulitis labs and diagnostics

A 
mild to moderateleukocytosis, 
elevated esr
stool and heme + in 25% of cases
sigmoidoscopy shows inflamed mucosa
may consider CT to evaluate for abcess
plain ab films are OBTAINED ON ALL PATIENTS TO LOOK FOR EVIDENCE OF FREE AIR - pneumoperitenouwm
70
Q

diverticulitis inpatient management

A

npo
IV fluids
IVABX (flagyl, cpro, ceftaidime clinda, ampicillin
if significan gi bleed present treat like PUD
20–30% of patients require sx

71
Q

cholycystitis what

A

associated with gall stones in 90% of cases

72
Q

cholycystitis when s and s

A

often after a large fatty meal
SUDDEN STEADY SEVER EPIGASTRIC PAIN, RO RIGHT HYPOCHNDRIUM
vomiting leads to relief

73
Q

cholysystitis exam

A

murphys sign: deep pain on inspiration, while fingers are placed under the R rib cage
RUQ tender to palpation, canfeel gallblader in 15% of cases
musclegaurding
fever

74
Q

cholecystitis exam

A 
WBC's 12-15K
serum Bili may be up
serum ALT,AST,LDH,and alk phos levels are all up
amylase ma be up
plain films show radioopaque gallstones
HIDA sccan
75
Q

cholecystitis gold standard exam

A

ULTRASOUND

76
Q

Cholysystitis management

A 
pain managemnt
ngt for decompression 
npo
crystoloid syloutions
Broad spectrum ABX like Piperacillin
surgical consult for lap choley
77
Q

Acute pancreatitis (autodigestion of pancreas by enzymes) causes

A

gallbladder disease, etoh, High calcium, High lipids, trauma, meds-sulfonamides, thiazides, lasix, estrogen, azathioprie (imuran)

78
Q

acute pancreatitis S and S

A

abrupt onset of steady sever pain EPIGASTRIC, WORSE BY WALKING AND LYING SUPINE, IMPROVED BY SITTING AND LEANING FORWARD, RADIATES TO THE BACK MOST COMMONLY BUT CAN GO ELSEWHER
nausea and emisis usually present, weakness sweating and anxiety in severe attacks
E

79
Q

acute pancreatitis exam

A

upper ab pain WITHOUT GAURGIND RIGIDITY OR REBOUND
distended ab
absentbowel sounds if associated with paralytic illius
fever
tacchycardia
pallor,cool skin
mild jaundice

80
Q

aacute pancreatitis with hemmorage

A

grey turner- flank discoloration

cullens sign- umbilical

81
Q

acute pancreatitis labs and diags

A

wbc elevation depends on degree
hyperglycemia
serum LDH and AST elevation
Serum Amylase 50-180 and ipase 14-289 elevated in 90% of cases BUN and coag my be up as well

82
Q

acute pancreatitis and calcium

A

levels below 7mg/dl associated with tetany , chvoseks sign or treseaus

83
Q

acute pancreatits elevated CRP

A

suggestive of pancreatic necrosis

84
Q

acute pancreatitis imaging

A

CT is better than ultrasound

85
Q

acute pancreatitis Ransons criteria- 5-6 risk factors +40% mortality, >7 risk factors +100% mortality

george washington go lazy after taken on admisisonn

A 
Greatr than 55years of age or 70 with gall stones
Wbc over 16K
Glucose over 200
LDH over 350
AST over 250
86
Q

ransons at 48 hours for acute pancreatitis

he broke CABE

A 
Hct drop of >10
BUN increase >5
Calcium <8
Arterial 02 <60
Base deficit >4
Estimated fluid sequestration >6000ml
87
Q

Acute pancreatitis tx.

A 
bed rest
npo
aggressive iv volume repletion
ng suction
pain control
pain free with bowel sounds can start clear liq diet
88
Q

bowel obstruction causes

A

adhesion, hernia, tumor, fecal impaction, illeus, volvuls

89
Q

bowel obstruction S and S

A 
cramping and periumblical pain
later pain is constant and diffuse
vomiting within minutes of pain (proximal obstruction) 
within two hours of pain is distal
minimal or no fever
90
Q

bowel obstruction physical findings

A 
minimal distention is proximal
ornounced distention is distal
mild tender but no peritoeal findings
high pitched, tinkling bowel sounds
cant pass stool or flatus
91
Q

bowel obstruction labs

A

normal labs initially
later may see dehydration level rise in wbc’s
plain films show DIALATED LOOPS OF BOWEL AND AR FLUID LEVELS

92
Q

air fluid level pattern in small bowel obstruction

A

HORIZONTAL IN SMALL BALL

FRAME PATTERN IN LARGE BOWEL

93
Q

bowel obstruction management

A 
fluid recuss
ngt suction
broad spectrum abx
surgery in ALL CASES OF COMPLETE OBSTRUCTION
partial obstruction may med manage
94
Q

UC definition

A

an idopathic inflammatory condition characterized bu diffuse mucosal inflammation of the colon, unlike chrons disease, UC invariably involves the rectum and may extend upward involving the whole colon. The diseae is characterized by symptomatic episodes and remissions

95
Q

UC signs and sx

A

BLOODY DIARRHEA IS THE HALLMARK SYMPTOM

96
Q

UC labs and diagnosis

A

stool studies are negative

sigmoidoscopy establishes the diagnosis

97
Q

UC management

A

mesalamie (canasa) suppositories or enemas for 3-12 weeks

hydrocortisone suppositories and enemas

98
Q

Mesenteric infarct-

A

a syndrom as a result of inadequate blood flow inthe mesinteric cir leading to ischemia and gangreen of the bowel

99
Q

UC appearance

A

cobblestone

100
Q

UC is inflammatory and starts from

A

bottom up

101
Q

Messinteric infarct causes

A 
arterial or venous embolus or thrombus 
atherosclerosis
smoking
usually occurs in older adults 
coagulopathy such as that from recent surgery (cardiac, AAA, increases the risk
102
Q

messinteric infarct S and S

A 
sudden onset cramp and colickly ab pain potentially after eating
pain out of proportion to exam findings
NV, Fever, ab gaurding and tenderness
hyperactive to absent BS, 
\+ perotoneal findings
shock
103
Q

messinteric infarct lab

A

elevated amylase, leukocytosis, ab films, CT

104
Q

messinteric infarct tx

A

emergent surgery

105
Q

appendicitis

A

inflamaiton of the appendix, precipitated by obstruction of the lumen, if untreated gangrene and perf can develop in 3 hours, most common presentationis men 18-30 years, affects 10% of the population.

106
Q

appy causes

A

fecalith, foreign body, inflammation, neoplasm

107
Q

appy signs and symptoms

A

vague colicky umbilical pain
pain shhifts to RLQ after several hours,
nausea with 1-2 episodes of vomiting LOTS OF EMISIS SUGGESTS ANOTHER DIAGNOSIS
pain is worse and is localized with coughing

108
Q

appy labs and diagnosis

A

RLQ gaurding WITH REBOUND TENDERNESS
local ab tenderness
pain worse with cough

109
Q

appy psoas sign (illiopsoas test

A

pain with R thigh extension

110
Q

appy obturator sign

A

pain with internal rotation of the flexed right thigh

111
Q

appy positive Rovsings sign

A

RLQ pain when pressure is applied to the LLQ

112
Q

appy fever

A

is low high fever suggest perf and another diagnosis

113
Q

appy and WBCs’

A

10k to 20k

114
Q

appy diagnosis

A

CT or ultrasound

115
Q

appy management

A

surgery
iv abx
iv fluids
pain managemnt

116
Q

gero considerations for GI

A 
decreased- jaw strength 
thirst and taste perception
gastric motility and delayed emptying 
increased transit time
impaired defication signal
decreased liver size and liver blood flow
117
Q

gi gero risk of

A

poor nutirition
altered metabolism of drugs
gerd
nsaid induced ulcers

118
Q

gi gero constipation

A

not a normal finding, most common causes include lack of fiber, deceased exercise, poor dentition, history of lax abuse, and impaired mental status

119
Q

gerd causes

A

dleayed emptying or incompetent lower esophegal sphincter

120
Q

gerd s and s

A 
retrosternal burning 
bitter taste in mouth
delching hicciups excessive salivation
frequently at night or recumbant
may be releived by sitting up water or food

exam is worthless

121
Q

gerd diagnostics

A

conside refferral for EGD, rule out cancer, barretts or PUD

122
Q

gernd non pharma

A

elevated HOB, avoid ETOH and caffine spices peppermint etc, stop smoking weight reduction

123
Q

gerd pharma

A

antacids prn
H2 blockers the tdines in high dose at night or bid
ppi zoles if h2 blockers are inneffective
gi surgical consult prn

issues and policy (22 decks)

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