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78 Cards in this Set

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WHAT TYPE OF TISSUE IS BLOOD?
CONNECTIVE TISSUE
WHAT ARE THE FUNCTIONS OF BLOOD?
1. TRANSPORT OF GASES, NUTRIENTS, & WASTE.
2. TRANSPORT OF PROCESSED MOLECULES.
3. TRANSPORT OF REGULATORY MOLECULES.
4. REGULATION OF PH AND OSMOSIS.
5. MAINTENANCE OF BODY TEMP.
6. PROTECTION AGAINST FOREIGN SUBSTANCES.
7. CLOT FORMATION.
WHAT IS BLOOD COMPOSED OF?
FORMED ELEMENTS AND PLASMA
WHAT IS THE NORMAL BLOOD VOLUME FOR BOTH MALES & FEMALES?
MALES 5-6 LITERS
FEMALES 4-5 LITERS
WHAT ARE THE COMPONENTS OF PLASMA?
PLASMA PROTEINS
IONS
NUTRIENTS
WASTE PRODUCTS
GASES
REGULATORY SUBSTANCES
WHERE ARE THE PLASMA PROTEINS AND WHAT ARE THEIR FUNCTIONS?
1. ALBUMIN- TRANSPORTS FATTY ACIDS; MAINTENANCE OF OSMOTIC PRESSURE & VISCOSITY.
2. GLOBULINS-TRANSPORT LIPIDS, CARBOHYDRATES, HORMONES, IONS, & ANTIBODIES
3. FIBRINOGEN- BLOOD CLOTTING
WHAT ARE FORMED ELEMENTS?
CELLS AND CELL FRAGMENTS OF BLOOD
DESCRIBE HEMATOPOIESIS IN EXCRUCIATING DETAIL.
FORMATION OF FORMED ELEMENTS OF THE BLOOD THAT IS RED BLOOD CELLS, WHITE BLOOD CELLS AND THROMBOCYTES. PROCESS OF BLOOD CELL PRODUCTION CONFINED TO RED MARROW.
WHAT DOES HPC GIVE RISE TO?
RBC
WBC
PLATELETS
WHAT ARE THE GENERAL CHARACTERISTICS OF WBC's?
-AKA LEUKOCYTES
-AMEBOID MOVEMENT (CYTOPLASMIC EXTENTIONS)
-DIAPEDESIS-PROCESS BY WHICH WBC BECOME THIN & ELONGATED AND SLIP BETWEEN CELLS OF BLOOD VESSELS
-CHEMOTAXIS- ATTRACTION OF WBC TO A CHEMICAL STIMULI
WHAT DOES THE TERM DIAPEDESIS MEAN?
PROCESS BY WHICH WBC BECOME THIN & ELONGATED AND SLIP BETWEEN CELLS OF BLOOD VESSELS.
DIFFERENCE BETWEEN GRANULOCYTES AND AGRANULOCYTES.
GRANULOCYTES-LARGE CYTOPLASMIC GRANULES
- NEUTROPHIL, BASOPHIL, EOSINOPHIL

AGRANULOCYTES- NO CYTOPLASMIC GRANULES
-MONOCYTES AND LYMPHOCYTES
DIFFERENCE BETWEEN ALL THE BLOOD CELLS.
THE PNEUMONIC DEVICE IS:
NEVER LET MONKEYS EAT BANANAS
1. NEUTROPHIL-NUCLEUS WITH 2-4 LOBES; GRANULES STAIN PINK OR REDDISH-PURPLE
2. BASOPHIL-NUCLEUS W/ 2 INDISTINCT LOBES; GRANULES STAIN BLUE-PURPLE
3. EOSINOPHIL- NUCLEUS OFTEN BILOBED; GRANULES STAIN ORANGE-RED OR BRIGHT RED
4. LYMPHOCYTE-ROUND NUCLEUS; CYTOPLASM FORMS A THIN RING AROUND THE NUCLEUS
5. MONOCYTE- NUCLEUS ROUND, KIDNEY OR HORSE SHOE SHAPED; CONTAINS MORE CYTOPLASM THAN DOES LYMPHOCYTE.
WHAT ARE THE GENERAL CHARACTERISTICS OF PLATELETS?
SMALL BITS OF CYTOPLASM SURROUNDED BY PLASMA MEMBRANE

LIFE SPAN 9-5 DAYS IN CIRCULATION

EXTENSIVE GLYCOCALYX
PREVENT BLOOD LOSS; PLATELET PLUG,
MAINTAIN HEMOSTASIS
WHAT ARE THE MECHANISMS FOR BLOOD HEMOSTASIS?
1. VASCULAR SPASM-IMMEDIATE BUT TEMPORARY CLOSURE OF BLOOD VESSEL RESULTING FROM CONTRACTION OF SMOOTH MUSCLE W/IN WALL OF BLOOD VESSEL.
2. PLATELET PLUG FORMATION-ACCUMULATION OF PLATELETS THAT CAN SEAL UP SMALL BREAKS IN BLOOD VESSELS.
3. COAGULATION- OR BLOOD CLOTTING- FORMATION OF A CLOT
ORDER OF PLATELET PLUG FORMATION MECHANISM.
1. PLATELET ADHESION- OCCURS WHEN VON WILLEBRAND FACTOR CONNECTS COLLAGEN AND PLATELETS.
2. PLATELET RELEASE REACTION IS RELASE OF ADP, THROMBOXANES,AND OTHER CHEMICALS THAT ACTIVATE OTHER PLATELETS.
3. PLATELET AGGREGATION- OCCURS WHEN FIBRINOGEN RECEPTORS ON ACTIVATED PLATELETS BIND TO ONE ANOTHER. A PLATELET PLUG IS FORMED BY THE ACCUMULATING MASS OF PLATELETS.
ORDER OF COAGULATION MECHANISM.
STAGE 1: DAMAGE TO TISSUE OR VESSEL ACTIVATES CLOTTING FACTORS, WHICH LEAD TO PRODUCTION OF PROTHROMBINASE.
STAGE 2: PROTROMBIN IS ACTIVATED BY PROTHROMBINASE TO FORM THROMBIN.
STAGE 3: FIBRINOGEN IS ACTIVATED BY THROMBIN TO FORM FIBRIN, WHICH FORMS THE CLOT.
DIFFERENCE BETWEEN EXTRINSIC AND INTRINSIC PATHWAYS.
EXTRINSIC CLOTTING PATHWAY- STARTS W/ TISSUE FACTOR, WHICH IS RELEASED OUTSIDE OF THE PLASMA IN DAMAGED TISSUE.

INTRINSIC CLOTTING PATHWAY- STARTS WHEN INACTIVE FACTOR XII, WHICH IS IN THE PLASMA, IS ACTIVATED BY COMING INTO CONTACT WITH A DAMAGED BLOOD VESSEL.
HOW IS CLOT FORMATION CONTROLLED?
ANTICOAGULENTS- PREVENT COAGULATION FACTORS FROM INITIATING CLOT FORMATION.
WHAT ARE THE MAJOR ANTICOAGULANTS?
ANTITHROMBIN-INACTIVATES THROMBIN

HEPARIN- RAPIDLY INACTIVATES THROMBIN

PROSTACYLIN- COUNTERACTS EFFECTS OF THROMBIN, CAUSED VASODILATION, INHIBITS RELEASE OF COAGULATION FACTORS
WHAT IS THROMBUS AND EMBOLUS?
THROMBUS-CLOT IN CARDIOVASCULAR SYSTEM FORMED FROM CONSTITUANTS OF BLOOD; MAY BE OCCLUSIVE OR ATTACHED TO VESSEL OR HEART WALL W/O OBSTRUCTION THE LUMEN.

EMBOLUS- PLUG, COMPOSED OF A DETACHED CLOT, MASS OF BACTERIA, OR OTHER FOREIGN BODY, OCCLUDING A BLOOD VESSEL.
HOW IS A CLOT RETRACTED AND DISOLVED?
1.CLOT RETRACTION- RESULTS FROM THE CONTRACTION OF PLATELETS, WHICH PULL THE EDGE OF DAMAGED TISSUE CLOSER TOGETHER.
2. SERUM, WHICH IS PLASMA MINUS FIBRINOGEN AND SOME CLOTTING FACTORS, IS SQUEEZED OUT OF THE CLOT.
3.CLOT DISSOLUTION- FACTOR XII, THROMBIN, TISSUE PLASMINOGEN ACTIVATOR, AND UROKINASE ACTIVATE PLASMIN, WHICH DISSOLVES FIBRIN (THE CLOT).
WHAT ARE THE GENERAL CHARACTORISTICS OF RBC'S?
-AKA ERYTHROCYTES
-700 TIMES MORE NUMEROUS THAN WBC'S
-17 TIMES MORE NUMEROUS THAN PLATELETS IN THE BLOOD
-MALES 5.4 MILLION, FEMALES 4.8 MILLION
WHAT IS THE STRUCTURE OF RBC'S?
BICONCAVE DISK;
NO NUCLEUS;
CONTAINS HEMOGLOBIN, WHICH COLORS THE CELL RED.
TRANSPORTS OXYGEN AND CARBON DIOXIDE
WHAT IS THE STRUCTURE OF HEMOGLOBIN?
-CONSISTS OF FOUR POLYPEPTIDE CHAINS AND FOUR HEME GROUPS
-EACH POLYPEPTIDE CHAIN CALLED GLOBIN IS BOUND TO ONE HEME.
-EACH HEME IS A RED-PIGMENT MOLECULE CONTAIN ONE IRON ATOM
WHAT DOES HEMOGLOBIN TRANSPORT?
THE HEME MOLECULES TRANSPORT OXYGEN AND THE GLOBIN MOLECULES TRANSPORT CARBON DIOXIDE AND NITRIC OXIDE. IRON IS REQUIRED FOR OXYGEN TRANSPORT.
WHAT IS THE DIFFERENCE BETWEEN OXYGENATED AND DEOXYGENATED HEMOGLOBIN?
OXYGENATED HEMOGLOBIN- HEMOGLOBIN IS EXPOSED TO OXYGEN, AND ONE OXYGEN MOLECULE CAN BECOME ASSOCIATED WITH EACH HEME GROUP. BRIGHT RED IN COLOR

DEOXYGENATED HEMOGLOBIN-HEMOGLOBIN CONTAINING NO OXYGEN, DARK RED IN COLOR
DESCRIBE THE PROCESS OF ERYTHROPOIESIS.
STEM CELL
1.PROERYTHROBLAST->EARLY ERYTHROBLAST->INTERMEDIATE ERYTHROBLAST->LATE ERYTHROBLAST(NUCLEUS EXCLUDED)->RETICULOCYTE->RED BLOOD CELL

SEE CHART PAGE 642
WHAT ARE THE DIETARY REQUIREMENTS FOR RBC PRODUCTION?
FOLATE
VITAMIN B
IRON
WHAT STIMULATES ERYTHROPOIESIS?
LOW BLOOD OXYGEN LEVELS,

SOME TYPICAL CAUSES OF WHICH ARE DECREASED NUMBERS OF RBC'S, DECREASED OR DEFECTIVE HEMOGLOBIN, AND DISEASES OF THE LUNGS.
DESCRIBE IN DETAIL AND IN ORDER, THE BREAKDOWN OF HEMOGLOBIN.
1.GLOBIN CHAINS OF HEMOGLOBIN ARE BROKEN DOWN INTO INDIVIDUAL AMINO ACIDS & METABOLIZED OR USED TO BUILD NEW PROTEINS.
2. IRON IS RELEASED FROM HEME OF HEMOGLOBIN. HEME IS CONVERTED TO BILIVERDIN, WHICH IS CONVERTED TO BILIRUBIN.
3. IRON IS TRANSPORTED WITH TRANSFERRIN IN BLOOD TO TISSUES FOR STORAGE OR TO RED BONE MARROW & USED IN PRODUCTION OF NEW HEMOGLOBIN.
4. FREE BILIRUBIN IS TRANSPORTED IN BLOOD TO LIVER
5. CONJUGATED BILIRUBIN IS EXCRETED AS PART OF THE BILE INTO SMALL INTESTINE
6 BILIRUBIN DERIVATIVES CONTRIBUITE TO COLOR OF FECES OR ARE REABSORBED FROM INTESTINE INTO BLOOD & EXCRETED FROM KIDNEYS INTO URINE
WHAT IS JAUNDICE?
YELLOWISH STAINING OF THE SKIN AND SCLERAE CUASED BY A BUILDUP OF BILE PIGMENTS IN THE CIRCULATION AND INTERSTITIAL SPACES.
WHAT IS THE DIFFERENCE BETWEEN INFUSION AND TRANSFUSION?
INFUSION-IS THE INTRODUCTION OF A FLUID OTHER THAN BLOOD, SUCH AS A SALINE OR GLUCOSE SOLUTION, INTO THE BLOOD.

TRANSFUSION-IS THE TRANSFER OF BLOOD OR BLOOD COMPONENTS FROM ONE INDIVIDUAL TO ANOTHER.
WHY WERE EARLY TRANSFUSIONS UNSUCCESSFUL?
BECAUSE THEY RESULTED IN TRANSFUSION REACTIONS, WHICH INCLUDED CLOTTING WITHIN THE BLOOD VESSELS, KIDNEY DAMAGE, AND DEATH.

(TRANSFUSION REACTIONS ARE CAUSED BY INTERACTIONS BETWEEN ANTIGENS AND ANTIBODIES)
WHAT ARE ANTIGENS AND ANTIBODIES?
ANTIGENS- ANY SUBSTANCE THAT INDUCES A STATE OF SENSITIVITY OR RESISTANCE TO INFECTION OR TOXIC SUBSTANCES AFTER A LATENT PERIOD; SUBSTANCE THAT STIMULATES THE SPECIFIC IMMUNE SYSTEM.

ANTIBODIES-PROTEIN FOUND IN THE PLASMA THAT IS RESPONSIBLE FOR HUMORAL IMMUNITY; BINDS SPECIFICALLY TO ANTIGEN.
WHAT IS AN AGGLUTINOGEN?
PROCESS BY WHICH BLOOD CELLS, BACTERIA, OR OTHER PARTICLES ARE CAUSED TO ADHERE TO ONE ANOTHER AND FORM CLUMPS.
WHAT IS AN AGGLUTININ?
ANTIBODY THAT BINDS TO AN ANTIGEN AND CAUSES AGGLUTINATION.
WHAT IS HEMOLYSIS?
DESTRUCTION OF RED BLOOD CELLS IN SUCH A MANNER THAT HEMOGLOBIN IS RELEASED.
KNOW THE DIFFERENCE BETWEEN A,B,AB, AND O BLOOD TYPES.
TYPE A- HAS A ANTIGENS & ANTI B ANTIBODY
TYPE B- HAS B ANTIGENS & ANTI A ANTIBODY
TYPE AB- HAS A & B ANTIGENS & NEITHER ANTIBODY
TYPE O - HAS NO ANTIGENS & BOTH A & B ANTIBODIES
WHAT IS THE MOST COMMON BLOOD TYPE? THE RAREST?
MOST COMMON- TYPE O


RAREST- TYPE AB
WHAT IS THE UNIVERSAL DONOR? UNIVERSAL RECIPIENT?
UNIVERSAL DONOR- TYPE O BECAUSE CAN USUALLY GIVE BLOOD TO OTHER ABO BLOOD TYPES W/O CAUSING ABO TRANSFUSION REACTION. HAVE NO ANTIGENS.

UNIVERSAL RECIPIENT-TYPE AB BECAUSE THEY HAVE NO ANTIBODIES
WHAT IS RH FACTOR?
Rh FACTOR ORIGINALLY FOUND IN RHESUS MONKEYS, Rh IS AN ANTIGEN ON RED BLOOD CELLS.
PEOPLE ARE RH+ IF THEY HAVE CERTAIN RH ANTIGENS (D ANTIGENS)AND RH- IF THEY DO NOT HAVE THE ANTIGENS

Rh+ MOST COMMON HAS RH ANTIGEN

Rh- NO Rh ANTIGEN *DO NOT GET ANTIBODIES UNTIL EXPOSED TO RH
HOW DOES Rh FACTOR AFFECT THE ABO BLOOD GROUP?
THE ABO BLOOD TYPE AND THE RH BLOOD TYPE ARE DESIGNATED TOGETHER. FOR EXAMPLE A PERSON DESIGNATED AS A POSITIVE IS TYPE A IN ABO BLOOD GROUP AND Rh-POSITIVE.
DESCRIBE IN ORDER AND IN DETAIL HDN?
HEMOLYTIC DISEASE OF THE NEWBORN- OR ERYTHROBLASTOSIS FETALIS:
1.BEFORE OR DURING DELIVERY RH POSITIVE RBC'S FROM FETUS ENTER THE BLOOD OF AN RH NEGATIVE WOMAN THROUGH A TEAR IN THE PLACENTA.
2. MOTHER IS SENSITIZED TO THE RH ANTIGEN AND PRODUCES ANTI RH ANTIBODIES
3.DURING SUBSEQUENT PREGNANCY W/ RH POSITIVE FETUS, RH POSITIVE RBC'S CROSS PLACENTA, ENTER MOMS CIRCULATION, STIMULATE ANTIBODIES AGAINST RH ANTIGEN. MOMS ANTIBODIES PRODUCE RAPIDLY
4. ANTI-RH ANTIBODIES FROM MOM CROSS PLACENTA, CAUSING AGGLUTINATION AND HEMOLYSIS OF FETAL RBC'S AND HDN DEVELOPS.
HOW ARE BLOOD TYPES CROSSMATCHED?
BLOOD TYPING DETERMINES THE ABO AND RH BLOOD GROUPS OF A BLOOD SAMPLE. A CROSSMATCH TESTS FOR AGGLUTINATION REACTIONS BETWEEN DONOR AND RECIPIENT BLOOD.
WHAT ARE NORMAL RANGES FOR BOTH MALES AND FEMALE IN A COMPLETE BLOOD COUNT?
MALES- 4.6-6.2 MILLION CELLS PER MICROLITER

FEMALES- 4.2-5.4 MILLION CELLS PER MICROLITER
WHAT IS ERYTHROCYTOSIS?
AN OVERABUNDANCE OF RBC'S.
WHAT DOES HEMATOCRIT MEASURE?
THE PERCENTAGE OF BLOOD VOLUME OCCUPIED BY ERYTHROCYTES.
WHAT IS THE NORMAL RANGE OF HEMATOCRIT?
MALES- 40%-54%
FEMALES- 38%-47%

HCT= % OF PACKED RBC'S
BUFFY COAT= WBC + PLATELETS <1%
PLASMA 55%
WHAT IS LEUCOPENIA?
LEUCOPENIA-IS A LOWER THAN NORMAL WBC AND CAN INDICATE DEPRESSION OR DESTRUCTION OF THE RED MARROW BY RADIATION, DRUGS, TUMOR, OR A DEFICIENCY OF VITAMIN B12 OR FOLATE
WHAT IS LEUKOCYTOSIS?
LEUKOCYTOSIS-IS AN ABNORMALLY HIGH WBC
WHAT IS LEUKEMIA?
LEUKEMIA- OFTEN RESULTS IN LEUKOCYTOSIS, BUT WBC'S HAVE AN ABNORMAL STRUCTURE AND FUNCTION.
HOW DO YOU MEASURE CLOTTING THE CLOTTING ABILITY OF BLOOD?
PLATELET COUNT- A NORMAL PLATELET COUNT IS 250,000-400,000 PLATELETS PER MICROLITER OF BLOOD

PROTHROMBIN TIME- IS THE MEASUREMENT OF HOW LONG IT TAKES FOR THE BLOOD TO START CLOTTING, WHICH IS NORMALLY 9-12 SECONDS.
WHAT IS THE NORMAL VALUE FOR PLATELET COUNT AND PROTHRMBIN TIME?
PLATELET COUNT- 250,000-400,000 PLATELETS PER MICROLITER OF BLOOD.

PROTHROMBIN TIME- 9-12 SECONDS.
BLOOD DISORDER



ERYTHROCYTOSIS
AN OVERABUNDANCE OF RBC'S RESULTING IN INCREASED BLOOD VISCOSITY, REDUCED FLOW RATES, AND IF SEVERE PLUGGING OF THE CAPILLARIES.
BLOOD DISORDER



RELATIVE ERYTHROCYTOSIS
RESULTS FROM DECREASED PLASMA VOLUME, SUCH AS THAT CAUSED BY DEHYDRATION DIURETICS, AND BURNS.
BLOOD DISORDER



PRIMARY ERYTHROCYTOSIS
OFTEN CALLED POLYCYTHEMIA VERA- IS A STEM CELL DEFECT OF UNKNOWN CAUSE THAT RESULTS IN THE OVERPRODUCTION OF RED BLOOD CELLS, GRANULOCYTES, AND PLATELETS. ERYTHROPOIETIN LEVELS ARE LOW AND THE SPLEEN CAN BE ENLARGED.
BLOOD DISORDER



SECONDARY ERYTHROCYTOSIS (POLYCYTHEMIA)
RESULTS FROM A DECREASED OXYGEN SUPPLY, SUCH AS THAT WHICH OCCURS A T HIGH ALTITUDES, IN CHRONIC OBSTRUCTIVE PULMONARY DISEASE, OR IN CONGESTIVE HEART FAILURE.
DECREASE O2 STIMULATES ERYTHROPOIETIN SECRETION, CAUSES INCREASE IN RBC PRODUCTION. HYPERTENSION CAN DEVELOP.
BLOOD DISORDER



ANEMIA
DEFICIENCY OF HEMOGLOBIN IN THE BLOOD.
-CAN RESULT FROM DECREASE # OF RBC, A DECREASE IN HEMOGLOBIN IN EACH REB, OR BOTH.
-SUFFER FROM LACK OF ENERGY, EXCESSIVELY TIRED AND LISTLESS, APPEAR PALE OR BECOME SHORT OF BREATH WITH SLIGHT EXERTION.
BLOOD DISORDER



IRON-DEFICIENCY ANEMIA
RESULTS FROM A DEFICIENT INTAKE OR ABSORPTION OF IRON OR FROM EXCESSIVE IRON LOSS
-NOT ENOUGH HEMOGLOBIN IS PRODUCED
-RBC'S ARE SMALLER THAN NORMAL
BLOOD DISORDER



FOLATE DEFICIENCY
-CAN ALSO CAUSE ANEMIA
AN INADEQUATE AMOUNT OF FOLATE IN THE DIET IS THE USUAL CAUSE OF FOLATE DEFICIENCY, WITH THE DISORDER DEVELOPING MOST OFTEN IN THE POOR, PREGNANT WOMEN, AND CHRONIC ALCOHOLICS.
-LACK OF FOLATE RESULTS IN FEWER CELL DIVISIONS.
-DECREASE RBC PRODUCTION
- CELLS GROW LARGER THAN NORMAL
BLOOD DISORDER



PERNICIOUS
NUTRITIONAL ANEMIA
CAUSED BY INADEQUATE AMOUNTS OF VITAMIN B12
-DECREASED RBC PRODUCTION
-RBC LARGER THAN NORMAL
-DECREASE IN INTRINSIC FACTOR
BLOOD DISORDER



HEMORRHAGIC ANEMIA
LOSS OR DESTRUCTION OF RBC'S
RESULTS FROM A LOSS OF BLOOD, SUCH AS CAN RESULT FROM TRAUMA, ULCERS, OR EXCESSIVE MENSTRUAL BLEEDING.
BLOOD DISORDER



HEMOLYTIC ANEMIA
IS A DISORDER IN WHICH RBC'S RUPTURE OR ARE DESTROYED AT AN EXCESSIVE RATE.
- CAN BE CAUSED BY INHERITED DEFECTS W/IN THE RBC'S.
-CAN BE CAUSED FROM DRUGS, SNAKE VENOM, ARTIFICIAL HEART VALVES, AUTOIMMUNE DISEASE, OR HEMOLYTIC DISEASE OF A NEWBORN
BLOOD DISORDER



APLASTIC ANEMIA
IS CAUSED BY AN INABILITY OF THE RED BONE MARROW TO PRODUCE NORMAL RBC'S.
-ACQUIRED AS RESULT OF DAMAGE TO RED BONE MARROW BY CHEMICALS OR RADIATION.
BLOOD DISORDER



THALASSEMIA
IS A HEREDITARY DISEASE FOUND PERDOMINANTLY IN PEOPLE OF MEDITERRANEAN, ASIAN, AND AFRICAN ANCESTRY.
-CAUSED BY INSUFFICIENT PRODUCTION OF THE GLOBIN PART OF HEMOGLOBIN MOLECULE.
-MAJOR FORM RESULTS IN DEATH BY AGE 20.
BLOOD DISORDER



SICKLE-CELL ANEMIA
HEREDITARY DISEASE FOUND MOSTLY IN PEOPLE OF AFRICAN ANCESTRY BUT ALSO OCCASIONALLY AMONG PEOPLE OF MEDITERRANEAN HERITAGE.
-RESULTS IN FORMATION OF ABNORMAL HEMOGLOBIN, WHICH RBC'S ASSUME A RIGID SICKLE CELL SHAPE AND PLUG UP SMALL BLOOD VESSELS.
- USUALLY FATAL BEFORE 30.
BLOOD DISORDER



VON WILLEBRAND'S DISEASE
MOST COMMON INHERITED BLEEDING DISORDER;
-OCCURS AS FREQUENTLY AS 1 IN 1000
BLOOD DISORDER



HEMOPHILIA
IS A GENETIC DISORDER IN WHICH CLOTTING IS ABNORMAL OR ABSENT

-MOST OFTEN FOUND IN PEOPLE FROM NORTHERN EUROPE AND THEIR DESCENDANTS.
- IS AN X-LINKED TRAIT AND IT OCCURS MOSTLY IN MALES.
BLOOD DISORDER



HEMOPHILIA A (CLASSIC HEMOPHILIA)
RESULTS FROM A DEFICIENCY OF PLASMA COAGULATION FACTOR VIII.

-OCCURS IN APPROXIMATELY 1 IN 10,000 MALE BIRTHS
-TREATMENT INVOLVES INJECTIONS OF MISSING CLOTTING FACTOR FROM DONATED BLOOD
BLOOD DISORDER



HEMOPHILIA B
IS CAUSED BY A DEFICIENCY IN PLASMA FACTOR IX.

-OCCURS APPROXIMATELY 1 IN 100,000 MALE BIRTHS
-TREATMENT INVOLVES INJECTIONS OF MISSING CLOTTING FACTOR FROM DONATED BLOOD.
BLOOD DISORDER



THROMBOCYTOPENIA
A CONDITION IN WHICH THE NUMBER OF PLATELETS IS GREATLY REDUCED RESULTING IN CHRONIC BLEEDING THROUGH SMALL BLOOD VESSELS AND CAPILLARIES.

CAUSES-INCREASED PLATELET DESTRUCTION CAUSED BY AUTOIMMUNE DISEASE, OR INFECTIONS, AND DECREASED PLATELET PRODUCTION RESULTING FROM HEREDITARY DISORDERS, PERNICIOUS ANEMIA, DRUG THERAPY, RADIATION THERAPY, OR LEUKEMAIS.
BLOOD DISORDER



LEUKEMIA
LEUKEMIAS ARE CANCERS OF THE RED BONE MARROW IN WHICH ABNORMAL PRODUCTION OF ONE OR MORE OF THE WHITE BLOOD CELL TYPES OCCUR.
-PATIENTS ARE VERY SUSCEPTIBLE TO INFECTIONS.
-EXCESS PRODUCTION OF WBC'S CAN INTERFERE W/ RBC & PLATELET FORMATION LEADING TO ANEMIAS AND BLEEDING
BLOOD DISORDER



SEPTICEMIA
OR BLOOD POISONING- IS THE SPREAD OF MICROORGANSIMS AND THEIR TOXINS BY THE BLOOD.
-RESULTS FROM INTRO TO MICROORGANISMS FROM MEDICAL PROCEDURE.
-CAN CAUSE SEPTIC SHOCK, WHICH IS THE DECREASE IN BLOOD PRESSURE THAT CAN RESULT IN DEATH.
BLOOD DISORDER



MALARIA
IS CAUSED BY A PROTOZOAN THAT IS INTRODUCED INTO THE BLOOD BY THE BITE OF THE ANOPHELES MOSQUITO.
-PART OF PROTOZOAN OCCURS IN RBC'S
-SYMPTOMS- CHILL AND FEVER PRODUCED BY TOXINS RELEASED WHEN PROTOZOAN CAUSED THE RBC'S TO RUPTURE.
BLOOD DISORDER



INFECTIOUS MONONUCLEOSIS
CAUSED BY A VIRUS (EPSTEIN-BARR VIRUS) THAT INFECTS THE LYMPHOCYTES (B CELLS).
-LYMPHOCYTES ALTERED BY VIRUS AND IMMUNE SYSTEM ATTACKS AND DESTROYS LYMPHOCYTES.
-SYMPTOMS OF FEVER, SORE THROAT, & SWOLLEN LYMPH NODES.
BLOOD DISORDER



ACQUIRED IMMUNODEFICIENCY SYNDROME (AIDS)
CAUSED BY THE HUMAN IMMUNODEFICIENCY VIRUS (HIV), WHICH INFECTS LYMPHOCYTES AND SUPPRESSES THE IMMUNE SYSTEM.
BLOOD DISORDER


HEPATITIS
IS AN INFECTION OF THE LIVER CAUSED BY SEVERAL KINDS OF VIRUSES.
-AFTER RECOVERING, HEP VICTIMS CAN BECOME CARRIERS
-W/ NO SIGNS OF DISEASE CAN RELEASE VIRUS INTO THEIR BLOOD OR BILE