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A&P 1 > Blood Homeostasis Coagulation > Flashcards

Blood Homeostasis Coagulation Flashcards

1
Q

Blood Composition

ALL

A

Formed Elements (45%)
Platelets (4.8%) [250-400 thousand]
RBCs (95.1%) [4.2-5.8 million]
WBCs (0.1%)…[5-9 thousand]
* Neutrophils (50-70%)
* Eosinophils (2-4%)
* Basophils (<1%)
* Monocytes (2-8%)
* Lymphocytes (20-30%)

Plasma (55%) aka fluid matrix
Electrolytes
Water (92%)
Wastes
Nutrients / Vitamins / Hormones
Gases (N2 , O2 , CO2)
Proteins (7%)
* Albumins (60%)
* Globulins (35%)
* Fibrinogen (4%)

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2
Q

Blood Composition

Plasma Only

A

Plasma (55%) aka fluid matrix
Electrolytes
Water (92%)
Wastes
Nutrients / Vitamins / Hormones
Gases (N2 , O2 , CO2)
Proteins (7%)
* Albumins (60%)
* Globulins (35%)
* Fibrinogen (4%)

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3
Q

Blood Composition

Formed Elements Only

A

Formed Elements (45%)
Platelets (4.8%) [250-400 thousand]
RBCs (95.1%) [4.2-5.8 million]
WBCs (0.1%)…[5-9 thousand]
* Neutrophils (50-70%)
* Eosinophils (2-4%)
* Basophils (<1%)
* Monocytes (2-8%)
* Lymphocytes (20-30%)

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4
Q

The Red Blood Cell

Importance in Structure

A

Biconcave disks- Malleability is imperative!
A-nucleate
Cytoplasmic Enzymes:
* Metabolize Glucose
* Form small amts of ATP
* Pliability of Cell Membrane
* Transportation of ions
* Ferrous Form of Fe
* Prevents oxidation of proteins

Contains Hemoglobin Molecules
* Hemoglobin must remain in RBC to function properly
* Ability to concentrate 34gram of Hgb per 100mL of cell fluid
* Metabolic limit of the cell
* Size of the cell

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5
Q

Red Blood Cell Size

A

Biconcave Disk
Width: 7.2-8.4um
Height (inner): 0.45-1.16um
Height (outer): 2.31-2.85um

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6
Q

RBC Production

A

During Gestation: Yoke Sac -> Liver -> Spleen/Lymph -> Bone Marrow
Up until 5 years: Bone Marrow of ALL bones
Slowing become fatty and leave the Tibia & Femur to do the work
After 20 years: Membranous Bones ( Vertebra, Sternum, Ribs, Ilia)

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7
Q

Genesis of Blood Cells

A

Erythropoietin = differentiator
* PHSC –> PHSC
* PHSC –> LSC –> Lymphocyte (B or T)
* PHSC –> CFU-S –> CFU-GM –> Granulocytes (Neutrophils, Eosinophils, Basophils) or Monocytes –> Macrocytes
* PHSC –> CFU-S –> CFU-M –> Megakaryocytes –> Platelets
* PHSC –> CFU-S –> CFU-B –> CFU-E –> Erythrocytes

PHSC = Pluripotent Hematopoietic Stem Cell
LSC = Lymphoid Stem Cell
CFU = Colony Forming Unit
CFU-S = CFU Spleen
CFU-GM = CFU Granulocutes, monocytes
CFU-M = CFU Megakaryocytes
CFU-B = CFU Blast
CFU-E= CFU Erythrocytes

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8
Q

Stages of RBC Differentiation

ALL

A

1st generation (Basophilic)
- Little Hgb

2nd/3rd generation (Polychromatophil/Orthochromatic)

  • Hbg fill cell (34%)
  • Nucleus condenses and is absorbed/extruded
  • ER is reabsorbed

4th generation (Reticulocyte)
- Basophilic material, GA, Mitochondria
- Diapedesis into blood capillaries from bone marrow
- If there are large numbers, there is a problem - RBC not maturing enough to carry on RBC function

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9
Q

1st generation RBC Differentiation

A

(Basophilic)
- Little Hgb

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10
Q

2nd/3rd generation of RBC Differentiation

A

(Polychromatophil/Orthochromatic)

  • Hbg fill cell (34%)
  • Nucleus condenses and is absorbed/extruded
  • ER is reabsorbed
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11
Q

4th generation of RBC Differentiation

A

(Reticulocyte)
- Basophilic material, GA, Mitochondria
- Diapedesis into blood capillaries from bone marrow
- If there are large numbers, there is a problem - RBC not maturing enough to carry on RBC function

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12
Q

Role of Erythropoietin

A

Tissue oxygenation is the most esential regulator of RBC production!
Anything to decrease oxygenation will stimulate erythropoietin for RBC production b/c we need more oxygenation.
* Low blood volume, anemia, low hemoglobin, poor blood flow, pulmonary disease

Kidneys and liver release erythropoietin
Hypoxia= inducible factor-I
Non-renal sensors can stimulate hormone release not just renal tissue hypoxia

Dec. tissue oxygenation –> erythropoietin —> hematopoietic stem cells –> proerythroblasts –> RBCs –> tissue oxygenation

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13
Q

Hematinics

A

Vitamins
B12 (cyanocobalamin)
Folate
Ascorbic acid (Vit. C)
Vitamin E
B6 (pyridoxine)
Thiamine
Riboflavin
B5 (pantothenic acid)
Metals
Iron
Manganese
Cobalt
Essential Amino Acids

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14
Q

Formation of hemoglobin

A

I. 2 succinyl-CoA + 2 glycine –> pyrrole
II. 4 pyrrole –> protoporphyrin IX
III. protoporphyrin IX + Fe++ –> heme
IV. heme + polypeptide –> hemoglobin chain (alpha or beta)
V. 2 alpha chains + 2 beta chains –> hemoglobin A

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15
Q

Hemoglobin Structure

A

Heme (mitochondria) molecules combine with Globin (ribosomes)
Tetramer!
Hgb A – most common- 2 alpha; 2 beta chains
4 iron molecules/Hgb
4 oxygen molecules (O2)/Hgb
250 million Hgb molecules/Erythrocyte!!!

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16
Q

When it’s not a tetramer…

A

It’s a dimer (only 2 chains in hemoglobin – different shape!)
Result of Hemolysis
Filtered by the kidneys – not good!
Stroma can clog the glomerulus –not good!
Stroma can clog small capillary beds – lungs, heart, brain- not good!
Reduced Hgb time in Circulation – not good!
Shifts OxyHgb Curve to the Left- not good!
Decreased O2 binding – not good!
“Free” Hgb scavenges NO = Vasoconstriction – not good!

Stroma = dimers
Tetramere = 4 globulin chains

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17
Q

Iron and Heme

A

Determines the ability of Hgb to hold on to O2
4-5g in the body - 65% in Hgb
Ferritin is stored iron
Hemosiderin is backup storage
Transferrin is a binder to transport iron

18
Q

RBC and metabolic waste

A

Picture slide :(
In the RBC…
Carbonic anydrase = enzyme in rxn below
CO2 + H2O —> H2CO3 (carbonic acid)
H2CO3 –> HCO3- + H+ –> Hb
Rxn also goes in reverse
Hb –> H+ + HCO3- –> H2CO3
H2CO3 –> CO2 + H2O (in presence of carbonic anhydrase)

RXN = reaction

19
Q

“Fun” Facts

How CO2 and O2 are transported

A

CO2 is transported…
* Bicarbonate Ions (70%)
* Hemoglobin (23%)
* Dissolved in Plasma (7%)

O2 is transported….
* Hemoglobin (98%)
* Dissolved in Plasma (2%)

20
Q

Oxygen Carrying Capacity

A

(1.34 x Hgb x SpO2) + (0.003 x PaO2)
Example:
Hgb = 12, SpO2% = 95%, PaO2 = 96mmHg
(1.34 x Hgb x SpO2) + (0.003 x PaO2) = ??
(1.34 x 12 x 0.95) + (0.003 x 96) = 15.56mL of O2/100mL blood OR 15.56mL of O2/dL <—-deciliter!!!

1.34 b/c 1g of Hgb can maximally bind to 1.34mL of O2
Henry’s Law = (0.003 x PaO2)

21
Q

ABO Blood System “Chart”

Agglutinogens and Agglutinins

A

Type A
* A agglutinogens (RBC surface proteins)
* B agglutinin (plasma antibodies)
* Can donate to A and AB
* May receive from A and O
* May not receive from B or AB b/c the B agglutinogens on the RBC surface of B and AB blood (donor) will bind with (agglutinate) the B agglutinin in the blood of a Type A person (receiver).

Type B
* B agglutinogens (RBC surface proteins)
* A agglutinin (plasma antibodies)
* Can donate to B and AB
* May receive from B and O
* May not receive from A or AB b/c the A agglutinogens on the RBC surface of A and AB blood (donor) will bind with (agglutinate) the A agglutinin in the blood of a Type B person (receiver).

Type AB
* AB agglutinogens (RBC surface proteins)
* NO agglutinin (plasma antibodies)
* Can donate to AB
* May receive from A, B, AB and O (universal receiver) b/c there are no agglutinins

Type O
* NO agglutinogens (RBC surface proteins)
* A and B agglutinin (plasma antibodies)
* Can donate to A, B, AB and O (universal donor) b/c it is a blood ninja with no agglutinin
* May receive from O
* May not receive from A, B or AB b/c the A and B agglutinogens on the RBC surface of A, B and AB blood (donor) will bind with (agglutinate) the A and B agglutinin in the blood of a Type O person (receiver).

Antigen = Agglutinogen - physical structure on RBC surface which causes an antibody rxn
Antibody = Agglutinin - protein produced in response to and counteracting a specific antigen
Agglutination = clumping of particles together when an antigen-antibody rxn occurs when an antigen is mixed with its corresponding antibody

22
Q

Antibodies

A

AKA Agglutinins
Plasma Antibodies
Almost completely absent at birth
Titers peak between 8-10 years old
Gamma Globulins (IgG & IgM)

23
Q

Transfusion Rxn’s

A

ppt text: Antibodies of recipient attack the antigens of the donor blood
Agglutination followed by delayed hemolysis d/t need for higher titers and IgM antibodies (hemolysins)

Brian’s text: after the initial agglutination in response to the newly administer donor blood, hemolysis is delayed, b/c the body needs both IgM antibodies specifically AND a higher titer of them, aka hemolysins. I think b/c IgM antibodies have 10 binding sides due their shape they produce a stronger transfusion rxn

24
Q

Rh Blood Types

A

Difference between ABO system & Rh system?
6 type of Rh factors (aka antigens)
C, D*, E, c, d, e
(everyone has 1 of each antigen)
If D, Rh +; is no D, Rh-

25
Q

Erythroblastosis Fetalis

A

Mom = Pam (Rh-); Dad = Jim (Rh+); Baby 1 = Cece (Rh+); Baby 2 = Phillip (Rh+).
1st pregnancy: Pam has uncomplicated pregnancy with Cece but develops Anti-Rh antibodies
2nd pregnancy: Pam’s anti-Rh agglutinins (antibodies) attacks Phillips Rh+ antigens (agglutinogens)….

Erythroblastosis Fetalis = Hemolysis/Agglutination -> Excess Bilirubin
Occured on 2nd exposure

Prevention: @ 28 weeks Alice gets treated with anti D antibody immunoglobulins (Rhogam).

26
Q

Hemolysis Concerns

A

400 ml of blood hemolyzed per day to cause jaundice in people with healthy livers

Most Severe Complication of Hemolysis:
Renal Shutdown
AA rxns release vasoactive toxins- decreasing GF
Circulatory Shock
Free Hgb “Dimers” clogs glomerulus

27
Q

Oxygen-hemoglobin Dissociation Curve

A

O2 extraction from Hgb to the tissues
Sigmoid Curve
Partial pressure of oxygen (mmHg) on x-axis & Oxyhaemoglubin (% saturation) SpO2 on y-axis

Left Shift: (Increased affinity)
Haldane Effect
* Decreased temp
* Dec. 2,3-DPG
* Dec. H+
* CO

Right Shift: (Decreased affinity)
Bohr Effect
* Increased temp
* Inc. 2,3-DPG
* Inc. H+

104 = partial pressure of O2 in alveoli (lungs)
40 = partial pressure after unloading in the capillaries / start of venous circulation
80 = partial pressure plateau on graph

28
Q

Hemostatsis

ALL

A
  1. Vascular Constriction (Spasm)
  2. Platelet Plug Formation
  3. Blood Clot (Coagulation)
  4. Fibrous Tissue
29
Q

Hemostasis

Vascular Constriction (Spasm)

A

Local Myogenic Spasm/Constriction
Autacoid factors from injured tissues & platelets
Nervous Reflexes
Thromboxane A2 (humoral factor) is released from platelets – causes vasoconstriction
Begins within minutes of injury and last up to 2 hours

Reduces Flow of Blood

30
Q

Hemostasis

Platelet Plug Formation

A

Cell membranes coated with glycoproteins (coat hangers) enable platelets to be “snagged” by roughened edges of the endothelium

Picture: Release of chemicals ADP, thromboxane A2, Ca2+, platelet factors shown at location of platelet plug

SWELL, SECRETE, STICK, STACK!!!!
* Platelet begin to swell with fluid
* Pseudopod protections, contractile forces release substances making the platelets sticky
* Secrete ADP & Thromboxane A2: activates nearby platelets
* Addition platelets adhere to the others (stacking) causing the formation of a platelet plug.
* Platelet plugs are designed for minute day to day perforations, and really are not “clots” per se
* The clot forms when fibrin threads fill in the “gaps” left in the plug…more on this later
* Once the clot forms, it is invaded by fibroblasts, connective tissue is formed, and the clot is dissolved

31
Q

Platelets

A

Platelet half-life = 8-12 days
Megakaryocytes Fragments
Eliminated by tissue macrophages primarily in the spleen
No platelets = petechiae
Contain:
Myosin, Actin, Thrombosthenin
Enzymes
Calcium Storage
ATP
Produces Prostaglandins
Produces Fibrin-Stabilizing Factor
Produces Growth Factor- for cell grow- mend vessel wall.
Surface Glycoproteins- repels from normal tissue; adheres to damaged tissue
Phospholipid membrane helps activate clotting process.

32
Q

Plasma Clotting Factors

ALL

Factor, Name, Function, Pathway

A

I. Fibrinogen. Converted to fibrin. Common
II. Prothrombin. Enzyme. Common
III. Tissue Thromboplastin. Cofactor. Extrinisc.
IV. Calcium ions (Ca++). Cofactor. All
V. Proaccelerin. Cofactor. Common
VII. Proconvertin. Enzyme. Extrinsic
VIII. Antihemophilic factor. Cofactor. Intrinsic
IX. Plasma thromboplastin component; christmas factor. Enzyme. Intrinsic.
X. Stuart-Prower factor. Enzyme. Common.
XI. Plasma thromboplastin antecedent. Enzyme. Intrinsic.
XII. Hageman factor. Enzyme. Intrinsic.
XIII. Fibrin stabilizing factor. Enzyme. Common.

Prekallikrein = fletcher factor
High Molecular Weight Kininogen = fitzgerald factor

All = intrinsic, extrinsic and common

33
Q

Extrinisic Pathway

A

“Due to external factors” or “non-blood factors”
Injured tissue that meets blood

34
Q

Intrinsic Pathway

A

“Blood activated factors”
Trauma to blood or exposure of blood to collagen
check out thrombin-positive feedback loop

35
Q

Final Common Pathway Prothrombin

A

Prothrombin activator complex is the rate limiting factor in clotting (usually!)
Prothrombin: Plasma Alpha 2 Globulin, 15mg/dL
Continuously formed by the liver…hepatic disease?
Vitamin K is necessary to produce prothrombin
You have less than a 24-hour supply at any given moment

36
Q

Final Common Pathway Fibrinogen

A

Fibrinogen is produced in the liver
Very big molecule – does not (should not-capillary leak?) leak into the interstitum
Thrombin is an enzyme which acts on fibrin to cause a fibrin monomer which link to other fibrin monomers
-Plasma globulins and platelets release Fibrin Stabilizing Factor which is also activated by thrombin – Fibrin Cross Linking activation

37
Q

Clotting Prevention

A
  • Smooth Endothelium
  • “Teflon” Coat of the Glycocalyx lining the Endothelium
  • Thrombomodulin on the Endothelium binds with Thrombin -> activates Protein C which INACTIVATES Factor V and Factor VIII
  • Thrombin gets absorbed in Fibrin Threads (deactivating thrombin)
  • Heparin activates AT III which inhibits Thrombin
38
Q

Lysis of Clots

A
  • After trauma, tissue plasminogen activator activates plasminogen automatically
  • Plasminogen is activated to plasmin
  • Plasmin digests fibrin threads, Factor V, Factor VIII, prothrombin and Factor XII
  • Plasmin is formed constantly, and would degrade clots we need except for alpha 2 antiplasmin
    • This factor binds with and inhibits plasmin
  • Plasmin is dose dependent: tissue activation causes more plasmin to be formed than inhibitor available
  • Plasmin removes millions of tiny clots which we otherwise would not clear
39
Q

Vasoconstriction

A

After vascular injury local neurohumoral factors induce a transient vasoconstriction.
Intact endothelium releases NO and prostacyclin to prevent platelet adhesion beyond the injury site

40
Q

*

Primary Hemostasis

A

Platelets bind via glycoprotein Ib (GP-Ib) receptors to von Willebrand factor (vWF) on exposed extracellular matrix (ECM) and are activated, undergoing a shape change and granule release. Released adenosine diphosphate (ADP) and thromboxane A2 (TxA2) induce additional platelet aggregation through platelet GpIIb-IIIa receptor binding to fibrinogen and form the primary hemostatic plug.

41
Q

Secondary Hemostasis

A

Local activation of the coagulation cascade [involving tissue factor and platelet phospholipids] results in fibrin polymerization, “cementing” the platelets into a definitive secondary hemostatic plug.

42
Q

Thrombus and Anti-thrombotic events

A

Counter-regulatory mechanisms, mediated by tissue plasminogen activator (t-PA, a fibrinolytic product) and thrombomodulin, confine the hemostatic process to the site of injury.

A&P 1 (10 decks)

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