Blood Homeostasis Coagulation Flashcards

Question

Erythroblastosis Fetalis

Answer 1

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).

Answer 2

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

Answer 3

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

Answer 4

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

Answer 5

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***

Answer 6

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

Answer 7

**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.

Answer 8

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

Answer 9

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

Answer 10

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

Answer 11

**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

Answer 12

**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

Answer 13

* 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

Answer 14

* 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**

Answer 15

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

Answer 16

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**.

Answer 17

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.

Answer 18

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