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GI/Hepatic > PUD > Flashcards

PUD Flashcards

1
Q

Etiologies of PUD

A

H pylori
NSAID induced
Stress ulcers

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2
Q

Site for H pylori induced PUD

A

Duodenum > stomach

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3
Q

Site for NSAID induced PUD

A

Stomach > duodenum

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4
Q

Site for stress induced PUD?

A

Stomach > duodenum

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5
Q

What are the sx of h. pylori

A

Epigastric pain common

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6
Q

What are the sx of NSAID/stress induced PUD?

A

Asymptomatic

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7
Q

H pylori ulcer depth

A

Superficial

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8
Q

NSAID induced ulcer depth

A

Deep

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9
Q

Duodenal ulcer time for pain

A

Worse at night

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10
Q

How does food affect duodenal ulcer

A

Relieved by food

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11
Q

How does food affect gastric ulcers

A

Made worse by eating

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12
Q

Associated sx of PUD

A

Heartburn, belching, nausea, bloating and anorexia

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13
Q

Nationalities most affected by H pylori

A

Africans

Latin Americans

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14
Q

Gen propreties of H pylori

A

Spiral shaped
pH-sensitive
G-

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15
Q

Where is H pylori typically found

A

Between the mucus layer and surface epithelial cells in the stomach

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16
Q

How does H pylori survive in the stomach

A

Urease production - neutralizes acid

Adherence pedestals - prevent being shed with the GI lining

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17
Q

How does H pylori cause GI injury

A

Direct damage
Altering host response
Causing hypergasterinemia which leads to increased acid secretion

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18
Q

Who do we test for H pylori?

A 
Active peptic ulcer disease
History of PUD
Gastric lymphoma
After resection for gastric cancer
Starting chronic NSAID therapy
Iron deficiency anemia
Idiopathic thrombocytopenic purpura
Long term low dose ASA
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19
Q

Diagnostic test for H pylori

A

Endoscopic
Urea breath test
Fecal antigen
Ab testing

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20
Q

What is tested in endoscopic exams

A

Histology
Rapid urease testing
Culture
Polymerase chain rxn

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21
Q

What Antibodies are being tested for in non-endoscopic tests for H pylori

A

Serum IgG to H pylori

Serum Ab to H pylori

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22
Q

When is it acceptable to test for H pylori eradications

A

Sx despite treatment
H pylori associated ulcer or MALT lymphoma
Resection for early gastric cancer
Test 4 weeks after the end of treatment
Eradication rates lower with 7 day regimens
No PPI for at least 1-2 weeks and no bismuth or abx for at least 4 weeks

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23
Q

First line treatment recommendations for H pylori

A

Clarithromycin Triple therapy
Bismuth Quadruple Therapy
Concomitant Quadruple therapy
Antisecretory therapy is generally continued at standard dose after initial 10-14 days of therapy

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24
Q

Clarithromycin triple therapy

A

PPI + Amox/flagyl + Clarithromycin x 14 days

Clarithromycin resistance < 15%

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25
Q

Bismuth Quadruple therapy

A

PPI + Bismuth + Flagyl + tetracycline x 10-14 days

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26
Q

Concomitant Quadruple therapy

A

PPI + Amox + Flagyl + Clarithromycin x 10-14 days
Can use prevpac + flagyl
Preferred over quadruple regimen because all medications are dosed twice daily

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27
Q

How does Bismuth help?

A

Healing d/t antibacterial and local protective effect, also stimulates PGs

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28
Q

What are the salvage therapies?

A

Bismuth quadruple therapy
Levaquin triple therapy
Concomitant quadruple therapy
Rifabutin triple therapy

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29
Q

Levaquin triple therapy

A

PPI + Levaquin + Amox x 10-14 days

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30
Q

Rifabutin triple therapy

A

Reserved for pts with multiple (> 3) treatment failures

PPI + Rifabutin + amox x 10 days

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31
Q

NSAID ulcers

A

Dose dependent

Use of chronic non-selective NSAIDs (also ASA)

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32
Q

What is mucosal injury a result of

A

Direct topical irritation (drugs are acidic in nature)

Inhibition of protective effects of mucosal PGs

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33
Q

What does COX-1 do

A

Produces PG involved in maintaining GI mucosal integrity and platelet homeostasis

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34
Q

What does COX-2 do

A

Produces PG involved in inflammation

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35
Q

Risk factors for NSAID ulcers

A 
Age > 65
Previous peptic ulcer
NSAID use or NSAID related dyspepsia
ASA including cardioprotective dosages
Concomitant use of NSAID + low dose ASA
Concomitant use of anticoagulant or antiplatelet agents
Concomitant use of oral bisphosphoantes
Concomitant use of SSRIs
Chronic or debilitating disorders
H pylori infection
Smoking/EtOH consumption
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36
Q

Complications of NSAID ulcers

A

GI bleeds
Perforation into peritoneal cavity
Gastric outlet obstruction

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37
Q

non-pharm treatment of NSAID ulcers

A

Reducing psychosocial stress
Avoid aggravating foods
Smoking cessation

38
Q

Pharm treatment of NSAID-induced ulcers

A

STOP NSAID if possible and treat with PPI qd for 4 weeks
Most ulcers will health with standard doses of PPI, H2RA or sucralfate
PPI + NSAID - when NSAID must be continued - PPI for 8-12 weeks

39
Q

Pharm prevention of NSAID ulcers

A

Misoprostol or PPI with NSAID or COX-2

COX-2 alone

40
Q

Why are H2RAs not used for NSAID ulcers?

A

Only prevent duodenal ulcers

41
Q

Non-salicylates that are non-selective?

A 
Indomethacin
Piroxicam
Ibuprofen
Naproxen
Sulndac
Ketoprofen
Ketoralac
Flurbiprofen
42
Q

Non-salicylates that are partially selective

A

Etodolac
Nabumetone
Meloxicam
Diclofenac

43
Q

Non-salicylates that are cox-2 selective

A

Celebrex

44
Q

Salicylates that are acetylated

A

ASA

45
Q

Salicylates that are non-acetylated

A

Salsalate

Trisalicylate

46
Q

What happens when cox-2s are taken with low dose ASA

A

Lose gastroprotective effect

47
Q

What is the max total daily dose of celebrex to minimize CV risk?

A

400mg/d

48
Q

What do the guidelines recommend for patients on low dose ASA and at low-mod risk for GI toxicity

A

misoprostol or PPI

49
Q

Which drugs decrease plavix effectiveness?

A

Nexium and prilosec

inhibit 2C19

50
Q

Which type of ulcers are sucralfate used for

A

Duodenal ulcers

51
Q

What are the ADRs for sucralfate

A

Constipation, nausea, dry mouth, dizziness and metallic taste

52
Q

How is sucralfate taken

A

On empty stomach

53
Q

What drugs have a reduced bioavailability when taken with sucralfate

A 
Warfarin
Dig
Synthroid
Phenytoin
Tetracycline
Quinolones
Theophylline
54
Q

What is misoprostol

A

Synthetic PG

55
Q

Misoprostol ADRs

A 
Diarrhea
Ab cramping
Nausea
Flatulence
HA
56
Q

Intra-abdominal infection

A

Peritoneal inflammation in response to micro-organisms resulting in purulence in the peritoneal cavity

57
Q

Uncomplicated intra-abdominal infection

A

Intramural inflammation of the GI tract without anatomic disruption

58
Q

Complicated intra-abdominal infection

A

Expands beyond the source organ into the peritoneal space

59
Q

Types of complicated intra-abdominal infection

A

Primary peritonitis

Secondary peritonitis

60
Q

Primary peritonitis

A

Also known as spontaneous bacterial peritonitis (SBP)
Bacterial translocation across the gut wall from the bloodstream, lymphatic system, indwelling peritoneal dialysis catheter, or fallopian tubes

61
Q

Secondary peritonitis

A

Microbial contamination through a perforation, laceration or necrotic segment of the GI tract

62
Q

Which peritonitis is often monomicrobial

A

Primary
Patients with cirrhosis
Patients on peritoneal dialysis

63
Q

Which bugs affect patients with cirrhosis?

A

G-

Enterococcal

64
Q

Which bugs affect patients on peritoneal dialysis

A

S aureus

65
Q

Which peritonitis is commonly polymicrobial

A

Secondary

66
Q

Which bugs are common for secondary peritonitis in the stomach and duodenum?

A

Strep

Lactobacillus

67
Q

Which bugs are common for secondary peritonitis in biliary infections

A

E coli
Klebsiella
Enterococcus

68
Q

Which bugs are common for secondary peritonitis in the small intestine

A 
E coli
Klebsiella
Lactobacillus
Strep
Diptheroids
Enterococcus
69
Q

Which bugs are common for secondary peritonitis in distal ileum and colon

A 
Bacteroides fragillis
Clostridium
E col
Enterobacter
Klebsiella 
Peptostreptococci
Enterococcus
70
Q

Examples of secondary peritonitis

A 
Appendicitis (most common)
Diverticulitis
IBD
Salpingitis
Biliary tract infections
Necrotizing pancreatitis
Neoplasms causing intestinal obstruction or perforation
Mechanical GI obstructions (hernias, adhesions)
Blunt abdominal trauma with rupture of intestine
Penetrating abdominal trauma
Endoscopy induced intestinal perforation
Abdominal surgery complications
71
Q

Tertiary

A

A persistent or recurrent infection at least 48 hours after appropriate management of a primary OR secondary peritonitis

72
Q

Clinical presentation of intra-abdominal infections

A 
Non-specific physical findings
Ab pain
Constipation
Diarrhea
Ab distention
73
Q

Management of intra-abdominal infections

A

Resuscitation
Source control
Abx treatment

74
Q

Resuscitation in intra-abdominal infections

A

Fluid replacement with isotonic IV fluids or blood products (if needed)
hemodynamic support

75
Q

Source ontrol in intra-abdominal infections

A

Drainage of abscess

Debridement if necessary

76
Q

Intra-abdominal infections abx treatment approaches

A

Treat until resolution of fever, leukocytosis, and/or ileus

Fixed duration 3-5 days

77
Q

Which abx have we seen icnreasing resistance?

A

Bacteroides fragillis and E coli to clindamycin and cefotetan

78
Q

When should empiris FQs and 1st and 2nd gen ceph be avoided until?

A

Antibiograms show > 80-90% susceptibility

79
Q

What is the DOC for pathogens producing extended spectrum beta-lactamases?

A

Carbapenems

80
Q

What is the most common intra-abdominal surgical emergency?

A

Appendicitis

81
Q

How is appendicitis diagnosed?

A

Diagnosed with physical s/sx and CT imaging

82
Q

What is surgical intervention for appendicitis reserved for?

A

Complicated infections with abscess or rupture

83
Q

Abx for appendicitis

A

Pip/tazo
Cefepime plus metro
Carbapenem

84
Q

Duration of abx in appendicitis

A

3-5 days

85
Q

Diverticulitis treatment

A

Bowel rest

Abx

86
Q

Diverticulitis abx for mild cases

A

PO abx (7-14 days)
Cipro (or levaquin) + metro
Bactrim plus metro

87
Q

Diverticulitis abx for severe cases

A

Pip/tazo

Carbapenem

88
Q

Spontaneous bacterial peritonitis (SBP) in peritoneal dialysis diagnosis

A

Clinical features and analysis of dialysate
Presume pt is infected if clinical features present
Should be treated empirically while waiting for results of dialysate analysis

89
Q

SBP in peritoneal dialysis treatment

A

Empiric treatment should cover G+ (vanc or 1st gen ceph) and G- (AGs) organisms

90
Q

SBP in peritoneal dialysis route of administration

A

Intraperitoneal
Give continuous or intermittent
Abx are stable for variable times after being added to the PD solution
Some abx can be mixed in the bag but not the same syringe

91
Q

Treatment for small/large bowel perforation

A

Pip/tazo
Cefepime plus metro
Carbapenem

92
Q

Treatment for rupture spleen

A

3rd or 4th generation cephalosporin

Vanc if MRSA suspected

GI/Hepatic (7 decks)

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