Cputhsc1

Front 1

Based on Michaelis-Menton kinetics (linear) at the saturation point of a reaction when the enzyme is working as fast as it can (Vmax), what is the only thing that varies

A. Substrate concentration
B. Enzyme concentration

Back 1

B. Enzyme concentration

Thus using excess substrate one can determine?

Hint 1

Enzyme concentration

Front 2

NADH absorbs light at what wavelength?

Back 2

340 nm

How is this useful in measuring enzyme activity?

Hint 2

It makes it easy to measure the formation or disappearance of NADH.

If a reaction does not utilize NAD/NADH then it can be coupled to the reaction (coupled enzyme assay)

Front 3

What is the purpose of a cofactor?

Back 3

Cofactors are substances that bind to an enzyme and enhance their activity.

There are inorganic cofactors = zinc, calcium, mag, iron

And organic cofactors, or co enzymes = NAD, protein S, pyridoxine (vit B6), etc.

Front 4

If a macroenzyme is bound to an antibody it has two effects on the enzyme, name them.

Back 4

It makes in incapable of functioning

And

Prevents it from being cleared in the blood

Hint 4

Accordingly, awareness of the presence of macroenzymes and procedures for their determination should be an integral part of diagnostic work-up, in order to obviate the use of unnecessary expensive and invasive diagnostic procedures. The patient’s physician should be informed on the presence of a macroenzyme in the patient’s serum. These data should be entered in the patient’s medical records and history form. On the other hand, the patient should be properly reassured that the occurrence of this enzyme form requires no specific therapeutic intervention.
It should be noted that data on the possible diagnostic significance of the macroenzyme occurrence remain scarce, vague and questionable. This fact should not be neglected, but the information on the reasons for the presence of macroenzymes and on the mechanisms of their formation should be continuously collected and reconsidered. Indeed, future research into the formation and detection of macroenzymes may hopefully result in defining some new diagnostic markers.

Front 5

Noncompetitive inhibition can not be overcome by increasing the substrate concentration. What type of inhibition can be overcome in the way?

Back 5

Competitive inhibition

Hint 5

An uncompetitive inhibitor alters two parts of the kinetics, name them.

Front 6

What is the definition of an international unit?

Back 6

The amount of enzyme that catalyzes the conversion of 1 micro mole of substrate per minute.

Front 7

Define katal.

Back 7

1katal = the amount of enzyme that catalyzes te conversion of 1 mole of substrate per minute

1IU= 16.7 nanokatals

Hint 7

The mole is a unit of measurement used in chemistry to express amounts of a chemical substance, defined as an amount of a substance that contains as many elementary entities (e.g., atoms, molecules, ions, electrons) as there are atoms in 12 grams of pure carbon-12 (12C), the isotope of carbon with atomic weight 12. This corresponds to a value of 6.02214179(30)×1023 elementary entities of that substance. It is one of the base units in the International System of Units, and has the unit symbol mol.[1]
The mole is widely used in chemistry, instead of units of mass or volume, as a convenient way to express the amounts of reagents and products of chemical reactions. For example, the chemical equation 2 H2 + O2 → 2 H2O implies that 2 mol of dihydrogen and 1 mol of dioxygen react to form 2 mol of water. The mole may also be used to express the number of atoms, ions, or other elementary entities in some sample. The concentration of a solution is commonly expressed by its molarity, the number of moles of the dissolved substance per liter of solution.
The number of molecules in a mole (known as Avogadro's number) is defined so that the mass of one mole of a substance, expressed in grams, is exactly equal to the substance's mean molecular weight. For example, the mean molecular weight of natural water is about 18.015, so one mole of water is about 18.015 grams. This property considerably simplifies many chemical and physical computations.
The name gram-molecule was formerly used for essentially the same concept.[1] The name gram-atom (abbreviated gat.) has been used for related but distinct concept, namely a quantity of a substance that contains Avogadro's number of atoms, whether isolated or combined in molecules. Thus, for example, 1 mole of MgB2 is 1 gram-molecule of MgB2 but 3 gram-atoms of MgB2.[2][3]

Front 8

Name the two liver transaminases.

Back 8

Aspartate aminotransferase (AST/SGOT)

Alanine aminotransferase (ALT/SGPT )

Which one is more specific?

Hint 8

ALT.
Confined mainly to the liver and kidney.

Front 9

AST is located in what organs (7)?

Back 9

Cardiac muscle
Liver
Skeletal muscle
Kidney
Brain
Lung
Pancreas

Where in the cell is AST found?

Hint 9

Cytoplasm (20%)
And
Mitochondria (80%)

ALT is only located in the cytoplasm.

Front 10

Heparin can elevate both liver transaminases to around how many times the baseline?

Back 10

3x

Front 11

In RENAL failure liver transaminases become lower or higher than healthy individuals.

Back 11

Significantly LOWER

Front 12

AST and ALT are both higher in men and African Americans, hemolysis raises both.

In children AST is slightly higher than ALT, this reverses by age 20.
This may reverse again with old age.
The ratio Of AST:ALT is called

Back 12

The deRitis ratio.

Front 13

LDH is present in numerous tissues and is traditionally separable into how many isoenzymes by electrophoresis?

Back 13

5 isoenzymes

Front 14

The fastest isoenzymes are LD1 and LD2.

These are found in greatest abundance in what tissues ( 3)?

Back 14

Heart
Red blood cells
Kidney

There is much more LD1 than 2.

Front 15

List the isotopes of LDH in order from highest to lowest concentration in normal CSF.

Back 15

LD1>LD2>LD3>LD4>LD5

1
2
3
4
5

Front 16

The slowest LDH isoenzymes are what (2)?
And where are they found (2)?

Back 16

The slowest are LD4 and LD5

They are found in liver and skeletal muscle

Therefore they will be elevated in liver damage.

Front 17

Where is LD3 found?

Back 17

Lymphocytes

and

Pancreas

Front 18

If an isoenzyme "6" is seen on electrophoresis of LDH its presence is thought to be associated with what?

Back 18

Hepatic vascular insufficiency( usually in the setting of cardiovascular collapse)

Front 19

The concentration of LDH isoenzymes in normal serum is
LD2>LD1>3>4>5

When LD1 is greater than LD2 three possibilities exist, what are they?

Back 19

Acute myocardial infarction
Hemolysis
Renal infarction

Front 20

If LD1and LD5 isoenzymes of LDH are elevated what are two explanations?

Back 20

1. Acute MI ith liver congestion

2. Chronic alcoholism that has been complicated by liver damage and megaloblastic anemia

Front 21

The best test to confirm that an elevated alkaline phosphatase is from the biliary tree?

Back 21

Gamma-glutamyl transferase or GGT

Front 22

Where is gamma-glutamyl transferase (GGT) found

Back 22

In the biliary epithelial cell, particularly those that line the small inter lobular bile ducts and bile ductules.

Thus, it is exquisitely sensitive to biliary injury.

GGT can also be elevated in (6)?

Hint 22

Steatosis
Diabetes
Hyperthyroid
Rheumatoid arthritis
Acute MI
COPD

Front 23

GTT is found to be around 2-3x the upper limit in heavy drinkers.

How long after abstaining from alcohol will levels be normal?

This is a good marker of alcohol consumption.

Back 23

3 weeks

Note: GGT is lower in women and higher if African-Americans

Front 24

GGT is a great marker to confirm that alkaline phosphatase is from the billiard tree, due to GGT in the biliary tree.

However, GGT is also in the smooth ER of hepatocytes. So GGT can be elevated due to excess toxins. In particular certain drugs, name a few (6).

Back 24

Warfarin
Barbiturates
Dilantin
Valproate
Methotrexate
Alcohol

Front 25

What is an alternative to GGT that is also found in the biliary epithelium.
It's highest levels are in cholestatic conditions.

It is specific, but not sensitive.mso it is stil second to GGT.

Back 25

5'-Nucleotidase

Front 26

Hyperammonemia is nearly always due to what?

Back 26

Liver failure.

However, in children one should suspect?

Hint 26

An inborn error of metabolism

Especially urea cycle enzyme deficiencies

Front 27

The sources, name two, of the body are?

Back 27

Skeletal muscles and gut

Bacterial in the GI tract breakdown protein and release ammonia. The liver removes the ammonia and discards it in the form of urea in urine.

Front 28

Name causes of elevated ammonia (3).

Back 28

Hepatic yet dysfunction
Too much collateral circulation
Excess protein in the gut ( for example, excess hemoglobin from a bleed)

Ammonia is neurotoxic.

Front 29

Ammonia measurement requires?

Back 29

A fresh blood sample, chilled during transport, and no hemolysis.

Patients should also refrain from smoking.

Front 30

There are two types of phosphatases: alkaline (optimum pH is 9)
and acid ( pH optimum is 5)

Acid phosphatases are found in greatest concentrations where (3 places)?

Back 30

Prostate
Red cells
Bone

Red cell phosphatase is distinguished from other Acid phosphatases by?

Hint 30

It's susceptibility to inhibition by 2% formaldehyde and resistance to inhibition by tartrate.

This is the same tartrate-resistant acid phosphatase (TRAP) that is found in hairy cell lukemia.

Non-TRAP (or prostate acid phosphatase) has been used as a serum marker for prostatic adenocarcinoma, but has been largely replaced.

Front 31

Alkaline phosphatase ( pH 9) is produced by four tissues, name them.

Back 31

Bone
Bile ducts
Intestine
Placenta

Therefore elevated alk phos is seen in biliary disease, bone disease, bone growth ( children), and pregnancy.

Separate reference ranges are needed in children and pregnancy.

When do we see decreased levels (2)?

Hint 31

Hypophosphatasia ( an inborn deficiency)
And malnutrition

Front 32

The regan isoenzyme is alk phos is observed in 5% of individuals with what condition?

Back 32

Carcinoma

It appears to be identical to placental alk phos.

Front 33

Bone alkaline phosphatase is produced by what cell type?

Back 33

Osteoblasts

And reflects bone-forming activity.

Front 34

It is important to get a fasting alkaline phosphatase for what reason?

Back 34

Intestinal alk phos can falsely elevate levels. Especially in Lewis positive type B or O secretors.

Ingesting a meal can elevate alk phos by 30% for 2-12 hours.

Front 35

Which type of bilirubin is water-insoluble?

Back 35

Unconjugated

Front 36

Another name for unconjugated bilirubin is:

Back 36

Indirect

Front 37

Which type of bilirubin is produced directly from the breakdown of heme?

Back 37

Unconjugated/Indirect bilirubin

Front 38

The process that occurs in the liver to cause bilirubin to be water-soluble is called?

Back 38

Glucuronidation

Front 39

Which type of bilirubin is secreted in bile?

Back 39

Conjugated/Direct

Front 40

What effect does intestinal bacteria have on bilirubin?

Back 40

Conversion to Urobilinogen

(which is yellow and gives stool/urine color)

Front 41

A patient with a cholangiocarcinoma causing complete biliary obstruction may demonstrate what characteristic stool finding?

Back 41

White, acholic stools

(Siver stool of Thompson)--how lame to have your eponym be about poop

Front 42

Bilirubinuria is always associated with which type of hyperbilirubinemia?

Back 42

If a patient has bilirubinuria, then the elevated bilirubin is CONJUGATED b/c indirect bili is not water soluble.

Front 43

A patient presents with jaundice and bright yellow urine that is 3+ positive for bilirubin on dipstick. A likely clinical scenario that could accompany this is:
a) Gilbert syndrome
b) Choledocholelithiasis
c) Crigler Najjar syndrome
d) loss of hepatocyte function due to drug effect

Back 43

b) A stone obstructing the bile duct is the only scenario listed that will cause conjugated bilirubinemia.

Crigler Najjar (failure of conjugation in hepatocyte), Gilbert (failure of hepatocyte to take up unconjug bili), and loss of hepatocyte function all cause indirect/unconjugated bilirubinemia

Front 44

Which of the bilirubin measurements is calculated, not measured?

Back 44

Indirect (Unconjugated): remember-this is the early stuff.

Front 45

The diazo-colorimetric method of hemoglobin measurement uses which of the following to calculate findings:
a) temperature
b) light scatter
c) Light transmisison at 540 nm
d) Turbidity
e) Color dye reaction

Back 45

Color dye reaction.

Front 46

What is purpose of adding an accelerant to the diazo-colorimetric method?

Back 46

Without accel, you measure mainly conjugated. With addition of accelerant, you maeasure conjug + unconjug (total). Subtract conjug from total and get (estimated) unconjugated.

Front 47

One more time:

Conjugated is to _________ as Unconjugated is to _______

a) direct, total
b) indirect, direct
c) direct, indirect
d) total, indirect

Back 47

Remeber: conjugated/unconjugated has to do with how the bili is in the body, while direct/indirect is the method of measurement. Indirect (Unconjugated) is the one you calculate *indirectly*

It's nice, because Indirect and Unconjugated both have prefixes, so you can remember they go together.

Front 48

Measuring absorbance by direct spectrophotmetry at 455nm can determine what?

Back 48

Total bilirubin

Front 49

What is the limitation of measuring bilirubin by direct spectrophotometry and how do we correct for this?

Back 49

Interference by hemoglobin can occur so we simultaneously measure hemoglobin level at its other peak and subtract them to get real answer

Front 50

What is delta hemoglobin?

Back 50

With prolonged elevation, conjugated bilirubin can actually bind to albumin (delta-bili). This sticks around longer, as it cannot be excreted by liver/kidney. Makes it look like hyperbili is still present.

Front 51

A patient with alcoholic cirrhosis and jaundice would be expected to have what changes in below parameters:

Type of hyperbili, AST/ALT, Alk Phos, Cholesterol, Pruritis

Back 51

Some unconjugated, but some conjugated; really high AST/ALT, not super-high Alk Phos, Normal cholesterol, no pruritis

Front 52

A patient with a bile duct obstruction would be expected to have what changes in below parameters:

Type of hyperbili, AST/ALT, Alk Phos, Cholesterol, Pruritis

Back 52

Almost all conjugated, Not super-high AST/ALT, really high Alk Phos, Increased Cholesterol, Itching +

Front 53

What is the half-life of Factor VII?

Back 53

12 hours

Front 54

A patient presents to an ER without CT or ultrasound equipment with jaundice and elevated PT. Before the workup can reveal whether he has cirrhosis or a bile duct obstruction, an simple medication can be given to help discern. What is it?

Back 54

Parenteral Vitamin K.

If the patient has cirrhosis, then Vit K should not help correct the factor levels much. If the patient has a stone, then the PT prolongation is likely due to a lack of absorption of Vit K (lack of bile salts) and should correct with IV Vit K.

Front 55

What pattern of gamma globulins do you expect to see in autoimmune hepatitis?

Back 55

polyclonal IgG increase

Front 56

What pattern of gamma globulins do you expect to see in primary biliary cirrhosis?

Back 56

polyclonal IgM increase

Front 57

What pattern of gamma globulins is common in all liver diseases?

Back 57

Impaired hepatic synthesis of protein with increased immunoglobulin synthesis results in an albumin to globulin ration <1.

Front 58

What leads to so-called physiologic jaundice of the newborn? What type of hyperbilirubinemia is it?

Back 58

Unconjugated hyperbilirubinemia. The gut lacks the bacteria to convert Conjugated Bili to urobilinogen and it can't be excreted via stool. Conjug bili is thus converted back to Unconjug by beta-gluconaridase in gut. Fetal clearance of the Unconjug bili is via placenta. At birth, if the baby cannot pass enough bili through stool then becomes jaundiced. Also, hepatic enzymes aren't full-force yet.

Front 59

Name the following characteristics of neonatal jaundice:
a) time of onset
b) time of peak
c) peak level and rate of increase

Back 59

a) onset at day 2-3 days
b) peaks at 4-5 days
c) peak of 5-6 mg/dL (usually) and at a rate of <5mg/dL/day

Front 60

Two common causes of marked elevation in newborn bilirubin:

Back 60

Hemolytic disease of newborn, sepsis

Front 61

What is the CNS damage caused by hyperbilirubinemia termed? Why does this happen in infants?

Back 61

Kernicterus

Underdeveloped blood-brain barrier

Front 62

A 7 day-old infant dies after severe hyperbilirubinemia. At autopsy, the cause is found to be due to biliary atresia. In addition, what CNS findings would you see?

Back 62

Yellow-stained subthalamic nucleus, hippocampus, thalamus, globus pallidus, cerebellar nuclei, and cranial nerve nuclei.

Front 63

Features in neonatal jaundice that raise the concern that it is not "physiologic:"

Timing of appearance and peak, length of jaudice, levels, type

Back 63

Appearance at <24 hours, rising bili past 1 week, persistance of jaundice past 10 days, level >12mg/dL, increase >5mg/dL/day, conjugated bili >2mg/dL. (Remember, Physiologic jaundice is more unconjugated--due to crappy liver enzymes).

Front 64

A newborn with biliary atresia develops jaundice. What type of jaundice is most likely, and why will phototherapy not work?

Back 64

The bilirubin is most likely conjugated (it's already been through the liver), and phototherapy works by converting unconjugated bili to conjug bili for water solubility and excretion.

Front 65

When should phototherapy be considered in the treatment of neonatal jaundice?

Back 65

As age increases, the threshold level increases. But it basically starts at 10mg/dL at 12 hours then increases 2mg/dL for each 12 hours of life.

Front 66

When should exchange transfusion be considered in the treatment of neonatal jaundice?

Back 66

>20mg/dL

Front 67

Timing and type of hyperbilirubinemia related to:
Physiologic jaundice of Newborn

Back 67

>24 hours but less than 10 days; unconjugated

Front 68

Timing and type of hyperbilirubinemia related to:
Breast milk Jaundice

Back 68

>7 days; unconjugated

Front 69

Timing and type of hyperbilirubinemia related to:
Polycythemia, Hemolytic disease of newborn, erythroblastosis

Back 69

<24 hours, unconjugated

Front 70

Timing and type of hyperbilirubinemia related to:
Hemoglobinopathies or RBC enzyme defects

Back 70

>7 days, unconjugated

Front 71

Timing and type of hyperbilirubinemia related to:
Bowel obstructions like CF, Hirschsprung, ileal atresis

Back 71

>7 days, unconjugated

(*unconjugated* because the gut bacteria don't see the conjugated bili to help it get changed to urobilinogen and excreted, but the enzyme β-glucuronidase is present to "unconjugate" the bili to get it reabsorbed.

Front 72

Timing and type of hyperbilirubinemia related to:

Inherited disorders of bilirubin metabolism

Extra: what are these disorders? (2)

Back 72

Unconjugated, >7days

Crigler-Najjar, Gilbert

Front 73

Timing and type of hyperbilirubinemia related to:

Biliary obstruction

Back 73

Conjugated, >7days

Front 74

Timing and type of hyperbilirubinemia related to:

TORCH infections

Extra: What are they?

Back 74

<24 hours, conjugated

Toxo, Rubella, CMV, Herpes, Others (Coxsackievirus, Syphilis, Varicella-Zoster Virus, HIV, and Parvovirus B19)

Front 75

Timing and type of hyperbilirubinemia related to:

Metabolic disorders such as storage diseases

Back 75

>7days, conjugated

Front 76

Timing and type of hyperbilirubinemia related to:

Disorders of bilirubin transport

Extra: What are they? (2)

Back 76

Conjug, >7 days

Rotor, Dubin-Johnson

Front 77

Timing and type of hyperbilirubinemia related to:

Allagille Syndrome

Back 77

Conjugated, >7days

Front 78

What is the main use of transcutaneous bilirubin measurements?

Back 78

Screening otherwise healthy newborn infants for elevations of bilirubin to evaluate those at risk for jaundice.

Front 79

In regards to drug-induced hepatitis, when do most events occur in relation to the drug dosage?

Back 79

Within first 4 months of administration.

Front 80

Which type of viral hepatitis is the most likely to become chronic?

Back 80

HCV

Front 81

What type of acute hepatic injury will raise the AST/ALT the most?

Back 81

Ischemic or toxic injury

Front 82

What level of AST will give you a 90% chance that the etiology of injury is toxic?

Back 82

>3,000 U/L

Front 83

A patient presents with AST of 600 U/L and an ALT of 600. Is the cause more likely alcohol or viral?

Back 83

Viral. Viral infections often raise the AST to greater than 10x the upper limit of normal, while EtOH rarely does this.

Front 84

A patient presents with AST of 300 and ALT of 145. Is the cause more likely alcohol or viral?

Back 84

Alcohol. EtOH often raises the AST 2x's higher than the ALT. Viral patterns are usually closer to 1:1.

Front 85

Which patients are more likely to have jaundice? Hep A, Hep b, Hep C, EtOH

Back 85

Hep A, EtOH

Front 86

Which levels correct first, bili or transaminases?

Back 86

Transaminases

Front 87

What is probably the best indicator of prognosis in acute hepatic injury?

Back 87

PT >4.0s

Front 88

What two isoenzymes make up serum amylase?

How do we differentiate?

Back 88

Salivary and pancreatic amylase

Electrophoresis, inhibition, or monoclonal antibodies

Front 89

If you put amylase on an electrophoresis gel how many bands do you see? Which are pancreatic and which are salivary?

Back 89

6, first three are salivary, second 3 are pancreatic

Front 90

How can we differentiate between salivary and pancreatic amylase using inhibition tests?

Back 90

Salivary amylase is inhibited by wheat germ lectin.

Front 91

When do serum amylase levels rise and normalize in acute pancreatitis?

Back 91

Rise within 2-24 hours, fall to normal in 2-3 days.

Front 92

Do high levels of amylase mean anything in the diagnosis of pancreatitis? What about prolonged elevation?

Back 92

High levels don't reflect severity, but do increase liklihood that pancreatitis is the cause. Prolonged elevation suggests pseudocyst formation or complication

Front 93

Why do most pancreatitis patients also have increased urine amylase?

Back 93

The amylase is normally cleared by glomerulus. (Keep in mind--kidney failure patients might have increased plasma amylase...) Can calculate fractional excretion of amylase.

Front 94

A 42 year-old gentleman presents with severe acute epigastric pain, nausea, and "stranding" (evidence of inflammation) of the pancreas on CT scan. Pancreatitis is the top of the differential, but serum amylase is barely elevated. What could be the cause?

Back 94

If his pancreatitis is caused by hypertriglyceridemia, TGs may interfere with measure of amylase assay.

Front 95

Name 10 non-pancreatic causes of hyper-amylasemia:

Back 95

diabetic ketoacidosis, peptic ulcer disease, acute cholecystitis, ectopic pregnancy, salpingitis, bowel ischemia, intestinal obstruction, macromaylasemia, renal insufficiency, opioid administration (?)

Front 96

What is macroamylasemia? What is the incidence?
What is the cause?

Back 96

1% incidence where apparently healthy individuals have elevated amylase and low urine amylase due to Ig-amylase complexes that are not cleared.

Front 97

Is lipase specific for the pancreas?

Back 97

Yes

Front 98

When does lipase rise and fall in acute pancreatitis?

Back 98

Rises like amylase in 2-24 hours of onset and remains elevated for 14 days.

Front 99

How is lipase better than amylase for pancreatitis diagnosis?

Back 99

Less renal clearance, so more predictable. Only pancreatic form exists.

Front 100

What is Ranson criteria used for in treatment of pancreatitis?

Back 100

Predict severity

Note: Lipase/Amylase levels do not predict severity.

Front 101

What two time frames are used to evaluate Ranson criteria?

Back 101

Admission and 48 hours following

Front 102

What criteria are used for Ranson criteria at admission?

Back 102

Age, WBC, Glucose, AST, LDH

Front 103

What criteria are used for Ranson criteria at 48 hours?

Back 103

Urea, Calcium, PaO2, Base deficit, fluid sequestration, hematocrit

Front 104

Most common causes of acute pancreatitis? (2)

Back 104

Alcohol and Gallstones

Front 105

What are some other causes of pancreatitis besides EtOH and gall stones?

Back 105

Hypertriglyceridemia, Hypercalcemia, Viral, inherited, CF, scorpion bite

Front 106

secretin-cholecystokinin (CCK) test is for

Back 106

pancreatic exocrine function

Hint 106

endoscope is introduced and the duodenal concentrations of pancreatic exocrine products (bicarbonate, amylase, lipase, trypsin) are measured after the intravenous administration of secretin and CCK

Front 107

fecal fat test is for

Back 107

pancreatic exocrine function, other causes of positive results

Hint 107

Severe ileal diseases (eg, Crohn disease) or ileal resection

Front 108

which is a better test, fecal chymotrypsin (bentiromide) or fecal elastase-1?

Back 108

The sensitivity and specificity of elastase-1 appears superior to that of chymotrypsin.

Front 109

Is the D-xylose test a measure of the pancreatic exocrine function?

Back 109

no, D-xylose test is a measure of small bowel mucosal absorptive capacity

Front 110

Which type of pancreatic cyst: Associated with pancreatitis, ovoid unilocular lesion with thick wall adjacent to pancreas

Back 110

pseudocyst

Front 111

Which type of pancreatic cyst: ↑Amylase ↓CEA ↑CA 19-9

Back 111

pseudocyst

Front 112

Which type of pancreatic cyst:
↓Amylase
↓CEA
↓CA 19-9

Back 112

Serous cystadenoma or Solid-cystic (solid-pseudopapillary tumor)

Front 113

Which type of pancreatic cyst:
↓Amylase
↑CEA
n1-↑CA 19-9

Back 113

Mucinous cystadenoma (mucinous cystic neoplasm) or Intraductal papillary mucinous tumor

Front 114

In normal subjects serum CK is of which isoform?

Back 114

MM, which comes from?

Hint 114

skeletal muscle

Front 115

CK-BB (CK1) is found primarily in the?

Back 115

Brain

Front 116

CK-MB (CK2) is found in which tissue(s)?

Back 116

Cardiac muscle is about 30% MB, skeletal about 1% MB.

Front 117

What is the ‘relative index’ that adds to the ability of the CK-MB assay to distinguish myocardial infarction?

Back 117

serum, CK-MB/total CK, 2% is the cutoff

Front 118

The immunoinhibition type of CK-MB immunoassay is susceptible to falsely elevated CK-MB due to

Back 118

hemolysis, the presence of CK-BB (in stroke), and macro-CK.

Front 119

Which type of serum CK is elevated in stroke?

Back 119

CK-BB

Front 120

What is macro-CK?

Back 120

a CK-Ig complex. On electrophoresis, it migrates between MM and MB. It is found in completely healthy elderly women.

Front 121

What is the significance of Mitochondrial CK?

Back 121

It is seen in patients with advanced, often disseminated, malignancies and is associated with a poor prognosis.

Front 122

Are assays for CK isoforms better than CK-MB?

Back 122

Assays for CK isoforms are not widely available, and published reports do not appear to display significant advantages over CK-MB.

Front 123

Why there is both an immediate release of cytoplasmic troponin (4-8 hours) and a sustained release (10-14 days)?

Back 123

While a small proportion of cardiac muscle troponin is free in the cytoplasm, the vast majority of it is bound to actin and myosin.

Front 124

What is the most sensitive of the cardiac markers and is the earliest marker of acute myocardial infarction?

Back 124

Myoglobin (Mgb)

Front 125

why the Altered Cobalt Binding (ACB) assay shows promise as a marker of transient ischemia?

Back 125

Ischemia-modified albumin has altered Cobalt Binding. It rises within minutes of myocardial ischemia and returns to baseline within 6 hours due to rapid hepatic clearance.

Front 126

What is the value of CRP in acute coronary syndrome?

Back 126

C-reactive protein (CRP) and high-sensitivity CRP (hsCRP) appear to be strong predictors for the development of ACS in healthy individuals, and to predict short-term prognosis following non-AMI ACS.

Front 127

the sensitivity of a single troponin test at 4 hours after onset of symptoms is

Back 127

50%, how to increase sensitivity?

Hint 127

two tests at 6 and 12 hours have a combined sensitivity of approaching 100%.

Front 128

If the cardiac troponin I is so sensitive and specific, why are we still measuring CK-MB?

Back 128

it is still important to measure serial CK-MBs to determine:
(1) whether the MB is going up or down; that is, whether the infarct is acute or resolving, and
(2) whether the MB comes down appropriately; that is, whether there is a complication of MI such as extension of the infarct

Front 129

How does serum CK-MB level change during an MI?

Back 129

Increased serum CK is detectable within 3–6 hours of an AMI, with a peak at 20 to 24 hours. Assuming there is not ongoing injury, CK returns to normal within 72 hours.

Front 130

How does serum cardiac markers change after a successful reperfusion?

Back 130

In successful reperfusion, all of the cardiac markers peak earlier than normal; although, their sequence of peaks parallels that of normal MI.

Front 131

What is the Biuret technique for?

Back 131

for determining total protein, how does it work?

Hint 131

In an alkaline medium copper salts form a purple complex with proteins.

Front 132

Proteins absorb ultraviolet light at which wave length?

Back 132

210 and 280 nm

Front 133

What are the bands on serum protein electrophoresis?

Back 133

albumin, α1, α2, β and γ.

Front 134

What will happen if albumin is congenitally absent?

Back 134

hyperlipidemia and mild edema

Front 135

Which is the fastest migrating protein in SPEP?

Back 135

Prealbumin

Front 136

What are major functions of prealbumin?

Back 136

It binds to T3, T4 (transthyretin) and vit A complex

Front 137

Elevations of prealbumin are seen in what conditions?

Back 137

Chronic alcohol abuse, Steroid therapy

Front 138

Elevations of alpha2 macroglobulin are seen in what conditions?

Back 138

Liver disease, nephrotic syndrome

Front 139

Decreased Ceruloplasmin is seen in which condition?

Back 139

Wilson disease,hepatic failure, Menke's syndrome

Front 140

Which protein is decreased in acute intravascular hemolysis?

Back 140

Haptoglobulin

Front 141

Transferrin can cross blood brain barrier as?

Back 141

tau-protein ( modified as asialated transferrin), normal transferrin

Front 142

what is the half life of prealbumin?

Back 142

48 hrs

Front 143

CSF protein electrophoresis will show?

Back 143

Sharp prealbumin band, double transferrin peaks,dim albumin

Front 144

In what conditions fibrinogen is present in serum?

Back 144

Dysfibrinogenemia,APL syndrome, heparin, vit K def

Front 145

Fibrogen appears at which location in SPEP?

Back 145

gamma and beta interface, may be misinterpreted as M protein

Front 146

Beta-gamma bridging is seen in which condition?

Back 146

Liver cirrhosis

Front 147

from which organ is CRP produced?

Back 147

liver

Front 148

what fraction of the population has CRP > 2mg/L?

Back 148

1/2

Front 149

what fraction of the population has CRP > 3mg/L?

Back 149

1/3

Front 150

Does the population distribution of CRP follow a Gaussian curve?

Back 150

No, It is a curve significantly skewed, with a dense cluster in the very lowest CRP levels and a long tail extending into the > 10 range.

Front 151

What the cutoff values for the three levels of CRP level?

Back 151

Normal <3mg/L, low-level elevation 3-10, high level >10.

Front 152

What is the high level CRP indicative of?

Back 152

acute inflammation

Front 153

Low level elevations of CRP are predictive of (2)?

Back 153

1. poor outcomes of cardiovascular events;
2. also correlated with mortality in non-cardiac diseases as well as in apparently healthy individuals

Front 154

Why is transferrin increased in an individual who does not have iron deficiency (2)?

Back 154

1. Pregnancy, 2.estrogen therapy

Front 155

Which form of serun transferrin may be superior to GGT as a marker for alcohol use?

Back 155

carbohydrate-deficient transferrin

Front 156

How many transferrin peaks do we observe in the CSF?

Back 156

Two peaks. Why?

Hint 156

transferrin and asialated transferrin (Tau protein)

Front 157

Is transferrin an acute phase reactant?

Back 157

no. It decreases in the acute phase, but later increases if the inflammation persists.

Front 158

What's the characteristic feature of serum protein electrophoresis in monoclonal gammopathy? (1)

Back 158

discrete, dark band (M-spike) usually in gamma region but can be seen in beta or alpha 2 regions.

Front 159

What is a monoclonal gammopathy and what's a another name for it?

Back 159

condition in which there's an immunochemically homogenous immunoglobulin in the serum. Another name is paraproteinemia

Front 160

What are some causes of a mononclonal gammopathy? (5)

Back 160

multiple myeloma, solitary plasmocytoma, MGUS, Waldenstroms macroglobulinemia, CLL/SLL

Front 161

How often do biclonal gammopathies occur and what's the cause?

Back 161

3-4% of cases, usually composed of IgA spikes having a single light chain, should be considered monoclonal

Front 162

What percentage of multiple myeloma patients have a hypogammaglobulinemia and what other finding are they likely to have?

Back 162

About 10%, they're more likely to have Bence-Jones protein (free light chains) in their urine

Front 163

When is immunofixation or immunosubstraction when the SPEP is negative for an M-protein? (3)

Back 163

When there's a strong clinical suspicion for multiple myeloma, there's systemic amyloidosis, or there's hypogammaglobulinemia

Front 164

What method is used to characterize the M-spike when it's found on SPEP?

Back 164

immunofixation or immunosubstraction

Front 165

What is the usual composition of an M protein?

Back 165

an intact immunoglobulin composed of 2 heavy and 2 light chains. Sometimes a light chain only and rarely a heavy chain only.

Front 166

What's the connection between systemic AL amyloidosis and monoclonal gammopathy?

Back 166

AL amyloidosis can occur when the M-protein produced has unusual (amyloidogenic) properties

Front 167

What test is used to monitor monoclonal gammopathy disease progression or efficacy of treatment?

Back 167

serum electrophoresis

Front 168

How is M protein quantification done and why is it useful? (2)

Back 168

carried by nephelometry (or turbidimetry) and used to classify disease and and follow disease

Front 169

Why are major immunoglobulins quantitated in multiple myeloma patients?

Back 169

to determine the degree of suppression

Front 170

Why is the quantity of serum free light chains important in monitoring multiple myeloma? (3)

Back 170

useful to follow individuals with light chain only disease, detect abnormalities in the kappa:lambda, and is extremely sensitive in detecting disease recurrence

Front 171

When does hyperviscosity syndrome develop, what are the symptoms (4) and when should serum viscosity be measured?

Back 171

-syndrome develops when serum viscosity is <3 cp -symptoms: nasal bleeding, blurred vision, retinal vein dilation (flame shaped retinal hemorrhages), and neurologic symptoms - serum viscosity should be measured when IgM M-protein > 4 g/dL or IgA/IgG > 6 g/dL

Front 172

What else should be looked for in patients with M proteins?

Back 172

cryoglobulinemia

Front 173

What's the difference between CSF and serum proteins?

Back 173

CSF normally has all of the same proteins but in smaller quantities

Front 174

What are the most characteristic features of normal CSF electrophoresis? (3)

Back 174

prominent pre-albumin band, double beta transferrin) band, dim albumin and alpha2 band

Front 175

What's the main purpose of CSF electrophoresis?

Back 175

support diagnosis of multiple sclerosis (oligoclonal bands) these bands should be absent from the patient's serum in a sample run concurrently

Front 176

What's the utility of urine protein electrophoresis in proteinuria?

Back 176

to determine the source of the protein

Front 177

What is a glomerular proteinuria pattern in urine electrophoresis and what type of renal pathology does it suggest?

Back 177

urine contains strong albumin, alpha1 and beta bands. Indicates glomerulonephritis where very large and very small proteins don't enter the urine (some preservation filtering and tubular resorption)

Front 178

What is a tubular proteinuria pattern in UPEP and what renal pathology does it suggest?

Back 178

urine has a weak albumin band, strong alpha1 and beta bands. Implies tubulointerstitial nephritis or acute tubular necrosis (impaired resorption of smaller proteins, normal glomerular filtration of large proteins)

Front 179

What is an overflow proteinuria pattern in UPEP and what renal pathology does it suggest?

Back 179

most commonly a monoclonal light chain (Bence Jones) but can also be due to myoglobin and hemoglobin. Implies a serum protein in excess of kidney's filtration/resorption capacity leading to overflow

Front 180

Define cryoglobulins and what's the method to detect them?

Back 180

-defined as immunoglobulins that precipitate reversibly at low temperatures. -to detect blood drawn,kept, clotted, and centrifuged at 37C, remaining serum stored at 37C (for at least 3 days) then centrifuged at 4C any precipitate is a cryoglobulin

Front 181

What are the 3 types of cryoglobulinemia recognized?

Back 181

Type I - monoclonal immunoglobulins Type II - mixture of monoclonal IgM and polyclonal IgG Type III - mixture of 2 polyclonal immunoglobulins

Front 182

What is the most common clinical condition associated with cryoglobulins? Name 4 other less common conditions

Back 182

#1 is hepatitis C infections others include lymphoproliferative diseases, chronic infections, autoimmune diseases (esp SLE), chronic liver diseases

Front 183

What are the clinical manifestations of cryoglobulinemia? (7)

Back 183

palpable purpura (constant feature usually over lower extremities), arthralgias, hepatosplenomegaly, lymphadenopathy, anemia, sensorineural deficits, and glomerulonephritis

Front 184

What are the renal complications of cryoglobulinemia and when do they usally manifest?

Back 184

nephrotic or nephritic syndrome with type II membranoproliferative glomerulonephritis on renal bx. Renal involvement trails by 4-5 years

Front 185

What's the basic pathologic lesion in cyroglobulinemia?

Back 185

vasculitis with large subendothelial immune complex deposition with a fibrillary or tubular structure on electron microscopy

Front 186

What's the goal and method of treatment of cryoglobulinemia? What's the success rate?

Back 186

Goal is immune modulation methods include alpha interferon, corticosteroids, and plasmapheresis. Remisssion achieved in 75% but 50% relapse

Front 187

Define hyponatremia

Back 187

serum sodium <135 mmol/L, considered severe when <120 mmol/L

Front 188

Under what clinical conditions is the diagnosis of SIADH most accurate? (5)

Back 188

when hyponatremia is irrefutable, urine sodium is >20 mmol/L, patient is euvolemic and has normal renal function, there's been no recent diuretic use, normal adrenal function

Front 189

What are the possible complications of correction hyponatremia too quickly? Too slowly?

Back 189

Central pontine myelinosis, cerebral edema

Front 190

What is pseudohyponatremia and what are 3 possible causes?

Back 190

serum osmolarity >280, may be due to hyperglycemia, hyperlipidemia, or hyperproteinemia

Front 191

What's the differential for hyponatremia when patient is hypovolemic? (5)

Back 191

Renal losses (urine Na+ >30 mmol/L), diuretics, medullary renal disease, Addison, and RTA type I

Front 192

What's the differential for hyponatremia when patient is euvolemic? (3)

Back 192

SIADH, psychogenic polydipsia, and drugs with ADH-like effect

Front 193

What drugs are known to have an ADH/vasopressin n-like effect? (4)

Back 193

desmopressin, SSRIs, TCAs, ectasy

Front 194

What's the differential for hyponatremia when patient is hypervolemic? (3)

Back 194

congestive heart failure, cirrhosis, nephrotic syndrome

Front 195

Under what conditions is hypernatremia usually found?

Back 195

A dehydrated person with physical inability to respond to their thirst response.

Front 196

What's the differential diagnosis for hypernatremia?

Back 196

iatrogenic sodium administration or water loss

Front 197

What is the differential diagnosis for hypokalemia? (3)

Back 197

GI losses, renal losses, transcellular shifts

Front 198

What urine K+ value characterizes hypokalemia due to GI loss and what are some possible etiologies? (4)

Back 198

Urine K < 30 mEq/day vomiting, NG tube, diarrhea, and villous adenoma

Front 199

What urine K+ value characterizes hypokalemia due to renal loss and what are some possible etiologies? (9)

Back 199

Urine K > 30 mEq/day diuretics, hypomagnesemia, antibiotics, mineralocorticoid excess, RTA types I and II, Cushing syndrome, congenital adrenal hyperplasia, and hyperrenism

Front 200

What's the possible etiology of transcellular shifts leading to hypokalemia? (2)

Back 200

alkalosis, correction of diabetic ketoacidosis

Front 201

What's a complication of correcting diabetic ketoacidosis?

Back 201

profound hypokalemia unless supplemental K is given

Front 202

What is pseudohyperkalemia?

Back 202

elevated potassium levels in absence of clinical evidence of hyperkalemia (doesn't need to be treated)

Front 203

What's a clue that hyperkalemia is due to in vitro release from red cells?

Back 203

visible hemolysis in the tube

Front 204

What chromosomal abnormality has been associated with passive transmembrane leak of potassium from red cells, without concomitant hemolysis?

Back 204

autosomal dominant abnormal gene on chromosome 16 (familial pseudohyperkalemia)

Front 205

What's the differential diagnosis for hyperkalemia? (6)

Back 205

acidosis, renal failure, potassium sparing diuretics, adrenal insufficiency, iatrogenic, rhabomyolysis

Front 206

Nearly all case of acidosis are associated with hyperkalemia except? (2)

Back 206

RTA types I and II in which K+ is low

Front 207

What electrolyte abnormalities characterize primary hypeparathyroidism? (4)

Back 207

increased Ca2+, decreased PO4, increased Cl-, and increased nephrogenous cAMP

Front 208

What's the effect o f PTH on renal tubules? (2)

Back 208

increasing Ca2+ resorption while increasing phosphate excretion

Front 209

What's the differential diagnosis of primary hyperparathyroidism? (3)

Back 209

parathyroid adenoma (most common), 4-gland hyperplasia, parathyroid carcinoma

Front 210

What is tertiary hyperparathyroidism?

Back 210

hyperparathyroidism that persists in post-renal transplant patients (parathyroids become autonomous)

Front 211

T/F hypercalcemia of malignancy is always caused by bone metastases

Back 211

F- can also occur in absence of bone metastases (humor hypercalcemia of malignancy)

Front 212

What is the most common mediator of humoral hypercalcemia of malignancy?

Back 212

PTH related protein (PTHrp)

Front 213

What lab findings are most suggestive of hypercalcemia of malignancy?

Back 213

increased nephrogenous cAMP in the presence of normal PTH

Front 214

What is the gene associated with familial hypocalciuric hypercalcemia?

Back 214

CASR gene on 3q

Front 215

What drugs are associated with hypercalcemia? (4)

Back 215

thazides, calcium containing antacids, calcium supplements, hypervitaminosis

Front 216

What endocrine disorders are associated with hypercalcemia? (3)

Back 216

hyperthyroidism, Addison, acromegaly

Front 217

What causes hypervitaminosis D and what is its effect on the kidneys?

Back 217

Caused by long term ingestion of vitamin supplements. Vit D enhances resorption of both calcium and phospate in the kidney (can lead to calciphylaxis)

Front 218

What granulomatous disease is associated with hypercalcemia and why?

Back 218

Sarcoid, the histiocytes of sarcoid have the capacity to activate vit D to the active form (1,25 di-hydroxy vitamin D)

Front 219

What are the clinical signs and symptoms of hypercalcemia? (8)

Back 219

nephrolithiasis, lethargy, hypo-reflexia, slowed mentation, nausea, vomiting, constipation, depression, and high peaked T waves on EKG

Front 220

What is calciphylaxis and what electrolyte abnormalities are associated with it?

Back 220

metastatic calcification of vessel walls and soft tissue, occurs when long term hypercalcemia and hyperphosphatemia occur concomitantly

Front 221

What forms of PTH are modern immunoassays able to detect? (4)

Back 221

Intact PTH (84 amino acids) N-terminal PTH, mid terminal PTH, and C-terminal PTH (all three of which are breakdown products produced in the parathyroids and in the blood)

Front 222

Which parathyroid forms have biological activity? (2)

Back 222

intact and N-terminal PTH

Front 223

Parathyroid Hormone (PTH) forms

Back 223

Biologic Activity Intact PTH + N- terminal PTH + Mid- region PTH - C-terminal PTH -

Front 224

What are the effect of PH change on ionized calcium measurement?

Back 224

Acidosis Increase Alkalosis Decrease

Front 225

What are the characteristics of the sample for ionized calcium measurement(5)?

Back 225

1) Must be from an artery 2) Must not be exposed to the air ( metabolism will change the PH) 3) Must not be drawn in calcium-chelating anticoagulants (EDTA, citrate) 4) Avoid prolong tourniquet 5) Must be kept cool and deliver to the lab rapidly

Front 226

What is the rule- of- thumb correction for Ca measurement in hypoproteinemia?

Back 226

0.8 mg/dl Ca per 1 g/ dl protein lost.

Front 227

Which tumors can secret PTH- related protein (PTHrP) (6)?

Back 227

SCC lung, head & neck, skin, cervix, esophagus and breast carcinoma.

Front 228

Secondary hyperparathyroidism

Back 228

Is due to peripheral resistance to the action of PTH (comonly seen in chronic renal insufficiency or vit.D deficiency), the Ca is low while the PTH is normal or high. It produces activation of osteoclasts, leading to brown tumors of bone (renal osteodystrophy).

Front 229

The effect of hypomagnesemia on PTH

Back 229

Acute hypomagnesemia cases increased PTH secretion but persistent or marked hypomagnesemia inhibits PTH secretion

Front 230

EKG changes in hypocalcemia(3)

Back 230

Lengthening of the QT interval, low voltage T waves, and dysarythmias

Front 231

D.D of Hypocalcemia (9)

Back 231

1) Vit. D deficiency 2) CRF 3) Drugs ( Heparin, glucagon, diuretics, aminoglycosides) 4) Hypoparathyroidism 5) Medulary thyroid cancer 6) Hypoproteinemia 7) Hyperphosphatemia 8) Pancreatitis 9) Massive transfusion

Front 232

Anion gap

Back 232

AG= Na - [ Cl + Hco3 ] Normal <12 Hypoalbuminemia can mask the anion gap Corrected anion gap= Na - [Cl + Hco3] + 2.5 (4 - albumin)

Front 233

Low anion gap causes (6)

Back 233

Paraproteinemia, hypoalbuminemia, hypermagnesemia, hypercalcemia, Lithium therapy, and hypophosphatemia

Front 234

Causes of metabolic acidosis with increased Anion Gap (7)

Back 234

Methanol, uremia, ketoacidosis( diabetic, starvation or Etoh), paraldehyde, lactic acidosis, ethylene glycol, salicylate

Front 235

Causes of metabolic acidosis with normal Anion Gap (7)

Back 235

RTA, diarrhea, recovery phase DKA, uterosigmoidostomy, NH4Cl, TPN, carbonic anhydrase inhibitors

Front 236

" BUN always underestimate GFR" False or True?

Back 236

True. Urea is freely filtered and partially reabsorbed by the nephrone; this reabsorption has a consequence that BUN always underestimate GFR. Reabsorption increases with hypovolemia, thus causes even more BUN understimation

Front 237

Creatinine underestimate GFR. False or True?

Back 237

False. Creatinine is freely filtered through the glomerulus, also a small amount of Creatinine is secreted by the tubules. Thus creatinine slightly overestimates GFR

Front 238

simplified GFR calculation formula

Back 238

CLcr = Ucr x Vur / Pcr,
Ucr: urine creatinine
Vur: volume of urine
Pcr: plasma creatinine

Front 239

The inverse relationship between GFR and creatinins is more linear in higher GFR. True or False?

Back 239

False. This relationship is more linear , when GFR is about half normal. Mild to moderate degrees of GFR impairment do not cause appreciable increase in the creatinine concentration.

Front 240

The Modificiation of Diet in Renal Disease (MDRD) formula for estimated GFR (eGFR) includes which variables?

Back 240

creatinine, age, sex, race

Front 241

True or False: Azotemia refer to a very high level of nonprotein nitrogen in the serum.

Back 241

False. It's BUN, not NPN.

Front 242

True or False: acidemia refers to arterial PH <7.0

Back 242

False, it's arterial pH<7.4

Front 243

True or False: alkalemia refer to arterial pH>7

Back 243

False, it's 7.44.

Front 244

Normal range of arterial blood pCO2

Back 244

40-44 mmHg

Front 245

Normal range of arterial blood bicarbonate

Back 245

24-28 mEq/L

Front 246

Normal range of anion gap

Back 246

3-10

Front 247

Normal arterial PaO2

Back 247

90-100 mmHg

Front 248

Normal arterial O2 saturation

Back 248

95%-98%

Front 249

Respiratory acidosis is due to

Back 249

too little elimination of CO2 by the lungs (hypoventilation).

Front 250

Respiratory alkalosis is due to

Back 250

too much elimination of CO2 by the lungs (hyperventilation).

Front 251

True or False: Compensation in primary respiratory disorders involves buffers and alterations in pulmonary handling of CO2.

Back 251

False, It's the renal handling of bicarbonate (HCO− 3).

Front 252

True or False: Compensation in primary metabolic disorders involves buffers and alterations in renal handling of bicarbonate (HCO− 3).

Back 252

False, It's the pulmonary handling of CO2.

Front 253

write out the Henderson-Hasselbach equation

Back 253

pH=pK+log(base/acid), what mainly constitutes the acid and base in the equation?

Hint 253

base: bicarb, acid, dissolved PaCO2

Front 254

co-oximeter measures which two serum proteins that pulse oximeter doesn't?

Back 254

methemoglobin and carbozyhemoglobin

Front 255

what form of hemoglobin that the all-mighty co-oximeter does not measure?

Back 255

sulfhemoglobin

Front 256

Is pulse oximeter the method of choice for detecting carbon monoxide poisoning?

Back 256

No, it's co-oximeter

Front 257

what serum measures are used in calculating the osmolal gap? (4)

Back 257

measured blood osmolarity, Na, Glucose, BUN

Front 258

Determine what type of acid-base disorder is this: pH and [HCO3] go same direction (bicarb usually < 25 mEq/L)

Back 258

Metabolic acidosis

Front 259

Determine what type of acid-base disorder is this: pH and [HCO3] go opposite direction (pCO2 usually > 44 mm Hg)

Back 259

Respiratory acidosis

Front 260

Determine what type of acid-base disorder is this: pH and [HCO3] go same direction (bicarb usually > 25 mEq/L)

Back 260

Metabolic alkalosis

Front 261

Determine what type of acid-base disorder is this: pH and [HCO3] go opposite direction (pCO2 usually < 40 mm Hg)

Back 261

Respiratory alkalosis

Front 262

how does the calculated anion gap change when there is hypoalbuminemia?

Back 262

the anion gap decreases, how to calculate the corrected anion gap?

Hint 262

corrected anion gap = anion gap +2.5(4-albumin)

Front 263

What is the normal BUN/creatinine ratio?

Back 263

10:1

When both BUN and creatinine are elevated maintaining this ratio is suggestive of what?

Hint 263

Intra-renal disease - glomerulonephritis and tubulointerstitial
Often refered to as renal azotemia

Front 264

When the BUN/creatinine ratio is elevated this suggests two possible problems, name them?

Back 264

Prerenal azotemia

And

Postrenal azotemia

Define these terms

Hint 264

Prerenal - when there is poor renal perfusion- hypovolemia, hypotension - and results are from BUN reabsorbtion being increased

Postrenal - results from renal obstruction

Front 265

A decreased BUN/creatinine ratio is rare and results from what two causes?

Back 265

Dietary insufficiency

And

Severe liver disease

Front 266

Name a protease inhibitor that is a better predictor than creatinine of future cardiac events in renal disease. It is independent of age, sex, or muscle mass.

Back 266

Cyststin C

Front 267

Normal proteinuria does not exceed how many mg/day?

Back 267

150 mg/day

This is mainly Tamm-Horsfall protein and small amounts of albumin.
The normal glomerulus filters protein based on what two properties?

Hint 267

Size and charge

Normally albumin does not freely cross the glomerular membrane.

Front 268

Significant proteinuria is usually defined as exceeding how many mg/day?

Back 268

300 mg/day

This is traditionally based on a 24-hour urine collection.

Front 269

What test can be used when a 24-hour urine is not possible?

Back 269

Urine protein:creatinine ratio

The urine protein assay is sensitive to all kinds of protein ( albumin, globulins, Bence-Jones), and has a low detection limit of 3 mg/dL.

A random urine sample, or spot urine, can be misleading, but the ratio is considered to be as good as the 24 hour urine)

Front 270

A urine dipstick is most sensitive to what protein?

Back 270

Albumin, the lower limit of detection is 18mg/dL

It is not sensitive to microalbuminuria, globulins, or Bence-Jones proteins.

Front 271

What two assays can be used to detect renal tubular dysfunction?

Back 271

B2-microglobulin
and
Lysozyme

These are freely filtered by the glomerulus and completely reabsorbed by the proximal convoluted tubule.

Their presence in urine suggests?

Hint 271

B2-microglobulin
and
Lysozyme

These are freely filtered then completely reabsorbed by the proximal convoluted tubule.

Front 272

Microalbuminuria is currently defined in terms of the albumin:creatinine ratio using what kind of sample?

Back 272

Spot urine, not 24-hour urine

Can detect as little as 0.3 mg/dL of albumin

Since the microalbumin assay is a homogeneous immunometric one, it is subject to what effect?

Hint 272

The hook effect. Or prozone effect.


In an agglutination or precipitation reaction, prozone or prezone is the zone of relatively high antibody concentrations within which no reaction occurs. In an agglutination test, a person's serum (which contains antibodies) is added to a test tube which contains a particular antigen. There are many types of different antibodies present in a persons serum, and there might be one particular antibody that will bind to antigen present in the tube. There are also other types of antibodies which would not bind the antigen. The antibody-antigen complex forms an agglutinate. In some cases, the concentration of antibody specific for a particular antigen is too low compared to other types of antibodies, and when this occurs, the small portion of agglutination that took place will be masked by larger aggregate of non-binding antibodies, and the mixture remain as fluid. The agglutination which took place is invisible, and this is called prozone. This can lead to false negative result. Therefore in each agglutination test, dilution of the antibody-antigen mixture is done to a certain level, until agglutination can be seen, or otherwise the test is negative.



How can one check this effect?

Front 273

The current recommendation of the national kidney foundation is annual testing for those individuals who are high risk, they include?

Back 273

People with diabetes, hypertension, or a family history of renal disease

Recommended screening includes what two measurements?

Hint 273

eGFR

And

Microalbuminuria screen (urine albumin:creatinine ratio), albumin is measured by the microalbumin assay.

Front 274

Chronic kidney disease is defined by one of two ways, name them.

Back 274

GFR > 60mL per 1.73m3 of body surface area, or

Albuminuria for 3 or more consecutive months

Front 275

There are 5 stages of chronic renal disease:
Stage one is proteinuria without decreased GFR
Stage two mild decrease in GFR
Stage three moderate
Stage four severe
Stage five?

Back 275

Renal failure, defined as?

Hint 275

GFR < 15 mL per minute per 1.73m3 or

Dialysis dependent

Front 276

The most common cause of renal cases acute renal failure is?

Back 276

Acute tubular necrosis

Acute glomerulonephritis may also cause renal ARF

Front 277

New onset of acute renal failure must have a battery of tests, these include a renal ultrasound, initial and serial BUN and creatinine, urine volume monitoring, BUN/creatinine ratio, urine osmolarity, and fractional excretion of sodium (FENa), urinalysis.

Back 277

Non-oliguric renal failure can occur in renal or Postrenal, but rarely Prerenal.

Front 278

Indications of dialysis includes (five)?

Back 278

Volume overload
Hyperkakemia
Metabolic acidosis
End organ damage due to uremia (pericarditis)
BUN > 100 gm/dL

Front 279

BUN/creatinine ratio, urine osmolarity, and fractional excretion of sodium (FENa)- this combination is useful is distinguishing renal from Prerenal. The FENa is almost always w (<1%) in Prerenal ARF. What is the exception?

Back 279

When the patient has been given a diuretic or has glycosuria.

The fractional excretion of urea can be an alternative.

Front 280

A lack of findings in urinalysis (or isolated byline casts) suggest?

Back 280

Prerenal ARF

Dysmorphic red blood cells and red blood cell casts suggest?

Hint 280

Glomerulonephritis


Pigmented casts suggest?

Front 281

Determination of the amniotic fluid bilirubin is part of the clinical evaluation of the pregnancy complicated by alloimmunization. The amniotic fluid bilirubin reflects?

Back 281

The degree of fetal hemolysis

Front 282

The concentration of bilirubin in amniotic fluid is proportional to absorbance. The maximal absorbance of bilirubin is at?

Back 282

450 nm

The difference between the actual absorbance and the norm 450) is plotted against the estimated gestational age.

Liley chart

Hint 282

This chart correlates with the previous chart as far as zone 1-3.

Unless the result falls in zone 3, serial measurements are taken.

If they are in zone 3 ( or in 2 and rising) then deliver if baby is term.

Front 283

What is hepatorenal syndrome?

Back 283

Development of progressive renal impairment in patients with severe end-stage liver disease, tere should be no other identifiable cause.

HRS has an incidence of about 5% of admissions for decompensated cirrhosis and about 50% over the course of cirrhosis.

HRS it thought to be due to what reason?

Hint 283

Dis regulation of renal blood flow.

Front 284

What is the most common cause of renal failure in a cirrhotic patient?

Back 284

Spontaneous bacterial peritonitis (SBP)

Nephrotoxic agents are also common ( NSAIDs, contrast)

Front 285

Renal biopsy in hepatorenal syndrome is essentially normal. An abnormal biopsy must be interpreted cautiously - many pts with cirrhosis have hepatitis viruses that can cause associated glomerulonephritis, and cirrhosis itself can lead to?

Back 285

An IgA like nephropathy

Front 286

What is the level of hCG in women with gestational trophoblastic disease compared to normal?

Back 286

Higher (usually complete moles hCG> partial moles)

Front 287

Which is more likely to be clinically diagnosed rather than histologically, partial or complete moles?

Back 287

Complete

Front 288

What's the characteristic clinical presentation for a complete mole? (5)

Back 288

Uterine enlargement greater than gestational age, vaginal bleeding, hypertension, absence of fetal heart tones, characteristic ultrasound

Front 289

Why must both types of molar pregnancies be monitored? (2)

Back 289

for 1) persistence of trophoblastic disease 2) development of malignant trophoblastic disease

Front 290

What's the risk of malignancy for molar pregnancies?

Back 290

<5% for partial moles and ~20% for complete moles

Front 291

1) What is the hCG monitoring schedule after the evacuation of a molar pregnancy? 2) How long after evacuation does hCG normally remain detectable?

Back 291

1) monitor weekly until hCG is undetectable for 3 consecutive weeks then monitor monthly for 1 year 2) hCG remains detectable for up to 10 weeks (in uncomplicated molar pregnancy)

Front 292

When is intevention warranted when monitoring hCG following evacuation of a molar pregnancy?

Back 292

If hCG levels plateau or rise then persistent GTD is suspected and may need chemotherapy following a metastatic workup

Front 293

1. T/F uterine choriocarcinomas are always preceeded by a molar pregnancy

Back 293

1. False, 1/2 follow a normal term pregnancy, 25% follow a normal spontaneous abortion, 25% follow a molar pregnancy

Front 294

What are the components of a "triple screen"? (3)

Back 294

hCG, AFP, and unconjugated estriol (uE)

Front 295

When is the triple screen normally performed and on what type of specimen?

Back 295

perfomed on serum drawn during 2nd trimester, ideally around 18 weeks

Front 296

What's the sensitivity of the triple screen for Down's syndrome?

Back 296

0.7

Front 297

1) What are the components of the "Quad test"? (4) 2) What is its sensitivity for detection of Down's syndrome?

Back 297

1) hCG, AFP, unconjugated estriol, and dimeric inhibin A 2) 80%

Front 298

What's the advantage of quad test over triple screen?

Back 298

Concentration of dimeric inhibin A is fairly stable throughout the 2nd trimester so it is less prone to error based on inaccurate gestational age

Front 299

1) What is the "integrated screen" for detection of trisomy and neural tube defects? 2) What is its sensitivity in detecting Downs?

Back 299

1) Pregnancy associated plasma protein A (PAPP-A) and hCG measured 1st trimester then AFP, unconj. estriol and inhibin A measured 2nd trimester and data combined 2) sensitivity 85% (90% if combined with measurement of nuchal fold thickness)

Front 300

What effects do the following maternal conditions have on prenatal screening for trisomy and neural tube defects? 1. diabetes 2. smoking

Back 300

1. both unconj. estradiol (uE) and hCG are decreased mildly 2. MSAFP increased, uE and hCG decreased

Front 301

What is the sensitivity of prenatal screening for Down's syndrome in twin gestations?

Back 301

50-70%

Front 302

1. What are the characteristic serum findings in prenatal screening for a fetus with trisomy 18 (Edward syndrome)? (3) 2. What percentage of cases with this pattern are actually affected? 3. What percentage of cases are detected with screening?

Back 302

1. decreased AFP, decreased hCG, decreased unconj. estriol 2. 10% 3. 80%

Front 303

What are the characteristic serum findings in prenatal screening for a fetus with neural tube defects?

Back 303

increased AFP, normal hCG, decreased unconj. estradiol

Front 304

What percentage of cases with increased maternal serum AFP are due to neural tube defects?

Back 304

0.1

Front 305

If an elevated maternal serum AFP is deemed to be caused by a neural tube defect what's the next step in the patient's workup?

Back 305

obtain amniotic fluid for AFP and acetylcholinesterase

Front 306

What is the sensitivity of maternal serum AFP for detecting neural tube defects in singleton and multiple gestations?

Back 306

singleton 90% multiple 30%

Front 307

1. What are the characteristic maternal serum findings when fetus has Down's syndrome? (4) 2. What follow up is recommended when they're found?

Back 307

1. decreased AFP, increased hCG (roughly 2 times normal), decreased unconjugated estradiol, decreased inhibin 2. high resolution ultrasound and amniocentesis for cytogenetics

Front 308

1.What is alpha fetoprotein (AFP)? 2. How do levels change in normal pregnancy? 3. What maternal characteristics require adjustments in AFP interpretation? (4)

Back 308

1. principle plasma protein in the fetus 2. rises progressively during 1st and 2nd trimesters 3. maternal weight, race, number of fetuses, and maternal diabetes

Front 309

How do the following affect AFP? 1. maternal weight 2. number of fetuses 3. maternal diabetes

Back 309

1. has a dilutional effect (falsely low values) 2. levels tend to be much higher 3. levels are much lower

Front 310

1. What unit is used to compare maternal serum AFP (MSAFP)? 2. what value indicates increased risk of neural tube defect? 3. What value is considered abnormal in maternal diabetes? multiple gestation?

Back 310

1. multiples of the median (MOM) 2. >2.5 MOM (present in >80% of cases) 3. diabetes >2.0 MOM, multiple gestations >4.5 MOM

Front 311

What conditions are associated with an increased maternal serum AFP? (13)

Back 311

neural tube defects, omphalocele, gastroschisis, renal anomalies, sacrococcygeal teratoma, cystic hygroma, hydrops fetalis, Turner syndrome, bowel obstruction, twins, wrong gestational age, fetal demise, fetal-maternal hemorrhage

Front 312

1. T/F decreased unconjugated estriol is sensitive for both Down syndrome and trisomy 18 2. What other congenital abnormalities is it associated with? (2)

Back 312

1. False weakly sensitive for Down syndrome but a good indicator for trisomy 18 2. also decreased in Smith-Lemli-Optiz syndrome (SLOS) and inherited (fetal) deficencies of steroid sulfatase

Front 313

1. Where is dimeric inhibin A produced? 2. what level of elevation is associated with Down syndrome

Back 313

1. it's a glycoprotein produced by the placenta 2. increased an average of 1.9 MOM in Down syndrome fetus

Front 314

What markers have demonstrated some (although limited) utility in predicting preterm labor? (3)

Back 314

serum estradiol, salivary estriol, screening for bacterial vaginosis

Front 315

Where is fetal fibronectin normally found and when can it be detected in cervicovaginal fluid?

Back 315

normally found at placental fetomaternal inferface. Can be detected briefly during early gestation then absent until just before labor

Front 316

1. What's the utility of fetal fibronectin in detecting preterm birth? 2. When should it be collected?

Back 316

1. its absence has a very high negative predictive value and can exclude preterm labor, its presence suggests onset of preterm labor but positive predictive is very low 2. greater than 24 hours after the last cervical exam or sexual intercourse

Front 317

What is the major phospholipid produced by mature type II pneumocytes and what are its major components?

Back 317

lecithin- majority is disaturated phosphatidylcholine (DPC), lesser amounts of phosphatidylglycerol (PG), phosphatidylinositol (PI), phosphatidylethanolamine (PE), and sphingomyelin

Front 318

1. During which gestational ages is fetal lung maturity assesment most critical? 2. When might it be indicated for term pregnancies?

Back 318

1. between 34-37 weeks gestation 2. poorly controlled maternal diabetes

Front 319

1. What is the best specimen for fetal lung maturity? 2. What would be considered a suboptimal specimen?

Back 319

1. Uncontaminated amniotic fluid obtained by amniocentesis 2. suboptimal specimen vaginal pool specimens which may be contaminated by blood or meconium

Front 320

T/F mosts tests for fetal lung maturity are better at predicting maturity than immaturity

Back 320

True - mature result is fairly reliable, immature result needs confirmation with another technique

Front 321

How do the the following change with increasing gestational age: 1. lecithin (L) concentration? 2. sphingomyelin (S) concentration? 3. L:S ratio?

Back 321

1. increases 2. remains the same 3. around 1:1 until 26 weeks then ration increases until ratio of 2:1 reached around 35 weeks

Front 322

1. What lecithin/sphingomyelin ratio indicates fetal lung maturity? 2. above the ratio in #1 what percentage of of premature infants will develop RDS? 3. below the ratio in #1 what percentage of of premature infants will develop RDS?

Back 322

1. 2:1 2. 2% 3. 60%

Front 323

How do the following influence the interpretation of the lecithin/sphingomyelin ratio? 1. maternal diabetes mellitus 2. presence of meconium 3. presence of blood

Back 323

1. ratio 2:1 doesn't ensure maturity (phosphatidylglycerol should be used) 2. falsely decrease the L:S ratio 3. normalizes the L:S to around 1.5

Front 324

Phosphatidylglycerol 1. when can it first be detected in the aminotic fluid? 2. what does its presence indicate? 3. T/F Its concentration is not effected by blood or meconium. 4. measurable by what 2 methods?

Back 324

1. around 36 weeks 2. fetal lung maturity 3. True (thus it is test of choice for contaminated specimens) 4. TLC or agglutination (equally reliable)

Front 325

1. What is the foam stability index? 2. How is it performed? 3. What value is considered indicative of fetal lung maturity?

Back 325

I1. ndication of concentration of surfactant in amniotic fluid (AF), which forms a film that can support the structure of a foam. 2. AF serially diluted with ethanol, highest concentration at which a complete ring of bubbles is seen is the foam stability index. 3. > 0.47

Front 326

1. How is surfactant lamellar body number density (LBND) measured? 2. What value is predictive of fetal lung maturity?

Back 326

1. the platelet channel of a cell counter can quantify them since they're about the same size as platelets 2. >50,000

Front 327

1. What is the disaturated phosphatidylcholine concentration used for? 2. what does it measure 3. In what clinical scenario is useful?

Back 327

1. it's an alternative to the lecithin/sphingomyelin ratio 2. determines the major component of lecithin directly 3. useful when only contaminated amniotic fluid specimen is available (unaffected by blood or meconium)

Front 328

1. What test is used most commonly to predict fetal lung maturity? 2. what value is considered mature? immature? 3. what effect does blood have on the values? 4. what value is considered mature even in the presence of blood?

Back 328

1. fluorescence polarization assay (FPA) 2. <260 considered mature, >290 considered immature 3. <0.5% blood values unaffected, greater amounts tend to have a parodoxical effect on the FPA values 4. <230 considered mature

Front 329

What effect does pregnancy have on maternal: 1. serum triglycerides? 2. albumin and total protein? 3. GFR? 4. transport proteins?

Back 329

1. increased by 40% (often causes a low-level ketosis) 2. decreased (hemodilution) 3. increased (due to increased blood volume) 4. increased (due to increased estrogen)

Front 330

What effect does pregnancy have on maternal: 1. BUN? 2. creatinine? 3. urate?

Back 330

1. decreased 2. decreased 3. decreased

Front 331

1. How does insulin resistance change during pregnancy? 2. What mediates this change?

Back 331

1. improved glucose tolerance until mid 2nd trimester then relative insulin resistance 2. human placental lactogen

Front 332

1. What is the incidence of DVT during the antepartum and postpartum period? 2. PE?

Back 332

1. 1/2000 antepartum and 1/700 postpartum 2. 1/2500

Front 333

1. What effect do autoimmune diseases have on pregnancy in general? 2. SLE? 3. Graves? 4. myasthenia gravis

Back 333

1. generally no effect 2. often exacerbated 3. common to have post-partum flareups 4. common to have post-partum flareups

Front 334

1. What neonatal complication can result from maternal idiopathic thrombocytopenic purpura (ITP)? 2. What must this complication be distinguished from? 3. What's a life threatening complication of either?

Back 334

1. ITP antibodies can cross the placenta causing neonatal thrombocytopenia 2. Neonatal alloimmune thrombocytopenia 3. neonatal intracranial hemorrhage

Front 335

1. What affect does pregnancy have on systemic lupus erythematosis? 2. Does it change throughout pregnancy?

Back 335

1. increases risk of flare ups 2. risk higher in early pregnancy and during puerperium, relative quiescence in latter half of pregnancy

Front 336

Why might it be difficult to distinguish a lupus flare up from pregnancy induced hypertension (PIH) and what test can aid the distinction?

Back 336

both can cause hypertension, edema, and proteinuria. Distinction can be aided by complement levels (low in SLE flare, normal in PIH)

Front 337

T/F mortality is increased in pregnant women with SLE

Back 337

true (most deaths result of pulmonary hemorrhage due to lupus pneumonitis)

Front 338

Why is it important to distinguish a lupus flare up from pregnancy induced hypertension (PIH)

Back 338

treatments very different (delivery for PIH and steroids for SLE)

Front 339

1. What is thought to be responsible for recurrent miscarriage, abortion, and preterm labor in SLE patients? 2. What's the treatment?

Back 339

1. lupus anticoagulant 2. anticoagulation (not corticosteroids)

Front 340

What conditions are neonates born to mothers with SLE at greater risk for? (3)

Back 340

IUGR, preterm labor, congenital heart block (mediated by Ro and La antibodies)

Front 341

1. How is the diagnosis of asymptomatic bacteriuria made? 2. what's the incidence in pregnant women? 3. what's the associated complication? 4. what's the most common causative agent?

Back 341

1. clean catch voided urine specimen with >100,000 bacterial colonies/mL 2. 10-20% (same as in nonpregnant women) 3. associated with development of UTI with high risk of pyelonephritis 4. Escherichia coli

Front 342

1. What is Sheehan syndrome? 2. What causes it? 3. What are the clinical symptoms?

Back 342

1. postpartum hypopituitarism 2. pregancy-associated pituitary enlargement and severe blood loss duing delivery 3. inability to lactate, lethargy, weakness, and weight loss

Front 343

1. Why is there an increased incidence of thyroid disorders during pregnancy? 2. What is responsible for the increase? 3. Which is more common in pregnancy hyper- or hypothyroidism? 3. What the best test of thyroid status in pregnancy?

Back 343

1. increased demand on thyroid due to increased thyroid-binding globulin and TSH like effect of hCG 2. hypothyroidism (esp in patients with borderline thyroid function or availability to iodine) 3. serum TSH

Front 344

What causes transient hyperthyroidism of hyperemesis gravidarum?

Back 344

high levels of hCG (thought to be most common cause of hyperthyroidism in pregnancy)

Front 345

A 25y/o female in late preganancy presents with nausea, RUQ pain, and jaundice. She eventually becomes confused. If acute fatty liver of pregnancy is suspected, what do you expect to see on histologic examination of the liver? What is the treatment of choice?

Back 345

Widespread microvesicular steatosis (especially around Zone 3-pericentrally), with little inflammation or hepatocellular necrosis.

Delivery of the baby

Front 346

What hematologic problem is common in acute fatty liver of pregnancy?

Back 346

DIC

Front 347

A woman in her 3rd trimester of pregnancy presents with jaundice and itching. If cholestasis of pregnancy is suspected, what laboratory findings can you expect? (6 things)

Back 347

Elevated Alk Phos (massively), increased GGT, increased 5'-nucleotidase, direct bilirubinemia (but less than 5mg/dL), normal or mildly elevated transaminases, increased bile acids *** (most characteristic)

Front 348

What are the typical histological findings in cholestasis of pregnancy?

Back 348

dilated canaliculi containing bile plugs, especially in pericentral (zone 3) region

Front 349

Name 4 tests that might be undertaken to evaluate "recurrent pregnancy loss:"

Back 349

Parental or abortus karyotyping, endometrial biopsy, thyroid function, lupus anticoagulant

Front 350

What is luteal phase defect defined as in regards to endometrial biopsy?

Back 350

endometrial histology that is 2 or more days discrepant with dates

Front 351

3 Clinical applications of Toxicology?

Back 351

Drugs of abuse screening, overdose management, therapeutic drug monitoring

Front 352

Define half-life:

Back 352

The time it takes for the drug concentration to reach 1/2 of the starting amount

Front 353

What is first-order kinetics?

Back 353

The rate of loss is exponential during drug elimination

Front 354

What is steady-state, when speaking of drug metabolism? (conceptually)

After how many doses does this usually occur?

Back 354

the amount of drug leaving the body equals the drug entering the body.

Typically reached after 5 doses given at an interval of 1 half-life each.

Front 355

When do the peak and trough of drug dosages occur?

Back 355

Peak: soon after a dose (typically)

Trough: just before a dose

Front 356

What is the most common thing that circulating drugs are bound to?

Back 356

Albumin

Front 357

Which part is the active component of the drug, free or bound?

Back 357

Free

Front 358

Increasing the amount of a protein that binds drugs into the circulation will do what to a drug's availability?

Back 358

Less free drug is available, and thus may have a weaker effect than anticipated for a dose

Front 359

A patient is taking Drug A, a drug with a narrow therapeutic window. He is prescribed a new Drug B. Three days later, he is admitted to the ER with toxicity of Drug A. What could be a mechanism involved in this that includes binding proteins?

Back 359

Likely Drug B displaced Drug A off of a binding protein, increasing the amount of Drug A available

Front 360

Which drugs remain tightly confined in the vascular space, lipophobic (aka-hydrophilic) or lipophilic (hydrophobic)?

Back 360

Lipophobic/hydrophilic

Front 361

The degree to which a drug can distribute into various body tissues (vasculature, adipose tissue, interstitium, etc) is defined as its:

Back 361

Volume of distribution

Front 362

What equation can calculate a drugs volume of distribution?

Back 362

Vd=D/C

where D= dose and C=resulting measured plasma concentration

Front 363

What is the most typical specimen received for drug screening (drugs of abuse)?

Back 363

Urine

Front 364

Urine drug of abuse screens have a low or high sensitivity?

Low or high specificity?

Back 364

High sensitivity

Low specificity

Front 365

What method is most frequently employed in drug of abuse screens?

Back 365

Immunoassay

Front 366

Why does every positive drug of abuse screen require confirmation?

Back 366

False positives due to cross-reactivity can occur

Front 367

What methods are typically used for confirmatory testing for a positive drug of abuse screen?

Back 367

Mass spectrometry and or gas chromatography

Front 368

What is "chain of custody?"

Back 368

A method insuring that a specimen that will have potential consequences is under control of someone or in locked storage at all times.

Front 369

Name 7 different checks that can be performed to evaluate a urine sample for adulteration:

Back 369

Color, Odor, Temperature, pH, Specific gravity, creatinine, nitrite

Front 370

What is the half-life of Cocaine?

Back 370

1:00:00

Front 371

How long is cocaine detectable in testing?

Back 371

24-72 hours

Front 372

Key metabolites of cocaine:

Back 372

benzoyl ecgonine methyl ester

Front 373

What is the half-life of heroin?

Back 373

0:03:00

Front 374

How long is heroin detectable in testing?

Back 374

72:00:00

Front 375

Key metabolite of heroin:

Back 375

6-acetyl morphine

Front 376

What is the half-life of amphetamine?

Back 376

0:30:00

Front 377

How long are amphetamines detectable in testing?

Back 377

72:00:00

Front 378

2 key metabolites of amphetamines:

Back 378

norepinephrine and phenylacetone

Front 379

What is the half-life of PCP?

Back 379

0:30:00

Front 380

How long is PCP detectable in testing?

Back 380

72:00:00

Front 381

2 metabolites of PCP:

Back 381

hyroxylated and gluconarated PCP

Front 382

What is the half-life of cannabis?

Back 382

8 hours (wow!)

Front 383

How long is cannabis detectable in testing?

Back 383

Weeks

Front 384

What is the key metabolite of cannabis?

Back 384

delta-9-THC-COOH

Front 385

What is physiologic basis of chest pain in cocaine users?

Back 385

Vasoconstriction with concurrent increased rate and blood pressure

Front 386

What happens to the specificity of myoglobin, CK-MB, and troponin I in cocaine-induced myocardial infarction?

Back 386

CK-MB and myoglobin specificity decrease due to skeletal muscle effects, but Troponin I stays the same

Front 387

Acute intoxication with opiates can lead to: (name 5 symptoms)

Back 387

Sedation, pinpoint pupils, constipation, bradycardia, and hypotension (also respiratory depression)

Front 388

What drug is commonly used to counteract opioid intoxication?

Back 388

Narcan (Naloxone) (also Nalmefene) are synthetic opioid antagonists that counteract the opioid effects

Front 389

Withdrawl from opiates commonly causes the following: (name 7 symptoms)

Back 389

increased lacrimation, rhinorrhea, diaphoresis, dilated pupils, tachycardia, irritability, restlessness

Front 390

What is methadone?

Back 390

A long-acting opioid that can be used to help withdrawl symptoms (less high, more sustained treatment of all withdrawl symptoms)

Front 391

What is clonidine's role in opioid withdrawl?

Back 391

It does not interact with the opiod receptors (like methadone does) but counteracts the symptoms through other mechanisms.

Front 392

Why does propoxyphene cause more symptoms than other opioids?

Back 392

It (and its metabolite) have a interference with calcium channels of the heart, very similar to quinidine.

Can cause cardiac conduction abnormalities and even seizures

Front 393

How do barbituates act on the CNS?

Back 393

They facilitate GABA (a depressant) effect in the CNS, especially in the medulla

Front 394

How do amphetamines (and methamphetamines) act on the CNS?

Back 394

Mediate release of dopamine

Front 395

What are long-term effects of meth and amphetamine use that are related to their mechanism of action?

Back 395

The release of dopamine eventually depletes and destroys the dopamine secreting cells of the substantia nigra and cause Parkinsonian syndrome (it's irreversible!)

Front 396

How does phencyclidine (PCP) act on the CNS?

Back 396

It acts on blocking catecholamine re-uptake

Front 397

What unique symptomatology often occurs with PCP use? (2 things)

Back 397

Its especially known for psychiatric effects. Horizontal nystagmus is very often seen.

Front 398

What other lab testing, besides a drug screen, must be carried out in those individuals suspected of having PCP intoxication?

Back 398

Glucose monitoring: often can cause hypoglycemia
CK and BUN: can cause rhabdomyolysis

Front 399

At what blood alcohol level does coma/death occur?

Back 399

>0.4 % BAC

Front 400

Outline the steps of alcohol metabolism:

In what organ does this occur?

Back 400

Liver

Ethanol metabolized by alcohol dehydrogenase to acetaldehyde.

Acetaldehyde is then converted by aldehyde dehydrogenase to acetic acid

Front 401

What type of tube should whole blood for alcohol testing be submitted in?

Back 401

Sodium fluoride and potassium oxalate will prevent increases (from fermentation) or decreases in the level

Front 402

What methodology is used for analyzing blood for alcohol content?

Back 402

Enzymatic method utilizing alcohol dehydrogenase

Front 403

What is the short-coming is using an alcohol dehydrogenase method for analyzing blood alcohol content?

Back 403

Only measures ethanol, will not pick up methanol

Front 404

What principle is used for analyzing breath alcohol?

Back 404

Since blood alcohol diffuses across alveolar septa and is excreted in expiration, the level can be measured in breath

Front 405

What is the ratio of blood:breath alcohol?

Back 405

12/31/1899 11:00:01

Front 406

What liver function test is often increased in chronic alcohol users?

When does it increase?

Back 406

GGT (gamma glutamyl transferase)

>4 drinks per day for more than 4 weeks

4 weeks of abstinence to decrease

Front 407

Wat is CDT? What is it being used for evaluating?

Back 407

Carbohydrate deficient transferrin: being investigated as a marker of heavy alcohol consumption. More specific than GGT, at least as sensitive as GGT. Raises sooner than GGT.

Front 408

Which 2 populations may not be as easy to monitor with CDT levels? Why?

Back 408

Women: they have naturally higher CDT, and it doesn't rise as much with alcohol.

Those with chronic liver disease--they have elevated levels of CDT without drinking being involved

Front 409

What RBC parameter measured by a CBC (or peripheral smear review!) is elevated with heavy alcohol consumption?

Back 409

MCV

Front 410

How is anion gap calculated?

Back 410

Sodium - (Chloride + BIcarb) = anion gap

Front 411

When is an increase in anion gap significant?

Back 411

20 mEq/L or higher is significant

Front 412

What is an important cause of decreased anion gap?

Why is this important?

Back 412

Hypoalbuminemia. For every 1gram decrease, there is a 2.5 mEq decrease in anion gap.

Important because this could "mask" an increase in anion gap!

Front 413

An increase in anion gap can lead typically to acidosis or alkalosis?

Back 413

Acidosis

Front 414

Numerous toxins cause anion gap metabolic acidosis: (listed are 12)

Back 414

Acetominophen, Salicylates, ascorbate, hydrogen sulfide, ethylene glycol, methanol, ethanol, formaldehyde, carbon monoxide, nitroprusside, epinephrine, paraldehyde

Front 415

What is a toxidrome?

Back 415

A set of symptoms that can suggest a particular agent or group of agents have been ingested

Front 416

toxidrome: Hyperthermia, dry skin, flushing, altered mental status, psychosis, mydriasis, constipation, what acronym?

Back 416

“hot as a hare, dry as a bone, red as a beet, mad as a hatter”, what category?

Hint 416

Anticholinergic, which drugs besides Atropine?

Front 417

Salivation, lacrimation, urination, diarrhea, GI cramps, emesis (); diaphoresis, miosis, and wheezing, what acronym?

Back 417

“SLUDGE”, what category?

Hint 417

Cholinergic, which drugs?

Front 418

Hypertension, tachycardia, mydriasis, anxiety, hyperthermia, what category?

Back 418

Adrenergic, which drugs?

Hint 418

Amphetamines, Cocaine, Pseudoephedrine Ephedrine, PCP

Front 419

Altered mental status, slurred speech, hypopnea/apnea, what type of drugs?

Back 419

1. Sedative, 2. Narcotic, names?

Hint 419

Barbiturates, Opiates

Front 420

Hallucinations, anxiety, hyperthermia, what type of drugs?

Back 420

Hallucinogenic, names?

Hint 420

LSD, PCP, Amphetamines, Cocaine

Front 421

In an overdose case, workup includes?

Back 421

1. tox screening; 2. calculate anion gap; 3. calculate osmal gap; 4. measure blood gas

Front 422

When is the anion gap significant in a overdose case?

Back 422

An increase in the anion gap to >20 mEq/L is significant.

Front 423

Roughly, how does alterations in albumin affect anion gap?

Back 423

for every 1 gram decrease in albumin, there is a 2.5 mEq decrease in the anion gap

Front 424

What are the chemicals that you will never realize that they will cause increased anion gap metabolic acidosis?

Back 424

ethylene glycol, methanol, ethanol, formaldehyde, nitroprusside, epinephrine

Front 425

In general, what type of agents will cause increased osmolal gap?

Back 425

all kinds of alcohols, ehtanol, methanol, glycerol, acetone, etc.

Front 426

When the same sample from a alcohol intoxication case was sent to lab A and lab B, lab A detected increased osmalol gap but not lab B?

Back 426

Lab A used freezing point depression osmometry, while Lab B has less-used vapor pressure osmometry.

Front 427

What do you call the difference between the saturation given by co-oximetry and the saturation given by the ABG analyzer?

Back 427

oxygen saturation gap

Front 428

Causes of an increased oxygen saturation gap (4)

Back 428

carbon monoxide poisoning (carboxyhemoglobin), methemoglobin, hydrogen sulfide poisoning (sulfmethemoglobin), and cyanide poisoning

Front 429

Why does the ABG analyzer falsely report a high oxygen saturation when there is carbon monoxide poisoning or sulfide poisoning?

Back 429

The ABG analyzer consider them to be oxyhemoglobin!

Front 430

An abnormally high venous oxygen content (arteriolization of venous blood) is seen in (2)

Back 430

cyanide and hydrogen sulfide poisoning

Front 431

How useful is the oxygen saturation gap when it refers to the difference between the percent oxyhemoglobin given by the ABG analyzer and that given by the pulse oximeter?

Back 431

it might reflect the presence of carboxyhemoglobin or methemoglobin, but the precise numbers are hard to predict

Front 432

Antifreeze contains which alcohol?

Back 432

Ethylene glycol

Front 433

rubbing alcohol contains which alcohol?

Back 433

isopropanol

Front 434

windshield washer fluid contains which alcohol?

Back 434

Methanol

Front 435

common Toxic Alcohol Poisoning agents all cause increased anion gap, true or false?

Back 435

False. Isopropanol doesn't.

Front 436

most common Toxic Alcohol Poisoning agents cause increased anion gap, true or false?

Back 436

False. Only ethanol might.

Front 437

in suspected methanol or ethylene glycol intoxication, what surrogate marker to use if direct tests are not available?

Back 437

Osmalol gap

Front 438

Which alcohol intoxication does not cause acidosis but does create an osmolal gap

Back 438

isopropanol

Front 439

What does the urine crystal look like in ethylene glycol intoxication?

Back 439

envelope-shaped, translucent, and birefringent, what's in it?

Hint 439

calcium oxalate

Front 440

which alcohol intoxication result in ocular toxicity?

Back 440

Methanol

Front 441

Lead is toxic to cells in which 2 ways?

Back 441

nonspecifically binds to and inhibits enzymes bearing sulfhydryl groups, many in the heme synthesis, and it is directly toxic to mitochondria.

Front 442

Iron deficiency and lead toxicity frequently coexist. The effect of iron deficiency is to enhance the toxic effects of lead in two ways:

Back 442

1.The final step in biosynthesis of heme, in which iron is incorporated into protoporphyrin, is further inhibited by a deficiency of iron.
2.In an attempt to upregulate intestinal absorption of iron, there is the unintended effect of increased absorption of lead.

Front 443

What shows in the peripheral smear of a lead poisoning?

Back 443

microcytic, hypochromic anemia with basophilic stippling

Front 444

What renal function changes (other than elevated BUN and creatinine) are seen in long-term lead toxicity?

Back 444

aminoaciduria, glycosuria, and phosphaturia, what causes these?

Hint 444

Mitochondrial toxicity leads to reduced ATP available to drive the numerous ATP-dependent channels involved in tubular epithelial function

Front 445

What is the cutoff for the blood lead level?

Back 445

10ug/dL

Front 446

If blood lead levels ‘rebound’ during treatment, what tests to use to distinguish false increase from true increase?

Back 446

free erythrocyte protoporphyrin or (FEP) or zinc protoporphyrin (ZPP) should not be increased in false rebound; they are intermediate products in heme synthesis

Front 447

Can we use capillary blood obtained from heel- or finger-sticks for lead levels?

Back 447

No. It's not accurate. Unless you test for FEP or ZPP, which is only sensitive for high level toxicity.

Front 448

name a few chelators used in treatment for lead poisoning

Back 448

dimercaprol (also known as British antilewisite or BAL), CaNa-EDTA, D-penicillamine, and succimer

Front 449

What level of blood CO will lead to coma and death?

Back 449

>50%

Front 450

Why infants are at greater risk for CO poisoning?

Back 450

CO has higher avidity for fetal hemoglobin

Front 451

venous blood is as good as arterial for CO level determination, true or false?

Back 451

TRUE

Front 452

The half life T½ of CO on 100% O2 is:

Back 452

1 hour

Front 453

What is the major organ disfunction of Acetaminophen toxicity?

Back 453

liver

Front 454

What is the Rumack-Matthew nomogram used for?

Back 454

To predict the risk in acetaminophen toxicity

Front 455

For an acetaminophen toxicity case, should be the initial blook sample drawn immediately after the patient arrives in the ER?

Back 455

No, it should be drawn 4 hours after the ingestion, for full absorbtion.

Front 456

When to administer N-acetylcysteine for acetaminophen toxicity cases?

Back 456

When the risk falls into the probable and possible hepatic toxicity categories in the Rumack-Matthew nomogram.

Front 457

In acetaminophen toxicity cases presenting late, samples drawn greater than 2–3 hours apart can be used to estimate the elimination half-life of acetaminophen in the patient. If the half-life is >4 hours, then hepatic necrosis is likely, why?

Back 457

patients with hepatic damage after overdose may exhibit a more prolonged acetaminophen half-life

Front 458

How does the serum bilirubin level affect the measured acetaminophen level?

Back 458

Hyperbilirubin cause elevated acetaminophen readings

Front 459

How does chronic ethanol use affect acetaminophen toxicity?

Back 459

Chronic alcohol use induces the P450 system, increases the proportion of acetaminophen processed to NAPQI, enhancing toxicity.

Front 460

True or False: Hyperbilirubinemia causes false negative Acetaminophen level?

Back 460

False.Hyperbilirobinemia causes "False Positive" Acetaminophen level mainly because of its broad spectrophotometric absorbanse.

Front 461

In which organ Acetaminophen is metabolized?

Back 461

Liver

Front 462

What are the two main pathways for handling acetaminophen in Liver?

Back 462

1) Mostly conjugation with glucuronide or sulfate to forme nontoxic metabolite. 2) A small amount is metabolized by P450 system into the toxic metabolite N-acetyl-p-enzoquinoneimine(NAPQI)

Front 463

How the liver detoxified the acetaminophen toxic metabolite(N-acetyl-p-enzoquinoneimine)?

Back 463

NAPQI is detoxified by glutathion

Front 464

True or False: Any agent that induces P450 system decreases acetaminophen toxicity?

Back 464

False.They increase the proportion of acetaminophen processed to NAPQI, enhancing toxicity, for example chronic ethanol use has this effect.

Front 465

What kind of liver pathology can we see in Acetaminophen toxicity?

Back 465

Centrilobular (zone 3) hepatic necrosis with periportal sparing that causes mostly by NAPQI metabolite.

Front 466

False or true: N-acetyl-p-enzoquinoneimine is only toxic for liver?

Back 466

False. Its formation within hepatocytes makes the liver primary target, but other organs may be affected.

Front 467

What is the mainstay of acetaminophen toxicity treatment?

Back 467

N-acetylcysteine (Mucomyst)

Front 468

What is N-acetylcysteine (Mucomyst) mechanism in acetaminophen toxicity? treatment?

Back 468

It promotes acetaminophen metabolism via the conjugation pathways, thereby decreasing the formation of the toxic metabolite NAPQI

Front 469

What are the usual ways for Cyanide poisoning?

Back 469

1) inhalation of smoke from a fire (present in insulation) 2) industrial exposure (present in pesticide nad other industrial materials) 3) Suicide or homicide attempt

Front 470

What is the Cyanide poisoning mechanism?

Back 470

It bindes to and inhibites cytochrome a3, thus uncoupling the electron transport system.

Front 471

True or False: Cyanide poisoning causes non anion-gap metabolic acidosis?

Back 471

False,it causes anion-gap metabolic (lactic) acidosis.

Front 472

What are clinical presentation of acute Cyanide poisoning?

Back 472

Cherry-red skin color, hyperpnea followed by apnea and loss of consciousness and bitter almond odor on patient's breathin.

Front 473

True or False: Cyanide is rapidly metabolized to thiocyanate which persists for a long period of time and is more reliable for the diagnosis?

Back 473

TRUE

Front 474

True or False:? A normal serum Lactate exclude cyanide poisoning?

Back 474

True, all patients exposed to Cyanide should have an elevated serum lactate and an anion gap metabolic acidosis

Front 475

False or True: Cyanide-poisoned patients have hypoglycemia?

Back 475

False, they have hperglycemia due to decreased utilization.

Front 476

How blood gases, performed by co-oximetry can be informative in Cyanide poisoning?

Back 476

First, if compared to venous blood it shows a decrease in the arterial- venous oxygen gap ( due to decrease utilization). Second, the co- oximeter can specifically measure carboxyhemoglobin and methemoglobin, removing them from the differential diagnosis.

Front 477

Cyanide poisoning treatment?

Back 477

Administration of sodium nitrate and amylnitrate leads to formation of methemoglobin, which binds available cyanide. Then sodium thiosulfate, which reacts with cyanomethemoglobin to form thiocyanate that can be cleared by kidney.

Front 478

Aspirin effects on acid-base balance?

Back 478

First, it directly stimulate the respiratory center within the medula oblaganta, promoting respiratory alkalosis. Second, it uncouples oxidative phosphorilation and inhibits Krebs cycle, shunting energy production towards anaerobic pathways with the development of a metabolic acidosis.

Front 479

The earliest sign of salicylate toxicity?

Back 479

Tinnitus and dizziness

Front 480

True or False:The acid- base disorder in salicylate toxicity is triphasic?

Back 480

True, 1) between 3-8 hours following ingestion, respiratory alkalosis due to stimulation of the respiratory center 2) between 12-24 hours creates a compensatory metabolic acidosis 3) alteration in metabolic pathways causes an increased anion gap metabolic acidosis

Front 481

True or false: Salicylate toxicity causes CNS stimulation?

Back 481

False, Salicylate toxicity causes CNS depression at third phase of toxicity that may contribute to hypoventilation and a compounding respiratory acidosis

Front 482

True or false: Mortality in salicylate toxicity is best correlated with the 8-hour plasma salicylate concentration?

Back 482

False, mortality is best correlated with the 6-hour plasma salicylate concentration

Front 483

Which salicylate concentration value has a high fatality rate?

Back 483

>130 mg/dl

Front 484

Chronic salicylate intoxication manifestations(3)

Back 484

Chronic metabolic acidosis, hypoglycemia, and possible hearing loss

Front 485

Whre are the possible ways to get an accidental arsenic toxicity?

Back 485

Through exposure to various pesticides, wood preservations, and leather tanning.

Front 486

In which industries there is a risk for arsenic gas intoxication?

Back 486

Production of metal alloys and semiconductor manufacture.

Front 487

What are the manifestations of arsenic gas inhalations?

Back 487

Arsenic gas is the most toxic form, capable of producing acute renal failure, hemolysis, and death within 24-48 hours.

Front 488

True or false: Ingested arsenic excreted in GI tract?

Back 488

False, Ingested arsenic excreted in urine

Front 489

In which tissues, arsenic can be distributed?

Back 489

Skin, nails, and hair

Front 490

Acute arsenic toxicity manifestation?

Back 490

Arsenic inhibits oxidative production of ATP. Thus intial toxicity is manifested in dividing tissue such as GI mocusa ( nasesa, vomiting, bloody diarrea, and abdominal pain), bone marrow (cytopenia with erythrocyte basofilic stippling similar to that seen in lead toxicity.

Front 491

Chronic arsenic toxicity manifestations

Back 491

Periferal neuropathy, skin hyperpigmentation, nephropathy, and hyperkeratosis ( particularly palms and soles, and transverse Mees lines in the nails.

Front 492

Which samples can be used for the diagnosis of chronic arsenic intoxication?

Back 492

Finger nails, hair, or urine

Front 493

True or false: A blood arsenic level is the most reliable test in arsenic intoxication?

Back 493

False, A blood arsenic level is highly unreliable, as the substance is rapidly cleared from circulation.

Front 494

Which test is the most reliable test in arsenic intoxication?

Back 494

Quantitative 24-hour urinary arsenic excretion: however, this result may be misleadingly elevated due to recent seafood ingestion

Front 495

TCAs mechanism?

Back 495

Blocking reuptake of dopamine and epinephrine from the synaptic space.

Front 496

True or false: many of the TCAs adverse effects relate to their cholinergic effect?

Back 496

False, it relates to their anticholinergic effect (not cholinergic)

Front 497

TCAs anticholinergic manifestations

Back 497

Dry mouth, constipation, urinary retension, papillary dilatation, hyperthermia, lethargy, confusion

Front 498

The major that are affected by tricyclic overdose

Back 498

The CNS and cardiac conduction system

Front 499

ECG manifestation of tricyclic overdose

Back 499

Widening of the QRS complex (QRS prolongation) that can lead to ventricular arrhythmias.

Front 500

True or false: the duration of the QRS is predictive of the likelihood of seizures?

Back 500

True, QRS interval longer than 0.1 seconds associated with a high risk of seizure

Front 501

Organophosphates and carbamates mechanism

Back 501

they inhibit acetylcholinesterase (that breaks acetylcholine) resulting in over stimulation of cholinergic process.

Front 502

The classicmanifestation of organophosphates and carbamates toxicity?

Back 502

Miosis, diaphoresis, excess salivation, lacrimation, GI hypermotility, bradycardia, and bronchospasm

Front 503

Lab diagnosis of organophosphates and carbamates toxicity?

Back 503

The level of erythrocyte cholinesterase activity.

Front 504

How long can we detect organophosphates metabolite in urine?

Back 504

Up to one week after exposure

Front 505

True or false: elemental mercury can easily absorb from GI tract

Back 505

False, Ingestion of elemental mercury is largely inconsequential, as GI absorption does not occure to any significant degree. In contrast, organic mercury (from the ingestion of fish) is readilly absorbed in the GI tract.

Front 506

Acute elemental mercury toxicity manifestations?

Back 506

Respiratory distress and renal failure

Front 507

Chronic mercury toxicity syndromes?

Back 507

Chronic elemental mercury toxicity causes two charactristic syndroms:acrodynia and erethism

Front 508

Acrodynia syndrome?

Back 508

Acrodynia (feer syndrome) in chronic elemental mercury toxicity manifest with autonomic symptoms (sweating, hemodynamic instability) and a desquamative erythematous rash on the palms and soles It is associated with incraesed urinary catecholamines and can in many ways mimic pheochromocytoma.

Front 509

Erethism syndrome?

Back 509

Erethism in chronic elemental mercury toxicity manifest with a central nervous disorder manifesting as personality change, irritability, and fine motor disturbances.

Front 510

Organic mercury toxicity manifestations?

Back 510

Visual field consriction, peripheral neuropathy, tremor, and hearing loss.

Front 511

True or false: inorganic mercury crosses the placenta, resulting in cardiac malformations

Back 511

False, inorganic mercury crosses the placenta, resulting in infants with sever neurologic impairment.

Front 512

True or fase: 24-hour urine collection is essential for diagnosis of organic mercury poisoning?

Back 512

False, 24-hour urine collection is essential for diagnosis of elemental (not organic) mercury poisoning. Organic mercury is not significantly excreted in urine.

Front 513

Suitable samples in organic mercury toxicity?

Back 513

Whole blood or hair analysis.

Front 514

Digoxin half life?

Back 514

36 hours

Front 515

True or false: Digoxin is primarily excreted by the kidney?

Back 515

True.

Front 516

Suitable time for Digoxin level samplng?

Back 516

8-12 hours after the last does

Front 517

True or false: serum digoxin level is the best way to evaluate the eficacy and the toxicity of digoxin?

Back 517

While serum digoxin level is important, both eficacy and the toxicity of digoxin may best measured by clinical parameters (heart rate, etc)

Front 518

Factors that incraese digoxin toxicity?

Back 518

Hypokalemia, hypercalcemia, hypomagnesemia, hypoxia, hypothyroidism, quinidine, and calcium chanel blockers.

Front 519

True or false: Quinidine can decrease the risk of digoxin toxicity?

Back 519

False. Quinidin in addition to enhancing end-organ effects of digoxin, frees digoxin from protein binding sites and impires digoxin clearance and enhances the risk of digoxin toxicity.

Front 520

Digoxin-like Immunoreactive substances (DLIS)

Back 520

DLIS or endogenous digoxin-like substance (EDLS) are found in the blood of some individual who are not taking digoxin and cause cross-reactivity. It is particularly common in neonates, pregnant women, liver and renal failure.

Front 521

True or false: Procainamid is cleared by the kidney

Back 521

False, it cleared by the liver

Front 522

What is the procainamid metabolite in the liver?

Back 522

N-acetylprocainamide (NAPA). The rate of procainamid conversion to NAPA is determined by concentration of hepatic acetyltransferase.

Front 523

True or false: High levels of NAPA are in slow acetylators

Back 523

False, In fast acetylator, who have genetically high levels of acetyltransferase, will higher level of NAPA NAPA

Front 524

True or false: The clearance of NAPA is prdominantly renal

Back 524

TRUE

Front 525

True or false: Only the metabolite of procainamide, NAPA is biologically active

Back 525

False, both procainamide and NAPA have bilologic activity, and the level of both should be measured.

Front 526

True or false: the drug-induced lupus effect of procainamide is dose-dependent

Back 526

Fase, the drug-induced lupus effect of procainamide is not dose-dependent

Front 527

Which organ is mainly responsible for clearing aminoglycosides from blood?

Back 527

The Kidneys

Front 528

The ideal time for the gentamycin trough and peak specimens drawning?

Back 528

The trough specimen is drawn immidietely before a dose, and the peak is drawn 30minutes after the completion of a does.

Front 529

The class IA antiarrythmic agents?

Back 529

Quinidine, disopyramide, and procainamide.

Front 530

The mechanism of class IA antiarrythmic agents?

Back 530

Blocking the sodium and potassium channels in cardiac conduction fibers.

Front 531

The typical manifestations of quinidine toxicity?

Back 531

Altered mental status, cinchonism (tinnitus, vertigo, blurred vision), a widening of the QRS complex, aprolonged QT interval, and hypotension ( without compensatory tachycardia)

Front 532

Common conditions related to the prolonged QT interval, CNS changes, and hypotension?

Back 532

Quinidine, TCAs, phenothiazines toxicity, and electrolyte abnormalities.

Front 533

Which organ clears quinidine?

Back 533

Liver

Front 534

The most reliable tool to predict quinidine toxicity?

Back 534

ECG. Quinidine levels are not routinely used to predict quinidine toxicity. IT is important to check and correct electrolyte levels.

Front 535

Phenytoin toxicity manifestations?

Back 535

Early manifestations of phenytoin toxicity include ocular dismotility (particularly horizontal gaze nystagmus), ataxia, and incoordination. More sever toxicity is associated with altered mental status and cardiac conduction disturbances.

Front 536

True or fase: oral phenytoin overdose has not been associated with significant cardiac conduction abnormality?

Back 536

True, in contrust to oral phenytoin, IV phenytoin overdose often produces a prolonged PR interval (AV block), hypotension and the arrhythmia.

Front 537

True or false: Arrhythmogenic effects of IV phenytoin intoxication is due to the propylene glycol diluent of phenytoin.

Back 537

TRUE

Front 538

Fetal hydantoin syndrome?

Back 538

The result of intrauterine exposure to phenytoin. It is carachterized by intrauterine growth retardation, microcephaly, mental retardation, midfacial hypoplasia, hypertelorism, a flattened philtrum, and shortened nose.

Front 539

The therapeutic range of lithium?

Back 539

0.4-1.2 mmol/L

Front 540

The lithium level at which the risk of adverse effects becomes extemely high?

Back 540

1.5 mmol/L

Front 541

True or false: Some toxicity can be seen in the lithium therapeutic range

Back 541

True, the margin between therapeutic effect and toxicity is a narrow one for lithium, and some toxicity can be seen in the upper reahces of lithium therapeutic range.

Front 542

True of false: For routine lithium monitoring, a sample should be taken at 12 hours following the last does?

Back 542

TRUE

Front 543

The litium half-life?

Back 543

It varies from 8-40 hours (depending largely upon age and renal function)

Front 544

When steady state would be expected after starting lithium therapy?

Back 544

Between 2 and 8 days.Checking levels after a period of 3 days to 1 week is recommended.

Front 545

True or false: Amiodarone levels should not necessarily be routinely monitored.

Back 545

TRUE

Front 546

The main Amiodarone metabolite?

Back 546

Desethylamiodarone

Front 547

The major risks due to amiodarone?

Back 547

Pulmonary toxicity (incidence of 1% annually), thyroid toxicity, hepatotoxicity (0.6%), and peripheral neuropathy (0.3%),

Front 548

Hyperthyroidism is the most common manifestation of the amiodarone thyroid toxicity?

Back 548

Fase, amiodarone thyroid toxicity apears with hypothyroidism in 5%-15%, and hyperthyroidism in 1%-2% of cases.

Front 549

Routine tests for monitoring the patients who are taking amiodarone?

Back 549

Thyroid and liver function tests, in addition chest X-ray and ECG

Front 550

The recommended intervals for the routine monitoring tests in amiodarone therapy?

Back 550

Thyroid and liver function tests, at baseline and every 6 months, chest X-ray and ECG annually.

Front 551

True or false: amiodarone increases the clearance of warfarin?

Back 551

False, it decreases the clearance of warfarin and can thereby prolong the INR.

Front 552

How amiodarone can affect the digoxin concentrations?

Back 552

Amiodarone increases digoxin concentration, and doses of digoxin must be reduced.

Front 553

The major lipids found in plasma?

Back 553

Cholestrol, triglyceride, and phospholipid.

Front 554

Triglyceride composition?

Back 554

TG is composed of 3 fatty acids extending from a glycerol group.

Front 555

Short, medium, and long fatty acids chain definition?

Back 555

Fatty acids are linear hydrocarbons that come in several lengths: short chain (4-6 carbons), mediumchain (8-12 carbons), and long chain (>12 carbons)

Front 556

Saturated, monounsaturated, polyunsaturated fatty acids definition?

Back 556

Saturated fatty acids: have only single bonds between carbons and thus have maximum number oa attached hydrogen bonds Monounsaturated FAs: have one double bond and thus one fewer hydrogen Polyunsaturated: have several double bonds and less hydrogen

Front 557

Phospholipid composition?

Back 557

Two fatty acids extending from a glycerol group, with the third spot on glycerol occupied by a phosphatidyl group ( such as phosphatidylcholine).

Front 558

Cholestrol composition?

Back 558

it is composed of 4 rings, a hydrogen side chain, and a hydroxyl group.

Front 559

Lipoprotein constituents?

Back 559

Cholestrol, triglyceride, and phospholipid, and apolipoproteins

Front 560

What kind of lipoproteins is made by enterocytes?

Back 560

Chylomicrons

Front 561

The chylomicrons function?

Back 561

It transports lipid from entrocytes to other somatic cells, particularly hepatocytes.

Front 562

The chylomicrons apolipoproteins?

Back 562

B-48, A-1, C, E

Front 563

The VLDL apolipoproteins?

Back 563

B-100, C, E

Front 564

The VLDL function?

Back 564

It is produced in the liver and is the vehicle for transporting of TG to somatic cells.

Front 565

What are major risks with amiodarone therapy?

Back 565

Pulmonary toxicity, hepatotoxicity, thyroid toxicity, peripheral neuropathy

Front 566

What test are recommended every 6 months of amiodarone therapy?

Back 566

Thyroid function tests, LFTs

Front 567

What test are recommended every year on amiodarone therapy?

Back 567

Chest Xray, EKG

Front 568

What effect does amiodarone have on warfarin treatment?

Back 568

It reduces Warfarin clearance and Prolong INR

Front 569

How much time is required for above mentioned effect to occur when used with warfain?

Back 569

7 weeks

Front 570

What effect does amiodarone have on digoxin treatment?

Back 570

digoxin concentartion is increased

Front 571

What major lipids are found in plasma?

Back 571

Cholestrol, triglycerides, phospholipids

Front 572

What are Triglycerides composed of?

Back 572

3 fatty acid extending from glycerol group

Front 573

What are saturated fatty acids?

Back 573

Fatty acids having single bonds between carbons and hydrogen ions

Front 574

What are monosaturated fatty acids?

Back 574

there is one double bond btw carbon and hydrogen

Front 575

Which lipoprotein transfers lipids from enterocytes to somatic cells?

Back 575

Chylomicron

Front 576

Lipids are ingested by hepatocytes by which receptor?

Back 576

apolipoprotein E

Front 577

What happen to ingested lipis in hepatocytes?

Back 577

They are converted to VLDL

Front 578

What apolioproteins are associated with VLDL?

Back 578

B-100,C and E

Front 579

What is the function of VLDL?

Back 579

Transports triglycerides to somatic cells

Front 580

What happens to VLDL in blood?

Back 580

It is converted to IDL the LDL by action of lipoprotein lipase

Front 581

What is the function of LDL?

Back 581

Transports cholestrol to somatic cells

Front 582

what apolioproteins are associated with LDL?

Back 582

B-100

Front 583

LCAT( lecithin cholestrol acyl transferase) is produced by which organ?

Back 583

Liver

Front 584

what apolipoproteins are associated with chylomicrons?

Back 584

B-48,A-1, C,E

Front 585

How is cholestrol measured?

Back 585

spectrophotometric method

Front 586

Calculate VLDL from TG?

Back 586

TG/5 if expressed in mg/dl, TG/2.2 if expressed in mmol/dl

Front 587

At what value of TG is this equation invalid?

Back 587

If TG isgreater than 400mg/dL, chylomicrons or beta VLDL is present

Front 588

How is HDL measured?

Back 588

By enzymatic sequence after removal of non HDL cholestrol

Front 589

What is Friedewald equation?

Back 589

LDL cholestrol= total cholesterol-HDL-TG/5

Front 590

When Is this equation invalid?

Back 590

If TG isgreater than 400mg/dL, chylomicrons or beta VLDL is present

Front 591

What are direct methods of LDL measurement?

Back 591

the methods are tedious. Ultracentrifugation, electrophoresis,homogenous assays

Front 592

What is the principle involved in ultracentrifugation?

Back 592

Liporoteins can be separated on the basis of difference in densities

Front 593

what is the pattern of separation of lipoproteins in electrophoresis?

Back 593

Chylomicron donot move from point of application,LDL migrates to beta region, VLDL in pre beta region, HDL goes to alpha region

Front 594

After refrigeration if plasma has creamy top layer, what does this indicate?

Back 594

Increased chylomicrons

Front 595

After refrigeration if plasma looks opaque, what does this indicate?

Back 595

increased HDL,VLDL or LDL

Front 596

What is major apolipoprotein in HDL?

Back 596

Apo-A1

Front 597

What is the consequence of high LDL or IDL?

Back 597

premature atherosclerosis

Front 598

What is the consequence of high TG?

Back 598

eruptive xanthomas

Front 599

tendinous xanthomas are seen in elevation of what lipoproteins?

Back 599

IDL ( raised TG and cholesterol)

Front 600

Xanthelesma are seen in elevation of what lipoproteins?

Back 600

LDL

Front 601

Acute pancreatitis is seen in elevation of which lipoproteins?

Back 601

chylomicrons, VLDL(TG= >5-10mmol/L)

Front 602

What are clinical features of familial LPL deficiency?

Back 602

xanthomas, pancreatitis

Front 603

What are clinical features of familial apo C-II deficiency?

Back 603

panreatitis

Front 604

what is phenotype of apolipoprotein deficiency?

Back 604

Type II b

Front 605

What is phenotype of dysbetalipoproteinemia ?

Back 605

Type III

Front 606

What are clinical features of familial combined hyperlipidemia?

Back 606

premature atherosclerosis

Front 607

what is predominant hypercholestrolemia?

Back 607

total cholestrol >200 mg/dL

Front 608

Which lipoprotein is predominantly elevated in predominant hypercholestrolemia?

Back 608

LDL

Front 609

What is the cause of familial hypercholestrolemia?

Back 609

LDL receptors deficiency

Front 610

What is low levell of HDL?

Back 610

< 35 mg/dL

Front 611

What is Tangier diease?

Back 611

It is autosomal recessive, low cholesterol, nl to increase TG, absent HDL and APO-A1

Front 612

What happen in Tangier disease?

Back 612

Cholestrol esters deposit in tonsils,lymphnodes, vessels, spleen with development of corneal opacities

Front 613

What are recommendations of 3rd Adult Treatment Panel Report?

Back 613

Fasting lipoprotein profile including total cholesterol, HDL, LDL and TG

Front 614

What is desirable total cholestrol?

Back 614

< 200

Front 615

What is desirable LDLl?

Back 615

<100

Front 616

What is desirable HDL?

Back 616

>60

Front 617

What is principle of capillary electrophoresis?

Back 617

Capillary tube is immersed in sample, volatge is applied and elution time is noted.

Front 618

What are advantages of capillary zone electrophoresis?

Back 618

small sample size, ability to automate procedure, very sensitive

Front 619

Which is equivalent to albumin in fetal blood?

Back 619

alpha feto protein

Front 620

What happens to albumin in inflammatory conditions?

Back 620

It decreases.

Front 621

Which protein is amyloid precursor protein in cardiac amyloidosis?

Back 621

prealbumin

Front 622

How does prealbumin enter CSF?

Back 622

It is secreted by choroid plexus

Front 623

Why prealbumin band becomes prominent in heparinsed patients?

Back 623

There is alteration of B-lipoproteins that migrates in prealbumin region

Front 624

What happens to pre-albumin in inflammatory conditions?

Back 624

It is decreased

Front 625

what is alpha2- macroglobulin?

Back 625

Protease inhibitor

Front 626

What happens to alpha2- macroglobulin in nephrotic syndrome and why?

Back 626

It is retained due to its large size so its concentration increase 10 fold

Front 627

A false poistive ceruloplasmin level is seen in what conditions?

Back 627

pregnancy, inflammatory conditions

Front 628

Does haptoglobulin binds to myoglobin?

Back 628

No

Front 629

Which form of transferrin is superior to GGT in diagnosing chronic alcholism

Back 629

Carbohydrate deficient transferrin

Front 630

C reactive protein in found in which region of SPEP?

Back 630

gamma region

Front 631

what vaues of CRP areassociated with cardiac events

Back 631

. 2-3 mg/L

Front 632

Symptoms of hypoglycemia can be classified into two types of responses: Fasting or Reactive

What is the cause of each?

Back 632

Fasting: caused by brain hypoglycemia, not rapid in onset

Reactive: caused by adrenergic activity, tends to be rapid

Front 633

How do the symptoms differ in reactive vs. fasting hypoglycemia?

Back 633

Fasting: mental status changes

Reactive: sweating, tachycardia, nervousness

Front 634

What are 4 different drugs that can induce hypoglycemia (classes, not specifics)?

Back 634

Alcohol, sulfonylureas and other oral hypoglycemics, insulin, and quinine

Front 635

What is nesidioblastosis?

Back 635

islet Beta cell proliferation

Front 636

What is Whipple's triad and what is it associated with?

Back 636

plasma glucose <45mg/dL, hypoglycemic changes, and correction of symptoms by glucose administration

Front 637

In a patient with a suspected insulinoma, what do you expect the insulin level to be?

Back 637

The absolute insulin level may actually be normal, but will be inappropriately high for the degree of hypoglycemia. Or it might be high.

Front 638

What should the insulin:glucose ration be in insulinoma?

Back 638

>180

Front 639

What are some causes of reactive hypoglycemia?

Back 639

The abnormal rapid-onset hypoglycemia following a meal can be caused by heriditary fructose intolerance, galactosemia, dumping syndrome (post vagotomy), rarely early type 2 diabetes

Front 640

Pancreatic islet cells secrete what two substances in equimolar amounts?

Back 640

Insulin and C-peptide

Front 641

Which substance secreted by pancreatic islet cells is metabolized faster?

Back 641

Insulin is metabolized faster than c-peptide.

Front 642

What is the primary clinical use of C-peptide?

Back 642

Since it hangs around so much longer than insulin but is secreted in equal amounts you can determine if insulin is being naturally released or exogenously administered.

Front 643

What is the shortcoming in using the C-peptide to evaluate for exogenous administration of insulin?

Back 643

Renal failure impedes C-peptide clearance and will result in elevated C-peptide levels

Front 644

How can proinsulin be used clinically?

Back 644

Proinsulin should represent less than 10% of the insulin level, so an elevated level may represent insulinoma

Front 645

Anti-insulin antibodies can be seen in what 3 clinical settings?

Back 645

Administration of insulin produces (rare), autoimmune insulin syndrome, and rarely insulinoma (actually all of these are rare)

Front 646

What is the cause of hypoinsulinemic hypoglycemia?

Back 646

Too much insulin (insulinoma or exogenous)

Front 647

What are the two types of hyperinsulinemic hypoglycemia?

Back 647

Ketotic and non-ketotic

Front 648

Non-ketotic hypoglycemia suggests what clinical settings?

How about ketotic hypoglycemia?

Back 648

presence of insulin-like activity such as in autoimmune hypoglycemia, starvation, liver failure

Ketotic: all other causes

Front 649

Since insulinoma may be associated with MEN1, what additional test should be performed?

Back 649

Serum calcium (remember PTH adenomas?)

Front 650

How can you diagnose hypoglycemia after death?

Back 650

Virtually impossible

You can detect insulin, peptide C, and proinsulin for several days after death

Front 651

What is the cause of Type 1 diabetes?

Back 651

autoimmune destruction of islet B cells

Front 652

What percentage of diabetics are type 1?

Back 652

~10%

Front 653

T/F

Autoantibodies are not part of the clinical picture in Type I Diabetes

Back 653

False

anti-GAD65, anti-ICA512, Anti-IAA can each be present

Front 654

What is the cause of Type 2 Diabetes?

Back 654

progressive insulin resistance with subseuent burn-out of islet cells

Front 655

What is the recommeded test to diagnose diabetes in nonpregnant persons?

What is the diagnostic level?

Back 655

Fasting plasma glucose

> or = 126 mg/dL is considered diagnostic

Front 656

A 60yo obese man presents with frequent urination, recent weight loss, poorly healing wounds, and fatigue. You suspect diabetes, however he has eaten breakfast that morning and a fasting glucose cannot be performed. What can you do?

Back 656

A random plasma glucose of >200mg/dL with symptoms of diabetes is diagnostic

Front 657

What is the diagnostic level for diabetes with the oral glucose tolerance test?

Back 657

75g of glucose is given and a 2 hour reading is taken. >200 mg/dL is diagnostic.

Front 658

What fasting plasma glucose level is defined as "impaired fasting glucose/pre-diabetic"

Back 658

99mg/dL

Front 659

What is the diagnostic level in the glucose tolerance test for "Impaired glucose tolerance"/prediabetes

Back 659

>139mg/dL at 2 hours after 75 grams

Front 660

How is the gestational diabetes oral glucose tolerance test different than the normal fasting glucose tolerance test?

Back 660

The amount of glucose is different

Front 661

What types of women can avoid glucose tolerance testing totally?

Back 661

young (<25y), healthy, normal pre-pregnancy weight, low-risk ethnicity, no family history and no prior OB complications

Front 662

What is the earliest screening for high risk women for GDM?

Back 662

a fasting plasma glucose (>126mg/dL) is diagnostic

Front 663

Non-high risk women and high risk women who "pass" their first screening should undergo what test next?

Back 663

At 24-28 weeks they should have a 100g load oral glucose tolerance test.

Front 664

What are the criteria for a positive 100g OGTT?

Back 664

Need two of the following:
>95 mg/dL fasting
>180 mg/dL 1hour
>155 mg/dL 2 hour
>140 mg/dL 3 hour

Front 665

Often, women are "pretested" before undergoing the full 3 hour/100g OGTT? What does this consist of?

Back 665

a 50g 1 hour OGTT: A measurement of >140mg/dL at one hour necessitates the 3 hour test.

Front 666

A 28 year-old woman is diagnoses with gestational diabetes and goes on to deliver a (large) healthy baby with no complications. What additional followup does mom need?

Back 666

Testing for GDM at 6-12 weeks postpartum

Front 667

Should the HbA1c test be used for diabetes diagnosis?

Back 667

NO

Front 668

What does the HbA1c test monitor?

Back 668

Long term glycemic control

Front 669

What is the American Diabetes Association recommended goal of therapy level of HbA1C?

Back 669

<7%

Front 670

Name 4 other lab values that are important to check in diabetics?

Back 670

Lipid disorders, microalbunemia, serum creatinine for estimated glomerular filtration rate, hypomagnesemia

Front 671

Who gets diabetic ketoacidosis?

Back 671

Insulin-dependent diabetics

Front 672

What are the 3 usual requirements for the diagnosis of DKA?

Back 672

hyperglycemia (>200mg/dL), ketosis, metabolic acidosis (venous pH < 7.3 or bicarb less than 15mmol/L)

Front 673

What are the urinalysis findings usually seen with DKA?

Back 673

glycosuria and ketonuria

Front 674

T/F: DKA is often associated with leukopenia.

Back 674

False. DKA is often associated with neutrophilia (that is not necessarily infectious in nature--unknown mechanism) But remember--DKA can be prompted by infection

Front 675

What are the three major serum ketones in DKA?

Back 675

acetone, acetoacetic acid, B-hydroxybutyrate

Front 676

What laboratory technique is used for measuring ketones?

Back 676

nitroprusside technique sensitive to acetone and acetoacetic acid but not B-hydroxybutyrate.

Front 677

What is the shortcoming in our laboratory analysis of ketones?

Back 677

Our nitroprusside technique measures only acetone and acetoacetic acid which accounts for only 20% of the serum ketones. B-hydroxybutyrate is converted to the other two measurable forms during treatment, so an apparent "bump" might be seen in the lab levels even with successful treatment

Front 678

What do you expect glucose level to be in DKA?

Back 678

>200mg/dL

Front 679

Is bicarbonate decreased or increased in DKA?

Is pH decreased or increased in DKA?

Back 679

Bicarb is down, pH is down (acidosis)

Front 680

Why is Potassium elevated in DKA?

Back 680

The Potassium is extracellular with the low pH, but the urinary excretion is increased, so true body potassium can be very LOW. When given insulin, the potassium can shift very quickly.

Front 681

What is the typical BUN level during DKA?

Back 681

increased due to severe volume depletion resulting in prerenal azotemia.

Front 682

Which patients get Hyperglycemic hyperosmolar nonketotic coma?

Back 682

Type 2 (non-insulin dependent) diabetics

Front 683

Which is more common, DKA or HHNC?

Back 683

DKA

Front 684

Which has higher mortality, DKA or HHNC?

Back 684

HHNC

Front 685

What is the typical glucose level in HHNC?

Back 685

at least 600mg/dL (may be >1000!)

Front 686

What is the typical osmolarity in HHNC?

Back 686

>330 mOsm/L

Front 687

What is the pH/Bicarb level in HHNC?

Back 687

normal

Front 688

What is the ketone level in HHNC?

Back 688

normal

Front 689

What is the potassium level in HHNC?

Back 689

may be elevated with true total body deficit (as in DKA)

Front 690

What is the BUN level in HHNC?

Back 690

Very elevated secondary to dehydration

Front 691

What is Syndrome X?

Back 691

Metabolic syndrome, the insulin resistance syndrome referring to the cluster of hyperlipidmia, impaired glucose tolerance, central obesity, increased CRP, HTN--association with cardiac disease

Front 692

Why is it not cost-effective to screen for cancer with tumor markers?

Back 692

The sensitivity of a test is dependent on the prevelence in the population, thus if you screen everyone you negate the good points of the test

Front 693

What is the "Hook effect" in immunoassay?

Back 693

When very high concentration overwhelm binding capacity of both capture and signal antibodies, thus yielding a low or even negative result.

Front 694

Why is the Hook effect a concern in tumor marker testing?

Back 694

Widely metastatic disease can have super high tumor marker levels, and lead to the Hook effect

Front 695

How can you adjust for the Hook effect?

Back 695

Perform the assay at multiple dilutions

Front 696

What are heterophile antibodies?

Back 696

Antiblodies that may be present in the patient that have wide reactivity with antibodies of other species.

Front 697

How can one adjust for heterophile antibodies?

Back 697

heterophile blocking reagents, remove immunoglobulins, serial dilutions

Front 698

What are other situations that may show elevated PSA (besides cancer)?

Back 698

BPH, prostatitis, prostatic infarct, and following needle biopsy of the prostate

Front 699

What is the level of PSA that, beyond which, is rarely associated with benign disease?

Back 699

10ng/mL--above this level you will typically not see a benign process

Front 700

What is the approximate percentage of men that will be found to have prostatic carcinoma with elevated PSA (>4.0 ng/mL)?

Back 700

30-40% of men

Front 701

1. What is the benefit of age specific PSA? 2. At what expense is the benefit obtained?

Back 701

1. increases sensitivity of PSA for younger men and increases specificity for older men 2. decreased sensitivity in older men

Front 702

1. What is the definition of PSA density? 2. What value is considered abnormal? 3. T/F PSA density improves the performance of PSA

Back 702

1. PSA divided by the estimated prostatic volume 2. > 0.15 3. false

Front 703

1. What is PSA velocity? 2. What level is considered abnormal? 3. PSA velocity does increase sensitivity and specificity but what is its limitation?

Back 703

1. rate of change of successive PSA measurements 2. >0.75 ng/mL/year 3. biologic variation of PSA from non-malignant causes

Front 704

In what form does PSA normally circulate?

Back 704

1. 75-90% is bound to protease inhibitors mostly alpha-1-antichymotrypsin but also alpha-2-macroglobulin and alpha-1-protein inhibitor

Front 705

Free PSA can be measured, how does it correlate with prostate cancer?

Back 705

low free PSA fraction (increased bound fraction) = low likelihood of cancer, high likelihood when free PSA < 10%

Front 706

Which PSA measurement should be taken only after several weeks have passed since urethral instrumentation and digital instrumentation

Back 706

% Free PSA

Front 707

What volume of prostatic fluid is the advantage of % free PSA seen over total serum PSA?

Back 707

< 60 cc

Front 708

T/F Free PSA is stable and specimens need not be separated and frozen.

Back 708

False- specimens that can't be processed within 2 hrs should be separated and frozen

Front 709

In what form is PSA released from glandular cells and how is it broken down?

Back 709

Initially pro-PSA --> 7 aa leader peptide clipped --> mature PSA. Anomalous clipping can lead to several additonal pro-PSA forms.

Front 710

Detection of what molecules has led to improved diagnosis of prostate cancer in men with PSA in 2.5-4.0 range?

Back 710

pro-PSA and truncated forms due to anomalous clipping (both are increased in prostate cancer)

Front 711

What is benign PSA (bPSA) and why is it clinically useful?

Back 711

form of PSA first isolated in transistion zone of benign prostatic hyperplasia (BPH). Can discriminate BPH from non-BPH prostate enlargement

Front 712

In prostate cancer what does preoperative serum PSA quantity reflect?

Back 712

tumor volume and stage (roughly)

Front 713

1. What is the expected serum PSA level following radical prostatectomy? 2. How are levels used after surgery?

Back 713

1. should drop to undetectable levels 2. used to screen for tumor recurrence or metastases

Front 714

After what time period does the correlation between PSA and tumor recurrence strengthen?

Back 714

after 5 years

Front 715

What is the definition of PSA recurrence per the American Society for Therapeutic Radiology and Oncology (ASTRO)? (2)

Back 715

3 consecutive increases PSA or a single rise so great as to trigger the initiation of hormone therapy

Front 716

When is the date of treatment failure in prostate cancer?

Back 716

the midpoint between the post-radiation nadir PSA and the first of three consecutive increases

Front 717

T/F Biochemical treatment failure and clinical failure in prostate cancer occur at approximately the same time.

Back 717

False - biochemical failure precedes clinical failure by approximately 6-18 months

Front 718

What may be a better indicator of pending treatment failure in prostate cancer than serum PSA quantity?

Back 718

PSA doubling time

Front 719

What factors affect CEA levels in patients with colorectal cancer? (7)

Back 719

tumor stage, tumor grade, tumor ploidy, tumor site, obstruction, liver function, and smoking

Front 720

What's the relationship between CEA level and colon cancer tumor grade?

Back 720

Inversely related i.e. well differentiated tumors = higher CEA and vice versa

Front 721

What percent of tumors at the following stages have elevated CEA levels? 1. confined to colon 2. positive nodes 3. distant metastases

Back 721

1. 25% 2. 50% 3. 75%

Front 722

T/F Left sided colon cancers have higher CEA levels than right sided tumors.

Back 722

TRUE

Front 723

How does bowel obstruction affect CEA?

Back 723

higher CEA levels

Front 724

T/F diploid colorectal tumors produce higher CEA levels than aneuploid

Back 724

FALSE

Front 725

How does liver dysfunction affect CEA?

Back 725

increases CEA

Front 726

How do the median CEA levels of smokers compare to nonsmokers?

Back 726

higher

Front 727

How does preoperative CEA affect patient outcome?

Back 727

higher CEA = worse predicted outcome

Front 728

Post-treatment surveillance of CEA (serial measurements): 1) sensitivity and specificity to detect recurrence? 2) sensitivity to liver metastases? 3)overall sensitivity to locoregional metastases?

Back 728

1) 80% and 70% 2) 94% 3)60%

Front 729

What other neoplastic conditions are associated with CEA elevations? (7)

Back 729

gastric adenoCA (esp. well-differentiated intestinal type), breast cancer, lung cancer, pancreatic adenoCA, medullary thyroid CA, cervical adenoCA, and urothelial carcinoma

Front 730

What nonneoplastic conditions are associated with elevated CEA? (7)

Back 730

smoking, peptic ulcer disease, inflammatory bowel disease, pancreatitis, hypothyroidism, biliary obstruction, and cirrhosis

Front 731

CEA levels above __ ng/mL are rarely due to benign disease?

Back 731

10

Front 732

What's the mainstay for detection of follicular and papillary thyroid carcinomas (so called differentiated)?

Back 732

serum thyroglobulin

Front 733

Which thyroid tumors are NOT associated with increased thyroglobulin?

Back 733

anaplastic and medullary

Front 734

What's the half-life of circulating thyroglobulin and how long before it becomes undectectable following total thyroidectomy?

Back 734

65 hours, approximately 1 month

Front 735

How is thyroglobulin normally cleared from circulation?

Back 735

Catabolism in the liver and recycling in the thyroid

Front 736

1. What percentage of normal individuals have anti-thyroglobulin antibodies? % with thyroid carcinoma? 2. how does this affect estimation of serum thyroglobulin and what assay allays this problem?

Back 736

1. 10% normal, >20% with carcinoma 2. usually results in underestimation, assays are available to detect thyroglobulin antibodies

Front 737

1. What is an alternative to serum thyroglobulin measurement as a tumor marker? 2. What would an increase of the above answer suggest?

Back 737

1. serial quantitative serum anti-thyroglobulin antibody 2. antigenic stimulation, suggesting recurrence

Front 738

1. Under what conditions is thyroglobulin assay sufficiently specific? 2. Addition of what can enhance the assay's specificity after the above requirement(s) have been met?

Back 738

1. ablation of all functional thyroid tissue (total thyroidectomy followed by radioactive iodine) 2. TSH can be administered or thyroxine replacement can be withheld prior to testing

Front 739

Tumor-associated trypsin inhibitor (TATI) has been used as a marker with what neoplasms?

Back 739

mucinous ovarian carcinoma, urothelial carcinoma, and renal cell carcinoma

Front 740

Tumor-associated trypsin inhibitor (TATI): 1. method of clearance? 2. affect of renal failure on serum levels? 3. how does degree of elevation correlate with severity of disease? 4. poor prognosis associated with what value? 5. What inflammatory condition is associated with elevated levels?

Back 740

1. kidneys 2. elevated 3. direct relationship i.e. higher levels = greater severity 4. >70 micrograms/L 5. pancreatitis

Front 741

1) What percentage of stage I ovarian mucinous tumors are associated with increased Tumor-associated trypsin inhibitor (TATI)? 2) Stage IV?

Back 741

1) 40% 2) nearly 100%

Front 742

1) What percentage of pancreatic adenoCA are associated with increased Tumor-associated trypsin inhibitor (TATI)? 2) What condition limits its specificity in pancreatic adenoCA?

Back 742

1) 85-95% 2) pancreatitis

Front 743

1. Tumor-associated trypsin inhibitor (TATI) is elevated in what percentage of gastric carcinomas? 2. TATI can complement which tumor marker in gastric CA?

Back 743

1. 60% (infiltrative signet ring type) 2. CEA which is only elevated in intestinal type

Front 744

1) Elevated tumor-associated trypsin inhibitor (TATI) what percentage of urothelial carcinoma 2)sensitivity for renal cell carcinoma

Back 744

1) varies with tumor stage from 20% low stage to 80% advanced stage 2) 70% (most likely elevated in advanced stage)

Front 745

CA-125 1) elevated and used for monitoring in what neoplasm? 2) why hasn't it proven useful for screening?

Back 745

1) non-mucinous epithelial ovarian neoplasms 2) elevated in only 50% of pts with stage I disease, poor positive predictive value in unselected women

Front 746

CA 125 elevations associated with which: 1) nonneoplastic conditions? (6) 2) non-ovarian neoplasms?(5)

Back 746

1) pregnancy, fibroids, benign ovarian cysts, pelvic inflammation, ascites, endometriosis 2) endometrium, fallopian tube, pancreas, breast, and colon

Front 747

CA-125 1) what level is considered normal? 2) what happens to levels in postmenopausal women? 3) normal values in black and Asian women compared to others? 4) how does it fluctuate with menstrual cycle?

Back 747

1) < 35 U/mL 2) decreases 3) lower 4) increases slightly during follicular (proliferative) phase

Front 748

How does CA-125 help differentiate pelvic masses in postmenopausal women?

Back 748

levels > 65 U/mL has a positive predictive value of > 95% for ovarian malignancy

Front 749

Rising CA-125 following treatment suggests relapse. This precedes clinical evidence of disease by how long?

Back 749

3-6 months

Front 750

What preoperative CA 125 level is considered unfavorable in terms of prognosis?

Back 750

> 65 U/mL

Front 751

How does CA 125 level correlate with prognosis... 1) half-life of CA 125 following chemotherapy? 2) time to normalization after chemo?

Back 751

1) patients with half-life >20 days have improved survival 2) patients whose level normalized within 3 cycles have improved survival

Front 752

CA-125 greatest utility is in women with known ovarian malignancy 1) what trend in CA 125 following initial treatment suggests treatment efficacy? 2) rate of fall correlates best with? 3) increase during treatment suggests? 4) increase following treatment suggests?

Back 752

1) falling levels 2) duration of disease-free survival 3) treatment failure 4) disease recurrence

Front 753

1) Persistent elevation of CA 125 above what level predicts residual disease? 2) With what specificity?

Back 753

1) > 35 U/mL 2) 95%

Front 754

How does CA 125 level correlate with prognosis... 1) half-life of CA 125 following chemotherapy? 2) time to normalization after chemo?

Back 754

1) patients with half-life >20 days have improved survival 2) patients whose level normalized within 3 cycles have improved survival

Front 755

What are CA 27.29 (aka BR 27.29) and CA 15-3?

Back 755

they're different epitopes of a single antigen - the protein product of breast cancer associated MUC1 gene

Front 756

Which is the preferred serum marker for breast cancer CA27.9 or CA15-3 and why?

Back 756

CA27.9 due to enhanced sensitivity and specificity. Elevated in ~30% low stage disease and 60-70% of advanced-stage disease

Front 757

What benign conditions are associated with elevated: 1) CA27.9 and CA15-3? (3) 2) CA 15-3 only?

Back 757

1) benign ovarian cysts, benign breast disease, and benign liver disease 2) cirhosis, sarcoidosis, and lupus

Front 758

CA 27.9 may be elevated in what non-breast malignancies? (5)

Back 758

colon, stomach, pancreas, prostate, and lung

Front 759

ER and PR assays: 1) performed almost exclusively by what method? 2) how are they graded?

Back 759

1) immunohistochemistry 2) according to the proportion of cells expressing intense nuclear staining

Front 760

1. What are the 2 methods for determining Her-2 status? 2. What's the purpose of testing?

Back 760

1. immunohistochemistry and FISH 2. determine suitability for treatment with trantuzumab

Front 761

1) What's the best marker for pancreatico-biliary adenoCA? 2) what is its greatest utility in the above disease? 3) what other malignancies can be associated with elevations of this marker? (2) 4) in what benign conditions might it be elevated? (3)

Back 761

1) Cancer Antigen (CA) 19-9 2) monitoring treatment response 3) esophagus and intestines 4) pancreatitis, cholestasis, cholangitis, and cirrhosis

Front 762

1) What percentage of individuals with CA 19-9 levels > 100 U/mL have benign disease? 2) > 1000 U/mL

Back 762

1) ~3% 2) virtually none

Front 763

1) What blood antigen is CA 19-9 identical to? 2) what group of individuals don't produce it?

Back 763

1) Lewis blood group antigen 2) Lewis-negative

Front 764

1) What is the major component of fetal serum? 2) Where is it synthesized?

Back 764

1) Alpha Fetoprotein (AFP) 2) yolk sac, fetal liver, and fetal GI tract

Front 765

1) What's the normal level of AFP in adults? 2) Values above ___ are rarely associated with benign disease?

Back 765

1) under 5.4 ng/mL 2) 500 ng/mL

Front 766

In what benign conditions is AFP normally elevated? (3)

Back 766

pregnancy (usually not >100 ng/mL), hepatitis, and cirrhosis

Front 767

1) AFP has utility in detection of what tumors? (2) 2) it may be sporadically elevated in other tumors, most notably what?

Back 767

1) hepatocellular carcinoma and yolk sac tumors 2) hepatoid variant of gastric cancer

Front 768

How is AFP used in yolk sac tumors?

Back 768

magnitude of AFP correlates with prognosis (levels > 10,000 ng/mL associated with poor prognosis)

Front 769

1) What's the reported rate of AFP elevation in hepatocellular carcinoma? 2) is this true in the Western world? why or why not?

Back 769

1) 80% 2) no, in other areas tumors may be detected when quite large at time of diagnosis

Front 770

What conditions are associated with elevated Human Chorionic Gonadotropin (HCG)? (4)

Back 770

pregnancy, trophoblastic disease, and choriocarcinoma, and marijuana use (low level elevation)

Front 771

In what percentage of seminomas is HCG elevated?

Back 771

0.15

Front 772

1) Where is Beta2-Microglobulin (B2M) expressed? 2) when and where is it released? 3) why is it a good but nonspecific tumor marker?

Back 772

1) surface of most nucleated cells, non-covalently linked to class I MCH molecules 2) released into the extracellular fluid when cells die 4) elevated whenever there's increased cell turnover

Front 773

Beta2-Microglobulin 1) independent prognostic factor in what disease? 2) can be used to monitor what process? 3) how is cleared?

Back 773

1) multiple myeloma 2) renal transplant rejection 3) by kidneys (nonspecifically elevated in renal insufficiency)

Front 774

Lipid-Associated Sialic Acid in Plasma (LASA-P) is a nonspecific tumor marker elevated in what kind of malignancies? (5)

Back 774

hematolymphoid neoplasms, tumors of the breast, GI tract, lung and ovary

Front 775

Name three conditions in which alkaline phosphatase would be elevated?

Back 775

Osteogenic sarcoma
Bone metastisis
Paget disease of the bone

Front 776

Alkaline phosphatase is the most sensitive marker for what condition concerning the liver?

Back 776

Hepatic metastisis

Front 777

In the case of primary intra-abdominal carcinoids alkaline phosphatase correlates with what?

Back 777

Prognosis

Front 778

Which of the following types of carcinoid tumors is most commonly associated with high levels of serotonin?

A. Foregut
B. Midgut
C. Hindgut
D. Atypical carcinoids
E. no specific type is associated with high serotonin

Back 778

B. Midgut

Front 779

Which of the following tumors is associated with elevated plasma chromogranin A levels?

A. Pheochromocytoma
B. Carcinoid tumor
C. Pancreatic islet tumor
D. Small cell neuroendocrine tumor
E. all of the above

Back 779

E. all of the above

Front 780

Name several neuroendocrine tumors (5- list not all inclusive)

Back 780

Carcinoids
Islet tumors
Medullary thyroid carcinomas
Pheochromocytomas
Neuroendocrine

Front 781

What cells are carcinoid neoplasms composed of?

Back 781

Enterchromaffin cells

Endocrine cells (EC). The secretions are seen here as eosinophilic granules (SG).

Also shown in this image are two Paneth cells, an entirely different type of secretory resident cell of the intestine; and one that's not any sort of endocrine cell at all, despite some similarities of appearance. Paneth cells secrete their product into the lumen; and their granules (PCG) are much larger and coarser than those of the true endocrine cells.

Front 782

Which immunohistochemical pattern is most consistent with medullary thyroid carcinoma?

A. Calcitonin (-), CEA (-), thyroglobulin (+)
B. Calcitonin (+), CEA (-), thyroglobulin (+)
C. Calcitonin (+), CEA (+), thyroglobulin (+)
D. Calcitonin (+), CEA (+), thyroglobulin (-)
E. Calcitonin (-), CEA (+), thyroglobulin (+)

Back 782

D. Calcitonin (+), CEA (+), thyroglobulin (-)

Front 783

Carcinoid neoplasms are capable of producing what neurotransmitter?

Back 783

Serotonin

What is the rate limiting step in the biosynthesis of seratonin?

Hint 783

Conversion of tryptophan to 5-hydroxytryptamine by tryptophan hydroxylase

Front 784

What cell takes up 5-hydroxytryptamine and stores it in its secretory (dense) granules?

Back 784

Platelets

Front 785

Is seratonin cleared by the kidneys or liver?

Back 785

Liver
Seratonin is dumped into the portal system.

Front 786

What are the symptoms of carcinoid syndrome?

Back 786

Diarrhea
Flushing
Wheezing

What two chemicals can be assayed in a urine sample to detect possible seratonin excess?

Hint 786

5-HIAA (a serotonin metabolite)
Serotonin

These can be falsely elevated if the patient has been consuming what food?

Front 787

Platelet serotonin appears to be the most accurate marker for the detection of what tumor?

Back 787

Carcinoid

Front 788

Plasma calcitonin is useful to detect what type of carcinoma?

Back 788

Medullary carcinoma


At the center and to the right is a medullary carcinoma of thyroid. At the far right is pink hyaline material with the appearance of amyloid. These neoplasms are derived from the thyroid "C" cells and, therefore, have neuroendocrine features such as secretion of calcitonin.

Front 789

What is the normal level of calcitonin in a individual?

Back 789

<10ng/L, some affected individuals have leves this low, provocative testing using what type of drugs (3) can make the test more sensitive?

Hint 789

Pentagastrin
Omeprazole
Or calcium
This test may need to be done in families with MEN II

Current assays for calcitonin measure what form?

Front 790

Thyroglobulin is not elevated in medullary carcinoma.

True or false?

Back 790

TRUE

Front 791

CEA is commonly elevated in __________ carcinoma. Higher values correlate with greater dedifferentiation and suggests a worse prognosis.

Back 791

Medullary

A 28 year old male has suffered from FUO, high blood pressure, diarrhea, and rapid heart rate for several years. Examination revealed enlarged cervical lymph nodes and thyroid nodularity. A biopsy was taken, as were several blood tests. After determining he carried a specific genetic mutation he was diagnosed with Sipple Syndrome (MEN 11-B).



A mutation in what gene was found?

RET
STAT 1
BCR/ABL

Hint 791

RET

The cause of most medullary thyroid carcinoma cases is unknown. However, some are associated with MEN (multiple endocrine neoplasia). One of these diseases is Sipple Syndrome (MEN 11-B). It is an autosomal dominant inherited syndrome that includes bilateral C cell (medullary) carcinoma, pheochromocytoma and hyperthyroidism. Both males and females carrying this gene usually become symptomatic in their thirties. The cancer cell of origin is the C cell which is the producer of calcitonin.

Front 792

Paragangliomas and pheochromocytomas originate from what cell type?

Back 792

Chromaffin cells

These cells are capable of secreting what molecules?

Hint 792

Catecholamines

Front 793

Norepinephrine cen be converted to epinephrine by the action of what enzyme?

Back 793

PNMT

Phenolethanolamine-N-methylTRANSFERASE

Tumors also have the capability to convert norepinephrine to epinephrine. Therefore adrenal tumors will secrete both norepinephrine and epinephrine. Is this true for extra-adrenal tumors?

Hint 793

No.

What do they secrete?

Front 794

Norepinephrine is metaboilzed to normetanephrine. Most normetanephrine is conjugated to sulfate and excreted in urine, and some is metabolized to what compound?

Back 794

VMA. Or. Vanillylmandelic acid

Epinephrine is also metabolized to VMA, however the intermediate is what compound?

Hint 794

Metanephrine

Front 795

Fractionation of catecholamines or metanephrines can be useful in what way in diagnosing a pheochromocytoma?

Back 795

It can help with suggesting a location (paraganglioma ((extra-adrenal mainly secrete norepinephrine)) vs. pheochromocytoma)

Front 796

Certain anti hypertensive drugs can interfere with the following assays: urinary VMA, urinary metanephrines, urinary catecholamines, plasma metanephrines, or plasma catecholamines, which of the following are included in this list?


A. Imipramine
B. Reserpine
C. Guanethidine
D. Nitroglycerine
E. MAO inhibitors
F. All of the above

Back 796

F. All of the above

Imipramine
Reserpine
Guanethidine
Nitroglycerine
MAO inhibitors

Front 797

Which of the following tests is considered most accurate for initial screening for a pheochromocytoma?

A. urinary VMA
B. urinary metanephrines
C. urinary catecholamines
D. plasma metanephrines
F. plasma catecholamines

Back 797

D. Free (unconjugated) Plasma metanephrines

Why is this?

Hint 797

Plasma metanephrines better reflect long-term catecholamine secretion.

This is because catecholamines are released in an episodic nature, so plasma catecholamines have poor sensitivity.

What test can be done to clarify equivocal serum and urine tests?

Front 798

What two metabolites are found in most cases of neuroblastoma?

Back 798

Vanillylmandelic acid
and
Homovanillic acid

HVA is the final metabolic product of what two compounds?

Hint 798

DOPA and dopamine