Lab Medicine Flashcards
1
Q
Broad categories of testing for pancreatic fxn (5)
A
- Pancreatic insufficiency syndromes
- Pancreatic excess syndromes
- Pancreatic inflammation
- Pancreatic Cancer
- Sialadenitis
2
Q
Pancreatic insufficiency syndromes
A
Gestational diabetes DM - Diagnosis and management - DKA - Hyperosmolar hyperglycemia nonketotic syndrome - CF
3
Q
Pancreatic excess syndromes
A
Insulinoma – mostly benign in nature
Zollinger-Ellison syndrome
4
Q
Pancreatic inflammation
A
Acute pancreatitis
Chronic pancreatitis - pseudocysts
5
Q
Options for Testing
A
- Finger stick blood sugar (FSBS)
- random or fasting (at least 2 hrs)
- Glucose Tolerance Test
- HgbA1c
- Fructosamine
- c-peptide
- Liver enzymes - AST/ALT, amylase, and lipase
- Calcium
- Serum ketones
- Stool fat – Sudan staining
6
Q
Fasting time for lipid panel vs. FSBS
A
12 hrs vs. 2 hrs
7
Q
What is a glucose challenge test?
A
- at 24-28 weeks gestation
- administered 50 gm glucose (<140 mg/dl considered no gestational diabetes).
- obtain baseline and one hour after.
- if positive, a complete OGTT is conducted with 100 gm over 3 hours
8
Q
There is an increased chance of developing gestational diabetes if you:
A
- Have had gestational diabetes during a previous pregnancy.
- Have previously given birth to a baby who weighed more than 9 lb (4.1 kg).
- Are younger than age 25 and were overweight before getting pregnant.
9
Q
How to take oral glucose tolerance test (OGTT)
A
Take baseline BS, then drink Glucola (75 gms glucose), then take BS at 1, 2 and maybe 3 hours later.
10
Q
OGTT results
A
Fasting: 60 -100 mg/dL
1 hour: less than 200 mg/dL
2 hours: less than 140 mg/dL
11
Q
What level is concern for prediabetes or diabetes?
A
Between 140 - 200 mg/dL considered “impaired glucose tolerance” or “prediabetes.”
A glucose level of 200 mg/dL or higher is diabetes.
12
Q
Diagnosis of diabetes
A
- Pertinent symptoms and random plasma glucose > or = 200
- Two fasting plasma glucoses > or = 126
- 75g OGTT 2 hour plasma glucose > or = 200
13
Q
Hemoglobin A1c - normal, what is it
A
< 6.5%
Generally considered to reflect average BS over preceding 3 months
14
Q
What is microalbuminuria? Why use it?
A
- It’s not just a dipstick urine, it’s a quantitative measure of the proteins leaking from diabetes-induced glomerular damage over time.
- Once it gets above 30, you start to have an impact on the kidneys.
15
Q
Define DKA (3 parts to condition)
A
*Diabetic ketoacidosis
An increase in the serum concentration of ketones > than 5 mEq/L, a blood glucose level greater than 250 mg/dL, and an arterial pH less than 7.3.
-Ketonemia and ketonuria are characteristic
16
Q
Hyperosmolar Hyperglycemia Nonketotic Syndrome
A
- High sugars (>700 to >1100)
- Serum osmolarity >325 mOsm
- No ketones
- Not initially comatose, but confused & sleepy
- Seen in the elderly
- Increased risk of thrombosis
- REHYDRATE!
- Slow reduction in BS
17
Q
Presenting complaints of someone with pancreatitis (5)
A
- Look sick – note in general appearance
- Nausea
- Weight loss
- Loss of appetite
- Abdominal pain
- Location and nature
- Radiating to back
- Body posture
18
Q
Acute Pancreatitis Causes (5)
A
- Chronic alcoholism
- Biliary obstruction – gallstones, CA
- Hypertriglyceridemia (>1,000/dL)
- Autoimmune – SLE
- Infection – viral, bacterial, fungal, parasitic
19
Q
Clinical Features of Acute Pancreatitis
A
Medical emergency with acute abdomen, intense abdominal pain with upper back radiation, peripheral vascular collapse, and shock from explosive activation of the systemic inflammatory response.
20
Q
Cause of death in acute pancreatitis
A
Death from shock, ARDS, or acute renal failure
21
Q
Acute pancreatitis labs
A
- marked elevation of the serum amylase during the first 24 hours
- followed within 72-96 hours by a rising serum lipase
- hypocalcemia may result from precipitation of calcium soaps in the fat necrosis; if persistent is a poor prognostic sign.
22
Q
Common sequelae of acute pancreatitis
A
sterile pancreatic abscess from liquefaction of the tissue and pancreatic pseudocyst, and retroperitoneal drainage of pancreatic enzymatic secretions.
23
Q
Why does hypocalcemia occur in acute pancreatitis?
A
- When you have pancreatitis, you have cellular breakdown, amylase and lipase increase, but because the pancreas is loaded with enzymes it starts to digest itself.
- Because of that, you wind up with the potential to develop cysts of necrotic eaten up pancreas and saponification of calcium.
24
Q
Pancreatitis Types
A
- Acute (5,000 case/yr, 10% mortality)
- Chronic
- Hemorrhagic
- Cullen’s sign
- Grey-Turner’s sign
- Extravasated pancreatic juice
25
Lab tests for pancreas inflammation: pancreatitis
- Amylase
- Lipase
- Calcium
- CMP (ALT and alk phos)
- CBC
- Lipid profile (triglycerides)
- ABG
26
Pancreatitis – Lab Findings
* Elevated amylase (NL 25-160 U/L)
* Higher is more specific to pancreas
- -Bowel wall: <300
- -Sialadenitis (salivary): ~300-800
- -Pancreas: 500 to 10,000
27
Assessment of severity of acute pancreatitis (Ranson's criteria)
3 or more:
1. age > 55 years
2. WBC > 16,000
3. Glucose > 200 mg/dl
4. Base deficit > 4 mEq/l
5. LDH > 350 IU/l
6. AST (SGOT) > 250 IU/l
28
Assessment of severity of acute pancreatitis (Ranson's criteria) - mortality
Mortality ↑ with development within 48 hours of:
1. decrease in hemoglobin > 10%
2. BUN increase > 5 mg/dl
3. Arterial PO2 < 60 mmHg
4. Calcium < 8 mg/dl
5. Fluid sequestration > 6 L
29
Chronic pancreatitis
- May be silent, or recurrent attacks of pain may occur at scattered intervals.
- Precipitated by alcohol abuse, overeating, and drug use.
30
Chronic pancreatitis - lab elevations
May have mild elevations of serum amylase and lipase; in the long run the destruction of acinar cells precludes such diagnostic clues.
31
Chronic pancreatitis - late complications
- Diarrhea (malabsorption)
- Steatorrhea
- Diabetes
- Pseudocyst
32
Fecal Leukocytes
- Detects WBCs in stool
- Cost ~$15
- Normal is negative
- Ordinarily you have a very low # of segmented neutrophils in stool [positive is >3 segs/hpf (high powered field)]
33
Fecal Leukocytes
- Inflammatory (shigella, salmonella, entamoeba, campylobacter, inflammatory bowel disease)
- Versus non-inflammatory (rotavirus, Norwalk virus, vibrio cholera, cryptosporidium, giardiasis)
34
Stool Culture & Sensitivity (C&S)
-Costs for routine ~$60 for routine and individual pathogens
-Routine (salmonella, shigella, enteropathic E. coli
Specific)
-C. jejuni (associated with Guillian-Barré), V. cholera
35
Tests for Clostridium difficile
- C. difficile toxin: ~$70, detects presence of toxin A (ELISA) or B (culture)
- Cause of pseudomembranous colitis (clindamycin any others)
- Test for toxin A quick and preferred
- Test for toxin B takes 48 hours
36
Helicobactor pylori
- Cost ~$60
- Measure antibodies to H. pylori in serum
- Takes ~20 minutes
- Results = likely, uncertain, unlikely
- Can’t test after treatment
37
H. pylori other and more direct options
- urea breath test (quick and cheap)
- stool H. pylori antigen test
- endoscopic biopsy for C&S
38
Where does H. pylori produce ulcerations?
Stomach and proximal duodenum.
39
What patient population has high % of H. pylori?
Hispanics
40
Carcinoembryonic Antigen
- CEA is glycoprotein found in GI epithelium in early fetus, but not after birth
- Test used if colon CA found or after surgery looking for return of CA
41
False positive CEA
other CAs, 20% of normal smokers have low level
42
Sweat Chloride
- Test for cystic fibrosis
- Pilocarpine is iontophoresed onto forearm, sweat collected, and assayed for chloride
- Positive for CF if chloride is >60mmol/l
- Can do as early as 4 weeks of age
- Not painful
43
Hepatocellular disease
Diseases of the liver cells
44
Cholestatic disease
Diseases of the biliary tree
45
Hepatocellular disease S&S
- No symptoms
- Fatigue, malaise
- Anorexia nausea
- Jaundice
- Pruritus
- Bruising and bleeding (vitamin K dependent clotting factors are liver-derived)
- Hematemesis
- Abdominal pain and swelling
- Confusion coma
46
Cholestatic disease S&S
- No symptoms
- Fatigue malaise
- Anorexia nausea
- Jaundice
- Major pruritis (when bilirubin builds up in your skin, it’s pruritic)
- Major abdominal pain and pancreatitis
- Gray or clay colored stools
47
Physical Signs – Hepatocellular & Cholestasic
- Nothing
- Hepatic enlargement
- Tender liver
- Nodular liver
- Jaundice
- Edema
- Hypotension and tachycardia
- Spider angiomata
- Nail clubbing
- Splenomegaly
- Palmar erythema
48
Estimating Prognosis Using Child Pugh
- Total bilirubin, mg/dL
- Serum albumin, g/dL
- Prothrombin time, prolongation (s)
- Ascites
- Hepatic encephalopathy
49
Unconjugated bilirubin is also known as
indirect bilirubin
50
Conjugated bilirubin is also known as
direct bilirubin
51
Breakdown of hemoglobin to bilirubin
Macrophages in spleen (and liver) break down hemoglobin into globin and heme. Heme is catabolized to biliverdin. Biliverdin reduces to bilirubin.
52
Which form of bilirubin is not filterable?
Unconjugated, because it's bound to albumin
53
Which form of bilirubin is water soluble and filtered in urine?
Conjugated, because it's bound to a diglucoronide molecule
54
green pigment seen in ecchymosis
Biliverdin
55
yellow pigment seen in ecchymosis
Bilirubin
56
Term for Yellow skin and sclera
jaundice and icterus, from elevation of bilirubin in serum, also itches
57
Dipstick Urinalysis Bilirubin
- Negative is normal
- Indicates the need for further evaluation for liver dysfunction and biliary obstruction
- -Conjugated bilirubin is water soluble (only type seen in urine)
- -Unconjugated bilirubin is water insoluble and cannot pass through the glomerulus (will not see in urine)
58
Dipstick Urinalysis Urobilinogen
- Normal is 0.2-1.0
- Urobilinogen is the end product of conjugated bilirubin after it has passed through the bile ducts and been metabolized in the intestine
- Urobilinogen is reabsorbed into the portal circulation, and a small amount eventually is filtered by the glomerulus
59
Causes of increased & decreased urobilinogen in dipstick urinalysis
Increased urobilinogen
- -Hemolysis
- -Hepatocellular disease
Decreased urobilinogen
- -Antibiotic use
- -Bile duct obstruction
60
If the duct is blocked at the ampulla by calculus or tumor:
1. Doesn’t affect amount of unconjugated formed.
2. Doesn’t stop conjugation, but conjugated can’t enter intestine
3. Unconjugated level is normal, conjugated rises due to “spillage”
4. No conjugated in gut, no stercobilin to color stool
5. Also, no conjugated in gut, no conversion to urobilinogen…now none to reabsorb
6. Result is excess conjugated in urine and no urobilinogen
61
Reporting Bilirubin
- Most times report total and direct levels.
- Can calculate indirect by subtracting direct from total.
- Urine tests for urobilinogen and conjugated bilirubin.
62
Hemolytic Jaundice
- Hemolytic anemia
- Sickle cell anemia*
- Absorption from hematomas
- -In patients with trauma
- -Hemolyzed blood being reabsorbed in his body, same as hemolytic reaction.
- Excessive erythropoiesis
- -Disease causing this is hemachromatosis and polycythemia vera.
63
Biliary Obstruction
- Bile duct stone
| - Cancer head of the pancreas
64
Intrahepatic cell damage
- Hepatitis A, B, and C
- Mononucleosis
- CMV – cytomegalovirus (yellow, RUQ pain. Get Hep panel + CMP + Monospot)
- Cirrhosis
- Liver tumors
- Drug-induced injury
65
Newborn jaundice
* Treat > 15 mg/dL before 48 hrs old
* > 18 mg/dL before 72 hours old
* >20 mg/dL anytime
66
Complications of > 25 mg/dL in newborns
hearing loss, intellectual disability, death - kernicterus
67
Jaundice due to breast milk
- Mom’s milk contains enzymes that deactivate baby’s enzymes
- -Can go to formula for 24-48 hrs
- -More frequent feedings
68
Bili Lights
- Production of bilirubin UDP glucuronyltranferase is physiologically delayed
- Unconjugated bilirubin is deposited in the skin
- Photolysis of unconjugated bilirubin to water soluble products
- Most newborns have some – 60%
- No longer than 2nd week of life
69
Alkaline phosphatase (Alk phos, ALP)
- Collection of isoenzymes that catalyze the hydrolysis of phosphate esters
- Fractionation of Alk Phos is available but rarely necessary
- ALP found in liver, biliary tree, and bone
- Placenta also Alk Phos up in third trimester
70
Extra/Intrahepatic Alk Phos
Extrahepatic > 5 times normal
- Obstruction (stones or tumor)
- Biliary tree
Intrahepatic < 3 times normal
-Hepatitis, cirrhosis
71
Bone Alk Phos
- From increased osteoblastic activity
- Metastatic tumors
- Paget’s disease (disordered bone growth and because it’s not well synchronized, Alk Phos will elevate)
- Fractures
- Normal bone growth during adolescence
72
Source Alk Phos
- Confirm Alk Phos is from liver with GGT (GGTP)
| - GGT goes up with Alk Phos in hepatic diseases, not bone
73
Gamma glutamyltransferase (GGT)
- Formally known as GGTP
- Catalyzes transfer of gamma-glutamyl groups between donor and acceptor molecules
-GGT is also very sensitive to liver damage due to alcohol intake that exceeds light consumption
74
Aspartate aminotransferase (AST)
- AST (formally SGOT)
- Catalyzes the transfer of the amino group of aspartic acid to alpha-ketoglutaric acid
```
Not specific to the liver, can be found:
Liver – predominate here
Heart
Skeletal muscle
Some kidney and brain
```
Confirm AST is from liver with elevated ALT (SGPT)
75
Alanine aminotransferase (ALT)
- Formally known as SGPT
- Catalyzes transfer of amino group of alanine to alpha-ketoglutaric acid
- Used to confirm AST is from liver
- Only rises slightly with heart or skeletal muscle
76
AST (SGOT) From Liver
- AST > 10 times think viral hepatitis (intra-hepatic)
| - AST< 10 times think extra hepatic obstruction, cirrhosis, tumor, mononucleosis
77
AST/ALT Ratio
> 1 think cirrhosis, tumor, extra hepatic obstruction
| < 1 think hepatitis, mononucleosis
78
Lactic dehydrogenase (LDH)
- Composed of 5 isoenzymes that catalyze pyruvate to L-lactate
- Found in heart, liver, skeletal muscle, kidney, lung, and erythrocytes
- Total LDH as reported is little use in establishing specific diagnosis
79
LDH Isoenzymes
- LDH1 in cardiac (LDH1/LDH2 ration >.85 indicator of MI)
| - LDH5 in Liver (there are better tests of liver function than this isoenzyme)
80
Prothrombin time
- goes up in liver disease
- -INR
- -The most sensitive indicator of liver disease
81
Liver ammonia conversion
- Ammonia (potential toxin) is byproduct of gluconeogenesis
- Liver converts ammonia into urea
- Also removes ammonia produced by intestinal bacteria from portal blood
- Urea is excreted in urine
82
Calcium exists in a free and bound state. Where are these found?
Most of the bound calcium is bound to albumin.
The free calcium is the metabolically active component.
83
A serum calcium level provides both free and bound quantities. Normal calcium & albumin.
Normal calcium level is 9.5-10.5 mg/dL
| Normal albumin level is 3.5-5.5 gm/dl
84
Evaluating albumin and calcium levels
For every 1 gm decrease in serum albumin, you must increase the serum calcium by 0.8 mg/dL
85
Patterns in liver enzymes - acute hepatitis
AST > 10-20
| Alk phos < 3
86
Patterns in liver enzymes - chronic hepatitis, cirrhosis, tumor
AST < 10
| Alk phos < 3
87
Patterns in liver enzymes - extra-hepatic obstruction
AST > 4
| Alk phos > 4
88
Patterns in liver enzymes -alcoholic cirrhosis, tumor, hepatic congestion
AST/ALT ratio > 1.0
89
Patterns in liver enzymes - acute hepatitis, infectious mononucleosis
AST/ALT ratio < 1.0
