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General Information
(Please remember that Video presentation of lectures are a luxury - occasionally technical problems may result in no tapes for a lecture - don't depend on these 100% to replace class). I have checked and student computer labs at the various campus, will have computers with audio capability. Videos will hopefully be in the appropriate WebCT course about one week (hopefully sooner) after the class - it takes time to transport between Boise and Pocatello, to encode and load. Announcements will be posted on CLS homepage when the videos are available.
Videos of the following classes are available:
- BIOS 411C - up to 9/17
- BIOS 411D - up to 9/18
- BIOS 411F - up to 9/18
- BIOS 411J - up to 9/16
- BIOS 411D - up to 9/18
- BIOS 411H - up to 9/18
If you haven't submitted bio - please do - Biography or similar information electronically - preliminary assignment
BIOS 411A - Phlebotomy, Section 1 - Pocatello
Skills are improving - venipunture with tube changes, hand-sticks with butterflies, and dermal sticks were the main focus. Week 4 objectives were posted. Assignment 1 was turned in and will be graded soon! Start to think about maybe an online quiz next week!! Next week we will be doing bleeding times, talking about arterial sticks and practice, practice, practice!!
New Assignment was posted in WebCT course - Please see CLS announcements or 411A - Section 1 bulletins.
BIOS 411A - Phlebotomy, Section 2 - Boise
Practical Lab Assignment posted. Hand in on Tuesday September 24. Keep up with weekly objectives. I may ask applicable questions during lab.
Students performed dermal punctures first on themselves and then on a partner. Students also performed venipunctures using multiple tubes. I am very impressed with EVERYONE. Technique and care is great! Tried to do spun HCT (technical difficulties with centrifuge); some made blood smears. Requisitions were utilized for patient identification and determination of which tubes to use.
Next lab: use of butterflies and if available, syringes. Please start making blood smears and dermal punctures for spun crits if centrifuge issue is overcome.
I am very pleased with everyone’s progress and look forward to placing
as many students as possible in a clinical setting.
(TOP)
BIOS 411B - Body Fluids - Pocatello and Boise
Will meet in approximately 3 weeks - Please check announcements for more details. Currently, you do not have access to the WebCT portion of the course.
We began to talk about regulations that influence clinical laboratory practice, starting with the history of regulations continuing on and into the 21st century. Several agencies involved specifically with clinical laboratory operations were mentioned. Next week, we will begin to talk about "Quality Health Systems" and clinical laboratory operations. Check the Assessment Activities module for this week's assignment. Sue may be in Boise next week!
BIOS 411D - Clinical Microbiology I
We finished up discussing infections of the CNS. We also discussed "Where are we?" and "Where should we be?". The students were reminded to be sure to take a look at the self tests associated with each page in the Microbiology course. Next week, we will begin to talk about organisms found in the blood. Sue Galindo may be in Boise next week!
BIOS 411F - Clinical Hematology I
The case studies we did this week hopefully illustrated the utility of
a flow chart for the evaluation of anemias. We looked at several anemias
- specifically iron deficiency and thalassemias. Iron deficiency will
account for about 90% of microcytic/hypochromic anemias, 9% of them will
be thalassemias and 1% others - such as siderocytic anemias.
Confirmatory tests for iron deficiency include iron-and iron binding
capacity which have a reciprocal relationship. There are no confirmatory
tests for mild alpha thalassemias but
electrophoresis is the the confirmatory test for the severe (three and
four deletion alpha thalassemias, the Beta thals and the mixed thals.
We looked at several of these (Minnesota WEB site). Next week I would like to get through cases of normocytic anemias starting with the other hemoglobinopathies (defects in chains due to amino acid substitutions.
BIOS 411H - Clinical Immunology/Serology/Transfusion Medicine I
Practice Quiz posted. This has a set of 60 questions to be answered in 70 minutes. This will not be officially graded. Go ahead and just take it; these are the type of questions that may be asked in certification examinations. I suspect that these questions will seem awful (if not – great!). Be assured that you will be able to answer these by the end of the two courses.
In conjunction with the objectives, lectures, assignments - my aim is for you to recognize the scope of knowledge that you need to become proficient in the area of immunology.
In lecture this week we covered Immunodeficiency (distinguished between Primary and Secondary with examples); Gammopathies (Multiple Myeloma), Protein electrophoresis (introduced method); and started Immunological methods. Discussed antibodies and antigens as reagents. Classification of immunoassays and reviewed precipitation methods, RID, Double Diffusion (Ouchterlony), Electroimmunodiffusion (Rocket-Laurell’s), Immunodiffusion, Immunofixation.
Course content module for Lab Methodology contains back ground information on immunology methods.
BIOS 411J - Clinical Chemistry I
We went over 4 case studies to illustrate the use of intracellular and
function markers in the
diagnosis of a few selected hepatic and pancreatic diseases.
- Pancreatitis - presenting with acute abdominal pain - surgical intervention contraindicated - to distinguish from other causes of acute abdominal pain: Amylase and Lipase. Like the cardiac markers there is a difference in the rate of rise and in the persistence of these markers. Amylase rises earlier but is cleared more rapidly - Lipase a little later but persists longer. Together almost 100% specificity and sensitivity. If Lipase unavailable - a two hour Amylase clearance test is a valuable tool. To distinguish from Ectopic pregnancy - Beta HCG - (we will discuss this one later. Hepatic markers may become elevated as activation of digestive zymogens and backup of fluid through common duct to liver occurs but this is late. GGT elevation occurs.
- Cholestasis - (obstructive disease - in this case gall bladder with stones) presenting also with acute abdominal pain may require surgical intervention primarily to prevent damage to pancreas. Hepatic markers will be elevated (AST, ALT, GGT. Alk Phos) indicating tissue damage. Liver Function markers (Albumin, Bilirubin Coagulation Proteins) may or may not be changed. In this case it was obvious that the liver was functional (conjugated or soluble bilirubin) and normal levels of albumin). There was an elevation in total and direct bilirubin and a prolongation of the Protime but the etiology was Post hepatic blockage. The enzymes support this conclusion - the Alkaline phosphatase was elevated to a greater degree than the transaminases. The reason for the prolonged Protime was lack of absorption of fat soluble vitamin K rather than inability of the liver to make the protein because of liver damage. Treatment is injectable vitamin K and surgical relief of the blockage. Further evidence supporting a diagnosis of blockage are to be found in the lack of increase of urobilinogen in the urinalysis in the presence of bilirubin and in the lack of color in the stools. Again the GGT was elevated but in a similar range as the acute pancreatitis.
- Acute hepatitis - in this case the viral markers indicated hepatitis
C as the etiological agent - but B and rarely A would have given the
same presentation as would other viruses and chemical causes. Acute
hepatitis especially in C and B may progress to chronic and then to
cirrhosis. As damage progresses, a decrease in liver function occurs (coagulation proteins, bilirubin conjugation and production of albumin). Increases in the Hepatic markers (AST, ALT, GGT, and Alk phos) indicate cellular damage occurring right now. The elevation of the transaminases to a greater extent than the Alkaline phosphatase (opposite of the case above) point to hepatic damage and specifically parenchymal or hepatocytes as opposed to biliary or ductile tissue.) When the ALT and AST are elevated to a similar extent the damage is
frequently reversible (observation - not hard and fast rule). When the AST is considerably higher than the ALT it indicates more severe damage with the leakage of mitochondrial AST. The GGT is again markedly elevated but similar to the other cases. In this case the albumin was low and the coagulation test elevated indicated enough hepatic damage to interfere with function. In this case fresh frozen plasma rather than vitamin K alone would be required to replace the coagulation factors. Albumin would have to be replaced immediately because the level of albumin in this patient is right at the point at which oncotic pressure can no longer be maintained.
- Alcoholic hepatic damage and cirrhosis - In the earlier admission
for this patient a similar picture to the acute hepatitis was seen,
with hepatic enzymes and liver function tests pointing toward hepatocyte
damage with loss of liver function. Viral hepatitis was ruled out and
a
careful history elicited the information that this individual routinely imbibed at least 5 martinis a day and had for some time. The GGT is again elevated similarly to the other cases and the transaminases to a greater extent than the alkaline phosphatase. Additionally the MCV (we
will discuss with CBCs) was elevated. Alcoholics frequently have nutritional deficiencies - B-12 and Folate deficiencies can give rise to a macrocytic anemia (high MCV). Alcoholism alone can do it through direct inhibition of nuclear division. On the second admission the liver enzymes had fallen to a more normal range, yet the liver function tests had deteriorated even further. In the face of a possible hepatic coma an ammonia level was run which was highly elevated. One student (don't know which one), correctly commented that the comatose state may have been due to the acidic state resulting from increased ammonia. The pronounced abdominal ascites and peripheral edema were due to the lack of albumin - additionally the ascites fluid accumulation in the abdomen could have been accentuated by the portal hypertension accompanying the hepatomegoly and scar tissue formation. Cirrhosis is also the end point of chronic hepatitis syndromes and a similar drop in liver enzyme levels can occur as the liver mass is replaced by scar tissue. As this happens, the true liver function tests
become more abnormal.
Many drugs and chemicals case hepatic damage which begins as cellular damage and as progression occurs results in loss of liver function. By the time loss of liver function detectable by laboratory tests occurs (albumin - coagulation factors- other proteins) a significant part of the liver mass has been destroyed. This is why with many drug treatments, the tests that are selected to monitor hepatic damage are the transaminases rather than specific proteins or true liver function tests. Remember the three transaminases (AST/ALT/GGT) for parenchymal damage with AST being more sensitive to mitochondrial damage- and Alkaline phosphatase to tubular damage. GGT is very sensitive because it can be induced and may rise out of proportion to the damage and is therefore the single most sensitive test, but is relatively nonspecific because you will see a rise in both tubular and parenchymal disease as well as severe pancreatitis. It is NOT included on any of the common chemistry panels and must be ordered specifically. AST/ALT/and Alkaline phosphatase are found in other tissues, so isolated increases in these need to be investigated further. Hemolyzed blood samples will elevate all three with ALT and ALP being raised higher than AST. Lesions in the Gut will give increases in AST and ALP over ALT.
We peripherally discussed Bilirubins. Bilirubin is the natural breakdown
product of the heme portion of the hemoglobin molecule. That process occurs
in the reticuloendothelial system. This bilirubin is insoluble in plasma,
binds to lipid membranes. It is conjugated to a glucuronide in the liver.
Once conjugated it is soluble and is excreted through the bile and also
back through the plasma and the kidney. When the lab gives you a value
for total bilirubin we do not distinguish
between processed and unprocessed (soluble or insoluble). When we give
you a direct bilirubin, that is the soluble portion which is that which
has been processed by the liver (for the most part - there are a few minor
soluble bilirubins without liver intervention but they are a very small
proportion of the total). The indirect is the unconjugated and its value
is derived by subtracting soluble from total. Urobilinogen is a further
breakdown of the bilrubin which occurs in the gut. It gives feces their
brown color and is soluble and circulates back across the gut and into
the urine, giving some of the yellow color to urine. In the case of common
duct or bile duct blockage therefore, the urobilinogen does not get made
and therefore the stools may be pale and the urobilinogen in the urine
does not increase.
For next week - read through the section that I have put on the WEB CT course describing the hepatic markers in more detail and read ahead for Renal function - DO NOT WORRY ABOUT THE ASSIGNMENTS -( Pharmacy students only)
PSCI 457 - Clinical Chemistry for Pharmacy Students
We went over 4 case studies to illustrate the use of intracellular and
function markers in the
diagnosis of a few selected hepatic and pancreatic diseases.
- Pancreatitis - presenting with acute abdominal pain - surgical intervention contraindicated - to distinguish from other causes of acute abdominal pain: Amylase and Lipase. Like the cardiac markers there is a difference in the rate of rise and in the persistence of these markers. Amylase rises earlier but is cleared more rapidly - Lipase a little later but persists longer. Together almost 100% specificity and sensitivity. If Lipase unavailable - a two hour Amylase clearance test is a valuable tool. To distinguish from Ectopic pregnancy - Beta HCG - (we will discuss this one later. Hepatic markers may become elevated as activation of digestive zymogens and backup of fluid through common duct to liver occurs but this is late. GGT elevation occurs.
- Cholestasis - (obstructive disease - in this case gall bladder with stones) presenting also with acute abdominal pain may require surgical intervention primarily to prevent damage to pancreas. Hepatic markers will be elevated (AST, ALT, GGT. Alk Phos) indicating tissue damage. Liver Function markers (Albumin, Bilirubin Coagulation Proteins) may or may not be changed. In this case it was obvious that the liver was functional (conjugated or soluble bilirubin) and normal levels of albumin). There was an elevation in total and direct bilirubin and a prolongation of the Protime but the etiology was Post hepatic blockage. The enzymes support this conclusion - the Alkaline phosphatase was elevated to a greater degree than the transaminases. The reason for the prolonged Protime was lack of absorption of fat soluble vitamin K rather than inability of the liver to make the protein because of liver damage. Treatment is injectable vitamin K and surgical relief of the blockage. Further evidence supporting a diagnosis of blockage are to be found in the lack of increase of urobilinogen in the urinalysis in the presence of bilirubin and in the lack of color in the stools. Again the GGT was elevated but in a similar range as the acute pancreatitis.
- Acute hepatitis - in this case the viral markers indicated hepatitis
C as the etiological agent - but B and rarely A would have given the
same presentation as would other viruses and chemical causes. Acute
hepatitis especially in C and B may progress to chronic and then to
cirrhosis. As damage progresses, a decrease in liver function occurs (coagulation proteins, bilirubin conjugation and production of albumin). Increases in the Hepatic markers (AST, ALT, GGT, and Alk phos) indicate cellular damage occurring right now. The elevation of the transaminases to a greater extent than the Alkaline phosphatase (opposite of the case above) point to hepatic damage and specifically parenchymal or hepatocytes as opposed to biliary or ductile tissue.) When the ALT and AST are elevated to a similar extent the damage is
frequently reversible (observation - not hard and fast rule). When the AST is considerably higher than the ALT it indicates more severe damage with the leakage of mitochondrial AST. The GGT is again markedly elevated but similar to the other cases. In this case the albumin was low and the coagulation test elevated indicated enough hepatic damage to interfere with function. In this case fresh frozen plasma rather than vitamin K alone would be required to replace the coagulation factors. Albumin would have to be replaced immediately because the level of albumin in this patient is right at the point at which oncotic pressure can no longer be maintained.
- Alcoholic hepatic damage and cirrhosis - In the earlier admission
for this patient a similar picture to the acute hepatitis was seen,
with hepatic enzymes and liver function tests pointing toward hepatocyte
damage with loss of liver function. Viral hepatitis was ruled out and
a
careful history elicited the information that this individual routinely imbibed at least 5 martinis a day and had for some time. The GGT is again elevated similarly to the other cases and the transaminases to a greater extent than the alkaline phosphatase. Additionally the MCV (we
will discuss with CBCs) was elevated. Alcoholics frequently have nutritional deficiencies - B-12 and Folate deficiencies can give rise to a macrocytic anemia (high MCV). Alcoholism alone can do it through direct inhibition of nuclear division. On the second admission the liver enzymes had fallen to a more normal range, yet the liver function tests had deteriorated even further. In the face of a possible hepatic coma an ammonia level was run which was highly elevated. One student (don't know which one), correctly commented that the comatose state may have been due to the acidic state resulting from increased ammonia. The pronounced abdominal ascites and peripheral edema were due to the lack of albumin - additionally the ascites fluid accumulation in the abdomen could have been accentuated by the portal hypertension accompanying the hepatomegoly and scar tissue formation. Cirrhosis is also the end point of chronic hepatitis syndromes and a similar drop in liver enzyme levels can occur as the liver mass is replaced by scar tissue. As this happens, the true liver function tests
become more abnormal.
Many drugs and chemicals case hepatic damage which begins as cellular damage and as progression occurs results in loss of liver function. By the time loss of liver function detectable by laboratory tests occurs (albumin - coagulation factors- other proteins) a significant part of the liver mass has been destroyed. This is why with many drug treatments, the tests that are selected to monitor hepatic damage are the transaminases rather than specific proteins or true liver function tests. Remember the three transaminases (AST/ALT/GGT) for parenchymal damage with AST being more sensitive to mitochondrial damage- and Alkaline phosphatase to tubular damage. GGT is very sensitive because it can be induced and may rise out of proportion to the damage and is therefore the single most sensitive test, but is relatively nonspecific because you will see a rise in both tubular and parenchymal disease as well as severe pancreatitis. It is NOT included on any of the common chemistry panels and must be ordered specifically. AST/ALT/and Alkaline phosphatase are found in other tissues, so isolated increases in these need to be investigated further. Hemolyzed blood samples will elevate all three with ALT and ALP being raised higher than AST. Lesions in the Gut will give increases in AST and ALP over ALT.
We peripherally discussed Bilirubins. Bilirubin is the natural breakdown
product of the heme portion of the hemoglobin molecule. That process occurs
in the reticuloendothelial system. This bilirubin is insoluble in plasma,
binds to lipid membranes. It is conjugated to a glucuronide in the liver.
Once conjugated it is soluble and is excreted through the bile and also
back through the plasma and the kidney. When the lab gives you a value
for total bilirubin we do not distinguish
between processed and unprocessed (soluble or insoluble). When we give
you a direct bilirubin, that is the soluble portion which is that which
has been processed by the liver (for the most part - there are a few minor
soluble bilirubins without liver intervention but they are a very small
proportion of the total). The indirect is the unconjugated and its value
is derived by subtracting soluble from total. Urobilinogen is a further
breakdown of the bilrubin which occurs in the gut. It gives feces their
brown color and is soluble and circulates back across the gut and into
the urine, giving some of the yellow color to urine. In the case of common
duct or bile duct blockage therefore, the urobilinogen does not get made
and therefore the stools may be pale and the urobilinogen in the urine
does not increase.
For next week - read through the section that I have put on the WEB CT course describing the hepatic markers in more detail and read ahead for Renal function -
Pharmacy Students only - DO NOT WORRY ABOUT THE ASSIGNMENTS
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Weekend!!! Be Safe - Have Fun |