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Clinical Medicine LAB - Professor Sample > Gastro V > Flashcards

Gastro V Flashcards

(90 cards)

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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
BAO results in gastric CA?
decreased - ↓ gastric CA - destroys some of the stomach wall then it can destroy the cells creating the stomach acid
26
Absent BAO result?
Absent: pernicious anemia - parietal cell destruction
27
MAO results ?
↑ ZE Syndrome, duodenal ulcer stimulate it and it goes even higher
28
Hemoccult indications?
Occult blood in stool ✪ used as screening exam for colon CA Can detect as little as 5ml of occult blood
29
Hemoccult interfering factors?
Bleeding gums following dental procedure Drugs that could cause GI bleeding Diet rich in red meat
30
Indications to run a Gastroccult?
Determines the presence of occult gastric blood and pH of Uses gastric aspirate or vomitus **looks for blood in vomit*
31
Gastroccult: interfering factors - False positives?
Under-cooked meat Raw vegetables
32
Gastroccult: interfering factors - False negatives?
Antacids Vitamin C
33
Liver and Pancreatic Function Testing?
``` AST ALT GGT Alk Phos Amylase Lipase Bilirubin Ammonia ```
34
AST (Aspartate aminotransferase) Function?
Not specific to the liver Catalyze transfer of amino acid groups Functions in protein synthesis Requires B6 as a cofactor
35
When is AST increased 5x normal?
MI Liver damage Shock Acute pancreatitis
36
When is AST increased 3-5x normal?
Obstruction in liver CHF Smaller MI Skeletal muscle damage
37
When is AST increased <3x normal?
Pericarditis Pulmonary infarction Cirrhosis
38
When is AST decreased?
Renal damage - it cannot be excreted B6 deficiencies **ast is less specific to the liver , ALT is more specific to the liver *
39
ALT test function?
Same as AST Much more specific to liver **TOAST with alcohol *
40
AST: ALT ratio >2.5 is classically associated with ?
alcoholic liver disease Liver: acute Hepatocellular injury Alcoholic hepatitis - main one Active cirrhosis
41
ALT distribution?
Large amount in hepatocytes Moderate amounts in heart, kidney, skeletal muscle Small amounts in RBCs
42
ALT increased when?
``` Inflammatory damage Obstruction of liver Hepatocellular disease Cirrhosis MI hepatitis ```
43
ALT decreased when?
Malnutrition
44
Measuring AST and ALT we are checking for ?
liver damage
45
Measuring AST and ALT: increased 20x normal when?
Viral or toxic hepatitis
46
Measuring AST and ALT: increased 3-10x normal when?
Bile duct obstruction MI Mono
47
Measuring AST and ALT: increased 0-3x normal when?
Pancreatitis | ETOH intake
48
GGT aka?
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
GGT function?
Transfer glutamyl groups Found in liver (some in pancreas, kidney, prostate, lung and breast)
50
When is GGT released?
When there is obstruction ETOH induced liver disease ** and is released when there is obstruction : gallstone pancreatitis or alcoholism ( causing inflammatory condition)*
51
When is GGT increased?
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
Amylase test function?
Measures pancreatic function Digestive enzyme that cleaves starches in glucose
53
Amylase distributed normally?
Normally in serum from pancreas and salivary gland
54
Amylase distributed in smaller amounts?
Smaller amounts in fallopian tubes, adipose, small intestine, and skeletal muscle
55
Amylase is also distributed from or when?
paranceteisis
56
Amylase rises in _____ hours and returns to NL in __________.
rises in 6-24 hours returns to NL in 2-7 days
57
Amylase increased is most commonly associated with ?
Acute pancreatitis Acute cholecystitis
58
Amylase increased is less commonly associated with ?
ruptured ectopic pregnancy, perforated peptic ulcer, intestinal obstruction
59
Amylase is decreased during?
Pancreatic insufficiency - pancreas is shot - burn out ability to make amylase and lipase
60
Lipase physiologic funciton ?
Cleaves triglycerides into fatty acids
61
Lipase is specific to ?
pancreas **Lipase is more specific to the pancreas than amylase *
62
When is Lipase released?
Response to pancreatic damage
63
When is Lipase elevated?
Pancreatic damage Pancreatic CA - can create excess lipase from the cells
64
Lipase rises in ___ hours?
24-36 hours
65
Lipase lasts __ days?
14
66
Explanation for Nl Lipase but Elevated Amylase?
Not pancreas ( you can r/o pancreatic problem) it is from IBD, intestinal obstruction or PUD
67
Where does bilirubin come from?
Red cell destruction Heme protein catabolism Bone marrow erythropoiesis
68
Indirect Bilirubin is conjugated or unconjugated?
unconjugated
69
When will you see an increase in Indirect Bilirubin? Prehepatic causes?
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
Direct Bilirubin is conjugated or unconjugated?
conjugated
71
When will you see an increase in Direct Bilirubin? Posthepatic causes?
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
Alkaline Phosphatase is actually up to __ different isoenzymes, collectively measured as ___.
60 ALP
73
ALP is produced by?
Bile cannalicular membrane of hepatocytes Bone, placenta, small intestine **liver and bone mostly *
74
What is an elevated ALP often associated with ?
biliary obstruction with cholestasis – and usually before a rise in bilirubin
75
Alk Phos. test function?
Used to monitor disease of the liver or bone
76
Alk. Phos. is found is many tissues like what?
Liver Bone (most frequent source of extrahepatic ALP) Biliary tract epithelium Placenta Intestinal mucosa
77
ALP isoenzymes ?
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
ALP isoenzymes: ALP-1 correlates with ?
Liver
79
ALP isoenzymes: ALP-2 correlates with ?
Bone
80
ALP isoenzymes: ALP-3 correlates with ?
Intestinal
81
ALP isoenzymes: ALP-4 correlates with ?
Placental
82
ALP for liver increased 5x normal from?
Bile duct obstruction Biliary Cirrhosis
83
ALP for liver increased 3-5x normal from?
Stone obstruction
84
ALP for liver increased <3x normal from?
hepatitis ( chronic - lower levels )
85
ALP for bone increased >5x normal from?
Paget's disease Hyperparathyroidism
86
ALP for bone increased 3-5x normal from?
Multiple myeloma CA mets to bone
87
ALP for bone increased <3x normal from?
Healing fractures
88
Children are naturally elevated in ALP - bone because of ?
growing bone
89
Ammonia physiologic function?
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
When is ammonia increased?
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 *

Clinical Medicine LAB - Professor Sample (36 decks)

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