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Clin Med- GI > Gallbladder/Pancreatic Lecture > Flashcards

Gallbladder/Pancreatic Lecture Flashcards

1
Q

Bile storage site

Concentrates bile

Contracts in response to cholecystokinin (CCK)

Filled when spincter or Oddi is closed

A

Gallbladder

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2
Q
A
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3
Q

Helps break up fats (for digestion in sm intestine, terminal ileum
and recycled to liver for re-excretion)

500-1500 mL secreted from liver each day!

A

Bile

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4
Q

Made up of:

  1. Bile salts (from cholesterol)
  2. Bilirubin (waste product from old worn out RBCs)
  3. Alkaline fluid
A

Bile

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5
Q

Cholecystic

A

Referring to gallbladder

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6
Q

Cholecystectomy

A

Removal of gallbladder

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7
Q

Cholecystalgia

A

Pain from gall bladder (aka biliary colic)

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8
Q

Acute cholecystitis

A

Inflammation (can be chronic)

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9
Q

What percentage of gallstones are cholesterol?

What percentage are calcium bilirubinate/ Ca salts?

A

Cholesterol 75%

Calcium 25%

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10
Q

“Pigmented” black/brown stones

A

Calcium bilirubiante stones

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11
Q
  1. Cholesterol supersaturation (bile gets supersaturated with cholesterol)
  2. Nucleation (Microscopic cholesterol comes together and crystallizes. Over time, additional layers of cholesterol added on)
  3. Gallbladder hypomotility (Slower emptying=more time for stone formation, ie pregnancy)
A

Causes of gallstones

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12
Q

Age (traditionally, over 40y/o)

Obesity (or rapid weight loss)

Sex: Female

Race (example: Native Americans)

(Female, Fat, Forty, Fair, and Fertile)

A

Risk factors for stones

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13
Q

Cholelithiasis

A

Stones in GB

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14
Q

Choledocholithiasis

A

Stone in bile duct

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15
Q

Oral contraceptives, Pregnancy, Diabetes/Insulin use, Hemolysis, Biliary parasites, Cirrhosis, Crohn’s, Hyperparathyroid Dz.

A

Contributing factors for gallstones

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16
Q

What % of ppl have gallstones and are asymptomatic

A

50-60% (most are never symptomatic)

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17
Q

Biliary colic (aching pain in the RUQ/epigastric)

Referred pain: to back, scapula, or R shoulder area

A

Symptoms of cholelithiasis

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18
Q

Best diagnostic (especially initial) for cholelithiasis

A

Ultrasound (95%)

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19
Q

Cystic ducts become blocked due to:

  • gallstones
  • sludge, infection cancer (less common)
A

Acute cholecystitis

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20
Q

Gallbladder blockage –> distention/edema –> ischemia

..this causes?

A

RUQ pain

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21
Q

RUQ and epigastric pain

R scapula/shoulder pain

N/V

Fever/Chills

A

Acute cholecystitis symptoms

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22
Q

Tenderness RUQ/epigastric area

+ Murphy’s sign

Possibe jaundice (late sign)

A

Acute cholestitits

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23
Q

Are plain radiographs good diagnostic images of gallstones?

A

NO..can only see about 25% (Ca containing stones are only about 25%)

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24
Q

Hepatobiliary IminoDiacetic Acid Scan

Radioactive tracer injected, followed thru liverGB

Best test, but usually not necessary

A

HIDA scan

..expensive! only use if odd presentation

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25
Q

CBC w/ diff:
Elevated WBC count (leukocytosis) 12-15k

Hepatic function tests:
LFT’s: elevated, sometimes

Alkaline phosphatase: usually elevated (at least a little)

Gamma-glutamyl transpeptidase (GGT): elevated

Bilirubin: elevated, especially in common duct stone

Amylase: elevated, sometimes

A

Labs in acute cholecystitis

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26
Q

Stone in common bile duct

  • usually migrates from gallbladder
  • less common: form in GBD
A

Choledocholithiasis

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27
Q

Can be asymptomatic (30-40%)
Biliary colic
Jaundice, pancreatitis, maybe cholangitis

ERCP (endoscopic retrograde cholangiopancreatography) can be used to DIAGNOSE and TREAT

A

Choledocholithiasis

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28
Q

Contraindication of ERCP?

A

Pancreatitis

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29
Q

ERCP is diagnosis and treatment ONLY if the stone is..

A

in common bile duct

(Choledocholithiasis)

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30
Q

Infection and inflammation of biliary tract

Due to obstruction, then infection
(retrograde infection: E.coli, Enterococcus, Klebsiella and Enterobactor)

A

Acute cholangitis

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31
Q

Potentially life threatning- can lead to sepsis/shock

Most often caused by choledocholithiasis

Signs/symptoms: RUQ pain, jaundice, fever (**Charcot’s triad)

A

Acute cholangitis

32
Q
  1. Abdominal pain (RUQ)
  2. Jaundice
  3. Fever
A

Charcot’s triad

(pathognomonic for Acute Cholangitis)

33
Q

How many blood cultures do you need for Acute Cholangitis?

A

TWO! different locations

34
Q

Labs:
CBC: leukocytosis
Hyperbilirubinemia
Alkaline Phosphatase: elevated / increasing
Blood cultures X 2

Tx:
Abx (to cover for gm negs, anaerobes, enterococci)
Removal of obstruction via ERCP

A

Acute cholangitis

35
Q

sits in retroperitoneum

Head near duodenum

Tail posterior to stomach, near spleen

During development two ‘buds’ get together and fuse

A

Pancreas

36
Q

2 portions of Pancreas

A

Exocrine and Endocrine portions

37
Q

Ducts –> duodenum

Acinar cells (95% of pancreas)

Lipase

Ductal epithelial cells

A

Part of exocrine portion or pancreas

38
Q

Secretes:

  1. Proteolytic enzymes (trypsinogen, chymotrypsinogen, procarboxypeptidase)..protein digestion
  2. Amylase…carbohydrate digestion
  3. Lipase…fat digestion (more sensitive on test)
A

Acinar cells (make up 95% of pancreas)

39
Q

Fat digestion is done by…

A

Lipase

40
Q

Amylase digests…

A

Carbohydrates

41
Q

Secretes:

Alkaline solution- water, electrolyes, sodium bicarb (NaHCO3)

  • majority of what pancreas secretes
  • 1-2 L a day
A

Ductal epithelial cells

42
Q

Where does the exocrine portion of the pancreas empty into?

A

Duodenum

43
Q

Where does the endocrine portion of the pancreas empty into?

A

Bloodstream

44
Q

Secretion –> bloodstream

Consists of:
Islets of Langerhans (1-2%)
Beta-Cells
Alpha Cells
Delta Cells

A

Endocrine portion of the pancreas

45
Q

These cells are responsible for insulin synthesis/secretion

A

Beta cells

46
Q

These cells produce glucagon

A

Alpha cells

47
Q

These cells produce somatostatin, serves to inhibit several processes including GH and TSH secretion

A

Delta cells

48
Q
  1. Digestion
  2. regulation of pH in intestines
  3. blood sugar regulation
A

Role of pancreatic secretions

49
Q

Pancreatitis usually results in _______ cell injury

A

Acinar

(can be acute or chronic)

50
Q

Can be related to an obstruction of the pancreatic duct (due to several different things, including stones & failure of the 2 parts of the pancreas to fully join during development: “pancreas divisum”)- 5-10% pop.

A

Pancreatitis

51
Q

The inactive proenzymes (like Trypsinogen) are activated early, while still in pancreas

Fat necrosis

Pancreatic enzymes digest itself

A

Possible causes of pancreatitis

52
Q

Gallstones (45%)

Alcohol (35%)

Together they make up about 80%

Idiopathic

MC: cholelithiasis or alcohol abuse

A

Causes of acute pancreatitis

53
Q

Trauma (ie MVA)
Drugs
Infections (mumps, EBV, CMV, HIV)
Peptic ulcer disease
Metabolic issues (hyperlipid, hyperCa)
Toxins (methyl alcohol)
Scorpion stings
Autoimmune
ERCP

A

Other causes of pancreatitis

54
Q

Valproic acid
Tetracycline
Metronidazole
Furosemide
Nitrofurantoin
Estrogens
Thiazides

A

Drugs that can cause pancreatitis

55
Q

If a gallstone is blocking the common bile duct and the pancreatic duct, what might happen?

A

Acute pancreatitis

56
Q

Upper abdominal pain/epigastric pain..may radiate to back
Rapid onset
Worse supine
Better leaning forward
N/V
Fever, chills

A

Acute pancreatitis

57
Q

PE: most tender epigastric
maybe distention, guarding

vitals: tachycardic, fever

A

Acute pancreatitis

58
Q

If gallstone is obstructing common bile duct in acute pancreatitis, what might develop?

A

Jaundice

59
Q
  1. Cullen’s sign= periumbilical ecchymosis
  2. Grey-Turner sign= flank ecchymosis
A

Signs of hemorrhagic pancreatitis

(these signs are rare, <1%)

60
Q

What is more sensitive and specific for acute pancreatitis

..amylase or lipase?

A

Lipase

61
Q
  • *increased** WBCs
  • *increased** amylase and lipase
  • *increased** LFTs

in severe dz..elevated glucose, decreased calcium

A

Acute pancreatitis

62
Q

Image of choice for acute pancreatitis?

A

CT!!!

63
Q

Bilirubin

ALT and AST

Alk-Phos (ALP)

Albumin

Prothrombin time

A

LFTs

64
Q

Helps assess severity of acute pancreatitis

A

Ranson’s criteria

65
Q

Age >55

WBCs >16

Glucose >200

ALT > 250 (6x norm)

LDH >350 (2x norm)

A

Ranson’s criteria

higher scores= more severe dz and increased chance of death

66
Q

Ranson’s score of 0-2

3-5

6+

A

0-2: low mortality. ~1%

3-5: 10-20% mortality

6+: 50% mortality

67
Q

Acute pancreatitis tx

A

NPO (esp NO ALCOHOL!)

Supportive..fluid, pain, nutrition

Correct electrolyte imbalance

68
Q

Inflammatory disease
Irreversible changes
Can lead to permanent loss of function

A

Chronic pancreatitis

69
Q

Causes of chronic pancreatitis

A
  1. Non obstructive (#1 cause is alcohol!!)
  2. Obstructive
    - benign..sphincter of oddi dysfunction
    - neoplasm
70
Q

Do gallstones cause chronic pancreatitis?

A

NO! only acute

71
Q

Epigastric/LUQ pain (episodic or continuous)
Diarrhea
Steatorrhea (as damage decreases lipase production)
diabetes (very late sign, as islets are damaged)

A

Chronic pancreatitis

72
Q

Gold standard of pancreatic function

(can dz early chronic pancreatitis)

A

Secretin stimulation test

73
Q

4th leading cancer death

5 year survival rate= 4%

s/s: wt loss, painless jaundice, pale stool, dark urine, Virchow’s node, Trousseau’s sign (migratory thrombophlebitis)

A

Pancreatic cancer

74
Q

Image of choice for pancreatic cancer

A

CT scan dual phase helical- head of pancreas

75
Q

Pancreatic cancer tumor marker?

A

CA 19-9 (75-85%)

76
Q

What happens to direct bili and alk phos levels in pancreatic cancer?

A

Increase!

77
Q

Tx= chemo/radiation (poor response)
Whipple surg
Palliative care

A

Pancreatic cancer

Clin Med- GI (8 decks)

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