Vol 28 / NO 2
FALL/WINTER 2014
Journal of Allied Health Professionals
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BALLOTED
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To be po 17, 2014
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IN
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INFORM
Presorted
Standard
US Postage
Paid
Lubbock TX
Permit No. 49
Articles
Acute Leukemia In Children:
A Review
Texas State Society of American
Medical Technologists
6
CE #31-303-14
By: Francis M. Torres
Fall/Winter 2014
Vol 28 / No 2
TABLE OF
CONTENTS
Features
Calendar of Events
The Challenging Function
of Delegates
10
A Look at Treatments
for Epilepsy
11
Candidates for 2015-2016
14
Blood aka River of Life
18
5
Photos16-17
Fall Registration
26
Hotel Registration
26
Departments
Officer’s Page
3
A Message from the President
4
District Councilor’s Message
4
Kimberly’s Corner
5
By: Benita Trainer
Angelina College Phlebotomy Student
Ballots must be postmarked by
August 17, 2014
Editorial opinions in articles printed in The New Texan
are those of the author, and are not the official policy of
the society.
The Editor reserves the right to edit all articles where
necessary.
Manuscripts submitted for publication should be
typewritten, double spaced with wide margins. No
manuscript will be returned unless specifically requested
by the author.
Changes of address of subscribers to The New Texan
must be in the hands of the editor one month before the
issuance of each number. Your old and new address
should be given. Advertising correspondence, requests
for information or other correspondence concerning
advertising may be addressed to Kim Meshell, P.O. Box
152023, Lufkin, Texas 75915
CE #31-304-14
by Elaine Allen
Home Office
American Medical Technologists
10700 W. Higgins Rd., Rosemont, IL 60018
847-823-5169
1-800-ASK-1AMT
(1-800-275-1268)
www.americanmedtech.org
2
The New TexaN
Fall/Winter 2014 / TxSSAMT
TxSSAMT Officers 2014-2015
President
VICE-President/editor
Norma “Taffy” Durfee, MT
P.O. Box 432 • Iola, Texas 77861
Work (936) 661-5140
nkd003@shsu.edu
Kim Meshell, CAHI, COLT, RMA, RPT
P.O. Box 152023 • Lufkin, Texas 75915
Home (936) 831-3729
Work (936) 633-5459
Cell (936) 465-2222
kim8569@hotmail.com
chairman of the
board/Co-Editor
MT Board Member
Michelle Jenkins, MT
1100 Carrington Court • Irving, Texas 75060
Home (972) 986-5133
Work (972) 518-6293
dimitrimj@netzero.net
Secretary
Katrina Fryar, MT
9338 FM 2549 • Bryan, Texas 77808
Cell (979) 777-7030
ag3kat@yahoo.com
Treasurer
David Finch, MT
1901 FM 2088 • Gilmer, Texas 75644
Home (903) 762-2419
Cell (903) 841-1884
dfinch@etex.net
Jean Palmer, CAHI, RMA
260 Willow Springs Drive • Coppell, Texas 75019
Home (972) 462-7826
Work (972) 403-6000
jeangonshpn@hotmail.com
Committee Chairs
employment chair
Pat Westbrook, MT
14330 Hollypark Drive
Houston, Texas 77015
Home (713) 453-2075
Work (713) 330-3000
pwest1@hal-pc.org
HISTORIAN/Hall of fame
Convention Chair
Vernell Boyd, MT
36119 B FM 149
Pinehurst, Texas 77362
(281) 259-2548
Cell (713) 826-3772
mamadowser@aol.com
Fall/Winter 2014 / TxSSAMT
Continuing education
chair
T.J. Weatherly, MT
158 Roucourt Loop
College Station, TX 77845
Cell (979) 255-9301
tjw80@yahoo.com
proctor chair
Jean Palmer, CAHI, RMA
260 Willow Springs Drive
Coppell, Texas 75019
Home (972) 462-7826
Work (972) 403-6000
jeangonshpn@hotmail.com
Legislative Chair
ASSISTANT Editor
Glenda Stephens, MLT
350 High Crest Drive
Point Blank, TX 77365
936-581-4672 or
106 Mineola Ct.
Lakeway, TX 78734
936-581-4672
Miranda Lankford
490 Joe Bailey Road
Apple Springs, Texas 75926
936-465-8984
Audit
Awards/membership
David Finch, MT
1901 FM 2088
Gilmer, Texas 75644
Home (903) 762-2419
Cell (903) 841-1884
dfinch@etex.net
Norma “Taffy” Durfee, MT
P.O. Box 432
Iola, Texas 77861
Work (936) 661-5140
Nkd003@shsu.edu
The New TexaN
3
A Message
from the
President
Taffy K. Durfee
Randy Swopes
W
e just returned from a great National AMT meeting in Chicago and I am proud to say that we had
11 delegates representing Texas. Viviana Pelton brought
some of her students and two of them, Kim Derschuck
and Celia McDonald participated in the student challenge
bowl. It was great to see new faces from Texas. Next year
the national convention will be held on the Kona Coast of
the Big Island of Hawaii. The dates will be June 22 thru
June 25, 2015, and the hotel rates will be $169 a night.
Our next fall meeting will be held in Mount Pleasant, Texas
and David Finch will be our conference host. The dates will
be September 19 and 20th at the LaQuinta Inn in Mount
Pleasant. This will be our first educational conference in
Mount Pleasant. The spring 2015 conference will be held
in Huntsville, Texas.
If you would be interested in hosting a state convention in
your area, just give Vernell Boyd a call at 713-826-3772.
She will help with the planning and details for hosting a
convention. We would love to hear from you.
Taffy K. Durfee
For Employment Information
Contact:
Pat Westbrook
14330 Hollypark Drive
Houston, Texas 77015
713-453-2075
4
The New TexaN
District
Councilor’s
Message
A
s we conclude the celebration of AMT’s 75th birthday,
the words describing our National Convention are: “a
good time was had by all”.
Central District did extremely well with awards this year.
District Achievement – Tonda Ellis, CMLA, RPT. Exceptional Merit Awards – Lia Spears ,MT. Pillar Awards – Art
Contino, AHI, RMA and Cecil Hunt, MT. Silver Service
Awards – Vernon Bass, MT and Kathy Sutton, MT. Cuviello
Award – Roxann Clifton, MT. Friend of AMT- George Raven. Norman Frankel Outstanding Student Awards, MLT
Student – Heidi Zuniga. Student Technical Writing Awards,
1st Place: Marcia S. Haverly, MLT Program, 2nd Place:
Tiffany Jackson, MLT Program, 3rd Place: Shelby McVicker, MLT Program. State Society Publication Awards – 3rd
Place: Kim Meshell. Because of all the officers and editors
diligent efforts, Central District was again perfect in Honor
Roll status. As a result of all this I was awarded the “Becky
Award”. I salute all of our winners.
Future Meetings include the Magnolia meeting in Gatlinburg, TN. on October 17th and 18th, 2014. 2015 National
Convention will take place in Hawaii. This meeting will be
casual attire. There will be no gift baskets for this year in
Hawaii. Gift cards will be given by states, in 2016 we will
return to baskets. The 2016 National Convention will be
held somewhere in the Southern Region. National Lab Assistants Week will be held the 3rd week of October.
Election of Board of Directors winners are Everett Bloodworth, MT, Ken Hawker, MT. and Deborah Westervelt,
RMA.
I look forward to attending one of your State Meetings.
Respectfully submitted,
Randy Swopes, MT, AMT
Central District Councellor
337-794-1164
2691 Whittington Rd., Westlake, La 70669
Fall/Winter 2014 / TxSSAMT
Kimberly’s
Corner
Kimberly Meshell
Howdy Texas!
H
Calendar
of
Events
Meetings or Conventions
ope y'all are having a fantastic summer. I just got back
from the AMT National meeting in Chicago. Loved it,
except for the flying part. We all know I hate to fly, I go into
a major panic attack. Had an exciting adventure when I was
there so look through the journal for the story of my chicken
dinner.... It's a hoot!
Fall 2014
September 19-20, 2014
LaQuinta Inn
Mt. Pleasant, Tx
Summer 2015
June 22-25, 2015
Kona, Hawaii
We have a lot going on. It is that time again for elections, so
please everyone vote. Your vote is important! You are the
heart of our society. We want to hear from you. The ballots
will be in the journal so please make sure you fill them out
and put in the mailbox. Remember, this is an organization
for the members, by the members and your vote counts!
Spring 2015
April 17-18, 2015
Comfort Suites
Huntsville, Tx
Fall 2015
TBA
We also have the next meeting coming up in Mount Pleasant, September 19-20 with a lot of great speakers. David
Finch has done a marvelous job getting together everyone
for this meeting. I hope to see everyone there.
We will also recognize our Hall of Famer-Ms. Pat Westbrook- very proud of her.
If you have any articles or stories for the journal, please let
me know.
I want to thank everyone for allowing me to be your editor,
I love it!
Kimberly
A New Way to Track Your
Continuing Education!
AMTrax is AMT's newest online CE tracking system. Simply
log in as a member on the AMT website (www.americanmedtech.org) and click on AMTrax under the Continuing
Education tab.
Benefits of AMTrax include:
w One easy and convenient place to track your CE and
related activities
w Track AMT as well as non-AMT activities
w Print your record anytime for your employer or state
licensing agency
w Easy way to demonstrate CCP compliance (for those
certified after 1/1/06)
w Passing scores on AMT online CE tests, like STEP Online,
automatically populate AMTrax
w It's FREE!
Fall/Winter 2014 / TxSSAMT
The New TexaN
5
CE #31-303-14
Acute Leukemia
A Review
By: Francis M. Torres
Children’s Hospital of San Antonio Hematology Laboratory
Introduction
L
eukemia is an abnormal proliferation of blood cells that
become cancer cells. It features variable damage to a
cell’s DNA that has lost its ability to regulate and repair. Out
of control leukocyte production from the bone marrow finds
its way to the peripheral blood and other territories and tissues such as the cerebrospinal fluid (CSF compartment) or
visceral organs. This represents the typical pathophysiology of acute leukemia, if untreated.
Epidemiology
In the United States, Leukemia and Lymphoma Society facts
published in 2013 report that approximately every 4 minutes
one person is newly diagnosed and every 10 minutes another succumbs to blood cancer (1). Approximately 3,000 new
cases of childhood leukemia are seen annually and 80% are
Acute Lymphoblastic Leukemia (ALL). Chronic leukemias
in children are very rare but when seen, most are Chronic
Myelogenous Leukemia (CML) which usually affects teenagers. Statistics indicate that males are more affected than
females and that Caucasians are more often afflicted in children; acute leukemia collectively represents 30% of malignancies in patients younger than 15 years of age.
The causes of leukemia are under continued investigation.
Firm advances have been elusive. Some studies have
shown that leukemia could be initiated during intrauterine
life, particularly the so-called congenital acute leukemia.
Some prenatal exposures are suspected as risk factors to
the development of leukemia. Genetic predisposition, environmental exposure and socioeconomic status are some
risk factors claimed to be linked to the development of pediatric acute leukemia. Some researchers have suggested
a relationship between birth weight and risk of developing
leukemia. Along with this line, birth weight is influenced by
genetic and intrauterine conditions. In a meta-analysis, babies born with a weight of over 4,000 g were found to be at
higher risk in developing childhood leukemia (2). However,
such proposals are in search of confirmation. Nonetheless,
it has been suggested that a well-balanced maternal diet
6
The New TexaN
during pregnancy may minimize the likelihood of neonatal
problems, including developing childhood leukemia.
The National California Childhood Leukemia Study group
published a population-based case-control study of the maternal dietary habits and risk of childhood leukemia. The
study has offered the conclusion that consumption of a
balanced diet including vegetables, protein sources, fruits,
provitamin A, carotenoids and antioxidants like glutathione
by pregnant women do not show an association to childhood AAA (3). During the first 2 years of life, children with
regular food consumption to banana, oranges, and orange
juice were not found to have an increased risk of developing
childhood leukemia (4).
Breastfeeding is known to be protective against infant infections because it boosts immunity. Some studies have
suggested that it decreases the risk of childhood leukemia
by 21% (5). There is no association between exposure to
the usual vaccinations such as BCG – Bacillus Calmette
Guerin, MMR – Measles, Mumps and Rubella, DPT – Diphtheria, Tetanus and Pertussis, and against Hepatitis. Common childhood diseases such as measles, mumps, rubella,
chicken pox and ear infections have not been found to be a
risk for the development of ALL (6). Children who are treated for other cancers with chemotherapy including cyclophsphamide, chorambucil, etoposide and teniposide have an
associated higher risk to development of AML in the following 5 – 10 years of treatment. (7)
Genetics
Normally, our genes, at a cellular level, dictate when to activate or inactivate cell divisions. Oncogenes and tumor
suppressor genes play a major role in tumorigenesis (8).
Permanent activation of cells to divide is secondary to oncogene activity in front of ineffective tumor suppressor genes;
such imbalance leads to cancer. Mutations of genetic material conducive to childhood cancer, as well as inherited
genetic abnormalities may result in DNA repair impediment.
These abnormalities, as well as the so-called tumor supFall/Winter 2014 / TxSSAMT
pressor gene syndromes and congenital immune deficiency
syndromes, may also include pediatric leukemia (9). The
defective gene that is incapable of DNA repair in Fanconi
Anemia or Ataxia Telangiectasia has been found to increase
the risk of leukemia and lymphoma (10,11). TP53 gene is
a tumor suppressor gene associated with Li-Fraumeni syndrome and when mutations in the gene occur, it may result
in ALL and usually the hypodiploid type (12-13).
Down syndrome increases incidence of ALL or AML in the
general population (14). Studies have demonstrated that
Trisomy 21 increases DNA damage leading to GATA1 (it
functions as a transcription factor for hematopoiesis) mutations (15,16). Infections with Epstein Barr virus, being more
frequently seen in patients with immune deficiency, are also
known to cause lymphoproliferative disorders like lymphoma (17). A constant effort to understand the genetic behavior of leukemia is being made by researchers and members
of medical teams aiming to clarify the mechanisms of leukemia and trying to prevent such malignancy, as well as the
achieve progress in the diagnosis and treatment.
Environmental
Environmental exposure plays an important role in the gene
mutations. Exposures to diagnostic X-ray (18), household
pesticides (19), paints, metals, and petroleum products
(20), frequent use of solvents to artwork and among those
children whose mothers lived in homes painted extensively in the year before the child’s birth (21) are some of the
suspected risk factors associated with childhood leukemia.
Benzene related exposure like automobile and industrial
emissions, active and passive smoke, dwellings nearby
auto repair garages and petroleum stations are reported
increased risk of childhood leukemia (22). A 7-year case
control study with National California Childhood Leukemia
Study found that paternal smoking is a greater risk of ALL
especially if both parents smoke (23). Exposures to high
levels of domestic radon (24) and prolonged exposure to
electromagnetic fields (EMF) could increase the risk of
childhood leukemia (25).
There are some studies that showed no association with
childhood leukemia. Studies, including folic acid supplement during pregnancy, daycare attendance and social activity in the first year of life (presumed to increase infectious
exposure) and cellular telephone use, were found not to be
associated with childhood leukemia (26).
Approach to Diagnosis
In children, the findings of anemia, protracted infection,
bleeding, hepatosplenomegaly, weight loss, loss of appetite, bone or joint pain, or lymphadenomegaly may accompany the presentation of leukemia. A thorough medical
history with thorough examination by the pediatrician or primary care provider would result in ordering an appropriate
Fall/Winter 2014 / TxSSAMT
laboratory diagnostic test to ascertain the cause or rule out
leukemia. As leukemia is concerned, specimens usually
tested are peripheral blood, bone marrow, cerebrospinal
fluid or sometimes material obtained from masses by fine
needle aspiration biopsy (FNAB). The laboratory technologist and the pathologist would be able to recognize leukemia based on cytomorphology, flow cytometric analysis and
cytogenetic findings. Algorithms in Figures 1.1 and 1.2 are
helpful guidelines for the orderly and correct approach for
the diagnosis of pediatric acute leukemia (27).
If the diagnosis of acute leukemia is confirmed from examination of peripheral blood and bone marrow, a diagnostic
lumbar puncture will be necessary in order to confirm involvement of the central nervous system (CNS), particularly
in cases of Acute Lymphoblastic Leukemia. Other studies
that complement the diagnosis of leukemia include blood
chemistries, urine analysis and imaging studies.
Prevention
Although the causes of childhood leukemia are not known,
the elimination of suspected risk factors or avoidance is
advisable. Pregnant women should eliminate or limit diagnostic X-ray studies and should avoid exposure to tobacco,
smoke, solvents, pesticides, high electromagnetic fields and
benzene chemicals. Paternal exposure recommendations
are also available but environmental or occupational-related
risks are less well known. For an infant or child, diet should
be nutritious and well-balanced, aiming to maintain homeostasis in the immune apparatus.
Any child exposed to known risk factors that develops clinical
signs and symptoms as described above should immediately
be seen by their physician and, if appropriate, laboratory exams should be included. Congenital or inheritable conditions
such as immune deficiency syndrome, as mentioned above,
should include a close follow up by a medical provider.
Once a child is diagnosed with acute leukemia a whole team
is available in well-organized pediatric hospitals that would
impart education to parents and patients. Understanding of
Clinical Laboratory & Diagnostic Services
Stephen R. Harlow, PhD, MT, ASCLS
Certified Laboratory Consultant
Managing Director
201 Laurence #108 • Heath, TX 75032
(214) 577-9311 • (972) 771-4588 FAX
sharlowphd@roninclinlab.com
The New TexaN
7
8
The New TexaN
Fall/Winter 2014 / TxSSAMT
Provided by: Francis M. Torres
Children’s Hospital of San Antonio Hematology Laboratory
Conclusion
This article is directed to laboratorian colleagues, the hope
that it will provide or expand understanding about the difficulties faced by families and the critical contribution of
laboratory workers, in dealing with a pediatric patient with
acute leukemia. Our work, combined with diverse teams in
a usual pediatric setting, with patience, understanding and
compassion would be our contribution to minimize the suffering of patients involved in pediatric acute leukemia. As
for me, I find a great deal of satisfaction in the work I do
by contributing my knowledge and skills in the hematology
laboratory at the Children’s Hospital of San Antonio and to
be of service to our children because “our children will always be first”. n
References
1. The Leukemia & Lymphoma Society facts 2013. Website: www.LLS.org
2. Hjalgrim H., Engels EA. Birth weight as a risk factor for childhood leukemia:
A meta-analysis of 18 epidemiologic studies Am J Epidemiol 2003; 158:724735
3. Jensen CD., Block G., Buffer P., Ma X., Selvin S., Month S. Maternal dietary
risk factors in childhood acute lymphocytic leukemia (United States). Cancer
Causes and Control. 15:559-570 (2004).
4. Kwan ML., Block G., Selvin S., Month S., Buffler PA. Food consumption
by children and the risk of childhood acute leukemia. Am J Epidemiol 2004;
160: 1098-1107
5. Shu XO., Linet MS., Steinbuch M., Wen QW., Buckley JD., Neglia JP.,
Potter JD., Reaman GH., Robison LL. Breast-feeding and risk of childhood
leukemia. J Natl Cancer Inst 1999;91:1765-1772.
6. MacArthur AC., McBride ML., Spinelli JJ., Tamaro S., Gallagher RP.,
Theriault GP. Risk of childhood leukemia associated with vaccination,
infection, and medication used in childhood. Am J Epidemiol 2008; 167: 598606.
7. Ibid 1.
8. American Cancer Society. Oncogenes, tumor suppressor genes, and
cancer. Website: www.cancer.org
9. Stieglitz E., Loh M. Genetic predisposition to childhood leukemia. Ther Adv
Hematol. (2013) 4(4)270-290
10. Buckley JD. Robinson LL, Swotinsky R, Garabrant DH, LeBeau M,
Manchester P, Nesbit ME, Odom L, Peters JM, Woods WG, et al., Occupational
exposure of parents of children with nonlymphocytic leukemia: a report from
the Children's Cancer Study Group. Cancer Res 49:4030-4037 (1989).
11. Infante-Rivard C, Labuda D, Krajinovic M, Sinnett D. Risk of childhood
leukemia associated with exposure to pesticide and with gene polymorphisms.
Epidemiology 10:481-487 (1999).
12. Homfeldt L., et al., The genomic landscape of hypodiploid acute
lymphoblastic leukemia. Nat Gent. Mar;45(3);242-52 (2013).
13. Powell BC., Jiang L., Munzny DM., Trevino LR., Strong LC., Wheeler
DA., Gibbs RA., Plon SE. Indentification of TP53 as an acute lymphocytic
leukemia susceptibility through exome sequencing. Pediatr Blood Cancer.
Fall/Winter 2014 / TxSSAMT
Jun; 60(6):E1-3 (2013).
14. Hasle C., Clemmensen I., Mikkelsen M. Risk of leukemia and solid tumors
in individuals with Down's syndrome. Lancet 355: 165-169 (2000).
15. Cabelof D., Patel H., Chen Q., Van Remmen H., Matherly L., Ge Y., et
al. Mutational spectrum at GATA1 provides insights into mutagenesis and
leukemogenesis in Down's syndrome. Blood 114: 2753-2763 (2009)
16. Ferreira R., Ohneda K., Yamamota M. Philipsen S. GATA1 function, a
paradigm for transcription factors in hematopoiesis. Mol Cell Biol. 2005,
25(4):1215-1227.
17. Saha A., Robertson E. Epstein-Barr virus associated B-cell lymphomas:
pathogenesis and clinical outcomes. Clin Cancer Res Mar 3, 2011 Published
OnlineFirst DOI: 10.1158/1078-0432.
18. Infante-Rivard C., Mathonnet G., Sinnett D. Risk of childhood leukemia
associated with diagnostic irradiation and polymorphism in DNA repair genes.
Children's health articles Environmental health perspective. 108 (6): 495-498
(2008).
19. Ma X., et al. Critical windows of exposure to household pesticides and
risk of childhood leukemia. Children's health articles Environmental health
perspective. 110(9):955-960 (2002).
20. McBride ML., Childhood cancer and environmental contaminants. Can J.
Public Health 1988, 89 (Supplement 1), S53-S62.
21. Freedman DM., et al. Household solvent exposures and childhood acute
lymphoblastic leukemia Am. J. Public Health 2001, 91(4), 564-567.
22. Buffer P., Kwan ML., Reynolds P., Urayama. Environmental and genetic risk
factors for childhood leukemia: appraising the evidence. Cancer Investigation,
1:60-75, 2005.
23. Chang JS., Selvin S., Metayer C., Crouse V., Golembesky A., Buffler PA.,
Parental smoking and the risk of childhood leukemia. Am J Epidemiol 2006;
163: 1091-1100?
24. Raaschou-Neilsen O, Andersen CE, Andersen HP, et al. Domestic radon
and childhood cancer in Denmark. Epidemiology 2008; 19(4):536-543.
25. Ahbom IC, Cardis E, Green A, Review of epidemiologic literature on EMF
and health. Environmental Health Perspective 2001; 109:911-933.
26. DynaMed. Acute lymphoblastic leukemia/lymphoma. Updated Feb 14,
2014 page 1-68.
27. Onciu M. Acute lymphoblastic leukemia. Hematol Oncol Clin North Am.
2009 Aug; 23(4):655-74.
Special thanks to Francis M. Torres & Children’s Hospital of San Antonio
Hematology Laboratory for providing editorial.
{CE questions continued on next page}
NATIONAL AMERICAN UNIVERSITY
National American University’s Austin campus is seeking
applications for adjunct faculty positions to teach Medical
Laboratory courses, Anatomy & Physiology, and other
Medical Assisting courses
• Applicants must be able to teach 1-2 days/wk in the evenings
• 3-5 years teaching experience preferred
• Minimum qualifications include a bachelor’s degree in a related field
(MD, PA, NP required to teach A&P)
• Certification and licenses must be current or able to reinstate
(ie, CMA, RMA, MT, RN)
• Applicants invited to interview will need to prepare a 15 minute
teaching demonstration to a small panel of staff/faculty
• Textbooks and instructor resources provided.
To apply:
the disease and the application of necessary therapies are
needed to adhere with knowledge and discipline. However,
we are all aware that such treatment includes complications
and adverse effects in the short and the long run. Under
ideal situations, the child and parents or guardians should
be informed and seek care in a qualified institution that includes groups like social services, nursing and psychologists working in coordination with medical teams. Joining
social media groups like Facebook and Twitter and other
organizations outside family and friends would also provide
the necessary support a family afflicted with a child with
pediatric acute leukemia.
Submit an employment application (http://www.national.edu/careers-nau),
letter of interest, current resume, and a copy of your college transcripts to:
Medical Assisting Program Coordinator
13801 Burnet Rd., Ste. 300
Austin, TX 78727
Fax/Email resumes to (512) 651-4705 or vvera@national.edu
EEO
The New TexaN
9
{continued from page 9}
Questions
Acute Leukemia in Children - CE #31-303-14
1. __________ __________
__________ is a chronic
leukemia which usually
affects teenagers.
2. T/F The definite cause(s)
of leukemia are well defined and well understood.
3. T/F Analysis showed that
babies born with a weight
of less than 4,000 g were
found to be at lower risk
in developing childhood
leukemia.
4. Which genes play a major
role in tumorigenesis?
(check all that apply)
a. Teniposide
b. Oncogenes
c. Glutathione
d. Tumor suppressor
5. Which gene is a tumor
suppressor gene that is
associated with Li-Fraumeni syndrome?
a. GATA1
b. Fanconi
c. TP53
d. Chorambucil
6. List at least 5 symptoms
that may accompany the
presentation of leukemia.
a. ____________________
b. ____________________
c. ____________________
d. ____________________
e. ____________________
7. List the specimen(s) used
for diagnostic analysis to rule
out leukemia.
a. ____________________
b. ____________________
c. ____________________
d. ____________________
8. G
ene mutations can be
caused by ___________
__________, including,
but not limited to, X-rays,
pesticides, paints and
benzene.
9. W
hat is the percentage of
newly diagnosed childhood leukemias are Acute
Lymphoblastic Leukemia?
a. Twenty
b. Thirty-five
c. Seventy-five
d. Eighty
10. ________ ________,
________ ________, and
________ ________ are
some risk factors claimed to
be linked to the development
of pediatric acute leukemia.
Please do not send money, these are free CEUs.
Send a copy of your answers and the identification form below to:
T.J. Weatherly
158 Roucourt Loop • College Station, TX 77845
American Medical Technologists Institute for Education
Reporting form for Continuing Education Hours
(Please print all information)
Last Name: ________________________________
First Name:________________________________
E-mail:____________________________________
q MT
q RMA
Check AMT Certification:
q MLT
q COLT
q RPT
q RDA
q CLC
q CAHI
AMT I.D. Number___________________________
(Do not put social security number on form)
10
The New TexaN
The Challenging
Function of
Delegates
By: Vernell Boyd, MT
A
t the recent 75th Anniversary of the American Medical
Technologists Convention in Chicago, I was asked to
write a report on “how serving as a delegate” has changed.
Where to begin? In the 70’s and 80’s, I remember attendance as being greater, even though membership total was
much less. State Societies had better participation--Texas
had FULL delegations--and all attending seemed to participate more in the elections and decision making. On banquet night, there was much political activity with delegates
soliciting votes from other states in order to elect their candidate-of-choice. Often, members signed up as candidates,
on the spot. The function of the Nominating Committee was
to interview all the candidates by asking them questions,
then make a recommendation based on their interview, for a
slate of Board Members. Their report placed their choices
in nomination. Others could be nominated from the floor.
Having served on the Nominating Committee for the past
two years, it seems the role of this committee is changing to
the point of only acknowledging the qualifications of those
wishing to serve on the Board. As it was announced this
year, the function of this committee is being evaluated and
it will possibly be different in years to come.
From past experience, delegates were more active and often investigated on their own, the qualities of those running
for the Board. AMT prides itself as being a “membership
run” organization. There is a “challenge” to each person
serving as a delegate to be informed and responsible for
choices that can make this organization “the BEST” !
To Future Delegates: Be informed, be responsible and accept the challenge of serving your best! You can make a
difference! n
Fall/Winter 2014 / TxSSAMT
A Look at Treatments for
By: Benita Trainer, Angelina College Phlebotomy Student
A
seizure is a sudden surge of electrical activity in the
brain. The electrical activity is caused by complex chemical changes that occur in nerve cells. Seizures themselves
are not a disease, but instead a symptom of many different
disorders that can affect the brain. Epilepsy is a chronic disorder that is characterized by recurrent and unprovoked seizures. Epilepsy is the fourth most common of all neurological disorders and the second most misunderstood. Epilepsy
affects people of all walks of life and of all ages. Over two
million people in the US alone have been diagnosed with epilepsy and one in six will develop it in their life time. Seventy
percent of epilepsy patients are able to control their seizures
with medications, however one third of patients live with uncontrollable seizures because no available treatment works
for them.
Once a person is diagnosed with epilepsy, the first choice
of treatment is usually medication. There are many different
anti-epileptic or anti-seizure drugs available. Different drugs
may work best with different types of seizures. If one fails,
another one may work better or with a combination of two or
more drugs at the same time. With all medications, however,
come side effects. Side effects from anti-seizure medications
vary from person to person as well as the type of meds administered and the dosage.
Awareness of diet therapy as a form of treatment for epilepsy
has expanded over the years but is rarely, if ever, the first
choice. The most well-known diet therapy is the Ketogenic
Diet. The Ketogenic Diet has been used for treatment of epilepsy since the 1920s and is used mainly for young children.
This diet is normally started in a hospital setting as it requires a
time of fasting in the onset. The patient has to adhere to a regimen of dietary restrictions and must maintain a strict schedule
for meal times. Small children who do not have free access to
the refrigerator and have parental control over meals tend to
have the most success. A clinical study performed at Johns
Hopkins Medical Institutions in Baltimore, Maryland found
that thirty three percent of patients with intractable epilepsy
had more than a fifty percent reduction in seizures as a result
of The Ketogenic Diet and fifteen to twenty percent became
seizure free. Many of the patients that remained on the diet
were able to decrease the amount of medications they were
taking or withdraw the meds completely.
An up and coming diet therapy is the Modified Atkins Diet or
The Atkins for Seizures Diet. The Modified Atkins Diet was
first studied at Johns Hopkins in 2002 and is still ongoing to
date. With this therapy, the initial phase of the original Atkins
Fall/Winter 2014 / TxSSAMT
Diet is maintained indefinitely. Unlike the Ketogenic Diet,
M.A.D. has no caloric or fluid restrictions and does not require
a hospital stay to start. This form of therapy can work well with
patients of all ages. Clinical studies have shown that sixty five
percent of patients had a fifty percent reduction in the amount
of seizures, thirty five percent had a ninety percent reduction
or better and twenty one percent became seizure free. The
percentage of patients who became seizure free rose in those
who continued on the diet longer than six months.
Both medication and diet therapies can greatly reduce the
number of seizures a patient has. In patients with intractable
seizures there are no known medications that have resulted
in the patient becoming seizure free. One also needs to compare side effects when trying to determine the right therapy
for yourself or a loved one.
Side Effects with medications
Mild and short term side effects Idiosyncratic side effects
n Fatigue n Rash
n Vision changes n Liver problems
n Headache n Pancreas problems
n Depression n Serious drops in white blood
n Confusion
cell and platelet counts
n Behavioral changes
n Peripheral edema
Dangerous Side Effects
n
Aplastic Anemia
n
Complete liver failure
Side Effects with Diet Therapy
Mild and short term side effects
n Weight loss (normally only in patients who are overweight when therapy starts)
n
n
n
Fatigue
Increase in cholesterol levels
Constipation
If you choose medication therapy to treat epilepsy, you will
have no trouble finding a long list of available drugs or of doctors that are willing to prescribe them. Should you be more
interested in diet therapy however, be ready to do your homework. Finding a Neurologist that will work hand in hand with a
dietician to implement diet therapy may be difficult. Diet therapy can reduce the number of visits to the Neurologist and
can also reduce the amount and cost involved in long term
prescription medications. In the long run, however, it may be
well worth the effort. n
Resources: The Epilepsy Foundation; Discovery.com; WEB MD; Johns
Hopkins Hospital; American Academy of Pediatrics; Atkinsforseizures.com
The New TexaN
11
Students
Delegate Report
By: National American University Student
T
he Lonestar Student Society returned safely from AMT’s
75th National Meeting in Chicago. Kimberly Derschuck,
Celia McDonald, and Ashley Rowe are all students of National American University in Georgetown. Since it formed last
year, the student society has been busy learning parliamentary procedures, creating a budget and calendar, and fundraising. For all of them, these types of activities are new.
The student society’s advisor, Viviana Pelton, is the Medical
Assisting Program Coordinator at National American University in Georgetown. She has now attended four national
meetings. “I first attended the AMT’s national meeting in Miami in 2011. I traveled alone and did not know anyone when
I arrived. I left feeling like I had just visited family. A feeling
that has only strengthened in intensity with each meeting.”
Viviana began getting involved at the state level in 2013. She
has served as a Texas delegate at the last two national meetings and has just recently hosted the TxSSAMT’s Spring Educational Program in Austin. “The Lonestar Student Society
was an instrumental part of its success,” Viviana said.
The AMT Home Office contacted members affiliated with
medical assisting schools, inviting them to participate in the
MA Challenge, a quiz bowl type event hosted by the California State Society of the AMT. Viviana approached Kim and
Celia about competing. Although excited at the opportunity,
the challenge of financing the trip was arduous. Numerous
fundraisers and support from the members of the TxSSAMT
ultimately contributed to the costs of airfare/transportation,
hotel, and meals for the three students.
On their last night in Chicago, the students spoke candidly to
Viviana about their experiences. Highlighted events included
the Welcome Party and the Awards Banquet, but the experience that held the most meaning was the overall feeling of
belonging and welcome throughout. All three students said
the AMT is now a fixed part of their profession. Furthermore,
future state and national meetings will be an attended event
well beyond their time as a student. Discussions evolved to
include future participation and involvement. Each student
hinted at their desire to serve the AMT organization by means
of membership in various committees and eventually elected
positions! n
Hall of Fame
Report and Recommendation for
By: TSSAMT Hall of Fame Committee
T
he Hall of Fame Committee recommends the induction
of PAT WESTBROOK, MT into the Texas Hall of Fame at
the Fall Conference in Mt. Pleasant, Texas on September 18,
2014 for her continued support and work for the Texas State
Society of the American Medical Technologists.
She has served faithfully in her elected offices as Secretary,
Vice President and President. She has served on numerous
State committees and always attends the national AMT Conventions. Her dedication on the national level is very commendable as she has served on many committees and as a
Texas delegate.
Here is a little bio about Ms. Pat!
Born in Lake Charles, Louisiana and raised in Texas. Attended University of Houston. Certified with AMT in 1972. Currently works as supervisor for Laboratory Services for Texas
Oncology at the Baytown Site.
12
The New TexaN
State offices held: President, Vice President, Secretary
State committees: Legislative, proctoring
State awards: Member of the year
National awards: Distinguished Achievement, Exceptional
Merit, Pillar
National committes: Scholarship, nominating, Proctoring,
State and Federal government affairs
We are so pleased to have Pat Westbrook as part of our
Texas Society. n
Congratulations Pat.
Fall/Winter 2014 / TxSSAMT
TxSSAMT Fall 2014 Continuing Education Program & Conference
LaQuinta Inn - Mount Pleasant, Texas
Friday, September 19, 2014
7:00 a.m. – 4:00 p.m.
Meeting Registration/Sign-In
7:50 – 8:00
Welcome Announcements – Taffy Durfee, MS, MT-TxSSAMT President
8:00 – 9:00
“Zoonotic Bacterial Pathogens Encountered in Rural Hospital Labs” - Joe (1.0 CE)
(1.0 CE) Strain, MT (ASCP), Specialist Clinic Microbiology
9:00 – 10:00
“It’s Your Hands: A Modern Approach to Infection Prevention”- Connie (1.0 CE)
(1.0 CE) Taylor, RN, Infection Control Nurse, Titus Regional Medical Center (TRMC)
10:00 – 11:00
“General Cancer Updates” - Rosa Cuencia, MD, Surgical Oncologist, Titus (1.0 CE)
(1.0 CE) Regional Medical Center (TRMC)
11:00 – 12:00
“Health Care Economic Update” - Terry Scoggin, COO, Titus Regional
(1.0 CE)
Medical Center (TRMC)
12:00 – 1:00
LUNCH – On Your Own (TxSSAMT Board Meeting)
1:00 – 2:00
“What You Need to Know About Emergency Medical Operations &
(1.0 CE)
Personal/Professional Disaster Preparedness” – Mark Mallory, Director,
EMS, Titus Regional Medical Center (TRMC)
2:00 – 3:00
“Lung Cancer Screening” – Gordon Downie, MD, Pulmonologist, Titus
(1.0 CE)
Regional Medical Center (TRMC)
3:00 – 4:00
“Phlebotomy Update: Expanded Roles of Phlebotomists” – Cindy Parsons,
(1.0 CE) Director, Med Lab Tech Program, Northeast Texas Community College
4:00 – 5:00
“The Benefits & An Overview of Hospice in the Community” – Sheri Cobb,
(1.0 CE)
Volunteer Coordinator, Cypress Basin Hospice
(8.0)
CE Daily Total
5:00 – 7:00
Business Meeting/Dinner/Hall of Fame Induction
7:00 – 9:00
TxSSAMT World Famous Auction (included with paid registration)
All members, attendees, speakers and guests are encouraged to attend. Remember to bring items to the
auction and help support the TxSSAMT Raymond Schiffer Scholarship and Awards Fund.
Saturday, September 20, 2014
7:00 a.m. – 4:00 p.m.
7:50 – 8:00
8:00 – 9:00
(1.0 CE)
9:00 – 10:00
(1.0 CE)
10:00 – 11:00
(1.0 CE)
11:00 – 12:00
(1.0 CE)
12:00 – 1:00
1:00 – 2:00 (1.0 CE)
2:00 – 3:00
(1.0 CE)
3:00 – 4:00
(1.0 CE)
(7.0)
Meeting Registration/Sign-In
Welcome Announcements – Kim Meshell, TxSSAMT, Vice President
“Exercise and Health Today” – Brad Burrows, DO, Family Practice, Titus
Regional Medical Center (TRMC)
“To Be Announced” – Kelvin Dunlop, Account Manager, McKesson Medical
Surgical Supplies
“What About the PSA Controversy?” – Rodger Stuart, MD, Urologist, Titus
Regional Medical Center (TRMC)
“Domestic Violence Awareness” – Teresa Wooten, Assistant Executive
Director, SAFE-T (Shelter Agencies for Families in East Texas)
LUNCH - On Your Own (TxSSAMT Board Meeting)
“HIPPA” – Speaker to Be Announced, Director, HIM, Titus Regional Medical
Center (TRMC)
“Current Trends in Health Care in the United States” – Dan McCauley,
DDS, FAGD, Mount Pleasant, Texas
“Therapeutic Drug Monitoring Review with Case Studies” – Stacey McVay,
MT (ASCP), Specialist, Chemistry, TRMC Laboratory
CE Daily Total
Thanks for your attendance! – Please travel home safely.
Visit us online at http://www.americanmedtech.org/BeInvolved/StateSocieties/Texas/MeetingandEvents.aspx
Note: Schedule is subject to change.
Fall/Winter 2014 / TxSSAMT
The New TexaN
13
Candidates for 2015-2016
Ballots must be postmarked by August 17, 2014
Taffy K. Durfee
Kimberly Meshell
I
H
am Taffy K. Durfee, president candidate for the Texas
Board of American Medical Technologists. My past positions on TXSSAMT include, president, vice-president, secretary, and member of the awards, audit and membership
committees. On the Texas state level, I have given numerous
lectures, written articles and worked as a proctor and moderator. As for the National AMT level, I have served on the credentialing, future planning, and nominating committees. I am
the secretary for AMTIE, and a current member of the EQS
educational committee. My educational presentations include
the National AMT meetings, the Magnolia conference and the
states of Tennessee and Michigan. Published articles include
the Palmetto, The Texan and the AMT events. Future contributions for this year include a presentation at the CLIA conference and the Arkansas AMT convention. I currently work
at Sam Houston University, in Huntsville, Texas. Previously, I
developed a Medical Technologist program for graduate level
students and taught phlebotomy training.
My goal in representing the Texas AMT is to bring the members together in education and to promote new membership
in our ever growing health care field. The need for continuing
education is growing and we need to keep the cost for these
educational conferences at a minimal. Texas has a promising
future for all in the health care field and we must continually
aid all of our members. n
ello! My name is Kimberly Meshell, vice president candidate for the Texas Board of AMT. My current position is
vice president/editor. My past positions include: secretary, editor, scholarship committee. I have hosted several meetings,
gave lectures, wrote articles and have been a moderator. On
the National level, I have been on the nominating committee,
student activity committee, publications and ran for the RMA
board position.
I currently work at Angelina College in Lufkin Tx. I have been
there for the past 16years and I am the Program Director over
the Phlebotomy, medical Assistant and CMLA programs. I
love working with the students and hope to continue to build
the programs to further educate them.
My goal is to bring more members to AMT not only to the
Texas society but also on the National level. I want to see
us grow in membership as our healthcare is growing. We
are currently working on bringing more programs to AMT and
hoping to get more people involved. I have several ideas for
the students that I am working on and I look forward to presenting them in the near future.
I hope to continue to serve on the Texas board and bring more
members together. I appreciate your vote. You as members
are the key to our society, so your vote counts. I hope to see
everyone at our future meetings. n
Jean Palmer, AS, RMA, CAHI
Katrina
I
atrina is the current Secretary for the Texas State
Society of AMT. She received the AMT Distinguished
Achievement Award in 2013 and hosted her first conference
in College Station, Spring 2012. Katrina has presented pathology and laboratory related topics at many of the conventions and contributed articles to the journal.
am a RMA and CAHI with over 30 years experience in the
healthcare field. I started my career in healthcare in the
Laboratory as a Lab Assistant and Phlebotomist. After several
years I decided to go to college and earn my Medical Assistant diploma and became a MA in 1997. I worked in Family
Practice and Pediatrics. I received my Associate degree of
science in 1998 after becoming an Instructor in a Career College. I now work in an Acute Episodic practice in a corporate
facility and am glad to be back in the field.
I also operate two businesses, a CPR certifying agency training in BLS and Heartsaver. I also create jewelry masterpieces, mostly dichroic glass but I dabble in other creations as
well.
I enjoy being a member of AMT and helping out. I am the
RMA state board representative, the state Proctor, and I am
the current Treasure of TxSSAMT and would appreciate your
support in the next election.
K
Katrina graduated with a bachelor’s degree in Genetics and a
minor in History in 2004 from Texas A&M University, College
Station, Texas. She was employed for two years at Texas
A&M as a research assistant in a protein folding laboratory
studying the conformational stability of various mutations
to Ribonuclease Sa. Currently, Katrina enjoys working as
a Pathologist’s Assistant at Brazos Valley Pathology. On
the weekends, Katrina, and her husband Ray, raise, train
and trial Australian Shepherds in the stock, agility, rally and
conformation venues. n
Thank you, Jean Palmer, AS, RMA, CAHI n
14
The New TexaN
Fall/Winter 2014 / TxSSAMT
AMT Legislative Report
Fall 2014
yummy!
O
n August 23, 2012, the centers for
Medicare and Medicaid Services
(CMS) issued a final rule establishing ‘meaningful use’ requirements
that providers must meet to receive
funding under the second phase
of the federal electronic health record (EHR) incentive. The CMS
Meaningful Use rule requires that
medical assistants be credentialed in order to enter orders into
the Computerized Physicians Order
Entry (CPOE) system for medication
and for laboratory and radiology services. AMT’s Registered Medical Assistants
(RMA) certification meets the condition of this
new rule.
The stage two Meaningful Use rule was adopted as part of a series of regulations
implementing the Health Information Technology for Economic and Clinical Health
Act (HITECH). Under that law, the doctors, healthcare professionals, and hospitals
can qualify for Medicare and Medicaid incentive payments when they adopt the
Meaningful Use Certified Electronics Health Records Technology (EHR). The HITECH Act also imposes Medicare payment penalties on providers who don’t meet
Meaningful Use standards by the year 2015.
The program is divided into three stages:
1) Stage One sets the basic functionalities electronic health records must include,
such as capturing data electronically, and providing electronic copies of health
informatioin.
2) State Two (which will begin as early as 2014) increases health information
exchange between providers, and promotes patient engagement by giving
patients secure online access to their health information.
3) Stage Three will continue to expand Meaningful Use objectives to improve health
care outcomes.
In each stage, CMS establishes a number of ‘core objectives’ and measures to
achieve those objectives. Objectives established at one stage are carried over,
often with modification, into the subsequent stages.
Why Hire AMT Certificants
◗ E
stablished in 1939, AMT has long been a nationally and
Internationally recognized agency, and is well respected in the industry.
◗ AMT’s exams are NCCA Accredited (National Commission for
Certifying Agencies).
◗ AMT carefully reviews credentials.
◗ AMT promotes high exam security.
◗ AMT encourages growth in the profession. n
Fall/Winter 2014 / TxSSAMT
Rocky Road
Cream Pie
Ingredients:
1pg. instant chocolate pudding mix
2 Tbs. unsweetened cocoa powder
1 1/2 c. milk1/4 tsp. almond extract
1/4 c. toasted almonds-chopped
1/2 c. miniature marshmallows
1 container frozen whipped cream
1pkg oreo crumb pie crust
Directions:
In large bowl, whisk together
pudding, cocoa powder, milk and
almond extract. Stir in almonds and
marshmallows. Cover and refrigerate for 30 minutes. Gently fold 1/2
c. whipped topping into pudding
mixture until blended. Evenly spread
over the mixture into pie crust.
Cover and refrigerate until 2 hours.
Spread remainder of whipped
topping over the pie.
Calories: 287
Protein: 3g
Fat: 14g
Trans fat:2g
Chol: 5mg
Carbs: 39g
Sodium: 356mg
The New TexaN
15
Meeting
foto pix
1
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2
3
4
9
12
The New TexaN
5
10
13
14
16
7
1 Entryway to the Drake Hotel
2Texas delegation at the
National convention
3Yvonne and son having a good
time at awards banquet
4Centerpiece at the Drake
Hotel, how stunning!
5District councilor Randy
Swopes getting an award at
the National convention
6Catholic church in Chicago,
beautiful
7 Art Contino with his award
8 Taffy and Sibyl with her award
8
11
9Art and Barbara at the town
hall session
10Kimberly and quilt winner
11 Viviana and Randy having fun
12 Members enjoying the meeting
13Vernell, Taffy and Pat at the
awards ceremony
14Taffy, Vernell,tj, Jean and
members
15Randy and Vernell modeling
scarves at the famous auction
16 Students modeling scrubs
171st timers, Jorge and
Melisia- so glad they came
Fall/Winter 2014 / TxSSAMT
15
16
19
17
22
20 21
24
23
25
27 28
31 32
18 Lake Michigan
19Members enjoying the state
conference
20 More scrubs being modeled
21Taffy with Viviana- what a
great meeting
221st timers, woohoo, we love
our new members
23 TJ escorting a beautiful sybil
24 Members having a good time
25 Sibyl at the spring meeting
26 Viviana doing a demonstration
27 Are we done yet? lol
Fall/Winter 2014 / TxSSAMT
28 Members having fun
29 Kimberly raffling off a quilt
30Members enjoying the awards
banquet
31 Texas student society ladies.
32 Miranda and Lonesha
331st timer- we love our new
members
34 Viviana and her students
35TJ and Taffy at TJ's baby
shower
36Members enjoying the awards
banquet.
18
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29
30
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The New TexaN
17
CE #31-304-14
aa River of Life
by Elaine Allen
B
lood is the life force of the human body; no part of
the human body could live without this amazing fluid.
Blood carries oxygen and nutrients to every living cell of the
living body. Blood fights germs and viruses that enter the
body. The blood helps the body get rid of wastes and also
acts as a cooling system of the body. With every beat of
your heart, blood performs these tasks so that you may live,
every second of your day.
Blood, long before modern medicine, has always been
viewed as the magical life force of all living things. This
belief began back during the caveman days, when humans
would notice when a living thing severely bleeds, that this
living thing would more often than not, die. Blood was often
celebrated as a magical tincture of the gods. Many pagan
religions would often depict the sacrificing of animals, and
in some incidents, people, to appease what they believed
to be gods. Blood was often used in magical potions. Over
the ages, many sayings of our time come from the ancient
beliefs of blood. It was often believed that a person could
become blood brothers or blood sisters by blending a few
drops of their blood together in a handshake. It was believed that to make a binding agreement that you would
write your signature in blood. A person who was angry was
said to be so mad that their blood boiled. Someone who
was born to a noble, or rich, family was said to be blue
blooded. Two warring factions, it would be said that there
was bad blood between them. It was also believed that
when someone was murdered, that their blood cried out to
the gods. Ancient medicine practitioners would often bleed
their patients to death using leeches or needless surgeries
to bleed out the bad spirits that were believed to be making
the patient ill.
Blood is often described as the transportation vehicle for
the organs of the cardiovascular system. This transport
around the human body is initiated by the pumping action of the human heart. Blood exits the heart via arteries,
which branch repeatedly until they become tiny capillaries.
By diffusing across the capillary walls, oxygen and nutrients leave the blood and enter the body tissues, where
carbon dioxide and wastes move from the tissues to the
bloodstream. As oxygen-deficient blood leaves the capillary beds, it flows into veins, which return it to the heart.
18
The New TexaN
The returning blood then flows from the heart to the lungs,
where it picks up oxygen and then returns to the heart to be
pumped throughout the body once again. The entire process of transporting blood across the body is repeated with
every beat of your heart.
Although blood appears to be a thick liquid, the microscope
reveals that blood has both cellular and liquid components.
Blood is a specialized type of connective tissue in which
livings cells, the formed elements, are suspended in a nonliving fluid matrix called plasma. The collagen and elastic
fibers typical of other connective tissues are absent from
blood, but dissolved fibrous proteins become visible as fibrin strands during the blood clotting process.
If a sample of blood is spun in a centrifuge, the heavier
formed elements are packed down by centrifugal force and
the less dense plasma remains at the top. Most of the reddish mass at the bottom of the tube is erythrocytes, the red
blood cells that transport oxygen. A thin, whitish layer called
the buffy coast is present at the erythrocyte-plasma junction. This layer contains leukocytes, the white blood cells
that act in various ways to protect the body, and platelets,
cell fragments that help stop bleeding.
Erythrocytes normally constitute about 45% of the total volume of a blood sample, a percentage known as the hematocrit. Normal hematocrit values vary. In healthy males,
the norm is 47%, with 5% difference range. In females,
the average hematocrit is 42%, with 5% difference range.
Leukocytes and platelets contribute less than 1% of blood
volume. Plasma makes up most of the remaining 55% of
the whole blood.
Blood is a sticky, opaque fluid with a characteristic metallic
taste. As children, we discover its saltiness the first time we
stick a cut finger into our mouth. Depending on the amount
of oxygen it is carrying, the color of blood varies from scarlet (oxygen-rich) to dark red (oxygen-poor). Blood is denser
than water and about five times more viscous, largely because of its formed elements. Blood is slightly alkaline, with
a pH between 7.35 and 7.45, and its temperature (38 C or
100.4 F), is always slightly higher than body temperature.
Fall/Winter 2014 / TxSSAMT
Blood accounts for approximately 8% of body weight. Its
average volume in healthy adults males is 5-6 L (about 1.5
gallons), somewhat greater than in healthy adult females
(4-5 L).Blood performs a number of functions, all concerned
in one way or another with substance distribution, regulating blood levels of particular substances, or body protection. Distribution functions of the blood involve delivering
oxygen from the lungs and nutrients from the digestive tract
to all body cells. Blood is involved in transporting metabolic
waste products from cells to elimination sites (to the lungs
for elimination of carbon dioxide, and to the kidneys for disposal of nitrogenous wastes in urine).Blood is also involved
in the transport of hormones from the endocrine organs to
their target organs and the regulation of functions of the
body. The blood maintains appropriate body temperature by
absorbing and distributing heat through the body to the skin
surface to encourage heat loss. Blood proteins and other
blood borne solutes maintain normal pH in body tissues by
acting as buffers to prevent excessive or abrupt changes in
blood pH that could jeopardize normal cell activities. Blood
acts as the reservoir for the body’s “alkaline reserve” of bicarbonate atoms and maintains adequate fluid volume in
the circulatory system. Salts (sodium chloride and others)
and blood proteins act to prevent excessive fluid from loss
from the bloodstream into the tissue spaces. As a result, the
fluid volume in the blood vessels remains ample to support
the blood circulation to all parts of the body.
ous homeostatic mechanisms. When blood protein levels
drop undesirably, the liver makes more proteins, and when
the blood starts to become too acidic (acidosis), both the
respiratory system and the kidneys are called into action to
restore the plasma’s normal pH. Body organs make dozens
of adjustments, day in and day out, to maintain the many
plasma solutes at acceptable life levels. In addition to transporting solutes around the body, plasma distributes heat
throughout the body.
Blood is a protector of the human body by preventing blood
loss. When a blood vessel is damaged, platelets, and plasma proteins initiate clot formation, stopping blood loss. The
blood also protects the body by preventing infections. Present in the blood are antibodies, complement proteins, and
white blood cells, all of which help defend the body against
foreign invaders such as bacteria and viruses.
Erythrocytes are small cells, about 7.5 micrometers (µm)
in diameter. Red blood cells look like biconcave discs, or
flattened discs with depressed centers. The thin centers
of RBCs appear lighter in color than around their edges.
Consequently, erythrocytes look like miniature doughnuts
when viewed through a microscope. Mature erythrocytes
are bound by a plasma membrane, but lack a nucleus, and
have no organelles inside the cell. The RBC are little more
than “bags” of hemoglobin, the RBC protein that functions
in gas transport. Other proteins present in the erythrocytes
are antioxidant enzymes that rid the body of harmful oxygen
radicals, but most of those function to maintain the plasma
membrane or promote changes in RBC shape. An example
of this is a protein called spectrin, which is attached to the
cytoplasmic face of its plasma membrane. Spectrin’s function in a net is deformable, which gives erythrocytes flexibility to change shape as necessary, to twist, turn, and become cup shaped. The flexibility spectrin nets offer is key to
ensure RBCs are carried with ease through capillaries with
diameters smaller than themselves, and then to resume into
their original biconcave shape.
Blood plasma is a straw-colored, sticky fluid. Although plasma is mostly water (about 90%), plasma contains over a
hundred different solutes. These solutes include nutrients,
gases, hormones, wastes, and products of cell activity, ions,
and proteins. Plasma proteins account for about 8% by
weight of plasma volume and are the most abundant plasma solutes. Except for hormones and gamma globulins,
most plasma proteins are produced by the liver. Plasma
proteins serve a variety of functions, but they are not taken
up by cells to be used as fuels or metabolic nutrients. Plasma solutes that are taken up by the cells to be used as fuels
are glucose, fatty acids, and oxygen. Albumin accounts for
some 60% of plasma protein and is the major blood protein
contributing to the plasma osmotic pressure (the pressure
that keep water in the bloodstream). Sodium ions are the
other major solute contributing to blood osmotic pressure.
The makeup of plasma varies all the time. Cells remove and
add substances to the blood every second. With a healthy
diet, plasma composition is kept relatively constant by variFall/Winter 2014 / TxSSAMT
The formed elements of blood, erythrocytes, leukocytes,
and platelets, have their own unique features. Two of the
formed elements of blood are not even true cells. Erythrocytes, or red blood cells, normally have no nuclei or organelles, and platelets cell fragments. Only leukocytes, or white
blood cells, are complete cells. Most of the formed elements
survive in the bloodstream for only a few days. Most blood
cells do not divide. Instead, blood cells are continuously renewed by division of cells in the bone marrow, where they
originate.
If you look at a stained smear of human blood under the
light microscope, you will see disc-shaped red blood cells
(RBCs), a variety of gaudily stained spherical white blood
cells, and some scattered platelets that look like debris.
Erythrocytes (red blood cells) vastly outnumber the other
types of formed elements in the blood.
The erythrocyte is a superb example of optimal structure
and function. The red blood cell picks up oxygen in the capillary beds of the lungs and releases the oxygen to tissue
cells across other capillaries through the body. Erythrocytes
transport some 20% of the carbon dioxide released by tissue
The New TexaN
19
cells back to the lungs. Each erythrocyte structure characteristic contributes to its gas transport functions; small size
and biconcave shape provide a huge surface area relative
to volume. RBCs have about 30% more surface area than
comparable spherical cells. Because no point within its cytoplasm is far from the surface, the biconcave disc shape is
ideally suited for gas exchange. Discounting water content,
an erythrocyte is over 97% hemoglobin, the molecule that
binds to and transports respiratory gases. Because erythrocytes lack mitochondria and generate ATP by anaerobic
mechanisms, red blood cells do not consume any of the oxygen they are transporting, therefore making erythrocytes
very efficient oxygen transporters.
Erythrocytes are a major factor contributing to blood viscosity. Women typically have a lower red blood cell count
than men. Women average 4.3 million cells per cubic millimeter of blood, verses men, who have 5.1 to 5.8 million
cells per cubic millimeter of blood. When the number of red
blood cells increases beyond the normal range, blood viscosity rises, and blood flows more slowly. As the number of
red blood cells drops below the lower end of the range, the
blood thins and flows more rapidly.
Erythrocytes are completely dedicated to their function,
which is their job of transporting respiratory gases of oxygen, and carbon dioxide, around their body. Hemoglobin,
the protein that makes red blood cells red, binds easily
and reversibly with oxygen. Most oxygen carried in blood
is bound to hemoglobin. Normal values for hemoglobin are
14-20 grams per 100 m of blood (g/100 ml) in infants, 13-18
g/100 ml in adult males, and 12-16 g/100 ml in adult females. Hemoglobin is made up of the protein globin bound
to the red heme pigment. Globin consists of four polypeptide chains, two alphas and two beta, each bound to a ring
like heme group. Each heme group bears an atom of iron
set like a jewel in its center. Because each iron atom can
combine reversibly with one molecule of oxygen, a hemoglobin molecule can transport four molecules of oxygen.
A single red blood cell contains about 250 million hemoglobin molecules, so each of these tiny cells can scoop up
about 1 billion molecules of oxygen. Hemoglobin is contained in erythrocytes, rather than existing free in plasma,
preventing it from breaking into fragments that would leak
out into the bloodstream, and from contributing to blood viscosity and osmotic pressure. The erythrocyte, being a bag of
hemoglobin, again proves the dynamic and efficient design
of the cell. Red blood cells are truly a highly specialized and
unique cell of the human body, proving day in and day out,
they are a necessary key element to life. Oxygen loading for
the red blood cells occurs in the lungs and the direction of
transport is from lungs to tissue cells. As oxygen- deficient
blood moves through the lungs, oxygen diffuses from the air
sacs of the lungs into the blood and then into the erythro20
The New TexaN
cytes, where it binds to hemoglobin. When oxygen binds to
iron, the hemoglobin, now called oxyhemoglobin, assumes
a new three-dimensional shape and becomes ruby red. In
the tissues, the process is reversed. Oxygen detaches from
iron, hemoglobin resumes its former shape and the resulting deoxyhemoglobin, or reduced hemoglobin, becomes
dark red. The released oxygen diffuses from the blood into
the tissue fluid and then into the tissue cells. About 20% of
the carbon dioxide transported in the blood combines with
hemoglobin, but it binds to the globin’s amino acids rather
than with the heme group. This formation of carbaminohemoglobin occurs more readily when hemoglobin is in the
reduced state, where it is disassociated from oxygen. Carbon dioxide loading occurs in the tissues and the direction
of transport is from tissues to lungs, where carbon dioxide
is eliminated from the body.
Leukocytes or white blood cells (WBCs) are the only formed
elements of blood that are complete cells, with nuclei and
the usual organelles. Leukocytes account for less than 1%
of total blood volume; leukocytes are far less numerous
than red blood cells. On average, there are 4800 to 10,000
white blood cells per cubic millimeter (mm3) of blood. Leukocytes are crucial to our defense against disease. The
white blood cells form a mobile army that helps protect the
body from damage by bacteria, viruses, parasites, toxins,
and tumor cells. Leukocytes have some very special functional characteristics. Red blood cells are confined to the
blood steam, and they carry out their functions in the blood.
But white blood cells are unique in that they are able to slip
out of the capillary blood vessels. This process of the WBCs
slipping out of the blood vessels is called diapedesis, which
means “leaping across” in Latin. The circulatory system is
simply the white blood cell means of transport to areas of
the body where they are needed to mount inflammatory or
immune responses. Signals that prompt WBCs to leave the
bloodstream at specific locations are adhesion molecules
(selectins) displayed by endothelial cells forming the capillary walls at sites of inflammation. Outside the bloodstream,
leukocytes move through the tissue spaces by amoeboid
motion. Amoeboid motion is caused by the white blood cell
forming cytoplasmic extensions that move the cells along,
like legs. The white blood cell follows the chemical trail of
molecules released by damaged cells or other leukocytes,
which is an event called positive chemotaxis. The chemical
trail left by the molecules allows the leukocytes to pinpoint,
and gather in large numbers at areas of tissue damage, and
infection, to destroy foreign substances or dead cells. When
white blood cells are mobilized for action, the body speeds
up their production and twice the normal number may appear within the blood within a few hours. A white blood cell
count of over 11,000 cells per cubic millimeter is called leukocytosis. This condition is a normal response to an infection in the body.
Fall/Winter 2014 / TxSSAMT
Leukocytes are grouped into two major categories on the
basis of structure and chemical characteristics. These two
major categories are defined by the names, granulocytes
and agranulocytes. Granulocytes contain obvious membranes bound with cytoplasmic granules. Agranulocytes
lack obvious granules. Each of these distinctive characteristics evident in the different groups of leukocytes can be
observed through a light microscope using a stained specimen. Many times students are asked to list leukocytes they
see in order from most abundant to least abundant. As a
general rule, this order is listed as neutrophils, lymphocytes,
monocytes, eosinophils, and basophils.
Granulocytes include neutrophils, basophils, and eosinophils, and they are all roughly spherical in shape. The
granulocytes are larger and much shorter lived than erythrocytes (RBCs). Granulocytes characteristically have lobed
nuclei. The nuclei are rounded nuclear masses connected
by thinner strands of nuclear material. The granulocytye’s
membrane-bound cytoplasmic granules stain quite specific
with Wright’s stain. Functionally, all granulocytes are phagocytes. A phagocyte is a cell that eats, or ingests, other cells.
Neutrophils are the most numerous of the white blood cells,
and account for 50 to 70% of the white blood cell population. Neutrophils are about twice the size of erythrocytes
(RBCs). The neutrophil cytoplasm stains pale lilac, and
contains fine granules that are difficult to see. These leukocytes are called neutrophils because their granules take
up both basic and acidic dyes. Hence, earning their name
which means “neutral-loving” in Latin. Together the two
types of granules give the cytoplasm a lilac color. Some of
these granules contain a potent “brew” of antibiotic-like proteins, called defensins. Neutrophil nuclei consist of three to
six lobes. This nuclear variability is often called polymorphonuclear leukocytes (PMNs) or simply polys. The Latin
translation of polymorphonuclear means “many shapes of
the nucleus”. Neutrophils are chemically attracted to sites
of inflammation and are active phagocytes. Neutrophils are
especially partial to bacteria, and some fungi. Bacterial killing is promoted in the body by a process called a respiratory
burst. In the respiratory burst, oxygen is actively metabolized to produce potent germ-killer oxidizing substances
such as bleach and hydrogen peroxide, and defensin-mediated lysis occurs. When the granules of the neutrophils
containing defensins are merged with a microbe containing
phagosome, the defensins form a peptide spear that pierce
holes in the membrane of the ingested foe. Neutrophils are
our body’s bacteria slayers. The numbers of neutrophils increase explosively during acute bacterial infections.
Eosinophils number 2 to 4% of all leukocytes found in blood.
Eosinophils are the same size of neutrophils. The deep
red nucleus of an eosinophil resembles and old-fashioned
telephone receiver. The eosinophil nucleus has two lobes
Fall/Winter 2014 / TxSSAMT
connected by a broad band of nuclear material. Large,
coarse looking granules, stained from brick red to crimson
with acid dyes, pack the cytoplasm. These granules are
filled with a variety of digestive enzymes. The eosinophils
back enzymes needed that digest bacteria. Eosinophils’
primary role in the white blood cells is to lead the counterattack against parasitic worms, such as flatworms, and
roundworms, that are too large to be eaten by the leukocytes. These worms are ingested in food, especially raw
fish. Parasitic worms also invade the body through the skin,
and then typically burrow into the intestinal or respiratory
mucosae. Eosinophils reside in the loose connective tissues at the same body sites, and when a parasitic worm
prey is encountered, the eosinophils gather around and release the enzymes from their cytoplasm granules onto the
parasite’s surface. The enzymes digest the parasite away,
breaking down the worm to be eliminated through the blood
stream. Eosinophils also lessen the severity of allergies by
phagocytizing, or eating, immune (antigen/antibody) complexes involved in allergy attacks. Eosinophils also inactivate certain inflammatory chemicals released during allergic reactions.
Basophils are the rarest of the white blood cells. Basophils
average only 0.5% to 1% of the leukocyte population. Basophils are slightly smaller than neurophils. Their cytoplasm
contains large, coarse histamine-containing granules that
have an affinity for the basic dyes. Basophil is translated
from Latin to mean “base-loving”. The basophil cells stain
purplish-black. Histamine is an inflammatory chemical that
acts as a vasodilator (makes blood dilate), and attracts
other white blood cells to the inflamed site. Drugs called
antihistamines counter this effect. The deep purple nucleus
is generally U or S shaped with two or three conspicuous
constrictions.
Mast cells are granulated cells that resemble basophils.
Mast cells are found in connective tissues. Mast cell nuclei tend to be more oval than lobed. These mast cells bind
like basophils to a particular antibody (immunoglobin E) that
causes the cells to release histamine. Mast cells are different from basophils in that they arise from different cell lines.
The second group of leukocytes is called agranulocytes.
Agranulocytes include lymphocytes and monocytes, white
blood cells that lack visible cytoplasmic granules. Although
agranulocytes are similar to granulocytes, that are distinct
and unrelated cell types. Their nuclei are typically spherical or kidney-shaped. Agranulocytes account for 25% or
more of the white blood cell population, and are the second
most numerous leukocytes in the blood. When lymphocytes
are stained for the light microscope, a typical lymphocyte
has a large, dark-purple nucleus that occupies most of the
cell volume. The nucleus is usually spherical, but may be
slightly indented. The nucleus is surrounded by a thin rim of
The New TexaN
21
pale-blue cytoplasm. Lymphocyte diameter ranges from 5
to 17 µm, but lymphocytes are often classified according to
size, as small (5-8) medium (10-12) and large (14-17). Only
a small portion of the lymphocytes exist in the blood stream.
Lymphocytes are named for the fact that most of these cells
are found firmly enmeshed in the lymphoid tissues, where
they play a major role in immunity. T lymphocytes (T cells)
function in the immune response by acting directly against
virus- infected cells and tumor cells. B lymphocytes (B cells)
give rise to plasma cells, which produce antibodies (immunoglobins) that are released to the blood.
Monocytes account for 3 to 8% of white blood cells, and
have an average diameter of 18 µm and are the largest
leukocytes. Monocytes have abundant pale blue cytoplasm,
and a darkly stained purple nucleus, which looks U or kidney shaped. When circulating monocytes leave the bloodstream and enter the tissues, they turn into highly mobile
macrophages with ravenous appetites for the germs they
were bred to kill. Macrophages, once inside the diseased
tissue are actively phagocytic, which means they seek out
and destroy the bad cells. Macrophages are crucial in the
body’s defense against viruses, certain intracellular bacterial parasites, and chronic infections. Macrophages are also
important in the activation of lymphocytes to mount the immune response.
Platelets are not cells in the strictest sense. They are small,
flexible aggregates of cellular material called cytoplasm.
The platelets help repair small blood vessels so blood does
not leak out. Platelets are about 1/4 the diameter of a lymphocyte and are cytoplasmic fragments of extraordinarily
large cells called megakaryocytes. There are usually about
500,000 platelets in each cubic millimeter of blood. In blood
smears, each platelet shows a blue-staining outer region
and an inner area containing granules that stain purple.
The granules contain an impressive array of chemicals
that act in the clotting process. Some of these chemicals
include: serotonin, Ca2+, a variety of enzymes, Adenosine diphosphate (ADP), and platelet derived growth factor
(PDGF).
Platelets are essential for the clotting process that occurs in
plasma when blood vessels are ruptured inside or outside.
By sticking to the damaged site, platelets form a temporary
plug that helps seal the break. Because platelets have no
cell nucleus, they age quickly and degenerate in about ten
days if they are not involved in clotting. When there is no clot
to plug, platelets circulate freely, kept mobile, but inactive
by molecules secreted by endothelial cells lining the blood
vessels. The platelets are formed in the bone marrow, and
regulated with the hormone called thrombopoietin. When
the thrombopoietin is secreted to make the platelets, the
bone marrow will grow a series of cells to produce megakaryocytes. The cytoplasm of the megakaryocyte becomes
22
The New TexaN
compartmentalized by membranes inside it. When the
megakaryocytes are ready to make platelets, the plasma
membrane will fragment, liberating the platelets. The platelets tear apart from the megakaryocyte similar to a postage
stamp tearing away from a book of stamps.
Normally, blood flows smoothly past the blood vessel lining (endothelium). When the blood vessel walls break, a
whole series of reactions is set into motion to accomplish
hemostasis. The Latin translation of hemostasis means the
“halting of blood”. Without this plug we would quickly bleed
out our entire blood volume from even the smallest cuts.
The hemostasis response is fast, localized, and carefully
controlled, and involves many blood coagulation factors, as
well as some substances that are released by platelets, and
injured tissue cells. During hemostasis, three phases occur
in rapid order. These three phases of clot formation are, in
order, vascular spasms, platelet plug formation, and coagulation, or blood clotting. Blood loss at the site is permanently
prevented when fibrous tissue grows into the clot and seals
the hole in the blood vessel.
The first phase of hemostasis is vascular spasms. This is
the constriction of the damaged blood vessel (vasoconstriction). Factors that trigger vasoconstriction include direct injury to vascular smooth muscle, chemicals released by endothelial cells, platelets, and reflexes initiated by local pain
receptors. The spasm mechanism becomes more and more
efficient as the amount of tissue damage increases. These
vascular spasms are most effective in the smaller blood
vessels. The value of vasoconstriction is clear. A strongly
constricted artery can significantly reduce blood loss for
twenty to thirty minutes, allowing time for platelet plug formation and blood clotting to happen.
The second phase of hemostasis is called platelet plug
formation. The platelets play a key role in homeostasis by
forming a plug that temporarily seals the break in the vessel wall. The platelets also help to orchestrate subsequent
events that lead to blood clot formation. Platelets do not
stick to each other or to the smooth endothelial linings of
blood vessels. When the endothelium is damaged and
underlying collagen fibers are exposed, platelets, with the
help of a large plasma protein called von Willebrand factor (VWF) synthesized by endothelial cells, adhere carefully to the collagen fibers, and undergo some remarkable
changes. They swell, form spiked processes, and become
sticky. Once attached, the platelets are activated by the enzyme thrombin and their granules begin to break down and
release several chemicals. Serotonin enhances the vascular spasm and Adenosine diphosphate (ADP), are potent
agents that attract more platelets to the area and cause
them to release their contents. Thromboxane A2 is a short
lived prostaglandin derivative that is generated during the
process, and stimulates both events. A positive feedback
Fall/Winter 2014 / TxSSAMT
cycle activates and attracts greater and greater numbers
of platelets to the area. Within a minute, a platelet plug is
built up, which reduces blood loss. The platelet plug is limited to the immediate area where it is needed by PGI2, a
prostaglandin produced by the endothelial cells. PGI2 inhibits platelet aggregation. Platelet plugs are loosely knit, but
when reinforced with fibrin threads, the platelet plug acts
like “molecular glue” for the aggregated platelets. Platelet
plugs are quite effective in sealing the small tears in a blood
vessel that occur with normal activity. Once the platelet plug
is formed, coagulation comes into play.
The third phase of hemostasis is called coagulation, or
blood clotting. During coagulation, the blood is transformed
from a liquid to a gel. This transformation caused by coagulation is a multistep process that leads to its critically important last three phases. The final reactions are:
1. A complex substance called prothrombin activator is
formed.
2. Prothrombin activator changes a plasma protein called
prothrombin into thrombin.
3. Thrombin catalyzes the joining of fibrinogen molecules
present in plasma to a fibrin mesh, which traps blood
cells and effectively seals the hole until the blood vessel
can be permanently repaired.
The complete coagulation process is much more complicated. Over 30 different substances are involved. Factors
that enhance clot formation are called clotting factors or
procoagulants. Vitamin K is a fat soluble vitamin and is required for the synthesis of four of the procoagulants made
by the liver. Factors that inhibit clotting are called anticoagulants. The clotting process depends on a delicate balance
between these two groups of factors. Most of these factors
are plasma proteins made by the liver that circulate in an
inactive form in blood until mobilized. Clotting may begin by
either the intrinsic or the extrinsic pathway. Both pathways
are usually triggered by the same tissue damaging events.
Clotting of blood outside the body, such as in a test tube,
is started only by the intrinsic mechanism. Prothrombin activator catalyzes the transformation of the plasma protein
thrombin to the active enzyme thrombin. Thrombin catalyzes the creation of fibrinogen (another plasma protein
made by the liver). As the fibrinogen molecules are aligned
into long, hair-like insoluble fibrin strands, the fibrin strands
glue the platelets together, and make a web that forms the
structural basis of the clot. Once in contact with fibrin, plasma becomes gel-like and traps formed elements that try to
pass through it. With calcium ions, thrombin also activates
factor XIII (fibrin stabilizing factor), a cross linking enzyme
that binds the fibrin strands tightly together and stabilizes
the clot. Clot formation is normally complete about five
Fall/Winter 2014 / TxSSAMT
minutes after blood vessel damage. The extrinsic pathway
involves fewer steps and happens more quickly than the
intrinsic pathway. Severe tissue trauma, for example, can
promote clot formation within 15 seconds.
Within 30 to 60 minutes, the clot is stabilized further by a
platelet induced process called clot retraction. Platelets
contain contracting proteins (actin and myosin), and they
contract much in the same manner as muscle cells. As
the platelets contract, they pull on the surrounding fibrin
strands, squeezing serum (plasma minus clotting proteins)
from the mass. This squeezing of the serum compacts the
clot and draws the rupture edges of the blood vessel closer
together. Even as clot retraction occurring, vessel healing
is taking place. Platelet-derived growth factor (PDGF) released by platelet degranulation stimulates smooth muscle
and fibroblasts to divide and rebuild the wall.
A clot is not a permanent solution to blood vessel injury.
The body undergoes a process called fibrinolysis which
removes clots when healing has occurred. This clean up
detail is crucial. Without fibrinolysis, blood vessels would
gradually become completely blocked. The natural “clot
buster” is a fibrin-digesting enzyme called plasmin, which
is produced when the blood protein plasminogen is activated. Large amounts of plasminogen are incorporated into a
forming clot, were it remains inactive until the body signals
reach it. The presence of a clot in and around the blood
vessel causes the endothelial cells to secrete tissue plasminogen activator (TPA). Activated factor XII and thrombin
released during clotting also serve as plasminogen activators. Most plasmin activity is confined to the clot, and many
plasmins that stray into the plasma are quickly destroyed
by circulation enzymes. Fibrinolysis begins within two days
and continues slowly over several days until the clot is finally dissolved. Blood clots to keeps us from bleeding to
death.
Blood tests, along with X-Rays, provide the first accurate
picture of a patient’s health. Our blood, like each and every one of us, is unique, and is used in forensic and DNA
testing. Blood has indeed earned its reputation for being
magical. Without blood, human beings would not be able to
live. With every beat of our heart, blood continues to carry
oxygen and food to our bodies. Our blood serves as our
protector, its cells sacrificing themselves so that we may live
another day. n
______________________________________________
1. The Human Body in Health and Illness, Third Edition By Barbara Herlihy,
Chapter 15 Blood, pages 263-278
2. Human Anatomy & Physiology, Sixth Edition, by Elaine N Marieb,
Chapter 17 Blood page 644-671
3.Laboratory Procedures for Medical Office Personnel, by Craig A Stepp,
and MaryAnn Woods, Chapter 10 Anatomy and Physiology of the Blood
pages 105- 112
{CE questions continued on next page}
The New TexaN
23
{continued from page 23}
Questions
BLOOD aka River of Life - CE #31-304-14
1. T/F A leukocyte is a white blood cell.
2. A _________ spasm is key to coagulation of the blood.
3.Agranulocytyes account for _________% of the white
blood cell population.
4. Match the cell with the description
c. “neutral-loving”
d. “leaping across”
12.The three stages of hemostasis are: ___________
___________, ___________, and ___________.
13.These cells are crucial in the body’s defense against
viruses, certain intracellular bacterial parasites, and
chronic infections.
a. Basophils
b. Erythrocytes
c. Thromboxane A2
d. Macrophages
4a. Red Blood Cell
(erythrocyte)
a. ingests other cells
4b. Phagocyte
b. ~ 2 – 4% of leukocytes, contain enzymes that
digest bacteria and parasites
4c.Eosinophil
c. aid in the clotting process
4d. Neutrophil
d. biconcave disc, ~ 7.5 micrometers in diameter
4e.Lymphocyte
e. normally account for 1% or less of the white blood
cells
14.These cells function in the immune response by acting
4f. Monocyte
f. lack visible cytoplasmic granules
4g.Basophil
g. most numerous of the white blood cells
4h.Agranulocyte
h. has a large nucleus that occupies most of the cell
volume that stains purple
a. erythrocytes
b. B lymphocytes (B cells)
c. T lymphocytes (T cells)
d. platelets
4i.Platelet
i. the largest leukocyte
4j. Granulocytes
j. c ontain obvious membranes bound with
cytoplasmic granules
5.Basophils make ___________ ___________ dilate, and
summon other ___________ to the inflamed tissue
area. Hint: Antihistamine counters this.
6. Granulocytes include _________, _________, and
_________, and they are all roughly spherical in shape.
7. T/F There are about 100 million red blood cells per
cubic cell millimeter of blood.
8.
T/F Clotting may begin by either the intrinsic or the
extrinsic pathway.
9.
T/F Red blood cells transport oxygen through the
veins to all parts of the living body.
10.Which type of cells help protect the body from damage
by bacteria, viruses, parasites, toxins, and tumor cells?
a. platelets
b. white blood cells
c. erythrocytes
d. von Willebrand factor
11. The Latin translation of diapedesis is
a. “halting of blood”
b. “base-loving”
24
The New TexaN
directly against virus- infected cells and tumor cells.
15. Clot formation is normally complete about (x) minutes
after blood vessel damage.
a. 15 minutes
b. 90 minutes
c. 5 minutes
d. 30 minutes
16.T/F A single red blood cell contains about 450 million
hemoglobin molecules.
Please do not send money, these are free CEUs.
Send a copy of your answers and the identification form below to:
T.J. Weatherly
158 Roucourt Loop • College Station, TX 77845
American Medical Technologists Institute for Education
Reporting form for Continuing Education Hours
(Please print all information)
Last Name: ________________________________
First Name:________________________________
E-mail:____________________________________
Check AMT Certification:
q MT
q MLT
q COLT
q RPT
q RMA
q RDA
q CLC
q CAHI
AMT I.D. Number___________________________
(Do not put social security number on form)
Fall/Winter 2014 / TxSSAMT
Kim’s
Chicken
Story.....
tidbits
Sunlight!
Did you know that
sunlight blocks the
effects of a sleep-inducing brain
chemical that builds up as the
day progresses? So if you feel
the blahs coming on, go sit outside or walk around
for 10 minutes and you should feel very alert.
Brainstorm!
I
wanted to share my famous chicken story from the Chicago meeting. On Tuesday July 8th, I went to dinner with
Taffy, Vernell, Pat, Michelle. We went to a steakhouse down
from the hotel. I ordered a chicken dinner, I did not realize
that it was the whole boneless chicken, literally. The waitress
did tell me but I was not paying attention or I would not have
ordered it. Anyway, I ate a small portion and took the rest
back to my hotel room for lunch on the next day. I decided to
go sight seeing with a new member and when I came back I
noticed that my bag with the chicken in it was gone. I called
the housekeeping supervisor and complained and he said
he would look into and call me back. I was upset because
the chicken cost me $30.00, more than I would have spent
on dinner. I go back out to explore again and when I come
back in, the chicken bag was back in my room. That made
me furious because 1.) I would not eat something that had
been taken from my room and 2.) because what if that bag
had some of my personal items in it. So, I called the manager downstairs and complained, she told me to come down
and they would give me my money back. I went downstairs
and told her that I didn’t feel right getting all my money back
since I did eat some of it. She started laughing and said “Ms.
Meshell, I'm sorry to be laughing but I investigated this and
your chicken was found in Lost and Found!” Housekeeping took my chicken dinner and put it in lost and found. Of
course, we all laughed about it and I did get my money back.
So that is the famous chicken story from Chicago! A picture
of the chicken on how big it was is included in this story.
Hope yall get a good laugh out of this! n
Fall/Winter 2014 / TxSSAMT
According to Princeton University
researchers they found that tired
folks who take a few moments
to brainstorm an idea over anything from how to save money
or what to have for dinner- become instantly more awake!
The researchers explained that
brainstorming triggers a flood of
excitement inducing brain chemicals that give you a second wind!
Coffee
and
Nutmeg!
Unique phytonutrients in nutmeg
can jumpstart the output of
energizing brain alertness,
concentration and feelings of
happiness in as little as 10
minutes! Lets add some nutmeg!
The New TexaN
25
Announcing the Fall TxSSAMT
Educational Program
Dates: September 19-20, 2014 – Mount Pleasant, Texas
Pre-Registration Form
Name:_________________________________________________________________________________________
Check One: q MT
Check One: q ASCLT
q MLT
q RMA
q NCA
q RDA
q ASCP
q RPT
q ISCLT
q CLC
q AMT
q CAHI
q COLT
q OTHER
Address:_______________________________________________________________________________________
City:___________________________________________________State:________________ Zip:_______________
AMT ID#_______________________________________________Phone:__________________________________
GENERAL REGISTRATION: (All Seminars) Friday & Saturday (One Day Only) Friday or Saturday
AMT Members $75.00 ($85.00 at door)
____________ $40.00 ($50.00 at door)
NonAMT Members $90.00 ($100.00 at door)
____________ $50.00 ($60.00 at door)
Military Personnel $20.00 ($25.00 at door)
____________ $10.00 ($15.00 at door)
Students with ID $20.00 ($20.00 at door)
____________ $10.00 ($10.00 at door)
Registration Total $ ____________
q RSVP if you are attending the Friday night social. No. Attending _____
Make checks payable to TxSSAMT and send registration to:
David Finch • 1901 FM 2088 • Gilmer, Texas 75644
(NOTE: Your receipt will be in your registration packet. No confirmations will be mailed.)
(TxSSAMT is not responsible for your personal reservations.)
LaQuinta Inn
1620 Rotan Ave. • Mount Pleasant, Texas 75455 • Ph. (903) 572-5514 or 1-800-531-5900
Directions:
Located just off I-30, 271 North Bypass
Across from Lowe’s
When making reservations,
Reference TxSSAMT Fall Educational Program
Price is $69.00 + Tax
Deadline for reservations at
LaQuinta Inn is September 3, 2014
26
The New TexaN
Program will provide 15 hours of Continuing Education
with a variety of subjects to be announced.
Also please plan to attend our
TxSSAMT Auction on Friday evening
benefiting educational scholarships.
Bring your auction items
and your checkbook!
Come join us for a fun
and educational time
Fall/Winter 2014 / TxSSAMT
Our Advertisers
Ronin Clinical Laboratory & Diagnostic Services - page 7
National American University - page 9
The New Texan Publication Committee
Editor: Kim Meshell, AHI, COLT, RMA
936-633-5459 • P.O. Box 152023 • Lufkin, Texas 75915
Assistant Editor: Miranda Lankford
936-465-8984
Co-Editor: Michelle Jenkins
972-518-6293
Graphic Designer: Rebekah Petty
Printer: Branch Media Pro
To Advertisers
The New Texan, Journal of Medical Technology, a publication of
TxSSAMT, is published 2 times a year in one index Volume per year.
Published under the direction of the editor and appointed associates,
the Journal is devoted to the publication of original articles (and review
articles) as well as observations in the fields of interest to medical allied
professionals.
The New Texan, has not only an aim, but a goal which is to serve
both our members and our advertisers through the Journal. We have
over six thousand members in our Texas organization who receive this
publication. Thus it serves as a constant reminder of the products or
articles advertised therein.
We feel that once you advertise in The New Texan, you will reap the
benefits of a close association with our members and will also enjoy the
increased sales of your product(s).
Title of Publication: The New Texan, Journal of Allied
Health Professionals.
Publisher: A publication of the Texas State Society
of American Medical Technologists
Type of Publication: Journal (8½” x 11”)
Issues: First and Second
Advertising Rates Per Issue
One Insertion
All Issues
Full Page $225.00
1/2 Page $200.00
1/4 Page $150.00
Outside Back Cover $275.00
Inside Front Cover $250.00
Inside Back Cover $250.00
Business Card $ 20.00 an issue
Mechanical Requirements
Width/Depth
Overall Size 8½” x 11”
Center Spread 10” x 16”
Full Page 7½” x 10”
1/2 Page 7½” x 5” or 3¾” x 10”
1/4 Page 3¾” x 5” or 2” x 7”
Circulation: (a) Controlled circulation of 6,000 third class mail permit.
Press run 6,000. (b) Circulation to all members of the Texas State Society
of American Medical Technologists. (c) Single column width. 33/8”; double
column width. 7 3/8”. (d) Depth of column - 10”. (e) Columns per page - 2.
(f) Column inches per page - 20.
Material requirements: Camera ready positive material.
Deadlines: First Issue - April 1. Second Issue - August 1.
No cancellations within 5 days of the closing date.
Agency Commission: Above rates net; any agency fees used, final fees
should be adjusted so that final payment agrees with above stated rates.
Terms: No cash discount, rated due 30 days following invoice.
If I can be of assistance to you or your organization, please contact me.
Kim Meshell • P.O. Box 152023 • Lufkin, Texas 75915
Home: (936) 831-3615 • Work: (936) 633-5459 • Cell: (936) 465-2222
kim8569@hotmail.com
Fall/Winter 2014 / TxSSAMT
The New TexaN
27
Greetings
from
Mount
INN & SUITES
Pleasant
Texas
September 19-20, 2014
LaQuinta Inn
1620 Rotan Ave. • Mount Pleasant, Texas 75455
Ph. (903) 572-5514 or 1-800-531-5900
Program will provide 15 hours of Continuing Education with
a variety of subjects to be announced.
Also please plan to attend our TxSSAMT Auction on
Friday evening benefiting educational scholarships.
Bring your auction items and your checkbook!
Come join us for a fun and educational time!
M
ount Pleasant was founded May 11, 1848 to serve as county seat for Titus County. The
city has a total area of 12.7 square miles and a population of around 16,500. It is located
near the beautiful Lake Bob Sandlin.
The Titus County Courthouse is located on the Downtown Square. One of the largest Dr. Pepper
Murals in the United States is also located on the Square along with Laura’s Cheesecake
Factory. Mount Pleasant is the first town in Texas to have a Walmart.
Directions:
LaQuinta Inn, 1620 Rotan Ave, Mount Pleasant, Texas 75455
Located just off I-30, 271 North Bypass Across from Lowe’s
When making reservations, Reference TxSSAMT Fall Educational Program
Price is $69.00 + Tax
Deadline for reservations at LaQuinta Inn is September 3, 2014
Mount Pleasant photos courtesy of City of Mount Pleasant, website http://www.mpcity.net
Announcing the
Fall Educational Program