Gastro V Flashcards

1
Q

H. pylori Indications?

A

Recurrent or chronic gastric or duodenal ulceration or inflammation

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2
Q

H. Pylori test explanation: Culture?

A

Mucous obtained through EGD

Chocolate or Skirrow’s medium

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3
Q

H. Pylori test explanation: Gastric mucosal biopsy?

A

Giemsa or Warthin-Starry stain

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4
Q

H. Pylori test explanation: Stool specimen?

A

Has to be fresh specimen (uses ELISA)

Not as accurate

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5
Q

H. Pylori test explanation: Serum testing ( ELSIA) detects?

A

Detects IgG, IgA, and IgM

**give you answer but do not tell you if active / acute infection

pos. IgM it does not mean you have acute infection it can mean you made ABS and cleared the infection

IgG stays around for awhile *

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6
Q

With H. Pylori serum Ig testing: when is IgA elevated?

A

Elevated at 2 months, decreases after treatment

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7
Q

With H. Pylori serum Ig testing: when is IgM elevated?

A

Elevated at 3-4 weeks, gone by 3-4 months

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8
Q

With H. Pylori serum Ig testing: when is IgG elevated?

A

Elevated at 2 mths, stays elevated for 1 year

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9
Q

H. Pylori test explanation: rapid urease test?

A

~95% accurate

Uses small sample of gastric mucosa :

Laid on gel
Laid on paper
Mixed in test tube

**Used while the doc is doing ther ECG with a small sample of gastric mucosa *

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10
Q

H. Pylori test explanation: Urea Breath test?

A

Nonradioactive labeled 13C urea is given to drink

If bacteria is present, will be converted to labeled CO2 which is then taken up by capillaries in the stomach and sent to the lungs for exhaling.

**good test to used after a person has been treated with H. Pylori to see if the infection is really gone or not
*

** it is urea so the bacteria is going to break it down to ammonia and CO2 and the carbon is labels and when they exhale we are looking for the radio labels carbon ( blow into a balloon) - looking for the presence of radio labels carbon = if it is positive then yes it is there but if it is negative then the urea is not breaking down it urea so we can assume there is not infection *

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11
Q

H. Pylori testing considerations?

A

H. pylori can be transmitted by contaminated endoscopes

False negatives

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12
Q

How do you get a False negative with H. Pylori testing?

A

Antacid therapy within 1 week prior to testing

PPI’s inhibit urea absorption

Bismuth or sucralfate will decrease uptake of urea during breath test

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13
Q

Gastrin Indications?

A

Peptic Ulcers

Zollinger-Ellison (ZE) Syndrome

G-cell Hyperplasia

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14
Q

Gastrin test explanation?

A

Serum test:

Levels of Gastrin

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15
Q

What interfering factors increase gastrin?

A

Peptic ulcer surgery (b/c persistent alkaline environment- stimulates Gastrin) - feedback loop is going to continue to make gastrin cause alkalinity

High-protein food

Hypoglycemia

Drugs creating alkaline environment (H2 blockers, antacids, calcium, caffeine)

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16
Q

What interfering factors decrease gastrin?

A

Anticholinergics

TCA’s

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17
Q

Gastrin testing can be diagnostic for what?

A

ZE syndrome

G-cell hyperplasia

Pernicious anemia - they have anti parietal cell ABS - misfunctioning parietal cells

Atrophic gastritis
Gastric carcinoma

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18
Q

What are the 2 gastric acid determination tests?

A

Basal Acid Output

Maximal Acid Output

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19
Q

Indications to run a Basal Acid Output test?

A

Obscure gastric pain

Loss of appetite

Weight loss

PUD

Gastritis

ZE syndrome

G-cell hyperplasia
early satiety

**basal level - baseline*

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20
Q

Contraindications to running a Basal Acid Output test?

A

Esophageal problems

Aortic anuerysm

Gastric hemorrhage

Heart problems (CHF)

Hypersensitivity to
Pentagastrin - stimulates stomach acid production- synthetic gastrin

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21
Q

Basal Acid Output Procedure?

A

Specimens obtained after ~10-15 minutes.

Specimens obtained Q 15 minutes x 90 minutes

1st 2 specimens are discarded

Saliva must be expectorated during the procedure

Total of 4 specimens

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22
Q

Maximum Acid Output indication?

A

If the BAO is abnl

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23
Q

maximum Acid Output procedure?

A

Pentagastrin is injected under the skin SQ

After 15 minutes, a specimen is collected Q15 minutes x 60 minutes
poststimulation specimens

**we want the maximum acid output they can produce *

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24
Q

BAO results if ZE syndrome?

A

elevated

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25
Q

BAO results in gastric CA?

A

decreased - ↓ gastric CA - destroys some of the stomach wall then it can destroy the cells creating the stomach acid

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26
Q

Absent BAO result?

A

Absent: pernicious anemia - parietal cell destruction

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27
Q

MAO results ?

A

↑ ZE Syndrome, duodenal ulcer

stimulate it and it goes even higher

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28
Q

Hemoccult indications?

A

Occult blood in stool

✪ used as screening exam for colon CA

Can detect as little as 5ml of occult blood

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29
Q

Hemoccult interfering factors?

A

Bleeding gums following dental procedure

Drugs that could cause GI bleeding

Diet rich in red meat

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30
Q

Indications to run a Gastroccult?

A

Determines the presence of occult gastric blood and pH of

Uses gastric aspirate or vomitus

**looks for blood in vomit*

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31
Q

Gastroccult: interfering factors - False positives?

A

Under-cooked meat

Raw vegetables

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32
Q

Gastroccult: interfering factors - False negatives?

A

Antacids

Vitamin C

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33
Q

Liver and Pancreatic Function Testing?

A
AST
ALT
GGT
Alk Phos
Amylase
Lipase
Bilirubin
Ammonia
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34
Q

AST (Aspartate aminotransferase) Function?

A

Not specific to the liver

Catalyze transfer of amino acid groups

Functions in protein synthesis

Requires B6 as a cofactor

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35
Q

When is AST increased 5x normal?

A

MI
Liver damage
Shock
Acute pancreatitis

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36
Q

When is AST increased 3-5x normal?

A

Obstruction in liver
CHF
Smaller MI
Skeletal muscle damage

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37
Q

When is AST increased <3x normal?

A

Pericarditis
Pulmonary infarction
Cirrhosis

38
Q

When is AST decreased?

A

Renal damage - it cannot be excreted

B6 deficiencies

**ast is less specific to the liver , ALT is more specific to the liver *

39
Q

ALT test function?

A

Same as AST

Much more specific to liver

**TOAST with alcohol *

40
Q

AST: ALT ratio >2.5 is classically associated with ?

A

alcoholic liver disease

Liver: acute Hepatocellular injury

Alcoholic hepatitis - main one

Active cirrhosis

41
Q

ALT distribution?

A

Large amount in hepatocytes

Moderate amounts in heart, kidney, skeletal muscle

Small amounts in RBCs

42
Q

ALT increased when?

A
Inflammatory damage
Obstruction of liver
Hepatocellular disease
Cirrhosis
MI 
hepatitis
43
Q

ALT decreased when?

A

Malnutrition

44
Q

Measuring AST and ALT we are checking for ?

A

liver damage

45
Q

Measuring AST and ALT: increased 20x normal when?

A

Viral or toxic hepatitis

46
Q

Measuring AST and ALT: increased 3-10x normal when?

A

Bile duct obstruction
MI
Mono

47
Q

Measuring AST and ALT: increased 0-3x normal when?

A

Pancreatitis

ETOH intake

48
Q

GGT aka?

A

GGT (gamma-glutamyltransferase)

**more confirmatory not used as a screening test*

** ordered a lot in GI to see if there is an obstructivee stone *

49
Q

GGT function?

A

Transfer glutamyl groups

Found in liver (some in pancreas, kidney, prostate, lung and breast)

50
Q

When is GGT released?

A

When there is obstruction

ETOH induced liver disease

** and is released when there is obstruction : gallstone pancreatitis or alcoholism ( causing inflammatory condition)*

51
Q

When is GGT increased?

A

Cholangitis/cholecystitis

Obstructive liver disease

Cirrhosis

Hepatitis

Pancreatitis

Renal cell damage

CA of prostate, lung, breast

ETOH-Can increase for up to 6 weeks - use this to monitor some alcoholism, if GGT is increased then they have been drinking

52
Q

Amylase test function?

A

Measures pancreatic function

Digestive enzyme that cleaves starches in glucose

53
Q

Amylase distributed normally?

A

Normally in serum from pancreas and salivary gland

54
Q

Amylase distributed in smaller amounts?

A

Smaller amounts in fallopian tubes, adipose, small intestine, and skeletal muscle

55
Q

Amylase is also distributed from or when?

A

paranceteisis

56
Q

Amylase rises in _____ hours and returns to NL in __________.

A

rises in 6-24 hours

returns to NL in 2-7 days

57
Q

Amylase increased is most commonly associated with ?

A

Acute pancreatitis

Acute cholecystitis

58
Q

Amylase increased is less commonly associated with ?

A

ruptured ectopic pregnancy,

perforated peptic ulcer,

intestinal obstruction

59
Q

Amylase is decreased during?

A

Pancreatic insufficiency - pancreas is shot - burn out ability to make amylase and lipase

60
Q

Lipase physiologic funciton ?

A

Cleaves triglycerides into fatty acids

61
Q

Lipase is specific to ?

A

pancreas

**Lipase is more specific to the pancreas than amylase *

62
Q

When is Lipase released?

A

Response to pancreatic damage

63
Q

When is Lipase elevated?

A

Pancreatic damage

Pancreatic CA - can create excess lipase from the cells

64
Q

Lipase rises in ___ hours?

A

24-36 hours

65
Q

Lipase lasts __ days?

A

14

66
Q

Explanation for Nl Lipase but Elevated Amylase?

A

Not pancreas ( you can r/o pancreatic problem)

it is from IBD,
intestinal obstruction or PUD

67
Q

Where does bilirubin come from?

A

Red cell destruction

Heme protein catabolism

Bone marrow erythropoiesis

68
Q

Indirect Bilirubin is conjugated or unconjugated?

A

unconjugated

69
Q

When will you see an increase in Indirect Bilirubin? Prehepatic causes?

A

unconjugated

Hemolysis

Internal hemorrhage

Gilbert’s (↓ in uptake of
bilirubin)

Crigler-Najaar (↓ in conjugation)

it is elevated b/c something is happening to it before it even hits the liver

70
Q

Direct Bilirubin is conjugated or unconjugated?

A

conjugated

71
Q

When will you see an increase in Direct Bilirubin? Posthepatic causes?

A

Obstruction ( CA)

Dubin-Johnson (↑ in bile)

Atresia of the bile duct

Common bile duct stones

Pancreatic CA

**this bili has already it the liver but it cannot be excreted by the small bowel or the kidneys it is going back into the circulatory system or the liver itself is conjugating it but we have something that is obstuctive like a Pancreatic CA putting pressure in bile ducts or stones or atresia of the duct *

72
Q

Alkaline Phosphatase is actually up to __ different isoenzymes, collectively measured as ___.

A

60

ALP

73
Q

ALP is produced by?

A

Bile cannalicular membrane of hepatocytes

Bone, placenta, small intestine

**liver and bone mostly *

74
Q

What is an elevated ALP often associated with ?

A

biliary obstruction with cholestasis – and usually before a rise in bilirubin

75
Q

Alk Phos. test function?

A

Used to monitor disease of the liver or bone

76
Q

Alk. Phos. is found is many tissues like what?

A

Liver

Bone (most frequent source of extrahepatic ALP)

Biliary tract epithelium

Placenta

Intestinal mucosa

77
Q

ALP isoenzymes ?

A

ALP-1
ALP-2
ALP-3
ALP-4

**only need to order the iso enzymes when we do not know here it is coming
*

78
Q

ALP isoenzymes: ALP-1 correlates with ?

A

Liver

79
Q

ALP isoenzymes: ALP-2 correlates with ?

A

Bone

80
Q

ALP isoenzymes: ALP-3 correlates with ?

A

Intestinal

81
Q

ALP isoenzymes: ALP-4 correlates with ?

A

Placental

82
Q

ALP for liver increased 5x normal from?

A

Bile duct obstruction

Biliary Cirrhosis

83
Q

ALP for liver increased 3-5x normal from?

A

Stone obstruction

84
Q

ALP for liver increased <3x normal from?

A

hepatitis ( chronic - lower levels )

85
Q

ALP for bone increased >5x normal from?

A

Paget’s disease

Hyperparathyroidism

86
Q

ALP for bone increased 3-5x normal from?

A

Multiple myeloma

CA mets to bone

87
Q

ALP for bone increased <3x normal from?

A

Healing fractures

88
Q

Children are naturally elevated in ALP - bone because of ?

A

growing bone

89
Q

Ammonia physiologic function?

A

Endproduct of protein metabolism

**ammonia is a endproduct / byproduce from protein metabolism , when it cannot be excreted by the liver ( ie. liver disease) we get build up of it in the serum and we get encephalopathyy ( pickled)?*

90
Q

When is ammonia increased?

A

Liver failure

Renal failure

** treatment - IV fluids, treat underlying problem, lactulose *

**if a family member is not acting right it is one of the first test you should run *