Exam Flashcards

1
Q

What should you always ask?

A
  1. eating/defecating make it better or worst
  2. last menstrual cycle
  3. what were you doing (trigger)
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2
Q

Most common surgical emergency of the abdomen**

A

acute appendicitis

r/o 1st!

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3
Q

acute appendicitis Sx

A
often inconsistent
only 50% class RLQ pain, N/V
Abdominal pain most common* (could be periumbilical/epigastric migrating to RLQ)
Sx usu <48hrs
N/V/D, constipation, anorexia
vomit AFTER onset of pain*
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4
Q

what should you worry about if vomiting precedes abdominal pain?

A

intestinal obstruction

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5
Q

McBurney’s point

A

RLQ tenderness 96% in acute appendicitis

2/3 of way from umbilicus to ASIS

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6
Q

Physical exam special tests for acute appendicitis

A

McBurney’s point
Rebound tenderness (Blumberg sign)
Rovsing sign: RLQ pain w/LLQ palpation
Obturator sign: RLQ pain w/int/ext rot of flexed R. hip
Psoas sign: RLQ pain w/extension of R. hip or flex of R. hip against resistance

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7
Q

Acute appendicitis labs

A

leukocytosis w/left shift 80-85% (unreliable in infants/elderly/preg)
elevated CRP

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8
Q

imaging study to eval for acute appendicitis

A

CT Abd/Pel w/oral contrast

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9
Q

Acute appendicitis Tx

A

NPO, IVF, Pain control, Antibiotics, consult surgery

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10
Q

what should you worry w/”pain out of proportion to exam***

A

mesenteric infarction
bowel is dying, surgical emergency! need to re-vascularize
often w/A.fib/CHF
CTA, MRA

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11
Q

imaging of choice for suspected rupture abdominal aortic aneurysm

A

U/S standard (pt unstable)
CT/CTA confirm if pt stable
high pre-hospital mortality

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12
Q

Classic triad for ectopic pregnancy*

A

abdominal pain
amenorrhea
vaginal bleeding

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13
Q

Imaging/labs for suspected ectopic pregnancy

A

hCG

U/S

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14
Q

when do MIs most often occur?

A

early in the morning, may only present w/indigestion

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15
Q

most common Sx of GERD/Esophagitis

A

Burning pain, worse w/lying down

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16
Q

abrupt onset of abdominal pain in PUD is worrisome of?**

A

ulcer perforation

Sx: gnawing/burning epigastric pain

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17
Q

Test of choice to Dx PUD*

A

EGD (esophagogastroduodenoscopy)

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18
Q

Biggest causes of acute appendicitis**

A

alcohol
gallstones
(constant boring pain)

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19
Q

Acute pancreatitis signs

A

Cullen sign

Grey-Turner sign

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20
Q

what can acute pancreatitis be caused by in the elderly?

A

pancreatic tumor

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21
Q

Biliary colic

A

sudden constant pain, 1-5hrs, may radiate to R scapula
gallstone temp block cystic duct
N/V
can develop into acute cholecystitis if untreated

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22
Q

acute cholecystitis

A
inflammation of GB wall
RUQ pain, radiate to R. scapula
N/V, anorexia, fever
Labs: leukocytosis, mild LFT elevation
U/S Dx, May need surgery
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23
Q

Charcot’s Triad (Ascending Cholangitis)

A

Fever
RUQ pain
Jaundice

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24
Q

biliary dyskinesia

A

recurrent RUQ pain in absence of gallstones

pain typically 30-60min after eating (spicy, greasy), last 1-4hours

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25
Q

most common cause of small bowel obstruction

A

intra-abdominal adhesions

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26
Q

acute gastroenteritis

A

self limiting
eval for dehydration
typically fever, vomiting first then diarrhea, anorexia
supportive care, no abiotic

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27
Q

C. diff colitis Tx

A

metronidazole (PO, IV)

vancomycin (PO only! IV doesn’t penetrate gut)*

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28
Q

most common type of peritonitis

A

secondary, identify source

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29
Q

Late complication of PID

A

Tubo-ovarian abscess

can be fatal if ruptures –> endotoxic shock

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30
Q

PID Dx criteria

A

lower abd tenderness
cervical motion tenderness
adnexal tenderness
often vaginal discharge

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31
Q

what can be the only presenting Sx of ovarian torsion*

A

lower abd pain

may resolve spontaneously, if not, can infarct

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32
Q

most nutrients are absorbed in…*

A

small intestines

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33
Q

Hepatitis A mode of transmission*

A

Almost exclusively fecal-oral

person to person

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34
Q

Hep A virus type*

A

SS RNA

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35
Q

When is Hep A transmission highest*

A

anicteric prodrome

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36
Q

What can destroy Hep A virus?

A

boiling water, chlorine, iodine

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37
Q

Increasing age in Hep A results in*

A

increasing adverse events

Sx variable w/age

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38
Q

Hep A prognosis

A

usu mild, self-limited illness

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39
Q

Icteric phase of Hep A

A

dark urine first
some have pale stools
Jaundice in adults
Hepatomegaly

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40
Q

Treat Hep A in developing countries*

A

sugar canes

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41
Q

Hep A IgG*

A

past infection; patient IMMUNE

OR vaccinated*

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42
Q

Post exposure prophylaxis of Hep A

A

immune serum globulin (Gammaguard) w/in 2wks of exposure

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43
Q

Hep B virus type*

A

DNA virus

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44
Q

Incubation period of Hep B

A

1-6mon! (while Hep A is 2-6wks)

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45
Q

Estimated global prevalence of Hep B

A

Est 1/3 of global popu infected

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46
Q

How is Hep B transmitted?

A
bodily fluids (blood, semen, vaginal secretions)
sexual, needles, PERINATAL,
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47
Q

Hep B Sx

A

acute phase: many asymp
viral prodrome w/icteric hepatitis (arthralgia, myalgia, transient skin rash, fatigue,)
jaundice last 1-3mon
anicteric hepatitis more to develop into chronic (more common)

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48
Q

Hep B core IgG

A

Past infection
NOT pos from vaccine
(Hep B Surface AB: HAD virus or vaccine)

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49
Q

Hep B E Ag

A

active viral replication, highly contagious

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50
Q

Heb B E AB

A

Carrier

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51
Q

Hep B Surface AB

A

HAD virus or vaccinated

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52
Q

Hep B: IF SURFACE ANTIBODY IS POS AND NOTHING ELSE*

A

VACCINATED FOR HEP B!!!* (immune)

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53
Q

Hep B: IF SURFACE AB IS POS AND CORE AB IS POS*

A

THEY HAD Hep B; BC DON’T GET POS CORE AB FROM VACCINE

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54
Q

Hep B Surface Ag

A

Acute or chronic (+6mon) infection

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55
Q

Hep B: Surface Ag Pos and E Ag pos*

A

Highly contagious infectious Hep B!

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56
Q

Hep B: Surface Ag Pos and E AB pos*

A

CHRONIC Hep B

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57
Q

What do all pts w/chronic Hep B (carrier or active) need?

A

screening regimen for hepatocellular carcinoma (HCC)

increased risk w/co-infection w/ Hep C or D

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58
Q

Hep B Tx

A

First line: pegylated interferon alpha, entecavir, tenofovir disoproxil fumarate (TDF)*
Goal: suppress viral load & boost patient’s immune response

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59
Q

Hep B lab values

A

ALT > AST

AlkPhos/GGT elevated (no more than 3x ULN)

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60
Q

What should you routinely screen for every women, every pregnancy, every time?*

A

Hep B surface antigen

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61
Q

Newborns born to mothers w/ chronic hepatitis B need…

A

hepatitis B immune globulin and hepatitis B vaccination within 12 hours of birth!

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62
Q

Hep C virus type

A

SS RNA

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63
Q

Most frequent cause for liver transplant in US

A

Hep C

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64
Q

Prognosis of Hep C

A

70-85% remain viremic –> can develop chronic Hep C –> fibrosis –> cirrhosis (25%) or hepatic carcinoma

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65
Q

Hep C transmission

A

needles (IVDU, tattoo), straw (intranasal cocaine), razor, blood infusion before 1990
sexual and maternal UNCOMMON

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66
Q

Dx Hep C

A

Check HCV PCR and HCV AB

Classic acute picture = HCV RNA positive but HCV AB negative (takes wks to mon to convert)

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67
Q

Hep C prognosis

A

good if treated

but incidence incr from opioid epidemic

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68
Q

Hep C Sx

A

most asymp, PE often normal, fatigue most common

Often not symp until advanced liver dz w/decompensation: mental status changes, edema, ascites, variceal bleeding

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69
Q

Is Hep C a protective AB?

A

NO! Can get Hep C again!

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70
Q

most common Hep C genotype

A

Genotype 1 (80% in US)

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71
Q

Hep C Tx Guidelines

A

Acute: just monitor for spontaneous clearing (min 6mon)
Chronic: depends on Genotype
WHO: TX ALL 12YO and older

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72
Q

Hep C Tx

A

protease inhibitor (eg sofosbuvir/simeprevir)

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73
Q

Hep D is only seen in…

A

Pts w/Hep B

worst prognosis, progresses to cirrhosis more rapidly, can lead to fulminant hepatic failure

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74
Q

Hep D Tx

A

supportive, Tx Hep B

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75
Q

Fatty Liver Dz types

A

alcoholic: reversible; any person who consumes >60g alcohol per day
non-alcoholic: commonly assoc w/metabolic syndrome
very common, 1/3 popu

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76
Q

fastest growing cause of liver disease in the Western world

A

Non-alcohol fatty liver dz

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77
Q

most common cause of chronic liver disease in US adults (followed by alcohol & hep C)

A

Non-alcoholic steatohepatitis

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78
Q

What is predicted to become leading cause of liver transplantation by 2030

A

NAFLD (no sepcific Tx: control diet, weight loss, alc abstinence)

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79
Q

Alcoholic liver disease stages

A

alcoholic fatty liver, alcoholic hepatitis, alcohol-related cirrhosis

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80
Q

Pathophysiology alcoholic liver dz

A

ETOH → activated Kuppfer cells → inflammation → fibrosis → cirrhosis

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81
Q

Alcoholic liver dz Lab values

A

AST>ALT (atleast 2x)

marked elevation of GGT (but not specific)

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82
Q

Most common autosomal recessive genetic disorder among Caucasians in the US

A

hemochromatosis

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83
Q

hemochromatosis

A

autosomal recessive, iron deposition in multiple organs, including the liver
75% asymp
test Transferrin

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84
Q

70-80% of those w/Autoimmune hepatitis are…

A

women
screen w/ANA
Tx: corticosteroids +/- azathioprine

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85
Q

What can you eval for in pts w/unexplained liver dz?

A

alpha 1 antitrypsin deficiency, even w/o resp Sx

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86
Q

Most common initial presentation of Wilson’s dz

A

cirrhosis

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87
Q

Wilson’s dz SxS

A

Kayser-Fleischer Rings
Chronic active hepatitis
Cirrhosis – most common initial presentation
Fulminant hepatic failure
Serum ceruloplasmin <20 mg/dL
Tx: Lifelong chelating agents (penicillamine)

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88
Q

Goblet cells

A

secretes mucus to protect mucosa from digestive enzymes and acid

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89
Q

Parietal cells

A

secrete HCl, intrinsic factor (absorbs B12 in sm int)

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90
Q

Chief cells

A

secrete pepsinogen (inactive form of pepsin - breaks down protein)

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91
Q

pernicious anemia

A

B12 deficiency

can result from gastric bypass surgery

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92
Q

Primary responsible agents for mucosal damage assoc w/PUD**

A

gastric acid and pepsin

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93
Q

Zollinger-Ellison syndrome

A

Rare: Caused by non-beta islet cell, gastrin-secreting tumor –> stimulates acid-secreting cells of the stomach –> gastric mucosal ulceration
primary tumor typ pancreas or duodenum

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94
Q

difference between stomach ulcer and erosion

A

ulcer is deeper, local inflammatory rxn, extends through muscularis mucosa

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95
Q

What doubles the risk of PUD?

A

H. pylori infection

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96
Q

Most cases of PUD are caused by**

A

H. pylori infection

NSAIDs (submucosal erosions, inhib cyclooxygenase, dec prostaglandins, and their protective effects)

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97
Q

H. pylori infection

A

produce urease to alkalize acidic stomach, colonization of stomach causes inflammation, impairs duodenal bicarb secretion, inc gastrin/pepsinogen production
promote gastric metaplasia in duodenum, increased susceptibility to acid injury, causing duodenal ulcers (can lead to gastric outlet obstruction)

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98
Q

most common symptoms of PUD

A

epigastric pain (gnawing, burning)

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99
Q

GASTRIC ulcers*

A

eating exacerbates the pain, little relief w/antacids

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100
Q

DUODENAL ulcers*

A

eating diminishes pain, relief w/antacids

nocturnal pain

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101
Q

Sudden onset of PUD Sx is worrisome for…

A

perforation

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102
Q

PUD Sx

A
MAY BE ASYMP
Dyspepsia (belching, bloating, fatty food intolerance, distention)
Chest discomfort
Heartburn
Hematemesis or melena if bleeding
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103
Q

Dx test for PUD

A

EGD (upper GI endoscopy)

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104
Q

if anemia in PUD…

A

alarm signal, endoscopy to rule out sources of chronic GI blood loss

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105
Q

H. pylori testing

A

Urea breath test

stool antigen test

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106
Q

What should you do after treating PUD?***

A

repeat endoscopy in 6-8wks to verify healing!

Non-healing ulcer is ca until proven otherwise***

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107
Q

Non-healing gastric ulcer is what until proven otherwise***

A

Gastric cancer

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108
Q

H. pylori Tx

A

1st line: Triple therapy regimen (10-14 days)
Clarithromycin: 500mg PO BID
Amoxicillin: 1g PO BID
Metronidazole: 500mg PO BID
PPI PO BID (eg esomeprazole, lansoprazole)

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109
Q

What is H. pylori infection associated with?

A

atrophic gastritis
MALT lymphoma
at risk for malignancy

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110
Q

PUD perforations can lead to…

A

fistulas
cause pancreatitis
need surgical eval

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111
Q

Best screening test for Zollinger-Ellison Syndrome*

A

fasting serum gastrin (pt ideally off PPI; serial measurements on diff days)

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112
Q

What can Zollinger-Ellison Syndrome be assoc w/?

A

multiple endocrine neoplasia - type 1

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113
Q

If pt has multiple ulcers or ulcers in weird places…

A

check gastrin level! (serial measurement on diff days)

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114
Q

Most common type of gastric cancer**

A

adenocarcinoma 90-95%*

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115
Q

What nodes are associated with gastric ca?

A
Sister Mary Joseph node (firm nodule in umbilicus)
Irish node (enlarged L axillary LN)
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116
Q

Dx tests for gastric ca

A

EGD for Dx (depth)

EUS/CT for staging (mets)

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117
Q

Gastric ca prognosis

A

3rd most common cause of ca-related death
often found as advanced dz
early dz asymp or mimic PUD

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118
Q

What can be the 1st sign of gastric ca?

A

Virchow’s node (L supraclavicular lymphadenopathy)

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119
Q

Boerhaave’s syndrome

A

esophageal rupture
urgent surgical eval
Dx w/imaging
broad spectrum abiotics (rapid sepsis)

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120
Q

Mallory-Weiss Tear*

A

mucosal tear due to retching, non-bloody emesis followed by bloody emesis
Longitudinal mucosal laceration at the gastroesophageal junction or gastric cardia*

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121
Q

Mackler’s Triad for Boerhaave Syndrome

A

lower chest pain
vomiting
subQ emphysema

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122
Q

Gastroparesis

A

Delayed emptying of the stomach due to an issue with motility, NOT a mechanical obstruction
DM a common cause*

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123
Q

Gastroparesis Tx**

A

Metoclopramide (Reglan) – acts on dopamine receptors in stomach/intestines/brain
**watch for tardive dyskinesias (stop medication to prevent permanent Sx)

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124
Q

Ligament of Treitz*

A

Landmark that determines UGI vs LGI bleed (determines Tx)

located: 4th portion of duodenum*

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125
Q

most common site of GI bleeding*

A

Upper GI tract

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126
Q

Iron deficiency anemia, (+) hemoccult in the elderly is…**

A

CANCER until proven otherwise*

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127
Q

testing required after heme (+) stool

A

EGD
Colonoscopy
^neg then eval small bowels

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128
Q

1 cause of Upper GI bleed**

A

Ulcer disease, erosions (esophageal, stomach, duodenum)

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129
Q

What are Mallory-Weiss tears often assoc w/?

A

alcohol

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130
Q

Portal hypertension*

A

Shunting of hepatic blood away from liver due to increased resistance typically from CIRRHOSIS*.

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131
Q

Bleeding Varices

A

Usu sudden, overt , major bleeding
75% esophageal**
in 50% of cirrhosis pts (can be fatal)

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132
Q

How to eval for UGI Bleed?

A

stabilize pt then EGD** (Dx AND Tx)

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133
Q

AIMS65 Score*

A
determines risk of in-hospital mortality from upper GI bleeding: greater than 2, high risk
Albumin <3 g/dl
INR >1.5
Mental status altered
SBP <90
Age >65yo
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134
Q

Where do diverticular bleeds most often occur?*

A

Right 50-90%
Ascending colon**
(not assoc w/diverticulitis, typically PAINLESS*)

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135
Q

Where does diverticulitis most commonly occur?*

A

primarily left colon

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136
Q

Most common source of lower GI bleed

A

Colon carcinoma (but often occult)

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137
Q

Most common source of OVERT lower GI bleed

A

Diverticular bleed

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138
Q

Most common LGIB in elderly

A

Diverticular bleed

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139
Q

Diverticular bleed prognosis

A
Many stop spontaneously (75%)
Typically PAINLESS (diverticulitis painful)
140
Q

Ischemic Colitis

A

Hematochezia (+) cramping abdominal pain
develops when blood flow to a part of your colon is reduced (predom NON-occlusive ischemia)
Tx: supportive, self-resolving

141
Q

Angiodysplasia

A

ACQUIRED vascular ectasia, degenerative, possibly from chronic venous congestion of the intestine; mostly elderly
self-limiting

142
Q

Where does angiodysplasia most commonly occur?

A

80% proximal colon

143
Q

Bright red rectal bleeding

Maroon Stools

A

Irritable Bowel Dz

144
Q

Which hemorrhoids are painful?*

A

External (distal to dentate line)

145
Q

What lab should you also order w/hematochezia

A

BUN/CREAT

146
Q

Pt. w/ h/o abdominal aortic graft who enter the ER with GIB must receive immediate surgical attention to r/o…

A

aortoenteric fistula (1%, rare, life-threatening)

147
Q

“Herald” bleed

A

episode of acute hemorrhage that ceases spontaneously-

148
Q

Postural hypotension in suspected GI bleed

A

(supine-to-upright fall in systolic BP of >10 mm Hg or increase in heart rate of >20 beats per minute) indicates moderate blood loss (10-20% of circulatory volume)

149
Q

Supine hypotension in suspected GI bleed

A

suggests severe blood loss (usually >20% of circulatory volume)

150
Q

Gold standard study for LGIB*

A

Colonoscopy

151
Q

UGIB & Treatment of Varices*

A

EGD with therapeutic banding/clipping/cauterization

152
Q

Tx for UGI bleeds secondary to esophageal varices

A

Intrahepatic Portosystemic Shunt (Reduces the pressure gradient between portal and systemic circulations)*
transjugular if also portal HTN

153
Q

False diverticula

A

only involve mucosa and submucosa (true: all layers)

154
Q

Diverticulosis

A

having non-inflamed diverticula

155
Q

Diverticula

A

small pouches created by the herniation of the mucosa into the wall of the colon through intestinal layers and smooth muscle

156
Q

Diverticulitis

A

inflammation of one or more diverticula

157
Q

Where does diverticula most commonly occur?*

A
sigmoid colon (highest intraluminal pressure)
(L more common in US but mostly false diverticula)
158
Q

Most common Sx of diverticulitis

A

LLQ pain 70%

159
Q

fecal matter in urine, think…

A

colovesicular fistula (could be a complication of diverticulitis)

160
Q

Best imaging study to eval diverticulitis

A

CT abdomen/pelvis

Colonoscopy contraindicated during acute ep bc high risk for rupture; can be used after to r/o malignancy

161
Q

What should you rule out w/diverticulitis?

A

Cancer

162
Q

What medications should you avoid in treating diverticulitis

A

NSAIDs
Corticosteroids
greater risk of perforation

163
Q

Meckel Diverticulum

A

Congenital abnormality that is a true diverticulum of the small bowel

164
Q

Rules of 2s for Meckel Diverticulum (PIMP)

A

2% of the population, within 2 feet of the ileocecal valve, 2 inches in length, two types of heterotopic mucosa (gastric and pancreatic), and presentation before the age of two.

165
Q

ALT correlates w/…

A

degree of abdominal adiposity

166
Q

AST increases w/…

A

skeletal muscle injury

167
Q

Is ALT or AST more specific for liver injury and death?

A

ALT (bc AST also found in mito of cardiac, skeletal muscle, blood cells)
(but normal ALT doesn’t mean no liver inflammation; damage reach certain point, stop leaking damaged enzymes)

168
Q

Slight elevations of transaminases (50-200)

A

Low-grade inflammation

169
Q

Huge elevations (+1,000) of transaminases

A

Acute liver injury/necrosis

170
Q

Tests indicating liver “plumbing problems”

A

Bilirubin
Alk Phos: bile duct inflammation (obstruction, autoimmune, infection); high levels = inflammation; low = no dz or pancreatic ca

171
Q

GGT

A

Specific to liver

172
Q

Indirect Bilirubin

A

product of breakdown of heme, NOT water-soluble. Bound to albumin and sent to the liver (won’t cause dark urine but may cause jaundice if high)

173
Q

Direct Bilirubin

A

conjugated in the liver → makes it water-soluble. Converted to urobilinogen (makes urine yellow)

174
Q

Bilirubin levels in PRE hepatic jaundice

A

elevated UNconjugated Bili

175
Q

Bilirubin levels in POST hepatic jaundice

A

elevated conjugated bili

176
Q

Bilirubin levels in hepatic jaundice

A

BOTH conjugated and unconjugated may be elevated

177
Q

Nutrition on LFTs

A

albumin low due to low nutrition status (but low albumin can also suggest chronic dz like ca, cirrhosis)

178
Q

TYLENOL MAX DOSE IN 24HRS*

A
3 grams (those w/o liver dz)
2 gram (Liver dz)
179
Q

alk phos elevated out of proportion to aminotransferases

A

Think obstruction (liver/bile ducts) - CHOLESTATIC

180
Q

aminotransferases elevated out of proportion to alk phos

A

Think liver inflammation - hepatocellular

181
Q

Isolated Hyperbilirubinemia - CONJUGATED**

A

think decreased excretion or leakage of pigment from hepatocytes
Dubin-Johnson Syndrome*
Rotor Syndrome*

182
Q

Isolated Hyperbilirubinemia - UNCONJUGATED**

A

Gilbert’s Syndrome: Bili goes up in period of stress*

Crigler-Najjar Syndrome*

183
Q

Most common cause of drug-induced liver injury**

A

Acetaminophen*

184
Q

Augmentin (amoxicillin/clavulanate) induced liver injury pattern on LFT*

A

Cholestatic pattern

185
Q

Ibuprofen induced liver injury pattern on LFT*

A

Mixed

186
Q

Diarrhea

A

passage of frequent (3 or more a day), small volume loose stools; alteration in normal absorption

187
Q

leading cause of malnutrition in children under five years old*

A

diarrhea

188
Q

Osmotic diarrhea causes*

A

Celiac Sprue/disease

Lactose intolerance

189
Q

what is not impaired in osmotic diarrhea?*

A

Electrolyte absorption is not impaired

190
Q

1 cause of secretory diarrhea*

A

Infections (eg S. Aureus, E.Coli, Vibrio Cholerae)

191
Q

Secretory Diarrhea

A
Diarrhea that occurs when excretion of water in the intestines exceeds absorption:
low stool osmolality
frequently electrolyte loss
usually does not resolve if fasting
often nocturnal
192
Q

Functional Diarrhea

A

Improvement at night and with fasting

Cause: Irritable bowel disease*

193
Q

1 parasitic cause of diarrhea in US and worldwide.

A

Giardia (NO fever usu)*

194
Q

Dx and Tx: Giardia

A

Stool O&P: 3 samples

Tx: metronidazole

195
Q

Entamoeba Histolytica

A

Parasitic infection - diarrhea
Common in tropical countries
Contaminated food or water

196
Q

Cryptosporidiosis

A

Parasitic infection - diarrhea
One of the most common causes of waterborne disease
Can live in humans and animals and passed in stool
Has a shell that allows it to survive for long periods of time and protect from chlorine disinfectants
Could be cause of chronic diarrhea in HIV/immunocompromised

197
Q

Tx Cryptosporidiosis

A

Nitazoxanide

198
Q

2 Most common Viral Causes of acute gastroenteritis*

A
Norwalk Virus (“winter stomach flu”): Common cause of acute gastroenteritis in the US
Rotavirus
199
Q

Most common GI disease in children 6-24 months

A

Rotavirus

200
Q

Fever absent bacterial infection

A

Staph

Clostridium perfringens

201
Q

Most common cause of Travelers diarrhea**

A

Enterotoxigenic E. Coli: ETEC

Food or water contaminated with animal/human feces

202
Q

Typhoid Fever

A

Severe form of salmonella (due to salmonella typhi)

life threatening

203
Q

Common bacterial cause of diarrhea in the USA

A

Campylobacter Jejuni

204
Q

(“rice water stool”)

A

Vibrio cholera (usu uncomplicated w/limited Sx)

205
Q

What do you not give to Enterohemorrhagic E.Coli (Shiga Toxin Producing)

A

Antibiotics - increased risk of HUS

206
Q

C. diff Tx

A

Metronidazole tx of choice for initial episodes and mild-moderate disease
Vancomycin or Fidaxomicin PO if severe or failure to Metronidazole
PO ONLY**

207
Q

INR that does not correct with parenteral vitamin K is suspicious for

A

severe hepatocellular injury

208
Q

1 clue to advanced liver disease that is missed by PCP*

A

the low platelet count (nl = 150K), esp if combined with prolonged INR!
pt has ADVANCED liver dz until proven otherwise

209
Q

most sensitive indicator of how the liver is functioning***

A

INR

210
Q

Acute Liver Failure

A

Acute hepatocellular injury + hepatic encephalopathy + prolonged PT (elevated INR)
LFTs are typically >10 x upper limits of normal

211
Q

Endocrine cells of pancreas

A

Alpha cells - Glucagon
Beta cells – Insulin
Delta cells - Somatostatin (inhibit insulin and glucagon release)
PP cell: pancreatic polypeptide hormone

212
Q

Causes of acute pancreatitis

A
Biliary tract stones
Drugs
ERCP
Ethanol abuse*
Metabolic
Idiopathic
Infections: viral, bac, fung
Ischemia
Parasites
Postoperative
Scorpion sting*
Trauma
213
Q

Causes of chronic pancreatitis

A
Autoimmune
Duct obstruction
Ethanol abuse*** (Most often the cause!)
Hereditary
Hypercalcemia* - 25%
Hyperlipidemia
Triglycerides* (play a big role in pancreatitis!) - 15%
Idiopathic
214
Q

most common cause of pancreatitis*

A

Gallstones

215
Q

“Female, Fair, Fat, Fertile, 40 yo”

A

Gallstones (cholelithiasis)

216
Q

second leading cause of pancreatitis**

A

ETOH

217
Q

most common identifiable cause of acute pancreatitis in CHILDREN

A

TRAUMA

218
Q

Pancreatitis - Presentation

A
Acute Onset of Abdominal Pain:
Usually Mid-Epigastric
Knife Like
Radiates to back (~50%)
May have lower chest pain (trouble taking a deep breath)
May have had previous episodes
Often assoc w/N/V
Later: abd fullness, GI bleed
(KEEP MI IN DDX)
219
Q

Pancreatitis PE

A
Typically seen “writhing” in pain
May not be able to find comfortable position: may have slight relief leaning forward
Febrile
Tachycardia
Tachypnea
Hypotension
Abdominal distension/ascites
220
Q

Signs of Pancreatitis

A

Cullen’s sign: periumbilical ecchymosis

Grey-Turner’s sign: flank bruising

221
Q

What lab study is specific for pancreatic dz*

A

Lipase (order daily ASAP)

Amylase nonspecific

222
Q

What electrolyte imbalance is present in 25% of pancreatitis*

A

hypocalcemia

223
Q

Hypoalbuminemia in pancreatitis

A

poor prognosis bc pt malnourished (cant eat, digest, or only drinking ETOH)
(Elevated LDH also poor prognosis)

224
Q

Daily Labs for pancreatitis

A

Amylase, Lipase
LDH
Ca
CBC

225
Q

thought to be the most sensitive test for pancreatitis, particularly chronic pancreatitis

A

trypsin (breaks down protein)

but not widely available

226
Q

Imaging studies for pancreatitis

A

abdominal U/S
Preferred: abd CT w/contrast
ERCP: for atyp causes

227
Q

ERCP urgent interventions in pancreatitis

A

Biliary sepsis
Biliary obstruction and severe pancreatitis
Ascending cholangitis
Progressivejaundiceorhyperbilirubinemia

228
Q

Pancreatitis Tx

A
DO NOT SEND PTS HOME (acute)
Maintain pt NPO
IV fluids* (helps)
Pain control – meperidine standard but shifting now to dilaudid (concern that morphine and its derivatives can cause spasm at sphincter of Oddi and increased biliary pressure, can make ab pain/Sx worst)
Anti-emetic – IV zofran, phenergan
Parenteral antacid (H2 blocker or PPI)
229
Q

1st line Tx of hypertriglyceridemia

A

Fibrates

230
Q

Ranson’s Criteria

A
Acute PancreatitisClinical Course scoring sys
            ≤ 2, 0% mortality
             3-4, 15 %
             5-6, 50%
             ≥7, ~95%
231
Q

Leading cause of chronic pancreatitis*

A

70% ETOH

232
Q

Most common type of pancreatic ca**

A

Ductal epithelium (adenocarcinoma)

233
Q

Best imaging study for pancreatic ca*

A

helical CT

234
Q

Pancreatic Cancer:Presentation

A

Unexplained weight loss (>5 pounds per month)
Biliary duct blockage (if head ofpancreasinvolved): Jaundice, Dark urine and light colored stool
Epigastric abdominal painradiating to back
Nauseaorvomiting
Anorexia
Weakness
(check Virchow’s node)

235
Q

Painless jaundice**

A

Pancreatic ca until proven otherwise!!

236
Q

Courvoisier’s Sign**

A

Non-tender, but distended, palpableGall Bladder

Associated withJaundice

237
Q

Pancreatic ca usu found at*

A

head of pancreas

238
Q

bile

A

produced by hepatocytes
bile acids, bilirubin, cholesterol, phospholipids, water, electrolytes
Emulsifies fats

239
Q

CCK

A

stimulates GB to contract

secreted from duodenal mucosa when fatty chyme enters

240
Q

Most common type of cholelithiasis*

A

cholesterol stones 80%

241
Q

What happens to your biliary system when pts stop eating

A

decreased enteral stimulation of the gallbladder (no CCK release) with resultant biliary stasis and stone formation

242
Q

Biliary colic

A

stones or sludge obstruct the cystic duct during GB contraction
Pain in epigastric/RUQ area with radiation to right scapula
Usually lasts 30-90 minutes, but up to 5hr
no fever or jaundice

243
Q

Imaging test of choice for gallbladder or biliary disease*

A

U/S (good for stones >2mm)

but CT and MRI/MRCP – superior for CBD stones

244
Q

Cholelithiasis Tx - symptomatic

A

cholecystectomy first-line

Asymptomatic stones – typically no intervention unless stones >2.5 cm or calcification of GB wall

245
Q

Acute Cholecystitis

A

Inflammation of the GB due to a stone impacted in the cystic duct (prolonged)

246
Q

Acute Cholecystitis PE

A

RUQ tenderness, fever, tachycardia, palpable GB/RUQ fullness (30-40%)
Murphy sign – tenderness and inspiratory pause with palpation of RUQ
Dx: U/S

247
Q

Diffusely calcified GB (“porcelain GB”)*

A

malignancy until proven otherwise

248
Q

Acute Cholecystitis Tx

A

Initial: bowel rest, IVF, analgesia, antibiotics, electrolyte correction
Antibiotics: piperacillin/tazobactam, ampicillin/sulbactam, or meropenem. If severe life-threatening cases, then imipenem/cilastatin; alt: 3rd gen ceph, Metronidazole

Laparoscopic cholecystectomy is standard of care for surgical treatment – early operation (within 72 hrs) is preferred (better outcomes)

Percutaneous drainage if surgery high risk

249
Q

Acalculous Cholecystitis population

A

very sick patients, elderly men

250
Q

Chronic Cholecystitis

A

repeated attacks of pain (biliary colic) that occur when gallstones periodically block the cystic duct.
GB can become thick-walled, scarred, and small
Tx: cholecystectomy

251
Q

Acute Cholangitis

A

Bile duct obstruction allows bacteria from duodenum to ascend; usu gram neg
Tx: antibiotics FIRST, then relieve obstruction w/ERCP

252
Q

Reynold’s pentad

A

Acute suppurative cholangitis:

Charcot’s triad plus confusion and hypotension

253
Q

What is Primary Sclerosing Cholangitis strongly assoc w/?*

A

STRONG association with IBD, especially ulcerative colitis***
thought to be autoimmune; Can lead to cirrhosis and portal HTN

254
Q

leading cause of chronic hepatitis and cirrhosis

A

Hep C

255
Q

As hepatic fibrosis progresses, steatosis…

A

regresses (may make diagnosis of NAFLD as cause more difficult)

256
Q

Medications that can cause chronic liver dz and cirrhosis**

A

Amiodarone

Methotrexate

257
Q

If pt has gastroesophageal varices on EGD, by definition they have clinically significant*

A

portal HTN

258
Q

Gastric varices*

A

less likely to bleed but if bleed then more severe - can be fatal

259
Q

Esophageal varices Tx

A

Tx: non-selective BB or banding

260
Q

serum-ascites albumin gradient (SAAG)**

A

Attribute ascites to peritoneal or non-peritoneal causes

SAAG = (albumin concentration of serum) – (albumin concentration of ascitic fluid)

261
Q

Non-peritoneal SAAG

A

SAAG > 1.1 g/dL
portal HTN, hypoalbuminemia (nephrotic syndrome, malnutrition), malignancy, pancreatic ascites, biliary ascites, trauma, myxedema

262
Q

Peritoneal SAAG

A
SAAG <1.1 g/dL
malignancy ascites (peritoneal implants), TB peritonitis, sarcoidosis, FBs, vasculitis (SLE, HSP), endometriosis, fungal or parasitic infections
263
Q

ascites Tx

A

Mild ascites: sodium restrictions, diuretics 1-2x/week

Moderate to severe ascites: aggressive diuretics, monitor electrolytes:
Spironolactone: K sparing
Furosemide

(often used in combo)

264
Q

Spontaneous Bacterial Peritonitis

A

Caused by translocation of GI tract bacteria across gut wall or by hematogenous spread of bacteria

265
Q

Spontaneous Bacterial Peritonitis Dx**

A

ascites: >250 PMNs per mm3 with positive culture (classic)

266
Q

culture-negative neutrocytic ascites

A

still significant mortality (still need abiotics!)

267
Q

Spontaneous Bacterial Peritonitis tx**

A

Cefotaxime x 5 days

repeat paracentesis in 48-72hrs

268
Q

Hepatic Encephalopathy is assoc w/

A

elevated ammonia level (normally detoxified by liver), but not always!
Tx: Lactulose, Rifaximin

269
Q

TIPS

A

Transjugular, intrahepatic, portosystemic shunt – connects portal vein to the hepatic vein, bypassing liver circulation

270
Q

10-25% of pts with cirrhosis HAVE…

A

Hepatocellular carcinoma (HCC), esp w/Hep B, C, etoh

271
Q

Crohn’s Disease*

A

Inflammation and ulceration of the GI tract that can involve the full thickness of the bowel* in a patchy, non-continuous distribution (skip lesions)**
(terminal ileum and colon most common)
chronic, recurrent condition

272
Q

Rectum involvement in Crohn’s Dz

A

rectum itself is relatively spared compared to the rest of the colon

273
Q

Complications of Crohn’s Dz

A

fistulae, abscesses, perianal disease, and strictures

274
Q

Crohn’s Dz Etiology

A

strong genetic component*

defect in immune response

275
Q

Common PE finding in Crohn’s Dz

A

FISTULAS* between colon/small bowel and other organs (bladder, vagina, rectum).

276
Q

Bloody Diarrhea, keep what on your DDx?*

A

Crohn’s Dz, Ulcerative colitis

277
Q

Sx of Crohn’s Dz

A

weight loss, lethargy, fever, and general malaise
N/V/D intermittent, could be bloody
pain usu RLQ, quality ranges

278
Q

PYODERMA GANGRENOSUM

A

cutaneous ulcerations in Crohn’s Dz

279
Q

When does Crohn’s Dz require urgent eval?**

A

High fever, severe abdominal pain, or symptoms of small bowel obstruction

280
Q

Dx test of choice for Crohn’s*

A

colonoscopy, biopsy affected areas

281
Q

String Sign on Small bowel series

A

Crohn’s Dz, colonoscopy

282
Q

Cobblestoning of small bowel

A

Crohn’s Dz, patchy lesions (fissures, elcers), severe case

Dx w/colonoscopy

283
Q

what test is 90% sensitive for detection of IBD

A

Fecal Lactoferrin

284
Q

40% to 80% of patients with ulcerative colitis is positive for…

A

p-ANCA

285
Q

ASCA

A

antibodies to baker’s yeast and brewer’s yeast found in up to 68% of patients with Crohn’s disease

286
Q

What medication should you avoid in Crohn’s Dz

A

NSAIDs

287
Q

Crohn’s Dz Tx

A

mild to mod: salicylate (5 ASA: 5 aminosalicylates), maintenance mesalamine
mod to sev: systemic corticosteroids (prednisone or Budesonide), consider immunosup maintenance (azathioprine)
Humira, Infliximab, methotrexate, tacrolimus f refractory
no immunosuppressants if infectious colitis on DDx

288
Q

any pt w/anemia, weight loss, and fever of unknown origin, consider

A

Crohn’s Dz

289
Q

where is the inflammation in ulcerative colitis?*

A

localized primarily in the mucosa and is uniform and continuous (not full thickness and patchy as in Crohn’s)*
Perirectal involvement is a typical feature of ulcerative colitis*
only colon and rectum involved

290
Q

Hallmark feature of ulcerative colitis**

A

bloody diarrhea

assoc w/tenesmus

291
Q

cigarette smoking in ulcerative colitis

A

protect against UC (but worsens in Crohn’s)

292
Q

Examples of 5-ASA (5-aminosalicylates)

A

Rowasa, Pentasa, Asacol

1st step Tx in IBD

293
Q

Anti-TNF’s

A

Remicade, Humira, Cimzia

block major step in inflammatory path, quick in IBD Tx but expensive

294
Q

Acute Dysphagia

A

Typically foreign body impaction in esophagus, such as food bolus, inability to swallow saliva
Tx: remove FB during endoscopy

295
Q

Causes of Chronic Dysphagia

A
Esophageal or Peptic Stricture
Esophageal Cancer
Eosinophilic Esophagitis
Esophageal Webs and Rings
Esophageal Motility Disorders
Systemic Sclerosis
Achalasia
Erosive Esophagitis
296
Q

dysphagia, dysphagia, dysphagia*

A

Esophageal Cancer: progressive dysphagia (solids to liquids)

Dx: endoscopy (Ct staging, PET distant mets)

297
Q

When reflux symptoms do not improve with acid suppression, consider*

A

Eosinophilic esophagitis (EGD and biopsy: >15 eosinophils per hpf; ring formation)

298
Q

Eosinophilic esophagitis tx

A

First line – inhaled corticosteroid (spray during breath hold then swallow) x 8 wks
Candida esophagitis – most common adverse reaction

299
Q

Esophageal Web – most common in

A
cervical esophagus (typically anterior) --> narrowing post-cricoid area
<2 mm thick tissue membrane protruding into lumen
(esophageal ring most common in distal esophagus)
300
Q

Plummer-Vinson Syndrome

A

(anemia + cervical esophageal web + dysphagia)

301
Q

Zenker Diverticulum

A

Pulsion diverticulum of the hypopharynx – herniation of esophageal mucosa (false diverticulum)
Rare, typically elderly population
Dx: barium swallow

302
Q

solids AND liquids dysphagia

A

Scleroderma

achalasia

303
Q

Achalasia*

A

Inadequate peristalsis in lower esophagus with tight LES (doesn’t relax)
progressive dysphagia for solids AND liquids**
“bird beak” esophagus*

304
Q

Esophageal Motility Disorders Tx

A

CCB or TCA (EG IMIPRAMINE)

305
Q

Alarming Sx in GERD (or risk for Barret’s)

A

GIB, IDA, unexplained wt loss, anorexia, dysphagia/odynophagia, intractable vomiting, new onset dyspepsia ≥ 60 yrs

306
Q

GERD Tx

A

H2 receptor antagonist: pepcid

then PPI instead

307
Q

Barrett’s Esophagus**

A
Replacement of the stratified squamous epithelium in the distal esophagus with metaplastic columnar epithelium
(Z line = junction between cell types)
risk of esophageal ca >30fold
Asymp, BUT many have GERD
Tx: indefinite PPI for all pts
308
Q

Celiac Disease

A

malabsorptive immune mediated disorder, triggered by environmental agent (gluten) in genetically predisposed individuals

  • Specifically intolerance to gliadin (alcohol-soluble fraction of gluten)
  • villous atrophy on sm int biopsy
  • Assoc with HLA-DQ2 and HLA-DQ8 gene loci
309
Q

What genetic disorders are assoc with Celiac Dz?*

A

Down syndrome, Turner’s syndrome and Type 1 Diabetes

310
Q

Classic Sx of Celiac Dz

A

foul-smelling diarrhea with floating stools and steatorrhea, flatulence
weight loss or other evidence of malabsorption (vitamin or nutrient deficiency, osteopenia)
*but most don’t come classically…

311
Q

Skin manifestation of Celiac Dz

A

dermatitis herpetiformis

312
Q

When should testing be done on pt w/suspected celiac dz

A

while pt on gluten rich diet

serologic eval: anti-tTG and/or IgA; endoscopy if pos

313
Q

How many specimens from duodenum to make Celiac Dz Dx?

A

6 biopsy specimens

314
Q

Hydrogen Breath Test

A

Lactose tolerance testing

315
Q

When is orthostatic BP suggestive of impending shock?

A

Decrease 10-20 mmHg systolic pressure with a reflex increase in pulse > 15 bpm

316
Q

Most common condition causing acute episodes of vomiting

A

viral gastroenteritis

317
Q

What can you assume w/pts on marijuana

A

Assume pt has some level of gastroparesis

Treatment: diet + promotility drugs (ex: Metoclopramide, Erythromycin) + glucose control

318
Q

Most urgent DDx to consider w/vomiting

A

MI

CVA/cerebral hemorrhage

319
Q

Mackler triad (Boerhaave’s syndrome)

A

chest pain
vomiting
subcutaneous emphysema due to esophageal rupture

320
Q

What is Crohn’s Dz at risk for?

A

4 to 20 fold inc risk of colon ca

321
Q

high risk genetic syndromes for Colorectal ca

A
Lynch Syndrome (HNPCC)
Familial Adenomatous Polyposis (FAP): nearly 100% develop <50yo
322
Q

USPTF screening guidelines Colon ca

A

50-75yo

323
Q

Irritable bowel syndrome Sx

A

Abdominal pain, usually lower quadrant, relieved by defecation
Bloating / Distention
Mucus in stools
Constipation
Diarrhea
Abdominal discomfort after eating
*strongly influenced by emotional factors

324
Q

Most common IBS subtype

A

IBS with predominant constipation (50%)

Functional, chronic constipation not explained by another disease

325
Q

IBS Dx test

A

Fecal calprotectin or fecal lactoferrin

326
Q

Meds that can cause constipation

A

Diuretics
Antacids
Antidepressants

327
Q

75% of hepatic blood supply comes from*

A

portal vein (and 50% O2)

328
Q

Functions of hepatocyte*

A
Glycogen storage
Decomposition of Red Blood Cells
Plasma Protein synthesis – albumin, alpha/beta globulins
Production of Non-Essential amino acids
Gluconeogenesis
Hormone production
Detoxification 
Bile production
Urea production – from Ammonia and CO2
(thousands of enzymes)
329
Q

KUPFFER CELL- FUNCTION

A

RBC Destruction – worn out cells (life span 100-120 days)
Aid in production of Antibodies/ plasma proteins and bile pigments
Phagocytic clearing of pathogens
Activation is responsible for early ETOH-induced liver injury

330
Q

Where is RBC broken down?

A

spleen

331
Q

Which form of bilirubin is water soluble?

A

conjugated bilirubin (direct bilirubin)

332
Q

determining jaundice etiology through lab values

A

look at direct bili levels (total high, indirect high)
Prehepatic: normal
Intrahepatic: low
Posthepatic: high

333
Q

acute onset of watery, nonbloody, voluminous diarrhea accompanied by nausea and vomiting

A

Enterotoxigenic Escherichia coli

334
Q

A patient has had problems with prolonged diarrhea. Stool cultures grow out Cryptosporidium. It is important to?

A

Test the patient for HIV

335
Q

treatment of choice for diarrhea caused by Giardia lamblia is?

A

Metronidazole

336
Q

most common cause of traveler’s diarrhea is adults?

A

E. coli

337
Q

Most commonly used NG tube for decompression

A

Salem Sump (dual lumen)

338
Q

When are NG tubes indicated?

A

treatment of ileus or bowel obstruction (decompression)
administer medications
enteral nutrition
contraindications: esophageal stricture, basilar skull fracture, esophageal varices
not recommended for long term enteral nutrition

339
Q

How to measure NG tube*

A

xyphoid to earlobe, then earlobe to nares
image w/XRay to confirm placement
tip of tube below diaphragm

340
Q

Meissner’s plexus

A

nervous plexus of submucosa; glands and smooth muscles

341
Q

Auerbach’s plexus

A

nervous plexus of muscularis externa; GI motility

342
Q

Retroperitoneal organs

A
S = Suprarenal (adrenal) glands
A = Aorta/Inferior Vena Cava
D = Duodenum (second and third segments)
P = Pancreas
U = Ureters
C = Colon (ascending and descending only)
K = Kidneys
E = Esophagus
R = Rectum
343
Q

What does the stomach absorb*

A

ETOH, Aspirin, NSAIDS

344
Q

Marasmus

A

Protein and calorie deficiency

NO edema

345
Q

Kwashiorkor

A

protein deficiency resulting in edema

346
Q

“Bird beak sign” on film

A

achalasia

347
Q

SENTINEL LOOP on film

A

short segment of adynamic ileus close to intra-abdominal inflammatory process (e.g., pancreatitis, appendicitis)