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IPAP Class 21-2 > GI Block 2 > Flashcards

GI Block 2 Flashcards

1
Q

Flexible Sigmoidoscope

A

Bedside transverse to descending colon and left colon.

Prep = enema (small amount)

Which is 85% of cancer

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2
Q

Colonoscopy

A

Gold standard to ID and TREAT

Prep = 8 hours prior w/ 1 gallon PEG (GOLYTE)

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3
Q

Virtual colonoscopy (CT colonography)

A

“Visual Only” - no prep

Indication for = Failed colonoscopy

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4
Q

Rigid sigmoidoscope

A

=rectum view

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5
Q

Anoscope

A

= anal view

Think hemorrhoids

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6
Q

Do ABX Associated Colitis patients experience diarrhea

A

Patients frequently experience diarrhea as a side effect of antibiotic administration
Due to alterations in colonic flora

This diarrhea is mild and self-limited

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7
Q

Colitis is an effect of what infection

A

C diff

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8
Q

Symptoms of ABX Associated colitis

A

Mild diarrhea to fulminant disease with mega colon

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9
Q

ABX associated colitis mode of infection

A

ABX disrupt normal bowel flora and allow c diff to flourish in the colon

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10
Q

Signs and symptoms of mild to moderate ABX Associated colitis

A

Mil to moderate diarrhea

  • fever
  • crampy abdominal pain
  • decreased appetite
  • malaise

Leukocytosis @ 15,000

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11
Q

ABX Associated colitis severe disease main signs and symptoms

A
  • severe abdominal pain
  • abdominal distention
  • fever
  • hypovolemia
  • lactic acidosis
  • hypoalbuminemia
  • Leukocytosis >15,000
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12
Q

Criteria for ABX associated colitis Fulminant Dz

A

ADMIT TO ICU

  • Hypotension severe
  • Shock (w/ progression multi system organ failure)
  • Fever greater than 101.3 F
  • Ileus or significant abdominal distention/pain
  • Megacolon >7cm diam (risk bowel perforation)
  • WBC greater than 35,000
  • Serum lactate levels > 2.2 mmol/L
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13
Q

ABX associated psuedomembranous colitis

A

Pseudo membrane on mucosal surface of bowel from severe inflammation ; raised yellow or off-white plaques up to 2 cm scattered

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14
Q

ABX associated colitis stool studies recommendation

A

hosp patients w/ ≥3 liquid stools w/in 24 hrs or outpatients w/ persistent diarrhea >1 week

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15
Q

ABX associated colitis tests and STUDY OF CONFIRMATION

A

Polymerase Chain Reaction (PCR) – study of choice = used in combo to confirm c diff

Immunoassay for glutamate dehydrogenase (GDH) = presence of C diff

Toxin Rapid Enzyme Immunoassays (EIAs) – confirmatory test to distinguish active toxin infection from colonization = detects presence of toxins [think c diff A and B test]

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16
Q

When is radiographic imaging warranted for ABX associated colitis

A

patients with clinical manifestations of severe disease or fulminant colitis

EVALS for : megacolon bowel perforation and surgical interventions

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17
Q

Preferred imaging for ABX associated colitis

A

CT of ABD and Pelvis

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18
Q

What is the radio sign of thickened colonic walls associated with mucosal damage from ABX associated colitis

A

Thumb printing

From C diff toxin

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19
Q

Main complication from fulminant disease

A

Toxic megacolon

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20
Q

What is treatment for nonfulimnat ABX Associated Colitis

A

Vancomycin PO

Fidaoxamycin

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21
Q

What colon diameter qualifies as a megacolon

A

7 cm

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22
Q

What symptoms do you suspect with toxic megacolon

A

Abdominal distention and diarrhea

Over 7cm

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23
Q

Is toxic colitis or acute toxic colitis obstructive

A

No and TOXICITY IS SYSTEMIC

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24
Q

What complication is most often associated with Ulcerative colitis

A

Toxic megacolon

IBD as well

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25
Q

Diagnostic criteria for toxic megacolon

A

Radio graph evidence

More than 7cm

[Atleast 3]
Fever
Pulse > 120 bpm  
Leukocytosis>10.5 
Anemia 
[Atleast 1]
Dehydration 
Altered mental status 
Electrolyte 
Hypotension
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26
Q

Treatment for toxic megacolon

A
  1. Bowel rest and decompression
  2. IV fluids and electrolyte
  3. Treat toxemia and precipitating factors
  4. Surgical consult
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27
Q

Characteristics of colonic diverticula

A

Most ASX
LEFT QUAD pain sigmoid and descending
Constipation

Vary in size and number

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28
Q

Where are colonic diverticula normally

A

Sigmoid and descending colon

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29
Q

Pathogenesis related to increased intraluminal pressure in colonic diverticula

A

Low fiber

Insufficient water intake

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30
Q

Treatment recommendations for diverticulosis

A

Non specific treatment or further necessary

Recommend increased dietary fiber and water

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31
Q

Characteristics of diverticula bleeding

A

Painless, gross hematochezia

  • bright red blood (squirts into the toilet)
  • no other symptoms
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32
Q

Patients with active diverticula bleed get what?

A

Resuscitation and stabilization FIRST

Then Endoscope

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33
Q

Patients with non active diverticular bleed will receive referral for what?

A

Scope

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34
Q

How do patients with diverticulitis present

A

ABD pain and TTP @ LLQ (sometimes with a mass)
Fever
N/V

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35
Q

Lab findings with diverticulitis

A

Leukocytosis on CBC

+/- stool occult blood

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36
Q

What diagnostic imaging is warranted for diverticulitis?

A

ABD CT only

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37
Q

Diverticular bleeding is characterized as

A

Bright red blood w/ squirting after bowel movements

Typically no other symptoms

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38
Q

Patients present with what for diverticulitis

A

ABD pain and LLQ tenderness
Fever
N/V

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39
Q

What type of meds are indicated for mild diverticulitis

A

Oral broad spectrum ABX

Metronidazole + [Ciprofloxacin OR TMP/SMX DS]

Alternate = Augmentin

7-10 day course

outpatient management

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40
Q

What type of diet is req’d for mild diverticulitis treatment

A

Clear liquid diet

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41
Q

Treatment of severe diverticulitis

A

NPO
IV Broad ABX
IV Fluid and electrolyte replacement
IV Pain management

Surgical Consult

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42
Q

Potential complications of diverticulitis

A

Perforation
Abscess Forms
Fistulization
Obstruction

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43
Q

If your pt fails to improve on ABX regimen when treating diverticulitis what should you do

A 
Suspect abscess 
Obtain CT (if complications could arise)
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44
Q

What is the order of acute colonic pseudo-obstruction

A

Hypomotility → gas accumulation → progressive dilation → possible perforation

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45
Q

Who is most common to be diagnosed with acute colonic pseudo obstruction

A

Postsurgical

Following trauma

Medical inpatients (respiratory failure, MI, CHF)

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46
Q

Signs and symptoms of acute colonic pseudo

A

Abdominal distension
Abdominal pain
Nausea & vomiting

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47
Q

What do plain films vs CT show for acute colonic pseudo obstruction

A

Plain films = colonic dilation ; usually cecum and right hemicolon

CT = rules out mechanical obstruction

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48
Q

Management steps in treatment for acute colonic pseudo obstruction

A

Consult with GI and or/ surgery

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49
Q

Where is volvulus most common

A

Sigmoid colon

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50
Q

Most common causes of sigmoid volvulus

A

Chronic constipation
Excessive use of laxatives
Excessive use of fiber
Chagas’ disease

OVER THE AGE OF 50

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51
Q

Presentation of sigmoid volvulus

A

N/V
ABD distention
Vomiting
Constipation

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52
Q

Physical exam of sigmoid volvulus

A

Distended abdomen with tympany to percussion

Tenderness to palpation

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53
Q

Treatment for sigmoid volvulus

A

Detersion via flexible sigmoidoscopy

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54
Q

Four major pathologic groups of colonic polyps

A

Mucosal Adenomatous
Mucosal Serrated
Mucosal Non-Neoplastic
Submucosal Lesions

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55
Q

What are the most common colonic polyps

A

Sporadic

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56
Q

Describe Adenomatous polyps

A

Most common 70 %

Tubular Tubulovillous Villous

Dysplastic

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57
Q

Hyperplastic extremely common low risk polyp

A

Serrated

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58
Q

Sessile polyps are greater risk of what

A

Adenomas

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59
Q

Juvenile polyps, hamartomas, inflammatory polyps – increased risk of cancer

A

Mucosal non neoplastic

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60
Q

Lipomas, lymphoid aggregates - no clinical significance
Pneumatosis cystoides intestinalis – air filled cysts
Carcinoid tumor - cancer

A

Submucosal lesions

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61
Q

When do polyps develop / colon cancer develop in hereditary colorectal polyposis syndrome

A

Polyps = 15 yrs old

Colon cancer = 40-50 yrs old

Requires genetic testing

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62
Q

Treatment chronologically for hereditary polyposis syndrome

A

Prophylactic colectomy, typically before age 20

Annual colonoscopy until colectomy

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63
Q

Three different hamartomatous polyposis syndromes

A

Peutz-Jeghers syndrome

Familial Juvenile Polyposis

Cowden disease

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64
Q

Common risk factors for colorectal cancer

A

Age [ above 45 yrs old ]

Family history

IBD

Dietary and Lifestyle Factors

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65
Q

Typical growth of colorectal cancer

A

Slow growing

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66
Q

What are the three types of tests for colorectal cancer screening

A

Stool based tests

Endoscopy tests

Radiographic tests

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67
Q

How does the fecal immuno chemical test and what does it detect

A

Uses antibodies to detect blood in stool

ANNUALLY [gFOBT is also ANNUAL]

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68
Q

Explain the FIT-DNA test and how often is it required

A

Combines the FIT with a test that detects altered DNA (cancer cells) in the stool

Every three years

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69
Q

What is the use of CEA antigen testing

A

Prognosis AFTER. Diagnosis

-marker of recurrence

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70
Q

Describe a colonoscopy

A

Visualization of entire colon

Detects cancer

Able to remove polyps

Requires full bowel prep and sedation

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71
Q

Describe a flexible sigmoidoscopy

A

Ever 5 yrs

Visualize retrosigmoid and descending colon

Laxative bowel prep

[CAN NOT REMOVE POLYPS]

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72
Q

CT. Colonography (visual)

A

Every 5 yrs

Less sensitive for polyps less than 1 cm

Light bowel prep no sedation

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73
Q

How often would one receive capsule colonoscopy

A

Every 5 yrs

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74
Q

Age of the average risk colorectal patient

A

45 and up

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75
Q

If pt has family members positive for colorectal cancer at what age and how often should they receive colonoscopy

A

Age 40

Every 5 years

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76
Q

Right colon symptoms of colorectal cancer

A

Iron deficiency anemia

Weakness or fatigue

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77
Q

Left colon signs and symptoms

A

Change in bowel habits

Stool streaked with blood

Obstructive symptoms

Constipation alternating with increased
stool frequency and loose stool

Colicky abdominal pain

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78
Q

Rectum signs and symptoms of colorectal cancer

A

Hematochezia
Tenesmus
Urgency
Decrease in caliber of stool (“ribbon stool”)

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79
Q

Signs of advanced or metastatic disease

A

Complete obstruction = ‘apple core lesion’

Weight loss

Fever, chill, night sweats

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80
Q

Work up for colorectal cancer

A

FOBT ( Guaiac or FiT)

CBC
CMP
UA

Colonoscopy

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81
Q

Stages of colorectal cancer

Stage I - 
Stage II - 
Stage III -
Stage III -
Stage IV -
A

Stage I - greater than 90%
Stage II – 70 - 85%
Stage III with < 4 positive lymph nodes - 67%
Stage III with > 4 positive lymph nodes - 33%
Stage IV – 5 -7%.

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82
Q

Hallmark symptoms of croons

A

ABD pain

Diarrhea with or with out blood

Fatigue

Fever

Growth failure

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83
Q

Terminal ileum ileitis

A

Small bowel Chrons disease

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84
Q

Ileocolitis

A

MOST COMMON

Small bowel + colon Crohn’s disease

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85
Q

What 2 classic signs do most crohns dz patients present with

A

Non penetrating colitis
Non-stricture disease

With further possible complications

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86
Q

What are the main complication risks in Crohn’s disease

A

May result in mucosal inflammation and ulceration, stricturing (obstruction), fistula development, and abscess formation

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87
Q

Symptoms from common intestinal obstruction complications of CD

A

Postprandial bloating
Cramping abdominal pain
Loud borborygmi

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88
Q

Penetrating disease and fistulization general pathology

A

Transmural bowel inflammation is associated with the development of sinus tracts

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89
Q

What does penetration of the bowel wall by sinus tract present as?

A

Phlegmon

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90
Q

Common sites for fistulas

A

Bladder [ENTEROVESICAL]
Skin [ENTEROCUTANEOUS]
Small bowel [ENTEROENTERIC]
Vagina [ENTEROVAGINAL]

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91
Q

FISTULA from recurrent UTI’s and pneumaturia

A

ENTEROVESICAL

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92
Q

Fistula that causes bowel contents to drain to the surface of the skin

A

ENTEROCUTANEOUS

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93
Q

Fistulas that may be aSX or present as a palpable mass

A

ENTEROENTERIC

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94
Q

Fistulas that pass as or feces through the vagina

A

ENTEROVAGINAL

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95
Q

What can a fistula of the retroperitoneum cause

A

Papas abscess or uretal obstruction

Hydronephrsosis

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96
Q

Perinatal disease anal fistula location

A

Lateral

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97
Q

Two extrainstestinal manifestations common in CD

A

Arhralgias or arthritis

Iritis or uveitis

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98
Q

What tests are elevated in lab testing Crohn inflammation

A

ESR

And

CRP

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99
Q

What is treatment for recurrent nonfulimnant ABX colitis disease

A

First = vancomycin for another 10 days

	fidaxcomycin (if not used previously)
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100
Q

What is treatment for recurrent nonfulimnant subsequent ABX colitis disease

A

Vancomycin taper (2-3 months)

Vancomycin 10 days then Rifaxmin for 20 days

Fecal Transplant if more than 3 occurrences

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101
Q

What is treatment for fulminant ABX colitis disease

A

Vancomyicin PO

Metronidazole IV

Vancomycin PR

SEVERE = colectomy surgical consult*

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102
Q

What fecal lab tests are available in CD

A

Stool culture and O and P

C diff testing

Fecal lactoferrin

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103
Q

What establishes the diagnosis for CD

A

Endoscopy

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104
Q

What can periodic endoscopy help assess

A

Under or over treating with medications

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105
Q

What does endoscopy of CD measure

A

Disease and active inflammation

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106
Q

What is used to evaluate strictures, fistulas, and ulcerations in Cd work up?

A

Barium upper GI series

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107
Q

If small bowel involvement detected in Cd what do you use to evaluate

A

Capsule endoscopy

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108
Q

What are the 4 different callsifications of CD

A

ASX
Mild-moderate
Moderate-Severe
Severe/Fulminant

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109
Q

Key diagnosis of mild to moderate CD

A

Ambulatory

normal eating and drinking

ENDOSCOPE LESIONS WHICH ARE NOT SEVERE

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110
Q

Moderate to severe CD presents as what?

A

Fever

Failed mild-mod treatment

Significant anemia

N/V without obstruction

ENDOSCOPE will see mod to severe active mucosal disease

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111
Q

Presentation of severe/fulminant disease

A

Significant weight loss

Persistent symptoms

High fever

ENDOSCOPY = severe mucosal disease

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112
Q

Controlling inflammation (induction) helps control what?

A

Symptoms

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113
Q

What are NSAIDs associated with in CD

A

Flares

Causes damage to small intestinal mucosa

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114
Q

Symptomatic treatment for CD

A

Antidiarrheals

Loperamide
Bile Acid Sequestrant = if terminal ileum involved

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115
Q

What med is given for authors ulcers associated with CD

A

Oral steroid

Kenalog in orabase (triamcinolone oral prep)

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116
Q

Mild to mod CD treatment =

A

Non systemic corticosteroid = Budesonide

Systemic Corticosteroid = Prednisone FOR FLARE TREATMENT

HIGH RISK = 5 ASA (Sulfasalazine)

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117
Q

Moderate to Severe CD treatment

A

Prednisone (oral)

Until resumption of weight gain and resolution of symptoms (7-28)

LONG TERM SIDE EFFECTS

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118
Q

If CD patients fail to respond to oral medications what should be considered

A

Hospitalization

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119
Q

What is the best maintenance therapy for CD?

A

Immunomodulators

Azathioprine
6-Mercaptopurine
Methotrexate

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120
Q

What is the best biological therapy to induce remission in mod to severe Crohn disease

A

Anti tumor Necrosis Factor

Infliximab
Adalimumab
Certolizumab

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121
Q

What is the most common surgical indication in CD

A

Resection of a segment of diseased intestine

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122
Q

What type of symptoms would qualify as admission criteria for CD

A

Obstruction

Infectious complications

Severe symptoms of diarrhea, dehydration, weight loss, or abdominal pain

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123
Q

What kind of condition is ulcerative colitis

A

Idiopathic with diffuse friability, erosions, and bleeding

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124
Q

What is the limit of UC

A

Mucosal layer

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125
Q

What is the Montreal classification of UC

A

Proctitis

Left sided colitis

Extensive colitis

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126
Q

What are common characteristics of UC

A

Exacerbations with periods of remission

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127
Q

UC has a significant risk for what?

A

Toxic Megacolon

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128
Q

Proctitis

Proctosigmoiditis

Distal colitis

Extensive colitis

Pancolitis

A

Rectum Mostly

Sigmoid and Rectum (but not up to transverse

Distal to transverse

Transverse + Sigmoid

Entire Colon

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129
Q

Hallmark sign of UC are what 2 things?

A

Bloody Diarrhea

Tenesmus

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130
Q

What is the fever temperature for moderate UC vs Severe

A

99-100

Over 100

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131
Q

Mild to Moderate UC clinical presentation

A

Gradual diarrhea onset w/ BLOOD and MUCUS

Fecal urgency

Tenesmus

LLQ pain (relieved by defecation)

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132
Q

Sever UC Clinical presentation

A

More than6 bloody bowel movements

Hypovolemia

Anemia

Hypoalbuminemia

LLQ pain

TTP on exam

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133
Q

Describe bowel movements in UC

A

Frequent and small in volume as a result of rectal inflammation

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134
Q

Common work up exam of UC

A

Volume status

Nutritional status

Abdominal tenderness

DRE = evidence of BRB

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135
Q

What helps differentiate IBD form IBS

A

Fecal leukocytes

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136
Q

With UC lab testing also be sure to test for what?

A

STI’s

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137
Q

What type of endoscopy is best for UC

A

Flexible sigmoidoscopy

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138
Q

What are biopsy features suggest UC

A

Crypt abscess

Crypt branching

Shortening and disarray

Crypt atrophy

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139
Q

Main difference in treatment for UC

A

5 ASA agents as mainstay of treatment

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140
Q

Ulcerative Proctitis treatment

A

Topical mesalamine (5-ASA ) = drug of choice

4-12 weeks

Suppository or enema

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141
Q

Ulcerative Proctitis treatment if topical 5 ASA is contrained

A

Topical hydrocortisone

If can not use this use oral mesalamine

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142
Q

Distal colitis treatment recommendations

A

Topical mesalamine

Topical corticosteroids

5 ASA

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143
Q

Mild to moderate distal colitis refractory treatment

A

Co therapy with oral and topical 5 ASA

Topical corticosteroid

Add prednisone if symptoms persist

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144
Q

If a distal colitis patient has frequent relapse what do you give them

A

Topical mesalamine if tolerable then by mouth if not

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145
Q

Mild to moderate extensive colitis treatment

A

Oral and Rectal 5-ASA for 4-8 weeks

Mesalamine
Sulfasalazine w/ folic acid [highest side effect profile]

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146
Q

If no improvement of extensive mild to mod colitis on oral and rectal treatment what do you add?

A

Oral corticosteroid

Prednisone or Methylpredinsolone

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147
Q

Mod to severe colitis treatment

A

Oral corticosteroid = first line

Treat 14 days then reevaluate

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148
Q

If oral steroid does not improve mod to severe colitis what do you do

A

Give immunomodulator

Anti TNF’s = INFLIXIMAB ; ADALIMUMAB ; GOLIMUMAB

Anti-integrin therapy = VEDOLIZUMAB

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149
Q

SEVERE fulminant pancolitis disease treatment

A

Inpatient care

Surgical consultation early
NPO
Parenteral fluid/electrolyte replacement
IV corticosteroids

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150
Q

What is important for treatment of UC

A

Long term therapy to prevent relapse

Oral mesalamine = daily administration

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151
Q

For UC in patients with more than 2 relapses in a year what two meds are indicated

A

Mercaptopurine

Azathioprine

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152
Q

How many years after diagnosis require colonoscopy biopsy ever 1-2 years?

A

8 years

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153
Q

What are absolute surgical indications for UC

A

Severe hemorrhage

Perforation

Carcinoma finding

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154
Q

What UC patient presentation requires admission

A

Severe disease manifested by anemia, eight loss and fever

Fulminant disease manifested by abdominal pain, distention, fever, tachycardia

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155
Q

How do you diagnose microscopic colitis

A

Diagnosis established by histopathologic examination of biopsy specimen

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156
Q

Two subtypes of microscopic colitis

A

Lymphocytic colitis – intraepithelial lymphocytic infiltrate

Collagenous colitis – colonic subepithelial collagen band >10 micrometers in thickness

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157
Q

What colonic subepithelial thickness is indicative of collagenous colitis

A

10 micro meters

158
Q

Risk factors for microscopic colitis

A

Female

Certain meds = NSAIDs , SSRI’S, Lansoprasole, Lisinopril, Simvastatin

159
Q

Clinical presentation of micro colitis

A

Chronic non bloody watery diarrhea

ABD pain

Fatigue

160
Q

What test is diagnostic for micro colitis

A

Colonoscopy with biopsy

161
Q

Treatment for micro colitis

A

Discontinue meds if necessary

Symptomatic care = Anitdiarrheals

162
Q

Persistent mico colitis treatment =

A

Budesonide x 4 weeks

163
Q

What type of syndrome is IBS

A

Idiopathic altered bowel habit in the absence of any organic cause

“Functional bowel disorder”

164
Q

What bio markers or confirmatory tests can diagnose IBS

A

NONE

based on symptom criteria

165
Q

What are 5 possible etiologies of IBS

A 
Abnormal motility 
Visceral hypersensitivity 
Intestinal inflammation 
Enteric infection 
Psychosocial abnormalities
166
Q

IBS is most commonly diagnosed after an episode of what?

A

Bacterial gastroenteritis

167
Q

IBS sings and symptoms

A

Crampy abdominal pain

Change in stool freq and form

Feeling of bloating

168
Q

What is the name of the fecal type chart to categorize stool

A

Bristol Stool Chart

169
Q

Classify IBS-C and IBS-D

A

Consitpation vs Diarrhea

170
Q

Somatic / psychological complications of IBS

A

Dyspepsia

Heartburn

Myalgias

Gynecological symptoms

Urolological symptoms

Anxiety/Depression

171
Q

What atypical symptoms (3) and lab abnormalities (3) in consistent with IBS

A

Rectal bleeding
Nocturnal abdominal pain
Weight loss

Anemia
Inflammation markers
Electrolyte disturbances

172
Q

What type of condition is IBS

A

Chronic - long standing

173
Q

What medical abnormalities should you ask about for a possible IBS diagnosis

A 
GI neoplasm 
IBD
Hyper/hypothyroidism
Malabsorption syndromes 
Psychiatric disorders

FAMILY HISTORY

174
Q

What questions should be asked about lifestyle changes when diagnosing IBS

A

Medication diet or exercise change

175
Q

What is a lifestyle questions that should be asked to diagnose IBS

A

Recent travel or illness

176
Q

Diagnostic criteria of IBS

A

More than 3 months of abdominal pain or discomfort and altered bowel habits

AND

Abdominal pain associated with 2 of the following

  1. Relief with defecation
  2. Onset associated with change in defecation frequency
  3. Onset associated with change in stool appearance
177
Q

Additional criteria to support IBS diagnosis

A 
Difference in stool frequency 
			 stool form 
			 stool passage 
Mucus 
Abdominal bloating 
		      Distention
178
Q

Physical exam findings of IBS

A

+/- mild abdominal TTP

could be exaggerated if psychosomatic symptoms are present

179
Q

Diagnostic testing in IBS D vs IBS C

A

D = test for celiac disease

C= plain abdominal films

180
Q

IBS treatment strategy

A

Educate patient that the length of disease is a psychosomatic vicious cycle

181
Q

Good diet for IBS

A

Regular meal pattern
Avoid large meals
Low FODMAPS

182
Q

Dietary modification for IBS-D

A

Trial of Lactose elimination

Gluten elimination

183
Q

Dietary modification of IBS-C

A

Increase fiber and fluid intake

184
Q

IBS treatment can improve in all subtypes with what?

A

Increased physical activity

185
Q

Adjunct pharmacological therapy for IBS

A

Dietary and lifestyle first

Antispasmodics 
Anti-constipation meds 
Antidiarrheals 
	SSRA 
	ABX
Psychotropic agents
186
Q

Indication for antispasmodics

A

Help with pain or bloating

Dicyclomine
Hyosycamine

187
Q

Anti consitpation for IBS-C medications

A

Osmotic laxatives = TRY FIRST

Lubiprostone for women greater than 18

Linaclotide

188
Q

Antidiarrheals for IBS-D

A

Loperamide

Bile salt sequestrants

SSRA

Alosetron 
Ondansetron

Rifaximin [ good for bloating]

189
Q

IBS with abdominal pain or bloating receive what psychotropic agents

A

TCA’s

Amitriptyline
Nortriptyline
Desipramine
Imipramine

190
Q

What are the steps of bilirubin synthesis and breakdown

A
  1. RBC’s are broken down to bilirubin and deposited in the bloodstream from hemoglobin
  2. Bilirubin binds to albumin transported to the liver
  3. Once in the liver it conjugates with glucuronide
  4. Transported into bile ducts then intestines
191
Q

What are LFT’s markers of

A

Hepatocellualr injury

Cholestatic disease

192
Q

Wha is commonly included in LFT’s

A

ALT
[transaminases]
AST

Alkaline phosphates
Total protein

Bilirubin
Albumin

193
Q

Other markers for eval of the liver

A

GGT
LDH
PT/INR
Platelets

194
Q

Hepatocelluar pattern of LFT’s

A

Elevation in the serum aminotransferases compared with the alk phosph

HIGH AST and ALT

195
Q

Where is AST commonly found

A

Skeletal muscle and erythrocytes

196
Q

Which is more specific for hepatic injustice ALT or AST

A

ALT

197
Q

What elevation os AST and ALT is seen in transaminitis and what does it indicate

A

2:1 elevation

  • ALCOHOL RELATED LIVER DISEASE*
  • WITH LEVELS OF GGT*
198
Q

Where are GGT enzymes found ( 5 )

A

Hepatocytes

Biliary epithelial cells

Renal tubules

Pancreas

Intestine

199
Q

Cholestatic pattern of LFT’s

A

Disproportionate elevation in alkaline phosphatase compared with aminotrasnferases

HIGH ALK PHOS

200
Q

ALP does what?

A

Liver and bone disease indicator enzyme that transports metabolites across cell membranes

201
Q

Where is hepatic ALP present

A

On the surface of bile duct epithelium

202
Q

Patho increase in portal pressure is due to what?

A

Pressure gradient between portal vein and IVC greater than 10 mmHg

203
Q

When is jaundice clinically apparent

A

Bilirubin is greater than 2 mg/ dL

First appearing in the conjunctive(sclera icterus)

204
Q

What type of bilirubin is a common jaundice characterization with increased plasma

A

Unconjugated (indirect)

205
Q

What diseases can Casey increased bilirubin production

A

Hemolytic anemia

Hemolytic reactions

Hematoma

Pulmonary infarction

206
Q

Impaired bilirubin uptake and storage occurs in what diseases

A

Posthepatitis hyperbilirubnemia

Gilbert syndrome

Crigler Najjar syndrome

Drug reactions

207
Q

Conjugated hyperbilirubinemia is an Issue of what

A

The liver

Hepatocellular disease
Biliary obstruction
hereditary Cholestatic syndromes

208
Q

What is the etiology of hemolytic unconjugated jaundice

A

Splenomegaly

209
Q

Conjugated Cholestatic syndromes

A

Jaundice

Pruritus

Light colored stools

210
Q

What does an ERCP work up do for Jaundice

A

Evaluate bile ducts if obstruction is suspected

211
Q

If you suspect a jaundice patient has biliary obstruction

A

Endoscopic retrograde Cholangiopancreatography

ERCP

212
Q

Define acute liver failure

A

Development of severe acute liver injury w/
Encephalopathy and impaired synthetic fx

Within 8 weeks of onset of disease

213
Q

Acute liver failure is due ot what most commonly

Risks increase with what disease

A

Acetaminophen toxicity

Diabetes

214
Q

Acute liver pain is in what general area

A

Right upper quadrant

215
Q

Lab findings for acute liver failure

A 
INR grater than 1.5 
Elevated aminotransferases 
Elevated alk phos 
Low platelet count 
Elevated ammonia 
Alleviated amylase and lipase 
Elevated BUN and creatinine
216
Q

What do you provide if you suspect acute liver failure in inpatient treatment

A

IV fluid and electrolyte replacement
Dietary monitoring
GI measures
= IV PPI or H2

217
Q

What are here most common causes of hepatitis in the US

A

ABC

218
Q

What happens during phase 1 of viral replication

A

ASX

Enzyme markers of hepatitis

219
Q

Viral hepatitis phase 2

A 
Prodromal phase 
	Anorexia 
	Athralgias 
	Urticaria 
	Alterations in taste
220
Q

What is a phase 2 symptoms that occurs in the prodromal phase

A

Aversion to cigarette smoke

221
Q

What is the third phase of viral hepatitis

A

Icteric phase

Predominant GI symptoms
Jaundice
Dark urine / Pale stools
Malaise

RUQ pain with hepatomegaly

222
Q

What is phase 4 of viral hepatitis

A

Jaundice symptoms resolve

Liver enzymes return to normal

223
Q

What type of transmission is Hep A

A

Fecal to oral but also contaminated food or water

Travel to endemic areas w/ poor sanitation

224
Q

Signs of Hep A

A 
ASX 
Fatigue 
Myalgia 
RUQ pain 
N/V

Distaste for cigarettes

225
Q

Physical exam of hep A

A

Mild
Low grade fever
Scleral icterus +/- jaundice
Hepatomegaly +/- splenomegaly

226
Q

Lab findings of Hep A

A

IGM anti HAV = acute infection , usual disappearance 3 -6 months

IgG anti-HAV may persist for years

LFT findings are ELEVATED AST and ALT

Elevation of ALK PHOS

227
Q

Treatment of Acaute hepatitis A

A

No specific
maintain hydration
Self limited recovery with in 2-3 months in most cases

228
Q

What is the mode of transmission for Hep B

A

Contact with body fluids sexual contact

Virus is present in saliva semen and vaginal juice

229
Q

Screening is recommended in Hep B for which high risk groups

A

Healthcare workers

IV drug users

Prisoners

230
Q

Chronic hep B patients have a substantial risk for what?

A

Cirrhosis and Hepatocellular carcinoma

231
Q

Acute Hep B vs Chronic Hep B disease presentation

A

Acute
ASX
Weight loss

Chronic 
Fatigue 
Jaundice 
Ascites 
Advanced liver disease
232
Q

Acute vs Chronic PE in HEP B

A 
Acute
Fever
Rash
Urticaria 
Icterus/jaundice 
Hepatomegaly

Chronic
Tender hepatomegaly
Signs of advanced liver disease

233
Q

Wha this the ALT AST serology in Hep B with acute infx

A

More than 10 times

234
Q

What is normally elevated in HEP B infx that indicated liver damage

A

Albumin
PTT/INR
CBC (platelets)
Bilirubin

235
Q

What does a positive HBsAg indicate

A

Acute or chronic infx

236
Q

What does a positive IgM anti-HBc indicate?

A

Acute infx

237
Q

What does a positive Anti-HBs indicate

A

Vaccinated

238
Q

Where is HBcAg

A

Intracellular antigen expressed in infected hepatocytes not detectable in serum

239
Q

Anti-HBc appears when and what is the significance

A

Shortly after HBsAg

Predominantly of the IgM class 
Meaning ACUTE
240
Q

A secretory protein that is processed from the pre core protein

Indicates viral replication and infectivity

A

HBeAg

increased likelihood to develop chronic HBV

241
Q

What parallels the presence of HBeAg

A

HBV DNA

242
Q

If Hep B is positive what serial testing should be done

A

HBsAg to condiment clearance or persistence at 6 months

243
Q

Acute Hep B treatment

A

Antiviral therapy ONLY for mod severe liver damage patients

Liver transplant IF SEVERE liver damage

Complete recovery suspected at 16 weeks

244
Q

Acute Hep B Prevention

A 
Screening 
Serologic testing pregnant pts 
Safe sex
Safe handling of blood and body fluids 
Vaccination

Hep B IG
[administered for known exposure followed by vaccination series]

245
Q

Hep C mode of infection ; what is the high risk

A

Blood
50% injection drug use

HIGH RISK = conversion to chronic state

246
Q

Hallmark AST and ALT of Hep C

A

Waxing and waning elevations

247
Q

Lab findings of Hep C

A

Hepatic LFT’s = higher ALT than AST

+Anti-HCV EIA = requires a + HCV RNA test to confirm viral RNA
(ACTIVE INFECTION)

Serial testing = acute or chronic

248
Q

Good treatment options for Hep C

A

Interferon == Ribavirin

Direct Acting Antivirals

249
Q

Hep D requires what?

A

Defective RNA requires HBV for transmission and replication

250
Q

What confirms diagnosis and indicates presenence of infection with Hep D

A

HDV-RNA

251
Q

What indicates acute Hep D and may persist in pts with HBV infection

A

Anti HDV IgM

252
Q

The most common cause of acute hepatitis world wide

A

Hep E

Fecal to oral transmission
Waterborne outbreaks

253
Q

What is the primary diagnostic test as confirmatory test for positive hepatitis E virus IgM

A

+ HEV-RNA

Greater than 3 months = chronic HEV

254
Q

What are makers of chronic HBV or HCV

A

Persistently elevated AST/ALT

Presence of HBsAg and anti-HBc

Anti-HCV

Liver biopsy findings

255
Q

Chorionic HBV and HDV treatment

A

Antivirals

  • Nucleoside or Nucleoside analog
  • Entecavir
  • Tenofovir
  • Lamivudine
  • Adefovir
  • Telbivudine

Pegylated interferon

256
Q

Chronic HCV treatment

A

Direct acting host targeting ANTIVIRAL agents

Ledipasvir
Sofosbuvir [Harvoni]

257
Q

Autoimmune hepatitis is common in

A

Women

258
Q

What extra hepatic manifestations are common in autoimmune hepatitis

A 
Arthritis 
Sjogren syndrome 
Thyoiditis 
Nephritis 
UC 
Coombs-positive hemolytic anemia

Increased risk of cirrhosis and cancer

259
Q

Non alcoholic fatty liver disease

A

Hepatic steatosis w/o significant inflammation

Can be diagnosed NONINVASIVE

260
Q

Nonalcoholic steatohepatitis

A

Hepatic steatosis in association with INFLAMMATION, FIBROSIS, hepatocellular injury

Requires biopsy for diagnosis

261
Q

Most common causes

A

Obesity
Diabetes
Hypertriglyceridemia (Insulin resistance)

262
Q

NAFLD has an association with what organ removal

A

Gallbladder

Cholecystectomy

263
Q

Patients with NAFLD complain of what vs NASH

A

NAFLD
ASX

NASH
Fatigue
Malaise
RUQ pain

264
Q

What is the AST ALT ratio in NAFLD

A

Elevated 1:1

W/ mild elevation in ALK PHOS

265
Q

MRI can do what for NAFLD

A

Identify fatty liver but can not distinguish from steatohepatitis

266
Q

Standard approach to assessing the degree of inflammation an d fibrosis in suspected NASH generally not recommended if ASX

A

Percutaneous liver biopsy

267
Q

Treatment of NAFLD

A

Lifestyle changes

Insulin sensitizing agents

268
Q

Who has worse prognosis in NAFLD

A

Elderly

Diabetes

Higher BMI

269
Q

Alcoholic steatosis Fatty liver may have what on physical exam

A

Hepatomegaly

270
Q

Transaminase elevation in alcoholic liver disease

A

2:1 AST : ALT
Elevated GGT
Referral for US and biopsy

271
Q

Treatment of alcoholic steatosis

A

Abstinence

272
Q

Alcoholic steatohepatitis transaminase ratio

A

2:1

273
Q

Other symptoms of alcoholic steatohepatitis

A

Muscle wasting

Abdominal distention and or ascites

274
Q

Lab findings of alcoholic steatohepatitis

A 
AST : ALT greater than or equal to 2:1 
Elevated serum bilirubin 
Elevated GGT 
Elevated INR 
Leukocytosis
275
Q

What should you obtain if you suspect alcoholic steatohepatitis

A

US and biopsy

276
Q

Late stage progressive hepatic fibrosis

A

Cirrhosis

Distortion of the hepatic architecture w/ NODULES

277
Q

Common cause of cirrhosis

A

Chronic viral hepatitis

ALD / NALD

Hemochromatosis

278
Q

What classification of cirrhosis is associated with ETOH

A

Micronodular

279
Q

What drinking habits are more at risk for cirrhosis

A

Chronic alcohol intake (30-50g/day) for more than 10 years

280
Q

The three stages of cirrhosis correlate with what?

A

The thickness of fibrous septa

281
Q

Clinical features of cirrhosis

A

Hepatocyte dysfunction
Portosystemic shunting
Portal hypertension

282
Q

Compensated cirrhosis presents mostly

A

ASX

Non specific symptoms = anorexia, weight loss, fatigue

283
Q

Deocmpensated cirrhosis symptoms

A 
Jaundice 
Pruritus 
Upper GI bleed 
ABD distention = ascites 
Confusion = hepatic encephalopathy
284
Q

The main General systemic manifestations of of cirrhosis

A

Decreased BP (MAP)

285
Q

Hyper dynamic circulation is initiated by what

A

Splanchnic and peripheral vasodilation

HIGH NO

286
Q

What is a put Medusae

A

Abdominal finding of cirrhosis

Umbilical vein opens and blood is shunted through to the abdominal veins centrally

287
Q

Cruveilhier baumgarten murmur

A

Venous hum of Portal HTN patients

Heard with stethoscope on epigastrum

288
Q

Endocrine function decreases in cirrhosis women vs men

A

Women
Chronic anovulation

Men
Gynecomastia

289
Q

HEENT findings in systemic cirrhosis

A

Hepatic Fetor= sweet breathe

Parotid gland enlargement = fatty infiltration edema

290
Q

2 neurological findings of systemic cirrhosis

A

Hepatic encephalopathy

Asterixis

291
Q

Most common cbc finding of early compensated cirrhosis

A

Thrombocytopenia

292
Q

Serum chem of cirrhosis

A

Hyponatremia

293
Q

Hepatic panel in cirrhosis should show what

A 
Increased AST/ALT 
ALK PHOS 
GGT
Bilirubin 
PT

Decreased Albumin

294
Q

What does an EGD help with cirrhosis confirmation

A

Observing esophageal varies and gastropathy

295
Q

Cirrhosis treatment requires what immunizations

A

HAV HBV pneumoccocal vaccines

Flu shot

296
Q

TIPS

A

Diversion of portal blood flow into hepatic vein

Reduces pressure gradient between portal and systemic circulations

Place a shunt!

297
Q

Spontaneous bacterial peritonitis has what abdominal symptom

A

Pain without tenderness

298
Q

Treatment of SBP

A

ADMIT

3rd gen cephalosporin
Ceftriaxone

299
Q

Prophylaxis SBP

A

Once daily ciprofloxacin

OR

TMP-SMX DS

300
Q

Azotemia in the absence of of parenchyma renal injury or disease with reduction in renal perfusion

A

Hepatorenal syndrome

301
Q

Serum creatinine of 1.5 mg/dL or higher is common in what syndrome

A

Hepatomegaly syndrome

302
Q

Oliguria, hyponatremia, and a low urinary sodium concentration are typical features

A

Hepatorenal syndrome

ADMIT TO ICU

303
Q

Systemic build up of ammonia is a compilacation of cirrhosis called

A

Hepatic encephalopathy

304
Q

Treatment of hepatic encephalopathy

A

LActulose = reduction in GI tract absorption

305
Q

What has shown efficacy in improved hepatic encephalopathy

A

Pre/Probiotics

By alteration of intestinal flora

306
Q

Untreated _______________ toxicity results in fulminant hepatitis and painful death syndrome

A

Acetaminophen

307
Q

How can you treat acetaminophen toxicity

A

N-acetylcysteine

308
Q

What can you order to observe normalization of values in toxic liver injury

A

Serial LFT’s

309
Q

Autoimmune destruction of bile ducts and cholestasis is AKA

A

Primary biliary Cholangitis

310
Q

What other autoimmune disorders are associated with primary biliary cholangitis

A

Sjogren syndrome
Autoimmune thyroid disease
Raynaud syndrome
Scleroderma

311
Q

Fatigue
Xanthomas
ASX hepatomegaly

A

Primary biliary cholangitis

312
Q

What symptoms occur later in primary biliary cholangitis

A

Jaundice
Steatorrhea
Portal HTN

313
Q

Lab findings in PBC

A

Cholestatic pattern

INCREASED ALK PHOS
Bilirubin
Transaminase
HIGH LIPIDS

314
Q

What markers of autoimmune diseae are present in PBC

A

Animitochondirla antibodies (AMA)

Antinuclear antibodies (ANA)

315
Q

Treatment for PBC

A

Ursodeoxycholic acid

*slows progression of disease*

Treat pruritis with Bile Salt sequestrants

316
Q

Diagnosis and genetic testing of hemochromatosis

A

Clinical aroun 50 years old

Incidental finding

Elevated AST and ALK PHOS

Elevated plasma iron and ferritin

317
Q

First line treatment and subsequent for hemochromatosis

A

Phlebotomy

Chelation with deferoxamine

Liver transplant

318
Q

Pathognomonic sign of Wilson dz

A

Kayser-Fleischer Rings

319
Q

What copper transport protein is low in Wilson’s disease

A

Serum ceruplasmin

320
Q

Copper Chelation Wilson disease treatment

A

Trientine

Penicillamine

Zinc

321
Q

Test of choice for Budd-Chiari syndome

A

Color Doppler US

322
Q

With budd-chiari syndrome you should suspect

A

Hepatic vein obstruction

323
Q

Progenitor hepatic abscess is

A

Traumatic implantation of bacteria through the abdominal wall

324
Q

Main clinical presentation of Phoenician hepatic abscess

A

Fever

Jaundice

325
Q

What tests are diagnostic for US

A

CT guided percutaneous drainage with culture of aspirate

326
Q

Benign liver neoplasm is AKA

A

Cavernous hemangioma

327
Q

Why do hepatocellular carcinoma pts sometimes have bone pain

A

Metastases

328
Q

What sudden sustained lab findings is indicative of hepatocellular carcinoma

A

Elevation of ALK PHOS

329
Q

Survival rate of HC

A

1 an 5 year survive rates = 23% and 5%

330
Q

What screening is warranted for hepatocellular carcinoma pts

A

Patients with :

1) Cirrhosis
2) Chronic HBV or HCV
3) Family he of HC

Hepatic US and Alpha feta protein level
Evry 6 months

331
Q

Gallstones present

A

ASX but may cause RUQ pain

Intermittent or partial obstruction

Lead to acute cholecystitis

332
Q

Acute attack preceded by a large fatty meal =

A

Acute cholecysitis

333
Q

Clinical presentation of acute cholecystitis

A

Sudden onset of persistent, steady RUQ pain

May radiate to shoulder and to back

Biliary colic that has not resolved after 4-6 hours

Nausea and vomiting frequent
Fever

334
Q

Physical exam findings of Acute Cholecystitis

A

RUQ TTP
Abdominal muscle guarding
Positive Murphy sign

335
Q

CBC reveals leukocytosis
UNCOMMON to have increased serum bilirubin

Elevations of ALK PHOS and AST ALT

NO CHOLESTATIC pattern

Elevated amylase

A

Acute cholecystitis

336
Q

First test for acute cholecystitis

A

RUQ US
Shows gallbladder wall thickening
Sonography Murphy sign

337
Q

Complications of acute cholecystitis (4)

A

Gangrenous cholecystitis
Perforation
Cholecystoenteric fistula
Gallstone Ileus

338
Q

Chronic cholecystitis may result in

A

Porcelain gallbladder

Intramural calcification of the gallbladder

339
Q

Treatment of acute cholecystitis

A

Admission for supportive care

Laparoscopic cholecystectomy

340
Q

Choledocholithiasis

A

Stones in the common bile duct

341
Q

Obstruction in common bile duct may lead to

A

Cholangitis (biliary tract infx)

342
Q

Severe biliary colic
RUQ epigastric pain
N/V
Jaundice

A

Clinical presentation of choledocholithiasis

343
Q

Lab findings of choledocholithiasis

A

Cholestatic pattern

High ALK PHOS and bilirubin and AST ALT

344
Q

Testing of choledocholithiasis

A

RUQ US = FIRST

ERCP = diagnosis and therapy

345
Q

Severe abnormal liver fx ALT level

A

ALT > 15 x normal

346
Q

Moderate abnormal liver fx ALT level

A

ALT 5-15 x higher than normal

347
Q

Mild abnormal liver fx ALT level

A

5 x higher than normal

348
Q

Treatment of choledocholithiasis

A

Refer to GI/Surgery

In general, bile duct stones, even small ones, should be removed, even in an asymptomatic patient

ERCP with stone extraction
Followed by laparoscopic cholecystectomy within 72 hours in patients with cholecystitis and within 2 weeks in those without cholecystitis

349
Q

Complications of choledocholithiasis

A

Ascending cholangitis

Pancreatitis

350
Q

Charcot triad of acute cholangitis symptoms

A

RUQ pain
Fever/Chills
Jaundice

351
Q

Reynolds’s Pentad of acute cholangitis

A

Charcots
Altered mental status
Hypotension

  • Indicates Acute Suppurative Cholangitis
    Surgical emergency!*
352
Q

Acute cholangitis

A

Bacterial infx of biliary tract as a result of obstruction invasion form duodenum

353
Q

Treatment of acute cholangitis

A

Treatment:

Admission
For supportive care and antibiotics

ERCP
For biliary drainage and removal of obstruction

Surgery
Only if ERCP fails or is unavailable
Cholecystectomy follows once infection is cleared
To prevent recurrence

354
Q

Asymptomatic Gallstone

Gallstone + Fever/Pain

Gallstone + Jaundice

Gallstone + Jaundice + Fever

Gallstone + Jaundice + Fever + AMS + Hypotension

A

Cholelithiasis

Cholecystitis

Choledolithiasis

Cholangitis

Supportive Cholangitis

355
Q

Key features to indicate bile duct cancer

A

Painless obstruction

W/ Dilated biliary tree

356
Q

Palpable gallbladder with painless obstructive jaundice is called what and also associated with what

A

Courvoiser sign

Pancreatic cancer

357
Q

When should you consider carcinoma of the biliary tract

A

Cholestatic pattern of biliary obstruction

W/ no explanation

AND

isolated intrahepatic mass on imaging and a normal serum level of alpha-fetoprotein

358
Q

What is the exocrine vs endocrine tissue of the pancreas

A

Acinar and duct tissue [Exocrine]

Islets of Langerhans [Endocrine]

359
Q

Acute pancreatitis is most commonly due to

A

Gallstones and chronic alcohol abuse

360
Q

Cystic fibrosis is a risk factor for what disease

A

Acute pancreatitis

361
Q

How does hyperlipidemia induce pancreatitis

A

Free fatty acids are released from serum tri’s in toxic concentration by pancreatic lipase in pancreatic capillaries

362
Q

Interstitial edema acute pancreatitis

A

Inflammation of pancreatic tissues without necrosis

363
Q

Necrotizing acute pancreatitis

A

Inflamed pancreatic tissues with necrosis

364
Q

Mild acute pancreatitis

A

No organ failure or systemic complications

365
Q

Moderate acute pancreatitis

A

Transient Oran failure or local or systemic complications that revolve within 48 hours

366
Q

Severe acute pancreatitis

A

Persistent organ failure with multiple organ involvement

367
Q

Clinical presentation of acute pancreatitis

A

Bilateral upper quadrant pain
“Boring with radiation to the back”

N/V

368
Q

Physical exam findings of acute pancreatitis (3)

A

Epigastric TTP

Cullens Sign

Grey Turner Sign

369
Q

Cullen sign

A

Edema and bruising around umbilicus

370
Q

Grey turner sign

A

Bruising of the flank with retro peritoneal or intra abdominal bleeding

371
Q

Lab findings in acute pancreatitis

A

Increased serum amylase and lipase

CBC = leukocytosis

CMP = elevated U=BUN

hepatic panel

Elevated CRP

372
Q

Diagnostic test of choose for acute pancreatitis

A

CT scan

373
Q

More points on the ransom criteria =

A

Higher mortality

374
Q

Treatment of acute pancreatitis

A

ERCP for gallstones

375
Q

Conventional pain contrail of mild acute pancreatitis

A

Meperidine (Demerol) = less likely to induce spasm of the sphincter of oddi

376
Q

Treatment of severe acute pancreatitis

A

Admit to ICU

Surgical consult

377
Q

Chronic pancreatitis = what pts?

A

Chronic alcoholics

378
Q

Chronic pancreatitis clinical presentation

A

LUQ

Anorexia

Weight loss

Constipation

Steatorrhea

379
Q

Diagnostic test for chronic pancreatitis

A

Eval of fecal fat

Plain films or CT to eval pancreatic calcification to rule out pancreatic cancer

380
Q

Secretin pancreatic function test

A

Stimulate the pancreas through administration of a meal or hormonal secretagogue

Normal secretory content observed

do this if you have clinical findings but not radiographic findings

381
Q

Chronic pancreatitis treatment measures

A

Non opioid pain control

Pancreatic enzyme supplementation

Low fat diet

REFER TO GI / PANCREATOLOGY

382
Q

Cant digest food , dyspepsia, cramping, bloating, watery diarrhea

Deficient exocrine pancreatic enzymes

A

Exocrine pancreatic insufficiency

383
Q

Most common etiologies of exocrine pancreatic insufficiency

A

Chronic pancreatitis

Cystic fibrosis

384
Q

Clinical presentation of exocrine pancreatic insufficiency

A

Water bulky fouls smelling diarrhea w/ steatorrhea

Weight loss

Abdominal pain bloating and flatulence

385
Q

What lab can eval for exocrine pancreatic insufficiency

A

Fecal elastase

386
Q

Mainstay of management of exocrine pancreatic insufficiency

A

Pancreatic enzyme replacement therapy

387
Q

Clinical presentation of pancreatic cancer

A

Abdominal pain
Jaundice
Weight loss
Vague LUQ pain

Courvoiser sign = nontender palpable gallbladder

388
Q

Lab findings on pancreatic cancer

A

Non specific

+/- amylase / lipase elevation or bilirubin

CA 19-9 = serum tumor marker

389
Q

Imaging study to eval jaundice in pancreatic cancer

A

US

390
Q

Imaging study to eval pain or weight loss in pancreatic cancer

A

Abdominal CT scan

391
Q

Imaging study to eval ducts in pancreatic cancer

A

ERCP

392
Q

Treatment of pancreatic cancer

A

Surgical resection

IPAP Class 21-2 (12 decks)

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