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IPAP 21-2 Soph Semester > GI Test 2 STUDY! > Flashcards

GI Test 2 STUDY! Flashcards

1
Q

What is a polyp and what are the 3 things they can lead to

A

a protuberance extending into the lumen of the colon

Typically asymptomatic, but may lead to
Bleeding (commonly)
Tenesmus
Obstruction

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2
Q

What are the 3 different types of polyps

A

Pedunculated (can get really large)
Flat
Sessile (most common)

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3
Q

What are the 4 major pathological groups of polyps

A

Mucosal Adenomatous (neoplastic)

Mucosal Serrated (neoplastic)

Mucosal Non-Neoplastic

Submucosal Lesions

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4
Q

What are the two types of neoplastic polyps

A

Adenomatous (most common) - malignant potential

Serrated:

  • Hyperplastic, very common, but no sig RSK. Skin tag.
  • Sessile serrated polyps have a similar risk/ greater risk to malignancy as Adenomatous polyps
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5
Q

Non- neoplastic polyps are a low risk for

A

Cancer

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6
Q

What are the mucosal non neoplastic polyps

A

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

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7
Q

What are the Submucosal lesions that have no cancer risk vs the one that does

A

Lipomas, lymphoid aggregates - no clinical significance

Pneumatosis cystoides intestinalis – air filled cysts

Carcinoid tumor - cancer

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8
Q

What polyps have the highest risk for cancer

A

Mucosal non-neoplastic

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

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9
Q

DO name: inherited DO, 100-1000 polyps, by age 15, cancer development is inevitable by age 40-50.

What is the Tx?

A

FAP ( familial Adenomatous polypsosis)

Treatment:
Prophylactic colectomy, typically before age 20
Annual colonoscopy until colectomy

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10
Q

hamartomatous polyps + oral mucocutaneous pigmented macules, increased risk of GI cancer

A

= peutz-jeghers syndrome ( hamartomatous polyposis)

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11
Q

multiple hamartomatous polyps, increased risk of GI cancer

A

Familial Juvenile Polyposis

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12
Q

hamartomatous polyps + lipomas throughout GI tract, increased risk of non-GI cancer

A

Cowdens Dz

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13
Q

Large polyps can cause

A

Bleeding,
GI obstruction
Intussusception

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14
Q

What is Lynch syndrome

A

Hereditary Nonpolyposis Colon Cancer (HNPCC)

Autosomal dominant condition

Increased risk of cancer:
Colorectal
Endometrial
Ovarian
Renal
Vesical
Hepatobiliary
Gastric
Small intestinal

Bethesda Criteria used for screening

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15
Q

What are the RSK FX for Colorectal Cancer

A

Age
-Incidence rises after age 45

Family history
-First degree relatives

Inflammatory Bowel Disease

Dietary and Lifestyle Factors

  • High fat, processed, red meat vs high fiber
  • Physical activity, obesity
  • Smoking
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16
Q

What can you add to your diet to decrease colorectal cancer

A

High fiber diets

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17
Q

What is the most common cause of large bowel obstruction in adults

A

Colorectal Cancer

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18
Q

What is the gold standard screen for colorectal cancer

A

Colonoscopy

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19
Q

What is the most common cause of occult GI bleeding in adults

A

Colorectal cancer

Tests:
FOBT and Iron deficiency anemia

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20
Q

What is the most commonly monitored tumor marker for colorectal cancer and how is it monitored

A

Carcinoembryonic antigen (CEA)

  • NOT a screening test
  • Useful for prognosis after diagnosis
  • Used as marker for recurrence after treatment
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21
Q

What is the test interval for colonoscopy?

For Flexible Sigmoidscopy?

A

Colonoscopy q 10 yrs

Flexible Sigmoidoscopy q 5 yrs

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22
Q

If a polyp is found with flexible sigmoidoscopy then what must be done next

A

Colonoscopy

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23
Q

What is the confirmatory test for colorectal test

A

BIOPSY!

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24
Q

At what age should African American begin getting screened for colon cancer

A

45 yo

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25
Q

What is the preferred cancer detection test

A

Anual FIT for blood

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26
Q

What is the option for pts who don’t want colonoscopy

A

CT Colonography (“virtual colonoscopy”)

Every 5 yrs

Used if colonoscopy not desired or contraindicated
Less sensitive for polyps <1 cm, flat adenomas, and serrated polyps

Requires bowel prep, no sedation

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27
Q

What are the CRC screening recommendations

A

Cancer prevention tests should be ordered first,
Preferred test is colonoscopy q 10 yrs at 45 yo

Cancer detection test- FIT blood test preferred or FIT DNA test

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28
Q

A pt with colon cancer with iron deficiency and weaknesss/ fatigue.. where is the cancer location

A

Right Colon likely

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29
Q

Pt with colon cancer with change in bowel habits, stool streaked with blood, and obstructive S/s ( constipation/ or increased frequency), + colicky abdominal pain

A

Left Colon most likely

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30
Q

Pt with colon cancer with hematochezia, tenesmus, BM urgency and decrease in caliber of stool “ ribbon stool”
Where is the cancer location

A

Rectum likely

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31
Q

What is the general W-up and Tx for colorectal cancer

A 
Work up: 
Fecal occult blood test (FOBT)
Guaiac or FIT
CBC
CMP
UA

Colonoscopy ( gold standard)

Treatment:
Surgical Resection
-Full or partial colectomy
Chemotherapy
Radiotherapy
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32
Q

What are the 5 stages of prognosis for colorectal cancer

A

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

For each stage, rectal cancers have a worse prognosis/ Survival rate ( SR)

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33
Q

What is the 1st line TX for C. Diff colitis

A

Oral Vancomycin

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34
Q

Antibiotic assoc colitis relapses require

A

7 week taper of Vanc

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35
Q

What is Crohns Dz

A

Chronic inflammatory disease

!Transmural process !

Variable locations - may involve the entire GI tract from mouth to anus

Variable severity of inflammation - mild to severe/fulminant disease

Worse in smokers!

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36
Q

What is the characteristic endoscopy finding in crohn Dz

A

Skip lesions

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37
Q

What are the Hallmark S/s of crohns

A 
Abdominal pain
Diarrhea +/- blood
Fatigue
Weight loss
Fever
Growth failure (younger patients)
Anemia
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38
Q

What are the main c/o of patients with Crohns

A

Cramp ab pain, RLQ, diarrhea, Wt loss, Growth delays

Malabsorption leads to Iron Def and B12 def.

Anorectal fístulas and bowel obstruction

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39
Q

What is the def of ileitis

A

SB only (terminal ileum (ileitis) – Crohns

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40
Q

What is ileocolitis

A

SB + colon Crohns

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41
Q

What are the RSKs of Crohns Dz complications

A

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

Ileal, ileocolonic, or proximal GI involvement
Extensive anatomic involvement
Deep ulcerations
Young age at diagnosis
Perianal/severe rectal disease
Penetrating or stenosis on presentation
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42
Q

What is phlegmon

A

walled off inflammatory mass without bacterial infection

may be palpable on physical examination

most often presents as an indolent process, and not as an acute abdomen

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43
Q

Penetration of Crohns Dz can lead to an intra abdominal abcess, which present how?

A

acute presentation of localized peritonitis with fever, abdominal pain and tenderness

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44
Q

What are the 4 common sites for fistula formation in crohns Dz

A

Bladder (enterovesical)
Skin (enterocutaneous)
Small bowel (enteroenteric)
Vagina (enterovaginal)

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45
Q

What complication is associated with fístulas to the retro peritoneum

A

Fistulas to the retroperitoneum may lead to psoas abscesses or ureteral obstruction with hydronephrosis

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46
Q

What are some extra intestinal manifestestions

A

Apthous ulcers, inflammatory skin conditions, Joint pains, MSK pains, Inflammations of the Iris or Uvula, can also effect the gall bladder increasing gall stones

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47
Q

What are the inflammations of the skin with Crohns

A

Pyoderma Gangrenosum and Erthyma Nodosum

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48
Q

Is there a specific lab work up for Crohns

A

NO

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49
Q

What does crohns look like on endoscopy

A

Cobblestoning of the mucosal surface

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50
Q

How is the managment of Crohns tracked

A

Colonoscopy and Endoscopys

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51
Q

How do you evaluate for small bowel involvement in Crohns

A

Capsule endoscopy

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52
Q

What is the DO criteria for Crohns

A

BIOPSY!

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53
Q

What level of Crohns is a pt that Responded to medical or surgical therapy
No current active disease

A

Asymptomatic remission

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54
Q

What level of Crohns is a pt that is Ambulatory, eating/drinking normally
<10% weight loss
No complications, dehydration, systemic toxicity, abdominal tenderness, painful mass
Endoscopy – lesions which are not severe

A

Mild- Moderate Crohns

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55
Q

What is the crohns level for a pt with Failed treatment for mild-moderate disease
Fever, weight loss > 10%, abdominal pain or tenderness, N/V without obstruction, significant anemia.
Endoscopy: Moderate to severely active mucosal disease

A

Moderate to Severe Crohns

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56
Q

What level of crohns is a pt with Significant/extreme weight loss and muscle wasting
Persistent symptoms despite steroids or biologic agents as outpatient
High fever, persistent vomiting, intestinal obstruction, involuntary guarding or rebound tenderness, or evidence of abscess
Endoscopy: Severe mucosal disease

A

Sever/ Fulminant Crohns

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57
Q

What is the Tx approach to Crohns

A

Avoid NSAIDs when possible

  • Often associated with flares
  • Cause damage to small intestine mucosa

Smoking Cessation

Stress Management

Treat Depression and Anxiety

Dietary Therapy

Anti diarrhea: Loperamide and Bile Acid Sequestrants

Oral Steroids for apthous ulcers: Kenalog

Glucocorticoids and Corticosteroids ( MILD or SEVERE)

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58
Q

Tax regimen for Mild to Moderate Crohns

A

isolated to the ileal and proximal colon: budesonide

Flares: predinose

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59
Q

What is the Tx of active Crohns that is moderate to severe

A

Prednisone

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60
Q

Pts who fail to respond to oral steroid therapy for chrons should be considered for…

A

Admission

Admit patient to inpatient ward (Internal Med)
IV Systemic Corticosteroids
bolus prior to starting infusion of infliximab
IV prednisone 40-60mg per day

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61
Q

What are the maintenance remission therapy drugs for Crohns Dz

A

Azathioprine
6-Mercaptopurine
Methotrexate

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62
Q

If immunomodualators do not work for Crohns what is the next step

A 
1st steroids 
Then immunmodulators 
Then TNFS like : 
Infliximab (Remicade)
Adalimumab (Humira)
Certolizumab (Cimiza)
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63
Q

What are the surgical indications for Crohns Dz

A

Resection of a segment of diseased intestine - most common indication

Penetrating disease - second most common

Recurrent intestinal obstruction

Abscess formation

Complex perianal fistula

SURGERY IS NOT THE 1st LINE

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64
Q

What is the admission criteria for Crohns Dz

A

Suspected intestinal obstruction

Suspected intra-abdominal or perirectal abscess

Serious infectious complication
-especially in patients who are immunocompromised due to concomitant use of corticosteroids, immunomodulators, or anti-TNF agents.

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

Severe or persisting symptoms despite treatment with corticosteroids

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65
Q

If a pt has mild or moderate chrons, what is the pharm approach

A

Short-term use if disease is confined to terminal ileum and right colon, since medication is formulated to be released in this area

-Budesonide

If the pt has flares: Prednisone

If the pt is high RSK: Sulasalazine

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66
Q

What is the difference of Crohns vs UC

A

Crohns: transdural

UC: Involves the mucosal surface of the colon, resulting in diffuse friability and erosions with bleeding

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67
Q

What are the Montreal classifications of UC

A
  • proctitis
  • left sided colitis
  • extensive colitis
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68
Q

Where does UC start and where does it progress

A

Starts in the rectum and advances proximally

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69
Q

What is the hallmark sign of UC

A 
Blood diarrhea (hallmark)
Rectal bleeding
Cramps
Abdominal pain
Fecal urgency
Tenesmus
Extraintestinal symptoms
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70
Q

A patient with 4 or less BM/ Day, WIth episodes of constipation, mild abdominal pain, and no signs of Systemic Dz, what severity UC

A

Mild

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71
Q

A pt with more than 4 BM/ day, abdominal pain and may be anemic from bloody stools, what severity of UC

A

Moderate

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72
Q

A pt with 6 or more BM/day, sever ab pain , systemic fever, anemia, elevated ESR and CRP, may have wt loss is what severity UC

A

Severe

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73
Q

What is the DOC for UC

A

Topical Mesalamine ( suppository or enema)

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74
Q

If no improvement at 4 weeks with mesalamine in UC, what drug can be added

A

Prednisone

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75
Q

In Severe colitis what is the 1st line

A

Oral corticosteroid x 14 days, consider adding anti-TNF

infliximab, adalimumab, or golimumab

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76
Q

What is the Tx option for moderate to severe ulcerative colitis in patients who have not responded, lost response, or been intolerant of other therapies

A

Vedolizumab ( Anti-integrity)

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77
Q

What is the approach to sever or Fulminant Colitis

A

Inpatient care

Surgical consultation early

NPO

Parenteral fluid/electrolyte replacement

IV corticosteroids

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78
Q

What is the maintenance Tx for UC

A

Oral Mesalamine

> 2 relapses a year:

Mercaptopurine or Azathioprine

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79
Q

What are the screening recommendations for UC

A

Colonoscopy with biopsies every 1-2 years, beginning 8 years after diagnosis

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80
Q

What are the absolute and relative surgical indications for UC

A

Absolute:
Severe hemorrhage
Perforation
Carcinoma

Relative:
Severe colitis unresponsive to maximal medical therapy
Less severe colitis but medically intractable symptoms or intolerable medication side effects

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81
Q

A pt with UC and rapid progression of S/s, with worsening ab pain, Distention, High fever and tachycardia, has what severity of UC

A

Fulminant

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82
Q

What is the characteristic pattern of microscopic colitis

A

Chronic water diarrhea, with every other cause R/o

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83
Q

What are the two subtypes of microscopic colitis

A

Lymphocytic colitis – Lymphocytic colitis is characterized by an intraepithelial lymphocytic infiltrate

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

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84
Q

Who is at most RSK for microscopic colitis

A

Women

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85
Q

What is the clinical presentation of Microscopic colitis

A

Chronic, non-bloody diarrhea that is typically watery
between four and nine watery stools per day

Abdominal pain

May also experience:
Fatigue, dehydration, weight loss

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86
Q

If diarheaa persists with microscopic colitis what is the DOC

A

Budesonide

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87
Q

What is IBS

A

Function Bowel DO

Absence of organic Cause

DO of exclusion

Idiopathic

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88
Q

What is the hallmark presentation of IBS

A 
Ab pain (often lower ab)  assoc w/ altered BM habits (Constipation/ Diarrhea) .
 Pain often relieved with defecation.
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89
Q

What is IBS-C

A

Constipation predominant

Patients typically report ≤ 3 BM/week, with straining

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90
Q

What is IBS-D

A

Diarrhea predominant

Patients typically report ≥ 3 BM/day, with urgency or fecal incontinence

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91
Q

What is the DO for IBS

A

≥ 3 months of abdominal pain or discomfort and altered bowel habits

AND

The abdominal pain is associated with 2/3 of the following

  • Relieved with defecation
  • Onset associated with change in defecation frequency
  • Onset associated with change in stool appearance
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92
Q

Pts with IBS should avoid what foods

A

Avoid sorbitol and fructose, gas producing foods, and cruciferous vegetables.

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93
Q

What should a IBS pt be recommended for Diet

A

Low fat, High fiber, unprocessed food diet

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94
Q

What diet modifications can be tried specifically with IBS-D

A

Trial of lactose elimination

Trial of gluten elimination

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95
Q

What diet modifications can be tried specifically with IBS-C

A

increase fiber, increase fluids

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96
Q

What is the 1st line Tx for IBS

A

Dietary and Lifesytle mods

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97
Q

Dicyclomine and Hyosyncamine are what agents

A

Antispasmodic

My help with pain and bloating in IBS

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5
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98
Q

What are lubiprostone and linaclotide

A

Anticonstipation medications

Osmotic laxatives- use first

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99
Q

What is in a normal LFT

A 
Alanine aminotransferase (ALT)
Aspartate aminotransferase (AST)
Alkaline Phosphatase
Total Protein
Bilirubin
Albumin
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100
Q

What is a hepatocellular pattern on LFT

A

Elevated AST and ALT compared to ALP ,

Says that the damage is in the hepatocytes

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101
Q

What does a 2:1 elevation in AST:ALT indicate

A

Alcohol related liver disease

Particularly in light of a elevated GGT

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102
Q

What does GGT tell you

A

Elevated GGT levels can be observed in a variety of nonhepatic diseases, including chronic obstructive pulmonary disease and renal failure

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103
Q

What does a cholestatic pattern on LFT tell you

A

Elevated ALK PHOS (ALP)

Says a stoppage of the flow ( cholestasis)

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104
Q

What is the pressure gradient between the portal vein and IVC that causes Portal HTN

A

Greater than 10 mmHg

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105
Q

What is the most common etiology of portal HTN

A

Cirrhosis

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106
Q

When is Jaundice clinically apparent

A

> 2 mg/dl appears first in the conjunctiva

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107
Q

Jaundice caused by unconjugated bilirubin is due to

A

overproduction of bilirubin

  • Hemolytic anemias
  • Hemolytic reactions
  • Hematoma
  • Pulmonary infarction

impaired bilirubin uptake by the liver

  • Posthepatitis hyperbilirubinemia
  • Gilbert syndrome
  • Crigler-Najjar syndrome
  • Drug reactions

abnormalities of bilirubin conjugation

108
Q

What does elevation of unconjugated and conjugated bilirubin tell you

A

hepatocellular disease
impaired canalicular excretion of bilirubin
biliary obstruction

Often referred to as conjugated hyperbilirubinemia, even though both fractions of bilirubin are elevated.

109
Q

What can cause conjugated hyperbilirubinemia

A 
Hepatocellular dysfunction
Hepatitis, cirrhosis
Biliary obstruction
Choledocholithiasis, biliary atresia, carcinoma
Hereditary cholestatic syndromes
110
Q

A pt with Normal stool and urine color
No bilirubin in urine
Splenomegaly if etiology is hemolytic disorder
And mild jaundice has what kind of bilirubin problem

A

Unconjugated

111
Q

A pt with jaundice, malaise, anorexia
low-grade fever, right upper quadrant discomfort
dark urine, amenorrhea
enlarged tender liver, spider telangiectasias, palmar erythema
ascites
gynecomastia

Has what kind of bilirubin problem

A

Conjugated

112
Q 
A pt with jaundice 
right upper quadrant pain
weight loss (suggesting carcinoma)
pruritus
dark urine
light-colored stools(acholic stools)
A

Biliary obstruction, Conjugatged

113
Q

What is the W-up for Jaundice

A

Lab studies:

  • Hepatic labs
  • CBC, CMP, UA

Radiographs
-Hepatic ultrasound

ERCP to evaluate bile ducts
-If obstruction is suspected

114
Q

What is an ERCP

A

An endoscopic technique in which a specialized side-viewing upper endoscope is guided into the duodenum, allowing for instruments to be passed into the bile and pancreatic ducts

Indicated in jaundiced patient suspected of having biliary obstruction.

115
Q

What is the most common cause of acute liver failure

A

Acetaminophen

116
Q

What is the INR in acute liver failure

A

> 1.5

117
Q

A pt with INR > 1.5, elevated Aminotranferease, elevated bilirubin and ALP, low platelet count, elevated ammonia, elevated amylase and lipase, elevated BUN and Cr

A

Acute liver failure

118
Q

What is the Tx approach to ALI

A

Acute liver injury/ failure

Admission for inpatient management
IV fluid and electrolyte replacement
Dietary monitoring
Gastroprotective measures (prevention of stress gastropathy)
IV PPI or H2
Other treatments as indicated based on etiology

119
Q

What are the 4 phases of hepatitis

A

Viral replication
Prodromal
Icteric
Convalescent

120
Q

What is phase 1 hepatitis

A

Phase 1 (viral replication phase)
Patients are asymptomatic during this phase
Laboratory studies demonstrate serologic and enzyme markers of hepatitis

121
Q

What is phase 2 hepatitis

A 
Phase 2 (prodromal phase)
Anorexia, nausea, vomiting
Arthralgias, malaise, fatigue
Urticaria, pruritus
Alterations in taste
Development of an aversion to cigarette smoke
122
Q

What is phase 3 hepatitis

A 
Phase 3 (icteric phase)
Predominant gastrointestinal symptoms
Jaundice
Dark urine, followed by pale-colored stools
Malaise
May develop RUQ pain with hepatomegaly
123
Q

What is phase 4 hepatitis

A 
Phase 4 (convalescent phase)
Symptoms and jaundice resolve
Liver enzymes return to normal
124
Q

What is the transmission and incubation period for HepA

A

Fecal oral

30 day incubation

Viral shedding in feces for up to 2 weeks prior to onset of S/s

125
Q 
A pt with Malaise, myalgia, arthralgia
Easy fatigability
Upper respiratory symptoms
Nausea & vomiting
Anorexia
Smokers develop distaste for cigarettes*
Low grade fever
Fever breaks - onset of jaundice (after 5-10 days)

What type of hepatitis

A

A

126
Q

What lab marker is elevated in acute Hep A

A

IgM anti HAV in acute

IgG HAV Ab in chronic

127
Q

What is the Tx approach to Acute Hep A

A 
Bed rest if needed
Symptomatic care
Antiemetic, antidiarrheal
Fluids regular meals
Avoid strenuous exercise or work
NO ALCOHOL OR HEPATOTOXIC MEDS
128
Q

What is the mode of transmission of Acute Hep B

A

Inoculation of infected blood or blood products

Sexual contact
-Virus present in saliva, semen, and vaginal secretions

HBsAg positive mothers may transmit to newborn during delivery

129
Q

What groups are at high risk for Acute Hep B

A

Healthcare workers
-Including staff at hemodialysis centers
IV drug users
Prisoners

130
Q

incubation period for Acute Hep B

A

6weeks to 6 months ave. 12-14 weeks

131
Q

What are the S/s and Lab findings for Acute Hep B (sub clinical, icteric, fulminant)

A

Sub clinical: malaise, arthalgia, fatigue, URI, N/V abdominal pain, anorexia, decreased desire to smoke

Icteric: Jaundince

Fulminant: Acute hepatic failure, encephalopathy, coagulapathy, jaundice, edema, ascites

LABS:

HB surface antigen, surface antibody, and core antibody

132
Q

A pt presents with a Postive HBsAg and negative Anti-HBs, their AntiHBc is IgM, what is their phase of HEPB infx

A

Acute hepatitis B

133
Q

A pt has negative HBsAG and positive antiHBs, the antiHBc is IgG, and both HBeAg and AntiHbe is negative,

What level of Hepatitis B do they have

A

Recovery/ resolved Hep B

note the HBsAG is negative, the Ig is IgG, which is long term

134
Q

What is the serologic hallmark of acute HBV infx

A

HBsAg

135
Q

When does anti-HBs appear

A

appears in most individuals after clearance of HBsAg and after successful vaccination against hepatitis B

136
Q

What does HBeAg

A

a secretory protein that is processed from the pre-core protein
indicates viral replication and infectivity

Persistence of HBeAg beyond 3 months indicates increased likelihood of chronic HBV

137
Q

How long does Anti-HBc persist for

A

For life

138
Q

What is the best way to determine viral replication of HEP B

A

HBV DNA

139
Q

What is the managment of acute HEPB

A

Supportive care

140
Q

What is tx for chronic HBV

A

Antiviral therapy, for pts with severe s/s, marked jaundice, inflammation of the liver, elevated ALT,

Rx: entecavir, tenofovir

141
Q

When can Tx be stopped for HBV

A

After two confirmed consecutive tests four weeks apart that the pt is cleared for HBsAG

142
Q

What are the modes of infx for Hep C

A

50% by injection drug use
Transfusion of infected blood
Body piercing, tattoos, hemodialysis
STI and Maternal transmission possible

143
Q

What is the incubation period for Hep C

A

6-7 weeks

144
Q

What are the S/s of hep C

A

Waxing and waning of AST/ALT

Fatigue, N, RUQ pain, Jaundince, dark urine, clay colored stools

145
Q

What are the screening and confirmatory test for HCV

A

Screen: HCV antibodies, with increased LFTs

Confirm: HCV RNA,

146
Q

What is the managment approach to HepC

A

Some can spontaneously recover,

PCR-RNA determines approach to Tx, Antivirals are the DOC

Ledipasvir- Sofosbuvir
Elbasvir- grazoprevir
(Drugs that end in vir)

Older regimen: Interferion or Ribavirin

147
Q

What is the prognosis of Hep C

A

Cirrhosis, Carnicoma of the liver, and liver failure

148
Q

What is the transmission of Hep D

A

Coinfection with Hep B, primarily parenteral

149
Q

What is the most common acute hepatitis world wide

A

Hep E

150
Q

What defines chronic viral hepatitis

A

Infection with HBV (+/- HDV) or HCV for greater than 3 months

Persistently elevated AST/ALT

Persistent presence of:
HBsAG and anti-HBc
anti-HCV

Or histologic findings on liver biopsy

151
Q

What is the antiviral regiment for chronic Hepatitis

A

Nucleoside or Nucleoside Analog
-entecavir, tenofovir, lamivudine, adefovir, telbivudine

Pegylated interferon

152
Q

What is autoimmune hepatitis

A

Form of chronic hepatitis due to autoantibodies

Much more common in women

Varying clinical presentation
-Some patients discovered incidentally

153
Q

What is NAFLD

A

Non alcoholic non fatty liver dz

Etiology: obesity, hyperlipidemia, glucocorticoid use, DM

Two types: fatty liver or steatohepatitis

154
Q

What is the most accurate test for NAFLD

A

Biopsy, microvesicular fatty deposits similar to alcoholic liver disease without the history of heavy alcohol consumption

155
Q

How is NAFLD usually discovered

A

Patients with NAFLD usually discovered because of elevated transaminase levels

Or incidental finding of hepatic steatosis on abdominal imaging ordered for another reason

156
Q

Lab findings in NAFLD

A

Lab findings:

  • Elevated transaminases
  • 1:1 AST:ALT ratio
  • Elevated ALK PHOS

Hepatic ultrasonography & biopsy
-Evidence of steatosis

157
Q

What is steatosis

A

Fatty liver dz

158
Q

What are the two subdivisions of NAFLD

A

Non-alcoholic Fatty Liver (NAFL)

Non-alcoholic Steatohepatitis (NASH)

159
Q

What is required to differentiate into NASH and NAFL

A

Liver biopsy

160
Q

Define NAFLD vs NASH

A

NAFL:
Hepatic steatosis without significant inflammation, hepatocellular injury, or fibrosis
Minimal risk of progression to cirrhosis
Can be diagnosed noninvasively (labs, imaging)

NASH:
Hepatic steatosis in association with inflammation and hepatocellular injury (ballooning hepatocytes), with or without fibrosis
Can progress to cirrhosis and liver failure
Requires biopsy for histologic confirmation

161
Q

Fever with ascites indicate

A

Bacterial peritonitis

162
Q

How does SAAG relate to ascites

A

(serum albumin) – (ascitic fluid albumin)

1.1 g/dL or higher : portal hypertension

Less than 1.1 g/dL : other cause

163
Q

What is a Transjugular Intrahepatic Portosystemic Shunt (TIPS)

A

Insertion of an expandable metal stent between a branch of the hepatic vein and the portal vein over a catheter inserted via the internal jugular vein

For treatment of portal hypertension as an etiology of ascites

164
Q

Most common agents of bacterial peritonitis

A 
E coli
Klebsiella pneumonia
Streptococcus pneumonia
viridans streptococci
Enterococcus species
165
Q

What is the Most important lab test is evaluation of ascitic fluid via paracentesis of the abdomen

A

Gram stain and culture

Cell count with differential

166
Q

What image study should be ordered If secondary bacterial peritonitis is suspected

A

Abdominal CT

167
Q

Tax approach to Bacterial peritonitis

A

Treatment: ADMIT
Empiric – IV 3rd generation cephalosporin
Ceftriaxone (Rocephin)
Specific treatment guided by culture and stain results

168
Q

Prophylaxis for bacterial peritonitis

A

Once-daily ciprofloxacin or TMP-SMX DS

Reduces rate of recurrence to < 20%

169
Q

What is Hepatorenal syndrome in cirrhosis

A

Occurs in 10% of patients with advanced cirrhosis

Represents the end-stage of a sequence of reductions in renal perfusion induced by increasingly severe hepatic injury

Prognosis is poor once this develops

Characterized by azotemia in the absence of parenchymal renal injury or disease

Serum creatinine of 1.5 mg/dL or higher

170
Q

What is hepatic encephalopathy

A

Neuropsychiatric abnormalities seen in patients with liver dysfunction
develops in 30 - 45% of patients with cirrhosis
Systemic build up of ammonia
Due to hepatocellular dysfunction and lack of hepatic ammonia clearance

171
Q

What are the two types of toxic liver injury

A

Direct hepatotoxicity (predictable):
Dose related severity
Latent period after exposure
Universal susceptibility

Idiosyncratic reaction:
Unpredictable and not dose related

172
Q

What is the Tx for acetaminophen liver injury

A

Treatment with N-acetylcysteine

173
Q

What is Rumack-Matthew Nomogram

A

Predictable, dose-related pattern and progression of injury seen on a graph for acetaminophen injury/ toxin

174
Q

What are the S/s of primary biliary cholangitis

A

Many asymptomatic at diagnosis

Diagnosis detected by hepatic panel abnormalities

Asymptomatic hepatomegaly

Vague, non-specific symptoms early

Fatigue is usual first symptom

Pruritus

Xanthamatous lesions of the skin or tendons

Jaundice, steatorrhea, portal HTN later

175
Q

What is the most signifigant lab test in Primary Biliary Cholangitis

A

Antimitochondrial antibodies (AMA) present in 95%

176
Q

What is the Tx approach to Primary Biliary Cholangitis

A

First rule out other etiologies of biliary tract obstruction
Carcinoma, cholangitis

Ursodeoxycholic acid

FDA approved pharmacotherapy for PBC

Slows progression of disease

Symptomatic treatment for pruritis

Bile salt sequestrants

Likely progression to liver transplantation

177
Q

What is hemochromatosis

A

Autosomal recessive disorder

Results in accumulation of iron as hemosiderin in the liver, pancreas, heart, adrenals, testes, pituitary, and kidneys
Hemosiderin – intracellular iron storage complex

May lead to cirrhosis and/or hepatic failure
Higher risk if high ETOH intake

178
Q

What are the S/s of hemochromatosis

A

Typical clinical onset after age 50

Diagnosis usually made earlier
Found incidentally on routine lab abnormalities
-Elevations in AST and ALK PHOS
-Elevated plasma iron and elevated serum ferritin

179
Q

What is the Tx goal of hemochromatosis

A

Treatment goal is to remove excess iron to prevent end-organ dysfunction and related complications

Treatment measures include:

  • Therapeutic phlebotomy – first line
  • Chelation with deferoxamine – for secondary iron overload or if phlebotomy ineffective/poorly tolerated
  • Liver transplant for advanced disease (cirrhosis or hepatocellular carcinoma)
180
Q

What is the 1st live Tx for hemochromatosis

A

Therapeutic phlebotomy

181
Q

What is the pathological sign for Wilsons Dz

A

Pathognomonic sign – Kayser-Fleischer Rings

Brownish or greenish ring at the corneo-scleral junction

182
Q

What are the lab findings in Wilson Dz

A

Low serum ceruloplasmin
High Urinary excretion of copper ( >40mcg/24hrs)
High copper concentration in the liver biopsy

183
Q

What is the Tx for Wilson Dz

A

Chelation

Trientine (triethylenetetramine)
Penicillamine
Zinc (Inhibits intestinal copper absorption)

Refer to GI and Neuro

184
Q

What is the most common cause of Portal HTN in a child

A

BuDD-Chiari syndrome

185
Q

What is Budd-chiari syndrome

A

Hepatic Venous Outflow Tract Obstruction
-Results in post-hepatic portal HTN

Primary Budd-Chiari:
-Obstruction due to a predominantly venous process (thrombosis or phlebitis)

Secondary Budd-Chiari:
-Compression or invasion of the hepatic veins and/or the inferior vena cava by a lesion that originates outside of the vein (eg, a malignancy)

186
Q

What is the study of choice for Budd-chiari syndorme

A

Color Doppler ultrasound

187
Q

What is the clinical presentation of Pyogenic Hepatic Abcess

A 
Fever
RUQ pain & TTP
Jaundice
Nausea, vomiting
Anorexia, weight loss, malaise

Laboratory Findings:
Leukocytosis on CBC
Positive blood cultures
Nonspecific abnormalities on hepatic panel

188
Q

What is the most common cause of hepatocellulr carcinoma

A

Cirrhosis

189
Q

A pt with Leukocytosis on CBC
Sudden & sustained elevation of ALK PHOS
Increase in alpha-fetoprotein indicates what liver problem

A

Hepatocellular carcinoma

190
Q

What pts should we screen for hepatocellular carcinoma

A 
Recommended for patients:
With cirrhosis
With chronic HBV or HCV
Family history of HCC
Hepatic ultrasound and Alpha-fetoprotein level 
Every 6 months
191
Q

Does cholelithiais effect men or women more

A

Women

192
Q

What are the 5 Fs of cholelithiasis

A 
Fat
Fair
Forty
Fertile (female) 
Flatulent
193
Q

What are the two signs that present with acute cholecystitis

A

Murphys sign, and Boas sign

194
Q

What is the physical exam presentation of Acute cholecystisis

A

Physical Exam:
Ill appearing patient, lying still on the exam table
RUQ TTP
Abdominal muscle guarding
Positive Murphy’s Sign
Jaundice is UNCOMMON
-Should raise suspicion for more serious process

195
Q

What are the Lab findings in Acute Cholecystitis

A 
CBC reveals leukocytosis
Increase in serum bilirubin is UNCOMMON
-Should raise suspicion for more serious process
Elevations of ALK PHOS and AST/ALT
-Non-specific elevations
-Should NOT reveal a cholestatic pattern
Modest elevation of amylase
196
Q

What are the common complications of acute cholecystitis

A

Gangrenous cholecystitis

  • Most common complication in diabetics or elderly
  • Presents with sepsis in addition to common symptoms

Perforation – common complication of gangrene

Cholecystoenteric fistula

Gallstone ileus
-Result of gallstone passing through a fistula – usually in the terminal ileum

197
Q

What are the S/s of chledocholithiasis and key lab findings

A

Severe biliary colic
RUQ or epigastric pain
Nausea and vomiting
Jaundice (may be intermittent – during attacks)

Cholestatic pattern of hepatic panel
-Higher elevations of ALK PHOS and bilirubin, than of AST/ALT

198
Q

What is a hepatocellular pattern

A

ALT or AST> ALP

199
Q

What is the cholestatic pattern

A

ALP> ALT or AST

200
Q

What is the Tx approach to Choldochlithiaisis

A

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

201
Q

What is Charcot triad

A

RUQ Pain
Fever/Chills
Jaundice

Acute cholangitis

202
Q

What is Reynolds Pentad and what does it indicate

A 
RUQ Pain
Fever/Chills (rigors)
Jaundice
Altered Mental Status
Hypotension

Indicates Acute Suppurative Cholangitis
Surgical emergency!

203
Q

What does C-reactive protein indicate

A

Levels of inflammation

204
Q

What is the Tx approach to Acute Cholangitis

A

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

205
Q

What is primary sclerosing Cholangitis

A

Increased immune response to intestinal endotoxins
-Results in diffuse inflammation of the biliary tract with fibrosis and stricture formation

Strong association with IBD
UC > Crohn

Presents as progressive obstructive jaundice
With fatigue, pruritus, anorexia, and indigestion

206
Q

What is the med term for asymptomatic gallstone

A

Cholelithiasis

207
Q

What is the med term for gallstone +fever/ pain

A

Cholecystitis

208
Q

What is the med term for a gallstone lodged causing jaundice

A

Choledocolithisais

209
Q

What is the med term for gallstone+ jaundice+ fever

A

Cholangitis

210
Q

What is the med term for a gall stone+ jaundice + fever + AMS+ HOTN

A

Suppurations cholangitis ( Reynolds triad)

211
Q

Who is most likely to present with Primary Sclerosing Cholangitis

A

A pt with ulcerative colitis

212
Q

What is courvoisier sign

A

Palpable gallbladder with painless obstructive jaundice
Also associated with pancreatic cancer

Indication of cholangiocarcinoma

213
Q

In a pt with s/s of biliary obstruction without an explanation ( no stones, no lesions) what should you suspect

A

Carcinoma of the Biliary Tract

214
Q

What are the specific lab findings in acute pancreatitis

A

↑↑Serum amylase and lipase (3x upper limit)
-Lipase increases earlier, remains elevated longer & has higher sensitivity for pancreatitis

CBC – Leukocytosis

CMP:
-Elevated BUN

Hepatic Panel
-Elevated ALK PHOS & Bilirubin

Elevated CRP – marker of inflammation

215
Q

What is the Radiograph of choice for Acute pancreatitis

A

CT scan

216
Q

What is the Tx for Acute Pancreatitis

A

Clear any obstructions with ERCP

Pancreatic rest- NPO
Bed rest
IV fluids

Pain control- meperidne >morphine ( causes less Oddi spasm)

217
Q

What is the Tx approach for severe Pancreatitis

A

Admission to ICU
Surgical consult
IV fluids and Monitoring
ABX

218
Q

What is the clinical presentation of chronic pancreatitis

A 
Recurrent episodes of LUQ and epigastric pain
Attacks may last hours to days
Anorexia & weight loss
Nausea & vomiting
Constipation
Flatulence
Steatorrhea!!!
219
Q

What is the DO testing for chronic pancreatitis

A

Eval fecal fat
Calcification on CT scans

Must R/o Pancreatic Cancer

220
Q

Tax approach to chronic pancreatitis

A 
Referral to GI/Pancreatology
Low fat diet
NO ETOH!! ( most common cause) 
Non-opioid pain control
Pancreatic enzyme supplementation
221
Q

What are the C/c of exocrine pancreatic insufficiency

A

Patients complain of dyspepsia, abdominal cramping bloating with flatulence, and watery diarrhea, may also complain about steatorrhea ( due to lack of lipase)

222
Q

What are the two most common etiológicos of exocrine pancreatic insufficiency

A

Chronic pancreatitis and cystitis fibrosis

223
Q

Steatorrhea is almost always associated with

A

Pancreatic DO

224
Q

What is the management approach to Exocrine pancreatic insufficiency

A

Enzyme replacement therapy

225
Q

A pt with abdominal pain, jaundice, Wt loss, LUQ pain, with a non tender- palpable gall bladder, is a 50 year old male, DM and smoker… what should you think

A

Pancreatic Cancer

226
Q

What is the serum tumor marker for Pancreatic Cancer

A

CA19-9

227
Q

Where does Diverticular dz most present

A

On the Left side of the abdomen, Left descending colon

228
Q

Where do most colon cancers occur

A

On the left side of the abdomen, Left descending colon

229
Q

What is the Gold standard of Colon imagining

A

Colonoscopy

230
Q

If a patient refuses a colonoscopy, what imaging method can you use

A

Virtual Colonoscopy

231
Q

True colitis is nearly always a result of infection with….

A

C. Diff

232
Q

A pt with watery, greening, foul smelling, mucus like diarrhea, with abdominal cramping and WBC < 15, 000 has what level of colitis

A

Mild- Moderate

233
Q

What are the DO criteria for Severe Colitis

A

Profuse Diarrhea, fever > 101.3, Hypoalbuminemia <3 g/ dl

And either Abdominal Pain (TTP) or Luekoctosis > 15, 000

234
Q

What defines Fulminant Collitis

A

HOTN, Fever >101.3, End organ failure, Ileus, WBC > 35, 000

235
Q

What is the SOC for ABX Colitis

A

PCR,

Then EIAs determine active or chronic

236
Q

What is the perferred imaging for ABX colitis

A

Abdominal CT, looking for the Thumbprinting

237
Q

What is the Tx approach to ABX assoc Colitis

A

Admit, Isolation, Correct fluid imbalances

MILD:
Metronidazole (cheaper) or Vancomycin (668 dollars)

Severe: Vancomycin

Fulminant: PO Vanc+ IV Metro+ PR Vanc (in 500 ml of NS enema)
(and early surgical consultation)

238
Q

What is the measurements for toxic vs megacolon

A

Megacolon is larger than 6 cm

239
Q

What is the DO criteria for Toxic Megacolon

A

Dilation of 6 cm

Plus Fever, Pulse >120, Luekocytosis > 10.5, Anemia

Plus: dehydration or AMS or Electrolyte Abnormal, or HOTN

240
Q

Tx for Toxic megacolon

A

Bowel rest, IV fluids, Tx the toxemia, and surgical consult

241
Q

What is a diverticulum

A

A sac like protrusion of the colonic wall

242
Q

What is the diet recommendation for Diverticulum

A

High fiber and fluids

243
Q

Pts with active diverticular bleeding need what approach

A

Resus and Stabilize, then endoscopy

Without bleeding: referral for scope

244
Q

How does a typical diverticulitis pt present

A

Abdominal Pain in the LLQ, Fever, N/V

245
Q

What is present of physical exam of diverticulitis

A

LLQ TTP, LLQ mass, Fever

Luekocytosis. , +/- occult blood

246
Q

What is the imaging of choice for diverticulitis

A

Abdominal CT!

247
Q

What is the managment approach to Diverticulitis

A

Conservative Managment :

Metronidazole plus Ciprofloxacin ( or TMP-SMX)

Alternative: Augmentin

X 7-10 days BID

Clear Liquid Diet

Severe managment:

Admit and Treat impatient

NPO, Broad spec ABX, Fluids, PAIN managment, Surgery Consult

248
Q

What are the common complications of diverticulitis and what is the managment

A

Per formation, Abscess, Fistualsa, or obstruction

Order a CT scan

249
Q

What is Olivies Syndrome

A

Acute colonic psuedo obstruction

250
Q

What is the most common site for a vulvulus

A

In the sigmoid colon

251
Q

What is the Tx approach to sigmoid volvulus

A

Detorsion with flexible sigmoidscopy

252
Q

What does an apple core lesion on Imaging suggest

A

Colorectal Cancer

253
Q

What are sinus tracts in Crohns Dz

A

Transmural bowel Inflamation is associated with the development of sinus tracts with Crohn’s disease

254
Q

What is perianal dz in Crohns dz

A

Large painful tags, anal fissures, and Perianal abscesses

255
Q

What are the lab findings in Crohns

A

Anemia, elevated platelets
Malnutrition

Inflammation
Fecal blood

256
Q

What drug should be used in high risk ASA Crohns dz pts

A

Sulfaslazine

257
Q

Which has more fístulas? Crohns or UC

A

Crohns

258
Q

What is the most common indication in the US for liver transplant

A

Chronic Hep C that progresses to cirrhosis and liver failure

259
Q

A pt with 2:1 elevation of AST/ ALT with a elevated GGT is what

A

Alcoholic fatty liver

260
Q

What endocrine s/s develop with sirrhosis

A

Amenorrhea and Gynomastica

261
Q

Lab findings in cirrhosis

A

Thrombocytopenia
Anemia
Luekocytosis or luekopenia
With evidence of renal failure Increase BUN, Cr

Elevated AST ALT

262
Q

S/s of hepatic encephalopathy

A 
Inversion of sleep wake cycle 
Personality changes 
Tremor, 
Somnolent
Slurred speech 
Agitation 
Confusion 
Coma
263
Q

What is azotemia

A

Characteristic finding in cirrhosis ( hepatorenal syndrome)

Serum Cr > 1.5

264
Q

Tx for hepatic encephalopathy

A

Admission and lactulose

265
Q

Tx for Primary Biliray cholangitis

A

Ursodeoxycholic acid

And bile salt sequestratnts

266
Q

Xanthomas are an indication of

A

Primary Biliary Cholangitis

267
Q

What is Ranson Criteria

A

A point system for severity of pancreatitis

IPAP 21-2 Soph Semester (20 decks)

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