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BIO 176 LAB + LEC > Hematopoietic Blood System 2 > Flashcards

Hematopoietic Blood System 2 Flashcards

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1
Q

describe LEUKOCYTES

A

FUNCTION:
- aid in DEFENSE AGAINST DISEASE
- can leave capillaries through DIAPEDESIS
- move through TISSUE by AMEBOID MOTION & POSITIVE CHEMOTAXIS

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2
Q

what is LEUKOCYTOSIS?

A

creation of a high WBC count over 11,000/mm3
- typical NORMAL RESPONSE to INFECTION

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3
Q

how do we CLASSIFY LEUKOCYTES?

A

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

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4
Q

what are our GRANULOCYTES?

A
  • BASOPHILS
  • EOSINOPHILS
  • NEUTROPHILS
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5
Q

what are our AGRANULOCYTES?

A
  • LYMPHOCYTES
  • MONOCYTES
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6
Q

what is the RELATIVE PERCENTAGE of LEUKOCYTES within our NORMAL BLOOD? Which classifications have the highest to lowest percentages?

A
  • Never Let Monkeys Eat Bananas
    • (N)eutrophils
    • (L)ymphocytes
    • (M)onocytes
    • (E)osinophils
    • (B)asophils
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7
Q

what is a DIFFERENTIAL (DIFF)?

A

test that aids in DIAGNOSING SPECIFIC CAUSE OF AN ILLNESS

can be variety of paths; either INFLAMMATION, AUTOIMMUNE DISORDERS, or INFECTIONS

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8
Q

how do LEUKOCYTES STAIN?

A
  • 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
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9
Q

describe our BASOPHILS

A

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

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10
Q

describe our EOSINOPHILS

A

EOSINOPHILS:
- have BRICK RED STAINING GRANULES
- often has a BILOBED NUCLEI
- responses similar to LYSOSOMES–in response to ALLERGIES and PARASITIC WORMS

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11
Q

describe our NEUTROPHILS

A

NEUTROPHILS:
- our most NUMEROUS WBCS
- has MULTIPLE LOBED NUCLEI with FINE GRANULES (containing HYDROLYTIC ENZYMES)
- have PHAGOCYTIC TENDENCIES–the BACTERIA SLAYERS

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12
Q

describe our LYMPHOCYTES

A

LYMPHOCYTES:
- our SECOND MOST NUMEROUS WBC
- has LARGE NUCLEI–CAN FILL UP ALMOST ALL THE CELL
- CRUCIAL TO IMMUNITY/IMMUNE RESPONSE

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13
Q

what are our THREE TYPES OF LYMPHOCYTES?

A
  • 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
  • NK CELLS:
    • kills VIRAL INFECTIONS
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14
Q

describe our MONOCYTES

A

MONOCYTES:
the largest LEUKOCYTE
- functions and transforms into a MACROPHAGE

FUNCTION:
- turns into an ACTIVE PHAGOCYTIC CELL–eating almost everything
- helps FIGHT CHRONIC INFECTION

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15
Q

how do WBCs move?

A
  • known as EXTRAVASION
    1. MARGINATION
      rolling and adhesion within LUMEN
    2. TRANSMIGRATION (DIAPEDESIS)
      across the endothelium
    3. MIGRATION
      movement from INTERSTITIAL SPACE towards the CHEMOTACTIC STIMULUS
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16
Q

what are some LEUKOCYTE DISORDERS?

A

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

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17
Q

describe THROMBOCYTES (PLATELETS)

A

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

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18
Q

what is THROMBOPOIESIS? what is THROMBOPOIETIN?

A

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

19
Q

definition of HEMOSTASIS

A

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

20
Q

describe the THREE STAGES of HEMOSTASIS

A
  1. 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

  1. 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

  1. 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)

21
Q

what is CLOPIDOGRREL (PLAVIX)?

A
  • used to reduce the risk of HEART DISEASE and STROKE
  • used together with ASPIRIN within HEART ATTACKS—after placement of CORONARY ARTERY STENT
22
Q

what are the VITAMIN K DEPENDENT CLOTTING FACTORS?

A
  • 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
23
Q

how is the LIVER important in terms of the clotting process?

A
  • CENTRAL role in clotting process–due to regulation of CLOTTING FACTORS
  • greater BLEEDING TENDENCY–INCREASED RISK in MORBIDITY + INVASIVE PROCEDURES
24
Q

compare the INTRINSIC and EXTRINSIC pathways of COAGULATION

A

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

25
Q

what happens after we reach the PROTHROMBIN ACTIVATOR?

A
  • 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
26
Q

describe CLOT RETRACTION

A

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

27
Q

define VESSEL REPAIR

A

VESSEL REPAIR:
- where VESSEL IS HEALING as CLOT RETRACTION OCCURS

STIMULATION:
stimulated by
- PLATELET DERIVED GROWTH FACTOR
- VASCULAR ENDOTHELIAL GROWTH FACTOR

28
Q

define FIBRINOLYSIS

A

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

29
Q

define THROMBOLYSIS

A

the breakdown of a THROMBUS

  • use of FIBRINOLYTIC DRUGS
    CLINICAL USE
  • seen in MI, PULMONARY EMBOLISMS, or ISCHEMIC STROKES
30
Q

what factors LIMIT CLOT GROWTH?

A

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)

31
Q

what are some disorders of hemostasis?

A
  • THROMBOEMBOLIC DISORDERS:
    • undesirable clot formation
  • BLEEDING DISORDERS:
    • abnormalities that prevent normal clot formation
  • DISSEMINATED INTRAVASCULAR COAGULATION (DIC):
    • involves both types of disorders
32
Q

what is a THROMBUS?

A
  • clot that develops and persists in UNBROKEN BLOOD VESSELS
    • can BLOCK CIRCULATION leading to tissue death
33
Q

what is an EMBOLUS?

A
  • EMBOLUS:
    • thrombus freely floating in the bloodstream
34
Q

what is an EMBOLISM?

A

an EMBOLUS obstructing a vessel

35
Q

what is THROMBOCYTOPENIA?

A

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

36
Q

describe HEMOPHILIA and IMPAIRED LIVER FUNCTION

A

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

37
Q

define DIC

A

Disseminated Intravascular Coagulation (DIC)
- where CLOTTING causes BLEEDING–creation of WIDESPREAD CLOTTING
- blocking of INTACT BLOOD VESSELS

EFFECTS:
- pregnancy complication
- INCOMPATIBLE BLOOD TRANSFUSIONS
- SEPTICEMIA

38
Q

define BLOOD GROUPS

A

based on the PRESENCE of ABSENCE of GLYCOPROTEIN and GLYCOLIPID ANTIGENS (AGGLUTINOGENS) on the SURFACE OF RED BLOOD CELLS

39
Q

what are our BLOOD TYPES?

A
  • 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
40
Q

what are Rh Blood Groups?

A

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

41
Q

describe ERYTHROBLASTOSIS FETALIS

A

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

42
Q

define TRANSFUSION REACTIONS

A

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

43
Q

how do we restore low blood volume?

A

use of NORMAL SALINE and MULTIPLE ELECTROLYTE SOLUTION aka RINGERS SOLUTION
- or PLASMA EXPANDERS
- begins to mimic the PLASMA ELECTROLYTE COMPOSITION

BIO 176 LAB + LEC (20 decks)

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