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Nichols + ??? 2 Flashcards

1
Q

Acinar Cell: Protective Mechanisms

A
  1. Inactive proenzymes
  2. Membrane enclosed
  3. Separate pathways
  4. Trypsin inhibitor
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2
Q

Acinar Cell: Acute Pancreatitis, mechanisms of injury

A
  1. Blockage of Secretion
  2. Co-localization of ZG and lysosomes
    • premature zymogen activation
    • autodigestion from within acinar cell
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3
Q

Cytokines and Acute Pancreatitis

A
  • Proteases activate complement
  • C3a and C5a recruit PMNs and macrophages
  • Inflammatory cells release cytokines (TNF-alpha, IL-1, PAF, NO)
  • Vascular injury and inflammatory responses
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4
Q

Local Effets

A
  • autodigestion of the pancreas
  • pancreatic swelling (edema)
  • fat necrosis and hemorrhage

pain, nausea, vomiting

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5
Q

Systemic Containment Response

A
  • circulation alpha1-antitrypsin (inactivates circulating proteases)
  • Circulating alpha-macroglobulin
    • binds to circulating trypsin
    • facilitates monocyte clearance of macroglobulin-tyrpsin complexes
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6
Q

Severe Pancreatitis: Inflammatory

A

Cause: TNF-alpha, IL-6

-fever, malaise, confusion

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7
Q

Severe Pancreatitis: Vascular

A

Cause: kallikrein - hypotension
thrombin activation - DIC, hemorrhage
elastase - hemorrhage
chymotrypsin - hemorrhage

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8
Q

Severe Pancreatitis: Respiratory

A

Cause: Phospholipase A2 - hypoxemia

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9
Q

Severe Pancreatitis: Metabolic

A

Cause: Fat Saponification - hypocalcemia

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10
Q

Acute Pancreatitis: Causes

A

gallstones & alcohol

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11
Q

Acute Pancreatitis: Symptoms

A

abdominal pain, nausea, vomiting

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12
Q

Acute Pancreatitis: Diagnosis

A
  • elevated serum amylase and lipase

- inflamed pancreas on CT scan

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13
Q

Acute Pancreatitis: Management

A

IV fluids, pain meds, remove stone (if causative)

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14
Q

Acute Pancreatitis: Etiologies

A

-miscellaneous
-autoimmune, hyperlipidemia, hypercalcemia, drugs, infection, iatrogenic, trauma, shock, genetic, scorpion bite
40% alcohol
40% gallstones

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15
Q

Hereditary Pancreatitis

A

tyrpsinogen mutation (arg to his) where degradation of trypsin cleavage is

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16
Q

Acute Pancreatitis: Diagnostic Criteria

A

2 of the 3

  1. abdominal pain, nausea/vomiting
  2. elevated serum amylase & lipase more than 3x upper limit of normal
  3. CT imaging showing pancreatic inflammation
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17
Q

Factors suggesting Pancreatitis is from Gallstone

A
  1. age >50
  2. female
  3. amylase > 4000 IU/L
  4. AST > 100 U/L
  5. alk. phos. >300 IU/L
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18
Q

Acute Pancreatitis: Supportive Management

A
  • close observation (hospital)
  • NPO
  • very aggressive IV fluid replacement
  • relief of pain
  • nutritional support (if prolonged)
  • antibiotics (if biliary pancreatitis)
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19
Q

Acute Pancreatitis: Predictors of Poor Outcome

A
  • admission hematocrit >44% with failure to decrease after 24hrs of IV fluids
  • admission BUN>25mg/dl with an increase after 24 hrs of IV fluids
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20
Q

Acute Pancreatitis: Clinical Prognosis CT

A
  1. Interstitial Pancreatitis (85%)
    • multi-organ failure rate < 10%
    • infection rate <1%
    • mortality ~3%
  2. Necrotizing Pancreatitis (15%)
    • multi-organ failure rate 50%
    • infection rate 15-20%
    • mortality 17%
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21
Q

Complications of Acute Pancreatitis

A
  • fluid collections
  • pseudocysts
  • fistulas (ascites, pleural effusions)
  • splenic vein thrombosis
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22
Q

Chronic Pancreatitis: Pathophysiology

A

-recurrent injury with tissue destruction and fibrosis

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23
Q

Chronic Pancreatitis: Cause

A

chronic alcohol

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24
Q

Chronic Pancreatitis: Symptoms

A

chronic abdominal pain
diabetes
steatorrhea

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25
Q

Chronic Pancreatitis: Diagnosis

A

imaging studies

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26
Q

Chronic Pancreatitis: Management

A

pain medications
insulin
enzyme supplements

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27
Q

Chronic Pancreatitis: Etiologies

A

80% alcohol

miscellaneous: cystic fibrosis, hereditary, tropical, autoimmune

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28
Q

Chronic Pancreatitis: Pathophysiology

A
  • chronic alcohol ingestion goes to recurrent bouts of pancreatitis and injury, and abnormal secretion (protein plugs and ductal obstruction - calcification)
  • the injury: stellate cell activation, fibrosis, pain & cell death, malabsorption diabetes
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29
Q

Chronic Pancreatitis: Pathology

A
  • little dark blue dots (lymphocytes), acini are gone, ducts still present (empty)
  • residual necrotic debris
  • early fibrosis
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30
Q

Chronic Pancreatitis: Clinical Presentation

A
  • chronic abdominal pain ~80%
  • malabsorption (steatorrhea) ~35%
  • diabetes ~35%
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31
Q

Chronic Pancreatitis: Causes of Pain

A
  1. increased pressure
  2. biliary strictures
  3. acute focal pancreatitis
  4. Neural Inflammation
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32
Q

Chronic Pancreatitis: Pain Managemetn

A

narcotics
acute exacerbations - abstinence, enzymes
neural inflammation -nerve block, splanchniectomy
ductal hypertension - drainage (stent/surgery)
pseudocyst pressure - drainage (stent/surgery)

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33
Q

Chronic Pancreatitis: Steatorrhea

A

-fat malabsorption occurs before protein or carbohydrate
-due to lipase deficiency
-treatment: reduce dietary fat intake
oral enzyme supplementation
acid suppression therapy

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34
Q

Chronic Pancreatitis: Diabetes

A
  • only seen in severe disease (>80% gland destroyed)
  • loss of both insulin and glucagon, difficult to control (brittle)
  • low insulin requirements
  • ketoacidosis is rare
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35
Q

Cystic Fibrosis: Pathophysiology

A
  • genetic disorder of defective chloride secretion
  • defective chloride secretion, inspissated secretory product, obstruction of ducts and lumens, infection, inflammation, tissue destruction
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36
Q

Cystic Fibrosis: Presentation

A

pediatric

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37
Q

Cystic Fibrosis: Symptoms

A

lung infection
chronic pancreatitis
hypertonic sweat

38
Q

Cystic Fibrosis: Diagnosis

A

sweat chloride test

39
Q

Cystic Fibrosis: Treatment

A

antibiotics

pancreatic enzymes

40
Q

Cystic Fibrosis

A
  • autosomal recessive
  • most common lethal genetic mutation in caucasians (~1:25)
  • most CF is caused by a 3 base pair deletion (F508) that affects the folding, processing, and functioning of CF gene product, the cystic fibrosis transmembrane conductance regulator
  • CFTR is a cAMP-activated chloride channel
41
Q

Cystic Fibrosis: Clinical Manifestations

A
  • obstructive/ inflammatory lung disease
  • chronic pancreatitis
  • hypertonic sweat
  • hepatobiliary tract disease
  • meconium ileus in infants
  • infertility
42
Q

Pancreas: Pathology

A
  • minimal pink fibrous tissue

- minimal thin secretions in ducts

43
Q

Cystic Fibrosis: Pathology

A

-numerous ducts severely distended with inspissated, dark pink secretions, atrophy of acini and mildly increased fibrous tissue

44
Q

Cystic Fibrosis: Diagnosis

A

Clinical Symptoms: frequent pulmonary infections (pseudomonas) diarrhea, malabsorption, failure to thrive, frequent episodes of dehydration
Testing: sweat chloride test, pulmonary function tests, genetic testing

45
Q

Cystic Fibrosis: Clinical Management

A
  • daily pulmonary toilet/inhalers
  • treatment of pulmonary infections
  • high dose pancreatic enzymes
  • gene transfer?
46
Q

Cystic Diseases of Pancreas

A
  • pancreatic cysts can be either benign or malignant
  • most common benign cyst-like lesion in pancreas is pseudocyst
  • serous ones have very little malignant potential whereas mucinous ones have malignant potential
47
Q

Benign Pancreatic Cysts

A
  • pseudocysts - very common (chronic pancreatitis)

- rare non-neoplastic cysts

48
Q

Cystic Neoplasms

A
  • serous cystic tumors (benign)
  • mucinous cyst neoplasms
  • intraductal papillary mucinous neoplasms
  • solid pseudopapillary neoplasms
49
Q

Cystic Diseases: Diagnostic Evaluation

A
  • imaging to assess cyst size
  • endoscopic ultrasound (structure, obtain fluid and tissue for analysis)
  • serum tumor markers (CEA for mucinous cystic neoplasm)
  • ERCP for intraductal papillary mucinous neoplasms
50
Q

Pancreatic Cancer

A
  • vast majority are adenocarcinomas of ductal origin
  • abdominal pain & weight loss
  • prognosis is poor unless caught VERY early
51
Q

Pancreatic Cancer Histology

A

90% are ducal adenocarcinomas
10% miscellaneous (cystic neoplasms, acinar cell neoplasms, lymphomas & sarcomas, neuroendocrine tumors) gastrinoma, insulinoma, glucagonoma

52
Q

Risk factors for pancreatic Cancer

A
  • cigarette smoking
  • alcohol in setting of chronic pancreatitis
  • hereditary pancreatitis
  • family history of pancreatic cancer
53
Q

Diagnosis of Pancreatic Adenocarcinoma

A

Features: weight loss, abdominal pain, jaundice
Lab Tests: elevated serum CA19-9 (tumor marker)
Imaging: mass of CT or MRI,endoscopic ultrasound with FNA

54
Q

Management Considerations of Pancreatic Cancer

A

-70% arise in the head of pancreas
-presentation: 40% metastatic (unresectable)
40% advanced local disease (unresctable)
20% organ confined (resectable), less than 1/2 can be cured
-Chemo & radiation therapy have limited effectiveness

55
Q

Surgery for Pancreatic Cancer

A 
Cure: for tail lesions (distal pancreatectomy)
-for head (Whipple resection)
Palliation: relieve biliary obstruction 
-relieve gastric outlet obstruction
-splanchnietomy for pain control
56
Q

Tumors of Small and Large Intestine

A
  • small intestine: rare
  • colon & rectum: more primary than any other organ
  • colon cancer mortality: 2nd only to lung cancer
  • 5% americans get CRC, 40% will die
  • 70% of colorectal tumors are adenocarcinomas
57
Q

Polyp

A

bump or nodule in the mucosa

  1. sessile
  2. pedunculated
  3. papilloma
58
Q

Non-neoplastic Polyps: Hyperplastic

A

sawtooth (serrated) lumens, due to overgrowth of mature cells in crypt bases, from KRAS mutation without APC mutation

59
Q

Non-neoplastic Polyps: Hamartoma

A

mass of mature, but disorganized tissue indigenous to site (Peutz-Jaghers syndrome)

60
Q

Non-neoplastic Polyps: Juvenile

A

retention in adults

-chronic inflammation, ulceration, dilated glands

61
Q

Adenomatous Colon Polyps

A

most common type

  • glandular structure can be tubular, villous, or tubulo-villous
  • has malignant potential
62
Q

Hyperplastic Colon Polyps

A
  • diminutive, dilated glands

- no malignant potential

63
Q

Inflammatory Colon Polyps

A
  • occur in long-standing IBD

- not neoplastic

64
Q

Epidemiology of Colorectal Cancer

A
  • most common GI malignancy
  • Higher incidence in developed countries
  • thought to be secondary to high fat, low fiber diet
  • Ca and folate in diet may be protective
  • Folate may have anti-cancer benefit early in adenoma sequence
65
Q

Increased Risk of Colorectal Cancer

A

-lack of physical activity
-red meat
-obesity
-cigarette smoking
-alcohol use
(diet & geography, age, family history, chronic colitis, adenoma, previous colorectal neoplasia)

66
Q

Decreased Risk of Colorectal Cancer

A
  • multivitamin containing folic acid
  • aspirin & other NSAIDS
  • postmenopausal hormone use
  • Ca supplementation
  • Selenium
  • Consumption of Vegetables, Fruits, and Fiber
67
Q

Presentation: Impact of Location

A

Ascending: Occult bleeding, anemia
Descending: Obstructive symptoms, overt bleeding
Rectum: Tenesmus, Pain, Bleeding

68
Q

Barium Enema in Diagnosis of CRC

A

show mass or constricting lesion

69
Q

Colon Cancer and Colonoscopy

A
  • locate lesion
  • remove polyps
  • biopsy of lesions
70
Q

Treatment of Colon Cancer

A
  • endoscopic polypectomy can be curative if cancer is localized to head of polyp
  • pre-op CT to look for metastatic disease
  • surgery is mainstay of treatment, involves removal of tumor and adjacent lymphatic
71
Q

Prognosis of Colon Cancer

A 
-worsens as extent of invasion increases 
Mucosa
Submucosa
Muscularis
Serosa
Lymph nodes 
Dukes
72
Q

Chemo in CRC

A
  1. Adjuvant Treatment in patients with positive nodes

2. Decreases recurrences and improves survival

73
Q

Colon Polyp Progression to CRC

A
  1. APC
  2. KRAS/BRAF
  3. p53, PIK3CA, loss of 18q
  4. P53
74
Q

Endoscopic Polyectomy

A

-removal of a stalked polyp with colonoscopy using cautery and a snare

75
Q

Tumor Suppressor Genes

A
  • genes that function normally in inhibition of cell growth

- abnormalities in tumor suppressor genes may be inherited

76
Q

Oncogenes

A
  • activation results in uncontrolled cellular proliferation
  • activation is usually from environmental stimuli
  • oncogenes are generally not inherited
77
Q

Colonic neoplasia

A

(polyps and cancer) results from the accumulation of mutations (inherited and/or sporadic) of cellular oncogenes, tumor suppressor genes, and DNA repair genes that cause dysregulation of normal cellular growth

78
Q

Familial Adenomatous Polyposis (FAP)

A

-autosomal dominant
>100 adenomatous polyps starting in (2nd & 3rd decade)
-all develop CRC without colectomy
-may also have gastric fundic gland polyps, duodenal adenomas and cancer, periampullary adenomas and cancer, desmoid tumors, and retinal pigmented lesions

79
Q

Genetic Etiology of FAP

A
  • one allele of the APC gene inherited in a mutated form (germ line mutation)
  • this mutation present in every cell of the colon
  • polyp growth begins when the second allele is somatically mutated thus causing loss of gene function
80
Q

Hereditary Non-Polyposis CRC (HNPCC)

A
  • germline mutation
  • accounts for 5% of CRC in US
  • proximal colon lesions are common
  • may also be associated with endometrial, ovarian, urinary, and gastric cancer
  • more common than FAP
81
Q

Diagnosis of HNPCC

A

1) one relative with CRC at age <50
2) CRC spans 2 generations
3) 3 relatives with HNPCC tumors - 2 must be first degree relatives of 3rd

82
Q

Goals of Screening for CRC

A

1) decrease mortality from colon cancer

2) prevent colon cancer by removing adenomatous polyps

83
Q

Colorectal Cancer Screening

A
  • average risk: asymptmatic, age >50, US Task Force recommended to stpo screening at age 75
  • High Risk: asymptomatic, personal history of adenomas or cancer, family history, hereditary cancer (FAP, HNPCC), IBD colitis
84
Q

Fecal Occult Blod in the Diagnosis of CRC

A

Phenolilc Guaiac (colorless) - peroxidase - Pigmented Quinone (turns in blue)

85
Q

Fecal Immunochemical Test (FIT)

A
  • responds to only human hemoglobin
  • does not detect UGI bleeding
  • requires 1 or 2 stool samples
  • may detect as little as 0.3gmHb/gm stool
  • more expensive than Guiac
  • more sensitive & specific than Guiac
86
Q

Virtual Colonoscopy

A
  • helical CT reconstructed into 3D images
  • studies on sensitivity & specificity have been variable
  • requires bowel prep
  • exposure to radiation
  • not widely available
  • role in screening is unclear
  • positive test requires colonoscopy
87
Q

Barriers to Colon Screening

A
  1. Limited access to medical care or colonoscopy
  2. Patient preference-bowel prep, time off from work for colonoscopy
  3. Risk and expense of screening test
    • best test for individual patient is test that gets done
    • only 65% of patients currently get screening between 50-75
88
Q

Colon Neoplasms: Benign Polyps

A

Adenomas: 2 Types

  1. Tubular: more pedunculated
  2. Villous: larger, more sessile, higher risk of malignancy
89
Q

Colon Neoplasms: Malignant Neoplasms

A

Adenocarcinoma: 2 Forms

  1. Polypoid
  2. Annular
90
Q

Malignant Small Bowel Tumors

A

-2% of all GI tract cancers
<0.4% of all cancers
-mean age diagnosis-65Y
-adenocarcinoma and carcinoid most common

91
Q

Signs & Symptoms of Small Bowel Tumors

A
  • vague, non-specific-delay in diagnosis of 8-12 months
  • crampy abdominal pain
  • weight loss
  • nausea/vomiting
  • GI bleeding/anemia
  • Jaundice with ampullary lesions
  • symptoms more likely with malignant lesions

GI (19 decks)

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