Normal Lab Values Flashcards

1
Q

Fecal Occult Blood Testing

A

Bleeding into gut, warns of cancer and other serious disease. Point of care kits may not pick up all pt with occult blood, so send stool specimen off if good history and physical suggests GI dz. Done every year on pt >50

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2
Q

Defer Fecal Occult Blood Testing if

A

Diarrhea, colitis, constipation, diverticulitis, ulcers, hemorrhoid flare ups, period. (dont want cross contamination)

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3
Q

Foods to avoid before Feccal Occult Blood Testing. Why?

A

Contiain heme or peroxidase (false +) or strong reducing agents (false -)
Beets, broccoli, Red meat, Vitamin C, horseradish

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4
Q

Stomach Anatomy and Physiology

A

storing, mixing, moving food into intestines
secrete IF for B12 absorption
Different areas/cells have diff fxn

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5
Q

Helicobacter pylori

A

microbe that is the cause of most stomach and duodenal ulcers, chronic stomach inflammation and long term stomach upset.

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6
Q

Urea Breath Test

A

for H. pylori.

C13 or C14 given by mouth. If H. pylori present, it breaks down urea to CO2, which the test detects

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7
Q

Biopsy Urease Test

A

for H. pylori
fragment of stomach or duodenal mucosa obtained on enoscopy dropped onto a gell that contains urea and pH indicator
ammonia generated from the urea by H. pylori changes the pH and color

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8
Q

Direct visualization, biopsy

A

for H. pylori
flagellated gram - rod
endoscopy - look for mucosal erythema, erosions granularity and nodularity
organisms can be seen on HandE or special stains in gastric mucin lining the pits

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9
Q

Seeing Helicobacter

A

Special stains: Geimsa, Diff Quick
Silver stains: Warthin-Starry, Gena, Dieterle silver
Immunohistochemistry and direct flourescent antibody testing used most often. KNOW WHAT Ab YOU NEED

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10
Q

Autoimmune Gastritis

A

immune mediated injury to gastric oxyntic mucosa
Gastric pH is alkaline or neutral (achlorhydria)
Serum pepsinogen likely reduced
Ab against H/K Atpase
IF Ab can also be present - low serum B12

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11
Q

Achlorhydria

A

decreased production of acid by parietal cells
most common atrophic gastritis
anti acid meds induce artificial achlorhydria
High serum gastrin, low serum pepsinogen
24 hr gastric acid profile (NG gube)

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12
Q

Hyperchlorhydria

A

gastric pH<2
remember gastrin stimulates acid production
Zollinger-Ellison syndrome= neuroendocrine tumor secreting gastrin.

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13
Q

Malabsorption vs Maldigestion

A

Malabsorption=SI not fxnl
Maldigestion= exocrine pancreas not fxnl
both present with discomort, diarrhea, weight loss
low serum albumin, low faat soluble vitamins

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14
Q

Fecal fat testing

A

both malabsorption and maldigestion fecal fat increased above 6g/day. have both qualitative and quantitative (72hr)

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15
Q

Pancreatic Insufficiency

A

Pancreas produces many enzymes for digestion, and many things gan cause pancreatic insufficiency
Fecal elastase 1 is current best screen. usually reduced if pancreatic fxn poor enough to cause illness

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16
Q

Small Bowel Insufficiency

A

Malabsorption due to celiac sprue/gluten enteropathy, Chron’s regional enteritis and others
prevents absorption of nutrients, despite them being well digested.
can screen for underlying condition of malabsorption and complications

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17
Q

Things you may screen for in Small Bowel insufficiency

A

B12, Vit D, Vit A; PTT, Celiac disease, cystic fibrosis, pancreatic fxn, methylmalonic acid, hydrogen breath test, xylose absorption test, lactose absorption

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18
Q

Other Testing for Small Bowel Insufficiency

A

Ultrasound, CT, endoscopy, ERCP endoscopic retrograde pancreatography

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19
Q

D-xylose test

A

Screen for small bowel insufficiency
sugar taken by mouth, if small bowel normal, it is found in blood and urine soon after
Draw blood at 2 hrs. Collect all urine for 5hrs
Test is not routinely used

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20
Q

D-xylose test: Results

A

High blood xylose and low urine levels suggests renal dysfxn
Low blood and urine levels suggest poor absorption (bacteria, parasites, short bowel, celiac)
Follow up with abnormal results

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21
Q

Blind Loop Syndrome

A

small bowel bacterial overgrowth syndrome
follows bypass surgery, bacteria overgrow where there is less movement of food
bacteria produce products that interfere with absorption of nutrients
LOOK FOR DEFECTS IN ABSORBING VARIUS SUGARS AND BILE SALTS. diagnosis= quantitating the bacteria

22
Q

Malabsorption/Maldigestion impact on other labs

A
Albumin, total calcium, and BUN =LOW
Cholesterol=LOW
PT prolonged (lack VitK)
Decreased levels of Vit A,D,E,K (fat soluble)
23
Q

Gluten and Gliadin Sensitivity

A

Serologic tests, Biopsy tests

Important - Patient must be consuming gliadin for test to be positive, otherwise false negative will result

24
Q

Serologic Tests for Gluten and Gliadin Sensitivity

A

tTG -IgA has highest sensitivity and specificity
EMA
DGP IgA and IgG antibody is specific for celiac
IgA and EMA tends to decrease in 3-6 months, so useful for monitoring pt compliance, but may be too low for initial diagnosis

25
Biopsy in Gluten sensitivity
Celiac disease= gross attenuated or absent vili | villous atrophy and cronic inflammation. count epithelial cells relative to lymphocytes
26
Dermatitis herpetiformis biopsy
some ppl with celiac will develop this biopsy erythematous skin including that adjacent to lesions initially neutrophils develop around abcess, eosinophils may move in as progresses granular IgA deposits along tips of dermal papillae
27
Lactose intolerance
lack of enzyme required to cleave lactose, unable to absorb it Diagnosis made based on history Hydrogen breath test (increased if +) Stool acidity measures lactic acid
28
Disaccharidase deficiency
congenital/genetic or acquired from damage to SI brush border food challenge, withdrawl then rechallenge various breath tests, biopsy of small bowel
29
Vasoactive intestinal poly peptide
can be produced ectopically by endocrine tumors and MEN-1 syndromes watery diarrhea, comfirmed by serum measurement
30
Stool Culture
used to detect enteral bacterial infections | plates checked at 24 and 48 hrs
31
Microscopic examination of stool
to detect ova and parasites in specimen. | 3 parts: direct wet mount, wet mount of stool concentrate, and preparation of permanent smear with staining
32
Immune methods to detect organisms
immunologic techniques to detect a host of bacteria, prtozoans and helminths in stool
33
Giardia Diagnosis
diagnosed on duodenal aspirate or biopsy when history is not classic. "bald professor" appearance under microscope
34
The Trasnaminases
AST/SGOT ALT/SGPT included in general metabolic panel for general screening released form hepatocytes that are even mildly injured. AST comes from many different kinds of cells. ALT is specific for liver and lesser extend sk. m.
35
Transaminitis
differential diagnosis when they are elevated, consider repeating test in two weeks off all alcohol and unneded meds, will "cure" may patients. otherwise assuming your patient complied, you'll need to consider several very serious treatable illnesses. proceed with lab workup
36
AST/ALT Ratio
normal 1.15:1 (and in individuals with liver disease not related to alcohol abuse) 2-6 associated with liver disease intra hepatic cholestasis >1.5 Acute viral hepatitis .5-.8
37
Bilirubin
Unconjugated (indirect) elevated, pt may have hemolysis or problem conjugating conjugated (direct) elevated, pt may have bile flow blockage both elevated probably damage to liver cells
38
Urobilinogen
measured routinely on urinalysis. produced by gut flora working on bilirubin, mostly removed by liver. high levels suggest hemolysis or hepatocellular insufficiency
39
Liver and alkaline phosphatase
elevated suggests cholestasis keep in mine physiologically higher in growing young adults, pregnancy, etc. CONTEXT important.
40
CFTR Chloride Transporter
deficiency causes cystic fibrosis. sweat chloride test immunoreative trypsinogen performed on drop of blood.
41
Wilson's disease
ATP7B copper transport required to remove excess copper is defective 24 hour urine copper level is very high in symptomatic patients. to confirm=genetic studies
42
HFE mutations - Hemochromatosis
Iron overload involving GI tract (liver, pancreas) transferrin saturation and serum ferritin to screeen. pitfalls - someone who takes an iron pill or someone who is ill from other causes
43
Alpha One antitrypsin deficiency
liver failure and emphysema serum antitrypsin assay. however, if patient is not in usu state of health, it will be elevated biopsy or genetic screening may be req'd
44
Autoimmune hepatitis
``` elevated antinublear antibodies. most common autoantibody is anti-f-actin anti LKM (liver kidney microsome) defines the less common variant ```
45
Primary Biliary Cirrhosis
small bile ducts are destroyed by autoimmunity | lab tests look for antimitochondrial Abs esp antibodies against pyruvate dehydrogenase
46
Alcohol Abuse
lab tests suggest heavy drinking, but wont give diagnosis elevated transaminases, esp AST:ALT ratio around 2 elevated red cell mean corpuscular volume is a warning (but has other causes) as liver failure advances, proonged PT, low albumin AST around 400-1000 suggests alcoholic hepatitis. gamma glutamyl transferase or ethylene glucuronide to monitor sobriety
47
Ethylene glucuronide
used in sobriety programs to monitor sobirety, bc made when person drinks alcohol, and stays in blood and urine for a day or more.
48
Metabolic Syndrome
more common cause of fatty liver/ elevated transaminases than alcoholism. lower MCV, AST/ALT ratio around usual 1.
49
Pancreatitis - Acute
medical emergency. physical exam and imaging are key. lab can vonfirm by finding elevated amylase and or lipase from injured cells. order blood and urine bc low urine despite high serum indicates macroamylasemia. (amylase autoantibody)
50
Serum amylase
diagnosis of acute pancreatits. valuse 4-6 times the upper reference range. Urine and serum levels rise parallel, but urine may remain higher longer
51
Serum lipase
acute pancreatitis lipase 5-10 times upper reference range rise within 4-8 hours, remain so for 7-14 days. levels not indicative of severity
52
Chronic Pancreatitis
loss of most of exocrine pancreas. diagnosis made on history, endoscopy, imaging, maldigestion labs less helpful, though many patients have low serum trypsin/trypsinogen bc many pancreatic acinar cells no longer present