Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

GI: Clin Med IIA > Disorders of the Pancreas > Flashcards

Disorders of the Pancreas Flashcards

1
Q

3 main parts of the pancreas

A

head
body
tail

Lies transversely in the posterior part of the upper abdomen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

what enzymes of the pancreas are considered exocrine

A
  1. pancreatic protease - proteins: trypsin, chymotrypsin
  2. lipase - TG
  3. amylase - carbohydrates
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

what are the endocrine hormones

A
  1. insulin
  2. glucagon
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

multiple spherical groups of epithelial cells embedded as nodules in the endocrine pancreas which are surrounded by a rich capillary plexus. Most numerous in the tail and make up 2% of the pancreas.

A

Islets of Langerhans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

3 cells of the Islets of Langerhans

A
  1. Alpha (15-20%): secrete glucagon which raises blood glucose levels by accelerating conversion of liver glycogen into glucose.
  2. Beta (60-70%): secrete insulin which influences carbohydrate metabolism enabling glucose utilization
  3. Delta (5-10%): secrete somatostatin which inhibits insulin and glucagon secretion
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

what secrete pancreatic enzymes into the pancreatic duct while epithelial cells lining the small pancreatic ducts secrete bicarbonate.

A

Acinar cells

proteases, lipase, amylase, bicarb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

what neutralizes acid coming into the small intestine from the stomach?

A

bicarb

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

what is the leading cause of gastrointestinal-related hospitalization in the US

A

Acute Pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

The peak age of incidence of acute pancreatitis occurs when?

A

in the 50s-60s; however, mortality increases with age.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

MC causes of acute pancreatitis

A
  1. gallstone (MCC)
  2. heavy alc intake - not binge
  3. other: HTG, Hypercalcemia, Trauma (Surgery or ERCP), Meds (sulfa drugs), Infections, Genetic Mutations
  4. 20% are “Idiopathic”
  5. Smoking, high dietary glycemic load, abdominal adiposity increase the risk pancreatitis, with older age and obesity increase the risk for a severe course
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

what may reduce the risk of developing acute pancreatitis

A

Vegetable consumption, dietary fiber, using statins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

what could specifically reduce the risk of non biliary pancreatitis

A

coffee

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

pathophys of acute pancreatitis

A
  • Edema or obstruction at ampulla of Vater (CBD meets PD) - Reflux of bile in pancreatic duct
  • Premature or overactivation of pancreatic enzymes
  • Autodigestion - accepted pathogenic theory resulting when proteolytic enzymes are activated in the pancreas acinar cell compartment rather than the intestinal lumen.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

what are the phases od the pathophys theory of acute pancreatitis

A
  1. Initial phase: intrapancreatic digestive enzyme activation and acinar cell injury.
    - acinar cell injury is the consequence of trypsin activation.
  2. second phase: activation, chemoattraction, and sequestration of leukocytes and macrophages in pancreas = enhanced intrapancreatic inflammatory reaction
  3. third phase: effects of activated proteolytic enzymes and cytokines, released by the inflamed pancreas, on distant organs.
    - Digestion of cellular membranes causing proteolysis, edema, interstitial hemorrhage, vascular damage, coagulation necrosis, fat necrosis, and cellular necrosis & death .
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Pathophysiology Of Gallstone Induced acute pancreatitis

A
  1. Early event is blockade of secretion of pancreatic enzymes while the synthesis of them continues
    - autodigestive injury to the gland
    - normal defenses of the pancreas are overwhelmed by pancreatic enzymes, particularly trypsin
    - Continuing synthesis of trypsin = activation of other enzymes = pancreatic autodigestion and damaging of acinar cells
  2. Microcirculatory injury happens d/t pancreatic enzymes that damage the vascular endothelium
    - vasoconstriction, capillary stasis, decreased oxygen sat, progressive ischemia
    - changes lead to increased vascular permeability and swelling of gland

activated pancreatic enzymes + microcirculatory impairment + inflammatory mediators = rapid worsening of pancreatic damage and necrosis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Pathophysiology in alcohol induced

A
  1. Alcohol increases synthesis of enzymes by pancreatic acinar cells to make digestive and lysosomal enzymes
  2. The exact mechanism is unknown
    - genetic and environmental factors is unknown
    - why only a small proportion of alcoholics develop pancreatitis are unclear
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q
  • Epigastric abdominal pain that radiates to the bacK - Worsens with activity and lying supine; Improves with leaning forward
  • N/V
  • Weakness, sweating, anxiety
  • Pain can persist several hours/days

this presentation is for what dx?

A

acute pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

what historial features may a pt have that may be the cause of acute pancreatitis

A
  • Hx of binge or heavy drinking just before sx.
  • Hx of biliary colic if d/t gallstone obstruction - Reaches max. Intensity in gallstone pancreatitis in 10-20 min
  • Hx of heavy fatty meal just prior to sx if due to “overactivation” of pancreatic enzymes.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

PE findings of acute pancreatitis

A
  • Epigastric Tenderness
  • Distended abdomen with absent bowel sounds if with ileus secondary to inflammation
  • Fever
  • Tachycardia
  • Tachypnea
  • Hypotension
  • Pallor, cool clammy skin
  • Jaundice - if ampulla of Vater blockage
  • Mass palpable d/t inflamed pancreas
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ecchymotic discoloration observed in the periumbilical region

A

although nonspecific, suggest the presence of retroperitoneal bleeding
Cullen’s sign - acute pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ecchymotic discoloration observed along the flank

A

Grey-turner’s sign - although nonspecific, suggest the presence of retroperitoneal bleeding

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

classifications for acute pancreatitis

A
  1. Acute interstitial edematous pancreatitis
    - Acute inflammation of pancreatic parenchyma and peripancreatic tissues, but W/O tissue necrosis
  2. Necrotizing acute pancreatitis
    - Inflammation associated WITH pancreatic parenchymal necrosis and/or peripancreatic necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Labs for acute pancreatitis

A
  1. Serum amylase
    - Rises w/n 6-12 h of the onset; nml w/n 3-5 d
    - Elevation of 3x ULN
  2. Serum Lipase - Most sensitive
    - Elevation of 3x nml
    - Rises 4-8 h of onset of sx; normal w/n 8-14 d
    - Elevations occur earlier and last longer compared with amylase
  3. CBC - leukocytosis
  4. CMP - elevated glucose, lyte abnml (N/V), alkaline Phos and ALT/AST (biliary pancreatits)
  5. lipids - HTG (severe hyperlipidemia)
  6. UA - proteinuria, glycosuria
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

which lab study is more sensitive as compared with amylase in patients with pancreatitis secondary to alcohol

A

serum lipase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

imaging for acute pancreatitis

A
  1. plain X-ray
    - “Sentinel Loop” - Dilated air filled small intestine near the pancreas
    - “Colon Cut-Off Sign” - Gas filled segment of transverse colon abruptly ending near pancreas due to functional spasm of descending colon secondary to pancreatic inflammation
    - Possible Ileus
  2. US - more helpful for stone in suspected biliary pancreatitis
  3. CT - enlarged and inflammation; complications: pseudocysts and abscesses
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

abrupt onset of deep epigastric pain, often radiation to back
Hx of previous episodes, often related to alcohol
N/V, sweating, weakness
abd tenderness and distention and fever
leukocytosis, elevated serume amylase and lipase

what are you suspecting?

A

acute pancreatitis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

how to dx acute pancreatitis

A
  1. Has characteristic abd pain and elevation in serum lipase/amylase 3x ULN = No imaging required
  2. Noncharacteristic abd pain, amylase/lipase <3x ULN, OR dx is uncertain = CT WITH contrast
    - Also to r/o other causes of acute abd pain
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

assessments of severity for acute pancreatitis

A
  • Ranson’s Criteria
  • APACHE II (Acute Physiology and Chronic Health Evaluation)
  • BISAP (Bedside Index for Severity in Acute Pancreatitis) - Simplest
29
Q

what is the Ranson’s criteria?

A

help predict the prognosis of acute pancreatitis.

5 signs can be documented at admission:
1. > 55 y/o
1. Blood glucose > 200 mg/dl
1. Serum LDH > 350 IU/L
1. AST > 250/UL
1. WBC count > 16,000

3+ = severe

Rest of Ranson’s signs are determined within 48 hrs of admission:
1. HCT decrease > 10%
1. BUN increases > 5 mg/dl
1. Serum Calcium < 8 mg/dl
1. PaO2 < 60mm Hg
1. Base deficit > 4 mEq/L
1. Estimated fluid sequestration > 6 L

0-2 = 1%
3-4 = 16%
5-6 = 40%
7-8 = 100%

30
Q

what is BISAP

A

Simple 5 Point Scale - utilized during first 24 hrs
1. BUN > 25 mg/dL
1. Impaired mental status
1. Systemic Inflammatory Response Syndrome (SIRS)
1. Age > 60
1. Pleural effusion

3+ = increased mortality and increased risk of complications

31
Q

complications of acute pancreatitis

A
  1. Prerenal acute kidney failure - severe volume depletion; Inadequate hydration = Acute Tubular Necrosis (ATN)
  2. Ileus - ?d/t retroperitoneal inflammation?
  3. Necrotizing Pancreatitis
  4. Pancreatic Abscess
  5. SIRS
  6. Pleural effusion
  7. ARDS - 3-7 d after onset; in pts requiring large volumes of fluid to maintain blood pressure and volume status
  8. Chronic Pancreatitis
  9. abscess
  10. Acute peripancreatic fluid collection
  11. Pancreatic Pseudocyst
32
Q

tx for mild acute pancreatitis

A
  1. Admit to hospital; “Rest” pancreas; resolves in 3 d
    - NPO (Complete bowel rest)
    - NG tube w/ vomiting and/or abd distention
    - IV fluids: early and aggressive - esp 1st 12-24 hrs
    - IV analgesia: opioids (Hydromorphone, fentanyl), Meperidine (Demerol) - TOC Historically
    - IV antiemetics and/or NG tube
    - Bed Rest
  2. Once sx resolve: Clear liquids, then low fat diet as tolerated; return of BS, largely pain-free
  3. gallstone → cholecystectomy once recovered - preferably during same visit
33
Q

caution when using Morphine for mild disease of acute pancreatitis as it may cause ?

A

sphincter of Oddi spasm

34
Q

tx for severe disease of acute pancreatitis

A
  1. Admit to ICU, same supportive measures as acute
    - large volume fluid resuscitation (6-8L/d)
    - If patient can’t tolerate oral foods for 5 d = enteral feeding
  2. Treat all associated complications: Hyperglycemia, Hypocalcemia, Hypomagnesia, Hypotension, Hypoxemia (with ARDS)
  3. Surgical consult - for biliary pancreatitis, abscesses, necrotizing, or pseudocysts.
  4. Abx ONLY if infection (abscess) - Imipenem
35
Q

how would an abscess complication from acute pancreatitis present?

A
  • Suppurative process characterized by rising fever, leukocytosis, and localized tenderness
  • Epigastric mass usually +6 wks into course of acute pancreatitis
36
Q

how would Acute peripancreatic fluid collection
from acute pancreatitis present?

A
  • Fluid collection develops in early phase, no well defined wall
  • Generally resolve spontaneously within 7-10 days
37
Q

how would a Pancreatic Pseudocyst
from acute pancreatitis present?

A
  • Encapsulated collection of fluid with well defined inflammatory wall
  • Occur >4 wks after onset
  • Fluid collections outside of the pancreas
  • Observation if asx; drainage if sx
38
Q

CT findings that are predictive of mortality of acute pancreatitis

A
  • Normal CT or mild pancreatic edema = good prognosis
  • Peripancreatic fluid - increase mortality 10% (increases likelihood of abscess and volume depletion)
  • Necrotizing pancreatitis - increase mortality 30% (increase risk of multi-organ failure)
39
Q

A syndrome involving inflammation, fibrosis, and loss of acinar and islet cells

A

Chronic Pancreatitis

pancreatic type abdominal pain, steatorrhea, derangements in pancreatic function and visible damage on imaging studies

40
Q

causes of chronic pancreatitis

A
  1. Alcoholism - MC
  2. Smoking alone or synergistically with alcohol
  3. Recurrent bouts of biliary pancreatitis
  4. Severe Hypertriglyceridemia
  5. Autoimmune
  6. Genetic mutations - 15%
  7. Idiopathic - 25%
  8. Obesity
  9. CF (MC in Child) - Thick mucus also clogs the pancreas and hinders the release of digestive enzymes. About 90% develop exocrine pancreatic insufficiency
41
Q

pathophys of chronic pancreatitis

A
  1. Persistent inflammation = permanent structural damage
    - May have stricturing or dilatation of pancreatic duct
    - Leads to decline in both exocrine and endocrine function
42
Q

presentation of chronic pancreatitis

A
  1. Chronic, steady or intermittent epigastric, LUQ pain- radiates to back; worse 15-20 min after eating
  2. Anorexia, weight loss
  3. N/V, Constipation, flatulence
  4. Pancreatic insufficiency
    - Exocrine - malabsorption symptoms and steatorrhea
    - Endocrine - overt DM late in course
  5. Intermittent acute “attacks”
    - Attacks may last only a few hours or as long as 2 weeks
    - Considered on a continuum with acute/relapsing pancreatitis/chronic
    - Pain may eventually be continuous evolving from episodic
  6. ~65% of pts have either osteopenia or osteoporosis
43
Q

what is the most common reason for hospitalization in chronic pancreatitis

A

pain

A change in pattern or sudden worsening of pain should also prompt a search for a complication of chronic pancreatitis - pseudocyst, Duodenal or biliary obstruction, Secondary pancreatic carcinoma

44
Q

The cause of pain in chronic pancreatitis is due to ?

A

increased pressure, ischemia, and inflammation of the pancreas

45
Q

lab findings for chronic pancreatitis

A
  1. Amylase, Lipase - slightly elevated or nml
    - d/t focal disease and fibrosis resulting in decreased abundance
    - Markedly elevated during attacks
  2. LFT’s - Elevated if biliary cause
  3. UA/serum glucose - Glycosuria
  4. Genetic testing, autoimmune workup (ANA, IgG levels, specific antibodies)
46
Q

imaging for chronic pancreatitis

A
  1. Plain X-rays - Calcifications in 30% of pts
  2. DX: CT (MC) - image entire pancreas and pancreatic duct (Pancreatic enlargement, pseudocysts, calcifications, atrophy, ductal dilation)
  3. endoscopic US - Dilated ducts, “honeycombing”
  4. ERCP - analyze pancreatic duct, most sensitive
  5. MRCP - Similar and less invasive than ERCP
47
Q

complications of chronic pancreatitis

A
  • Pseudocysts
  • DM
  • Exocrine deficiency (Malabsorption)
  • Opioid addiction
  • Disability and reduced life expectancy
  • Pancreatic Carcinoma (main cause of death)
48
Q

noninvasive tx/pharm for chronic pancreatitis

A
  1. Low fat diet
  2. Avoid alcohol
  3. Pain management
    - Caution with opioids (addiction)
    - Combo with NSAIDS, Tramadol, or Acetaminophen with TCA’s
  4. Pancreatic digestive enzymes
  5. Insulin for associated DM
  6. Treatment of any malabsorptive disorders
49
Q

invasive tx for chronic pancreatitis

A
  1. ERCP w/ stone extraction +/- stent placement - biliary cause
  2. ERCP w/ decompression of pancreatic duct - dilated in alcoholic pancreatitis
  3. Puestow procedure for dilated pancreatic duct - Effective pain relief
  4. Resection of head or tail (Whipple procedure)
  5. Surgical drainage of pseudocysts
  6. Pain management procedures: Celiac plexus block, Spinal Cord Stimulators
50
Q

what is the puestow procedure

A
  1. creating a longitudinal incision along the pancreas while the main pancreatic duct is filleted open longitudinally from the head to its tail
  2. The duct and pancreas are then attached to a loop of the small intestines (jejuneum)
51
Q

d/t pain is difficult to treat in chronic pancreatitis, this often leads to ?

A

opioid addiction

52
Q

carcinoma of the pancreas MC occurs in what location?

A
  • 75% in pancreatic head
  • 25% body and tail - Poorer prognosis
53
Q

MC type of carcinoma of the pancreas

A

adenocarcinoma (85%, ductal)

54
Q

RF for pancreas carcinoma

A
  1. Advanced age (rare before age 45)
  2. High fasting plasma glucose
  3. Tobacco use (greatest risk factor)
  4. Heavy alcohol use
  5. Obesity
  6. Chronic pancreatitis
  7. Family history/genetics
  8. New onset DM after the age of 45
  9. Prior abdominal radiation
  10. Certain breast cancer carriers (BRCA 2) have 7% risk of concurrent pancreatic cancer

Any older pt with new onset DM = pancreatic cancer is in the DDx!

55
Q

presentation of pancreas carcinoma

A
  1. Vague epigastric pain with radiation to back (MC)
    - gnawing, visceral with insidious onset
    - for 1-2 months before presentation - Can be worse after eating or lying supine
  2. Wt loss, anorexia, fatigue, N/D, hyperglycemia
  3. Acute pancreatitis w/o identifiable cause

Often asx until metastasis occurs….esp with body and tail masses.

56
Q

PE findings of pancreas carcinoma

A
  1. Painless Jaundice and Enlarged palpable gallbladder
    - d/t tumor of pancreatic head causing obstruction of common bile duct (Courvoisier sign)
    - Nontender put palpable distended gallbladder right costal margin
  2. Malabsorptive diarrhea
  3. If in tail, pain can be in LUQ
  4. advanced cases - a hard periumbilical nodule may be palpable (Sister Mary Joseph’s node)
57
Q

lab studies for pancreas carcinoma

A
  • Amylase, Lipase - normal to mildly elevated
  • Glycosuria, Hyperglycemia
  • Elevated LFT’s if CBD obstruction
  • +/- CA 19-9 tumor marker
58
Q

imaging for pancreas carcinoma

A
  1. CT - 1st line (detects mass in 80%)
    - Can do CT guided FNA for cytologic studes and tumor markers
    - Identifies metastases, delineates extent of tumor
  2. Endoscopic U/S, MRCP
  3. ERCP - confirmation if inconclusive CT (“double duct”)
    - Simultaneous dilation of pancreatic and common bile duct
  4. Open surgical exploration needed for bx if unable to get CT guided or ERCP guided bx.
59
Q

staging for pancreas carcinoma

A

TNM classification

  • Tis: carcinoma in situ;
  • T1: limited to pancreas, <=2 cm in greatest dimension
  • T2: limited to pancreas, >2 cm in greatest dimension
  • T3: extends beyond pancreas but w/o involvement of the celiac axis or the superior mesenteric artery
  • T4: involves celiac axis (celiac artery, with left gastric, splenic, and common hepatic artery) or the superior mesenteric artery (unresectable primary tumor)
  • N1, regional LN metastasis; M1, distant metastasis.
60
Q

tx for pancreas carcinoma

A
  1. if localized - Whipple Procedure - Radical pancreaticoduodenal resection
  2. Distal Pancreatectomy
  3. Total Pancreatectomy
61
Q

what is the whipple procedure

A
  1. Removal pancreatic head, duodenum, first 15cm of jejunum, CBD, gallbladder, and a partial gastrectomy
  2. 5 year survival rates in these patients: 25-30% (Only 10% in node positive patients)
  3. Surgery carries 4% mortality rate
  4. Often preceded by biliary stenting if with jaundice/CBD blockage
  5. Often followed by chemotherapy +/- chemoradiation
62
Q

how to determine suitability for surgery in pancreas carcinoma

A

staging laparoscopy before surgery

63
Q
  • Resection of tumor in body and tail.
  • Always do staging laparoscopy first - Only 13% of body and tail tumors resectable
  • Typically also combined with splenectomy
  • Surgery carries higher postoperative mortality rates

what type of procedure is this?

A

Distal Pancreatectomy

64
Q

what makes a pancreas carcinoma nonresectable?

A
  • Liver, peritoneum, and omentum mets
  • Encasement of superior mesenteric artery/vein
  • Extension into IVC
65
Q

tx for nonresectable pancreas carcinoma

A
  • Biliary stents (if sx of obstruction)
  • Chemo
  • Palliative treatment
66
Q

screening recommendation for pancreatic cancer?

A
  • Patients with FHx (1st degree) w/ pancreatic cancer should have screening CT age 40-45 or 10 years before onset of cancer in family member.
  • There is NO screening test for healthy adults for pancreatic cancer.
67
Q

Education of pts on PREVENTION of pancreatic cancer

A
  • Don’t smoke. People who smoke are twice as likely to get pancreatic cancer as non-smokers.
  • Limit alcohol. Heavy drinking can lead to pancreatitis, or chronic inflammation of the pancreas. Long-term pancreatitis increases the risk for pancreatic cancer.
  • Maintain a healthy weight. Someone with a BMI, or body mass index, of 30 or higher is considered obese.
  • KNOW YOUR FAM HX - Can get genetic testing if + first degree relative
  • Be familiar with common s/sx: Jaundice, Unexplained weight loss, Pain
68
Q

a procedure to diagnose and treat problems in the liver, gallbladder, bile ducts, and pancreas.

A

Endoscopic Retrograde Cholangiopancreatography
(ERCP)

69
Q

uses magnetic resonance imaging to visualize the biliary and pancreatic ducts non-invasively. This procedure can be used to determine whether gallstones are lodged in any of the ducts surrounding the gallbladder.

A

Magnetic Resonance Cholangiopancreatography (MRCP)

GI: Clin Med IIA (12 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions