Hematopoietic Blood System 2 Flashcards
describe LEUKOCYTES
FUNCTION:
- aid in DEFENSE AGAINST DISEASE
- can leave capillaries through DIAPEDESIS
- move through TISSUE by AMEBOID MOTION & POSITIVE CHEMOTAXIS
what is LEUKOCYTOSIS?
creation of a high WBC count over 11,000/mm3
- typical NORMAL RESPONSE to INFECTION
how do we CLASSIFY LEUKOCYTES?
GRANULOCYTES:
- these have VISIBLE CYTOPLASMIC GRANULES; can be STAINEd
- often have LOBED NUCLEI
AGRANULOCYTES:
- these have NO VISIBLE CYTOPLASMIC GRANULES; CANNOT BE STAINED
- have SPHERICAL or OVAL-SHAPED/KIDNEY SHAPED NUCLEI
what are our GRANULOCYTES?
- BASOPHILS
- EOSINOPHILS
- NEUTROPHILS
what are our AGRANULOCYTES?
- LYMPHOCYTES
- MONOCYTES
what is the RELATIVE PERCENTAGE of LEUKOCYTES within our NORMAL BLOOD? Which classifications have the highest to lowest percentages?
- Never Let Monkeys Eat Bananas
- (N)eutrophils
- (L)ymphocytes
- (M)onocytes
- (E)osinophils
- (B)asophils
what is a DIFFERENTIAL (DIFF)?
test that aids in DIAGNOSING SPECIFIC CAUSE OF AN ILLNESS
can be variety of paths; either INFLAMMATION, AUTOIMMUNE DISORDERS, or INFECTIONS
how do LEUKOCYTES STAIN?
- NEUTROPHILS:
- neutral—don’t attract either acid or base; quite neutral
- EOSINOPHILS:
- stain red or orange
- acidic in nature
- BASOPHILS:
- stain blue or purple
- basic in nature
- LYMPHOCYTES:
- stain dark
- MONOCYTES:
- horseshoe shape
describe our BASOPHILS
BASOPHILS:
- our RAREST WBCs
- have important BASOPHILIC GRANULES–containing HISTAMINE
HISTAMINE:
very important as an INFLAMMATORY CHEMICAL–acts as a VASODILATOR to attract WBCS to inflamed sites
describe our EOSINOPHILS
EOSINOPHILS:
- have BRICK RED STAINING GRANULES
- often has a BILOBED NUCLEI
- responses similar to LYSOSOMES–in response to ALLERGIES and PARASITIC WORMS
describe our NEUTROPHILS
NEUTROPHILS:
- our most NUMEROUS WBCS
- has MULTIPLE LOBED NUCLEI with FINE GRANULES (containing HYDROLYTIC ENZYMES)
- have PHAGOCYTIC TENDENCIES–the BACTERIA SLAYERS
describe our LYMPHOCYTES
LYMPHOCYTES:
- our SECOND MOST NUMEROUS WBC
- has LARGE NUCLEI–CAN FILL UP ALMOST ALL THE CELL
- CRUCIAL TO IMMUNITY/IMMUNE RESPONSE
what are our THREE TYPES OF LYMPHOCYTES?
- T LYMPHOCYTES (T CELLS):
- act against VIRUS-INFECTED CELLS and TUMOR CELLS
- B LYMPHOCYTES (B CELLS):
- gives rise to PLASMA CELLS — can PRODUCE ANTIBODIES
- protection from FUTURE INFECTIONS
- gives rise to PLASMA CELLS — can PRODUCE ANTIBODIES
- NK CELLS:
- kills VIRAL INFECTIONS
describe our MONOCYTES
MONOCYTES:
the largest LEUKOCYTE
- functions and transforms into a MACROPHAGE
FUNCTION:
- turns into an ACTIVE PHAGOCYTIC CELL–eating almost everything
- helps FIGHT CHRONIC INFECTION
how do WBCs move?
- known as EXTRAVASION
- MARGINATION
rolling and adhesion within LUMEN - TRANSMIGRATION (DIAPEDESIS)
across the endothelium - MIGRATION
movement from INTERSTITIAL SPACE towards the CHEMOTACTIC STIMULUS
- MARGINATION
what are some LEUKOCYTE DISORDERS?
LEUKOPENIA:
- an ABNORMAL LOW WBC COUNT (drug-induced)
LEUKEMIAS:
- the OVERPRODUCTION of ABNORMAL WBCs
(named depending on specific WBC being affected)
ACUTE LEUKEMIA:
- from STEM CELLS–affects CHILDREN
CHRONIC LEUKEMIA:
- prevalence in OLDER PEOPLE
describe THROMBOCYTES (PLATELETS)
THROMBOCYTES:
- important in terms of CLOTTING BLOOD (COAGULATION)
- can survive for only around 5 - 9 days
MEGAKARYOCYTES:
- seen within RED BONE MARROW
- begins to SPLINTER into 2000-3000 FRAGMENTS to create PLATELET PLUGS
- kept INACTIVE and MOBILE by NITRIC OXIDE (which is found within ENDOTHELIAL CELLS of our BV)
- allows for greater VASODILATION and GREATER BLOOD FLOW
what is THROMBOPOIESIS? what is THROMBOPOIETIN?
THROMBOPOIESIS:
- the FORMATION OF PLATELETS
THROMBOPOIETIN:
- hormone that activates MYELOID STEM CELLS to turn into PLATELETS
- MEGAKARYOCTES begin to RUPTURE into PLATELETS
FIBRIN:
- protein that is produced by PLATELETS
- this helps assist in the CLOTTING OF BV
definition of HEMOSTASIS
HEMOSTASIS:
- a fast series of REACTIONS for STOPPAGE of BLEEDING through COAGULATION
- blood changes from LIQUID into a GEL
- a type of POSITIVE FEEDBACK MECHANISM
- requires CLOTTING FACTORS
describe the THREE STAGES of HEMOSTASIS
- VESSEL SPASM
begins with ENDOTHELIAL MUSCLE CONTRACTION or aka VASOCONSTRICTION
- release of ENDOTHELIN and SEROTONIN
- release of NERVOUS REFLEXES/PAIN RECEPTORS
- creation of a LOCAL MYOGENIC SPASM
**NITRIC OXIDE and PROGLANDIN–makes sure no platelets begin to form in UNDAMAGED BV
- PLATELET PLUG FORMATION
release of CYTOPLASMIC GRANULES such as SEROTONIN, ADP, and THROMBOXANE A2
- ensures an INCREASE in VASOCONSTRICTION and PLATELET AGGREGATION
**release of COLLAGEN–promotion of PLATELETS to STICK
- stick to plasma protein VON WILLEBRAND FACTOR
- COAGULATION (CLOT FORMATION)
creation of COAGULATION CASCADE–use of PROCOAGULANTS (from LIVER)
- this is where the blood turns from LIQUID to GEL
- also has some help from FIBRIN for REINFORCEMENT
**PROCOAGULANTS–I - XIII (need VITAMIN K to synthesize FOUR CLOTTING FACTORS)
what is CLOPIDOGRREL (PLAVIX)?
- used to reduce the risk of HEART DISEASE and STROKE
- used together with ASPIRIN within HEART ATTACKS—after placement of CORONARY ARTERY STENT
what are the VITAMIN K DEPENDENT CLOTTING FACTORS?
- II (PROTHROMBIN)
- VII (SERUM PROTHROMBIN CONVERS. FACTOR)
- IX (CHRISTMAS FACTOR, PTC)
- X (STUART FACTOR, PROWER FACTOR)
- many work together to stop bleeding through CHEMICAL REACTIONS
- majority of CLOTTING FACTORS—produced within the LIVER
how is the LIVER important in terms of the clotting process?
- CENTRAL role in clotting process–due to regulation of CLOTTING FACTORS
- greater BLEEDING TENDENCY–INCREASED RISK in MORBIDITY + INVASIVE PROCEDURES
compare the INTRINSIC and EXTRINSIC pathways of COAGULATION
INTRINSIC PATHWAY:
- clotting factors ARE PRESENT within BLOOD
- SLOWER CLOTTING PATHWAY
- triggered by BLOOD TRAUMA or EXPOSURE to UNDERLYING TISSUES
EXTRINSIC PATHWAY:
- clotting factors are OUTSIDE BLOOD
- FASTER CLOTTING PATHWAY
- trigeered by ENDOTHELIUM-DERIVED PROTEIN FACTOR aka TISSUE FACTOR (TF) (FACTOR III)
FACTOR 10 (Xa)
- where Ca2+, PF3, and FACTOR V CONVERGE and make PROTHROMBIN
- creation of PROTHROMBIN ACTIVATOR–endpoint for both pathways
what happens after we reach the PROTHROMBIN ACTIVATOR?
- PHASE TWO: PATHWAY TO THROMBIN:
- PROTHROMBIN ACTIVATOR catalyzes the transformation of PROTHROMBIN to active enzyme THROMBIN
- PHASE THREE: COMMON PATHWAY TO FIBRIN MESH:
- THROMBIN:
- catalyzes FIBRINOGEN (soluble mesh) into FIBRIN (insoluble mesh)
- clot formation—will begin to CONSOLIDATE/TIGHTEN to pull edges of the damaged vessel together—the creation of a STABLE FIBRIN CLOT
- THROMBIN:
describe CLOT RETRACTION
CLOT RETRACTION:
- stabilization of the CLOT
- use of ACTIN and MYOSIN within platelets
CONTRACTION:
- pulling of FIBRIN STRAND (squeezes serum out)
- draws in RUPTURED BV EDGES
STIMULATION:
- stimulated by PLATELET-DERIVED GROWTH FACTOR
define VESSEL REPAIR
VESSEL REPAIR:
- where VESSEL IS HEALING as CLOT RETRACTION OCCURS
STIMULATION:
stimulated by
- PLATELET DERIVED GROWTH FACTOR
- VASCULAR ENDOTHELIAL GROWTH FACTOR
define FIBRINOLYSIS
FIBRINOLYSIS:
- REMOVAL OF UNNEEDED CLOTS after HEALING
- use of PLASMIN: a FIBRIN DIGESTING ENZYME
(converted from PLASMINOGEN–by the TISSUE PLASMINOGEN ACTIVATOR)
- often begins after TWO DAYS–continues for several
define THROMBOLYSIS
the breakdown of a THROMBUS
- use of FIBRINOLYTIC DRUGS
CLINICAL USE - seen in MI, PULMONARY EMBOLISMS, or ISCHEMIC STROKES
what factors LIMIT CLOT GROWTH?
TWO MECHANISMS:
- swift REMOVAL & DILUTION of CLOTTING FACTORS
- INHIBITION of activated CLOTTING FACTORS
FACTORS:
- ANTITHROMBIN and PROTEIN C
(inactivates THROMBIN)
- HEPARIN
(inhibits THROMBIN, enhances ANTITHROMBIN III)
what are some disorders of hemostasis?
- THROMBOEMBOLIC DISORDERS:
- undesirable clot formation
- BLEEDING DISORDERS:
- abnormalities that prevent normal clot formation
- DISSEMINATED INTRAVASCULAR COAGULATION (DIC):
- involves both types of disorders
what is a THROMBUS?
- clot that develops and persists in UNBROKEN BLOOD VESSELS
- can BLOCK CIRCULATION leading to tissue death
what is an EMBOLUS?
- EMBOLUS:
- thrombus freely floating in the bloodstream
what is an EMBOLISM?
an EMBOLUS obstructing a vessel
what is THROMBOCYTOPENIA?
the DEFICIENT NUMBER of CIRCULATING PLATELETS
- showing of PETECHAIE–appears due to spontaneous or widespread hemorrhage
CAUSE:
- the SUPPRESSION or DESTRUCTION of RED BONE MARROW
- platelet count low
TREATMENT:
- transfusion of CONCENTRATED PLATELETS
describe HEMOPHILIA and IMPAIRED LIVER FUNCTION
the INABILITY to synthesize PROCOAGULANTS
CAUSES:
- vitamin k deficiency
- hepatitis
- cirrhosis
HEMOPHILIA:
the INABILITY TO CLOT
CAUSES:
- can cause IMPAIRED FAT ABSORPTION and LIVER DISEASE
- prevention of liver to PRODUCE BILE
TREATMENT:
- FFP–giving the DERIVED FACTOR to PATIENT
define DIC
Disseminated Intravascular Coagulation (DIC)
- where CLOTTING causes BLEEDING–creation of WIDESPREAD CLOTTING
- blocking of INTACT BLOOD VESSELS
EFFECTS:
- pregnancy complication
- INCOMPATIBLE BLOOD TRANSFUSIONS
- SEPTICEMIA
define BLOOD GROUPS
based on the PRESENCE of ABSENCE of GLYCOPROTEIN and GLYCOLIPID ANTIGENS (AGGLUTINOGENS) on the SURFACE OF RED BLOOD CELLS
what are our BLOOD TYPES?
- TYPE A
has ANTIGEN A
has ANTI-B ANTIBODIES
compatible with AO - TYPE B
has ANTIGEN B
has ANTI-A ANTIBODIES
compatible with BO - TYPE AB
has ANTIGEN A & B
has NO ANTIBODIES
compatible with ABO - TYPE O
has NO ANTIGENS
has BOTH ANTIBODIES
compatible with O
what are Rh Blood Groups?
ANTI-RH ANTIBODIES:
antibodies that are NOT SPONTANEOUSLY FORMED in Rh- INDIVUDUALS
- formed if RH- INDIVIDUAL receives RH+ blood/ or if RH- MOM CARRIES RH+ FETUS
SECOND EXPOSURE:
- can lead to a typical TRANSFUSION REACTION
- can lead to ERYTHROBLASTOSIS FETALIS
describe ERYTHROBLASTOSIS FETALIS
this only occurs with RH- MOM and an RH+ FETUS
FIRST PREGNANCY:
- the RH- MOM is first EXPOSED to the RH+ BLOOD of the FETUS
- mom is then SENSITIZED and exposed to ANTI-RH ANTIBODIES
SECOND PREGNANCY:
- if by chance her second child is RH+, specific ANTI-RH ANTIBODIES will begin to DESTROY the RBCS of the second child
TREATMENT:
- use of REBIRTH TRANSFUSIONS and EXCHANGE TRANSFUSIONS
- RHOGAM–use of ANTI-RH TREATMENTS–prevention of SENSITIZATION
define TRANSFUSION REACTIONS
where there is MISMATCHED BLOOD INFUSED
the DONOR’S CELLS begin to be ATTACKED by the RECEIPIENT’S PLASMA AGGLUTINOGENS
- begins to CLOG VESSELS and RUPTURES/RELEASE of HEMOGLOBIN
RESULTS:
- decreased OXYGEN CARRYING CAPACITY
- decreased BLOOD FLOW
- result in RENAL FAILURE due to HEMOGLOBIN
how do we restore low blood volume?
use of NORMAL SALINE and MULTIPLE ELECTROLYTE SOLUTION aka RINGERS SOLUTION
- or PLASMA EXPANDERS
- begins to mimic the PLASMA ELECTROLYTE COMPOSITION
