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Patho Test 3 > Coagulation > Flashcards

Coagulation Flashcards

1
Q

What is the endothelium?

A
  • “practically imperceptible” the endothelial cells arrange themselves as a fine lining that has numerous life support function
  • blood will clot if it ever touches anything besides an endothelial cell
  • endothelial cells are responsible for keeping blood from clotting- by release anticoag factors (didn’t specify which ones)
  • endothelial cells also help relax smooth muscle (responsible for HTN and hypercoaguability)
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2
Q

What is blood flow like through blood vessel?

A
  • laminar flow through blood vessels. fast inside, slow outside
    • if any disruption in wall. causes turbulent flow
  • Turbulent flow is caused by numerous small currents flowing crosswise or oblique to the long axis of the vessel, resulting in flowing whorls and eddy currents
    • turbulent flow is much less efficient and also causes further damage to the blood vessels
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3
Q

How does platelet aggregation happen inside a blood vessel?

A
  • endothelial cells always touch eachother. if the basement membrane is exposed from some damage to endothelial cells, and blood is coming in contact with area below endothelial cells
  • VWF will bind to collagen in membrane and PLT bind to VWF, becoming partially activated and kicking off clotting cascade
  • fibrin, RBC and plt all form together to make clot
  • see videos for furhter explanation

Platelet adhesion and aggregation. Von Willebrand factor functions as an adhesion bridge between subendothelial collagen and the glycoprotein Ib (GpIb) platelet receptor. Aggregation is accomplished by binding of fibrinogen to platelet GpIIb-IIIa receptors and bridging many platelets together. Congenital deficiencies in the various receptors or bridging molecules lead to the diseases indicated in the colored boxes. ADP, adenosine diphosphate.

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4
Q

What is the intrinsic pathway?

A

activated by contact with basement membrane

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5
Q

What is the extrinsic pathway

A

activated by tissue factor which is presented by subendothelial cells

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6
Q

What is the common pathway?

A

results in the activation of prothrombin to thrombin which converts fibrinogen to fibrin. Cross-linked fibin (factor 13) holds platelets and RBC together to form a clot

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7
Q

What is fibrinogen/fibrin? Activator? function?

A
  • aka Factor I
  • Activator are facotr IIa and XIIIa
  • function- forms clot (fibrin); XIIIa assists formation of crosslinks
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8
Q

What is prothrombin/thrombin? Activator? Function?

A
  • Aka factor II
  • Activator- Xa, Va, Ca, platelet
  • function- activates I, V, VIII, XIII, PLT
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9
Q

What is tissue factor? Activator? Function

A
  • AKA factor III
  • Activator= tissue damage
  • Function- cofactor of VIIa (extrinsic pathway)
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10
Q

What is calcium’s role in coag? Factor? Function

A
  • AKA Factor IV
  • Function- cofactor of IIa, VIIa, IXa, Xa, protein C, protein S
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11
Q

What is von willebrand factor?

A
  • Activator- collagen
  • Function- binds to VIII mediates platelet adhesion
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12
Q

What is antithrombin III?

A

Inactivates IIa, Xa and others; enhanced by heparin!

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13
Q

What is plasminogen/plasmin?

A
  • activator- tPA and urokinase
  • Function- lyses fibrin, vWF, and others
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14
Q

What is tPA?

A

Tissue plasminogen activator

function- activates plasminogen

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15
Q

The clotting mechanism has a _____ feedback system.

A

positive

Thrombin (factor II towards the end) comes back to activate factor V and Factor VIII causing more clotting

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16
Q

How do we start clotting?

A
  • Extrinsic- need something else to clot (tissue factor (facotr III))
    • anything that is supposed to be in contact with blood has tissue factor, if it’s not supposed to be in contact with blood, it doesn’t have tissue factor
    • Factor III, VII activate
  • Intrinsic- have everything we need already
    • starts by factor XII when it touches collagen
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17
Q

What does warfarin act on?

A
  • causes synthesis of non functional VII and prevents activation of Xa
    • inhibits both intrinsic and extrinsic pathway
  • Warfarin also prevents II, IX, X formation
    • all Ca dependent factors
    • consider VII to be main one inhibited
  • Increases prothombin time ()PT)
  • will have effect on clotting status a couple of days later. only affects new factor VII
    *
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18
Q

What is heparin?

A
  • increases inactivation of thombin (IIa) which inhibits activation of factor VIII and inhibits the intrinsic pathway
  • Increases partial thromboplastin time (PTT)
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19
Q

What is EDTA?

A
  • Chelates Ca and prevents clotting
  • what’s in the lab tube to prevent lab samples from clotting
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20
Q

What does PT measure?

A

extrinsic pathway (VII)

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21
Q

What does PTT measure?

A

Intrinsic pathway (VIII, IX)

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22
Q

What stops us from clotting?

A
  • Fibrinolytic system
  • Vascular injury causes endothelial cell to release tPA (tissue plasminogen activator)
  • This converts plasminogen to plasmin
  • plasmin converts fibrin–> fibrin degradation products
    • takes strands and chops them up
    • when we break fibrin down, also produce D-dimer
  • Plasmin also breaks down fibrinogen and prevents further clotting
  • Near the damage- the clotting will overwhelm the damage
  • further from the damage- the plasmin will overwhelm the clotting
    • this keeps clotting where we need it
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23
Q

What can cause not enough clotting?

A
  • Hereditary clotting factor deficiencies
  • disorders affecting paltelet number
    • disorders resulting in plt produciton defects
      • congenital
      • acquired
    • acquired causes resulting in excess platelet destruction
      • nonimmune platelet destruction disorders
      • immune platelet destruction disorders
24
Q

What are disorders that can cause too much clotting?

A
  • Heretiable causes of hypercoagulability
    • thrombophilia d/t decrease antithrombotic proteins
    • thrombophilia d/t increase prothrombotic proteins
  • acquired causes of hypercoagulability
    • myeloproliferative d/o
    • malignancies
    • pregnnayc and OC use
    • neprhotic synrome
    • antiphopholipid antidoies
    • heart disease
25
Q

What is Hemophilia A?

A
  • Factor VIII deficiency
    • <1% present before severe bleeding (has to be missing 99% of factor VIII before issues)
  • X linked
  • prolonged PTT, PT normal (only intrinsic pathway affected, extinsic is working fine)
  • Txmt- give factor VIII each day and they’re ok
26
Q

What is hemophilia B?

A
  • Factor IX <1% of normal before
  • prolonged PTT, PT is normal (only intrinsic pathway affected)
  • X-linked
27
Q

What will happen in deficiencies in factor X, V, II (prothrombin)

A
  • autosomal recessive
    • very rare because these patients tned to die out and only carriers around
  • prolongation of PT and PTT (deficiency in common pathway so both extrinsic and intrinsic are affected and prolonged bleeding time)
28
Q

What happens with factor VII deficiency?

A
  • rare autosomal recessive
  • prolonged PT but normal PTT
29
Q

Factor XI deficiency

A
  • Autosomal recessive
  • affect 5% of ashkenazi jews
  • prolongation of the PTT
    • intrinsic pathway won’t work from factor XI but we do have other ways of activating this pathway besides factor XI
  • generally mild
30
Q

Factor XII deficiency?

A
  • Not associated with clinical bleeding- only affect intrinsic pathway
31
Q

Factor XIII deficiency?

A
  • Rare autosomal recessive disorder
  • normal results on PT, PTT, Fibrinogen level, plt count
  • not a big problem
32
Q

Hypofibrinogenemia and afibrinogenemia?

A

rare autosomal recessive

if not fibrinogen, not going ot clot and most likely die very quickly. low amount of carriers

33
Q

Dysfibrinogenmia?

A
  • usually no clinical disease
34
Q

What is von Willebrand disease?

A
  • autsomal dominant or autosomal recessive
  • often deficiency of vWF
  • rarely life threatening bleeding
35
Q

What is acquired factor VIII or IX inhibitors?

A

looks just like hemophilia A or B, but supplemental VIII or IX is destroyed. won’t help to give those factors

36
Q

What is congenital hypoplastic thrombocytopenia with absent radii?

A
  • Autosomal recesive
  • missing radius
  • also affect platelet numbers?
37
Q

Faconi anemia?

A
  • autosomal recessive- fairly well and bred out of gene pool earily
  • congenitla aplastic anemia iwth severe pancytopenia
    • genetic damage to bone marrow
  • often progresses to acute leukemia
38
Q

What is May-Hegglin anomaly?

A
  • ineffective platelet production
  • thrombocytopenia with giant platelets
39
Q

Wiskott-Aldrich syndrome?

A
  • xlinked
  • present with eczema, immunodeficiency and thrombocytopenia
  • congenital disorder resulting in PLT production defects
40
Q

Acquired causes resulting in platelet production defects?

A
  • Bone marrow damage
    • aplastic anemia or myelofibrosis with pancytopenia
  • vitamin B12 or folate deficiency
    • DNA synthesis needed for megakaryocyte production
    • don’t have enough platelets because we don’t have enough b12/foalte to make megakaryocytes
41
Q

TTP?

A

Thrombotic thrombocytopenic purpura

  • characterized by formation of platleet rich thrombi in the arterial and capillary microvasculature
  • deficiency of ADAMTS 13 protease
    • usual function is to cut ultra-large vWF multimers into smaller pieces
    • vWF is therefore not affective, and then vWF doesn’t mind to collgen/plt and doesn’t start clotting cascade
  • classically described as a complex of five signs
    1. fever
    2. renal failure
    3. thrombocytopenia
    4. microangiopathic hemolytic anemia
    5. neurologic abnormalities
  • preeclampsia with HELLP syndrome can evolve into TTP postpartum
  • TTP is a medical emergency
  • Treatment: plt and vwf (same as hellp)
  • develop lots of purple spots because capillary bleeding isn’t stopped
42
Q

What is hemolytic uremic syndrome?

A
  • similar ot TTP
  • Typically seenin children with bloody diarrhea due to infection with a particular strain of E coli that produces a shiga-like toxin
    • siga-liek toxin causes excessive clotting which causes RBC to be borkwn down
      • RBC” bleeding” and HGB pouring out. HGB is not supposed to be free in blood
      • free hgb goes ot kidneys, gets stuck in basement membrane, causing damage to kidney and now we have decreased GFR and increase in Urea
43
Q

HELLP syndrome?

A
  • thrombocytopenia is a frequent complicaiton of pregnancy
  • combination of Red cell hemolysis (H) elevated liver enzyme levels (EL) and low platelet count (LP) is present
  • postpartum TTP is a life-threaening illness with poor prognosis
  • associated with pre-eclampsia
  • treatment: with platelet and vWF will restore clotting temporarily
44
Q

Pathophys of DIC?

A
  • Starts with massive tissue destruction/epithelialinjury/sepsis which causes release of tissue factor (fromt dead cells/fragments of cells in blood)
  • causes widespread microvascular thombosis
    • activation of plasmin
      • firbinolysis
        • inhibition of thrombin, plt aggregation and fibrin polymerization
      • proteolysis of clotting factors
    • consumption of clotting factors and plateletes
  • causes vascular occlusion
    • causes microangiopathic hemolytic anemia
      • lots of hemolysis
      • ischemic tissue damage from clots everywhere
  • LABS:
    • D-dimer and other fibrin degradaiton products elevated in DIC
    • Fibrinogen is low
    • PT and PTT are prolonged d/t loss of clotting factors

call this causes uncontrolled bleeding.

basically uncontrolled clotting cascade, clotting/bleeding everywhere

very delicate balancing act between controlling bleeding/clotting

45
Q

What is post transfusion purpura?

A
  • d/o affecting plt number (immune plt destruciton d/o)
  • give someone blood, immune systme reacts to some component in blood and induces autoimmune destruciton of regular host platelets
46
Q

What is HIT?

A

heparin-induced thrombocytopenia

  • HIT type I (non immune HIT)
  • HIT type 2 (immune-mediated HIT)
  • Antibodies form the heparin-platelet factor 4 complex
  • 10-15% of patient receiving bovine unfractionated heparin develop an antibody
  • <6% of patients receiving porcine heparin develop antibodies
  • <10% of those who develop an antibody will experience a thrombotic event
  • immune mediated HIT occurs b/w days 5-10 of heparin use
47
Q

ITP?

A

Idiopathic thrombocytopenic purpura

  • d/o affecting plt number (immune plt destruciton d/o)
  • thrombocytopenia unrelated to drug exposure, infection or autoimmune disease is generally classified as autoimmune idiopathic thrombocytopenic purpura (ITP)

thrombocyopenia is also a common manifestation of autoimmune disease

48
Q

What is Virchow’s triad?

A

Virchow’s triad is what contributes to thrombosis

  • Endothelial injury- important in anticoag. endothelial cells secrete factors that prevent blood from clotting
    • if damaged, endothelial cells won’t secrete the anticoag factors
  • abnormal blood flow
    • endothelial injury will also cause abnormal blood flow, further contributing to thrombosis
  • hypercoagulability

Virchow’s triad in thrombosis. Integrity of endothelium is the most important factor. Injury to endothelial cells can also alter local blood flow and affect coagulability. Abnormal blood flow (stasis or turbulence), in turn, can cause endothelial injury. The factors may act independently or may combine to promote thrombus formation.

49
Q

Thrombophilia Due to Decreased Anti-thrombotic Proteins?

A

Hypercoaguability disorders are more survivable vs anticoagulant d/o.

  • Hereditary Antithrombin Deficiency
    • autosomal dominant
    • ~20 times more likely to develop venous thromboembolism (VTE)
      • slow moving blood is also more likely to clot d/t improperly activated thrombin
  • Hereditary Protein C and Protein S Deficiency
    • The risk of VTE is about the same as with AT III deficiency
    • Synthesis of both protein C and protein S is vitamin K dependent
      • protein C and S inactive V and VIII
      • warfarin also inhibits production of protein C and protein S
50
Q

Thrombophilia Due to Increased Pro-thrombotic Proteins

A
  • Factor V Leiden
    • genetic mutation that makes it very resistant to inactivation
      • causes hypercoaguability and more likely to clot
      • if everything else is working fine, then they’re ok
    • present in 5% of people of Northern European descent
  • Prothrombin Gene Mutation
    • causes increased levels of prothrombin
      • not a problem under normal condition but more likely to have thromboembolisms
    • occurs in about 4% of individuals of European descent
51
Q

What are myeloproliferative disorders?

A
  • acquired causes of hypercoagulability
  • polycythemia vera, essential thrombocytosis, and paroxysmal nocturnal hemoglobinuria
    • too many rbc and more factors to contribute to clot (polycytemia vera)
  • increased incidence of thrombophlebitis, pulmonary embolism, and arterial occlusion
  • risk of splenic, hepatic, portal vein, and mesenteric blood vessel thrombosis
    • more likely to be problematic where we have slow moving blood
52
Q

How do malignancies cause hypercoagulability?

A
  • Adenocarcinoma of the pancreas, colon, stomach, and ovaries
    • as tumor grows, cna end up with necrotic core, which loose like sepsis. as cells die, get into circulation and have tissue factor that causes hypercoaguability
    • tends to be localized around the cancer but not all of it will stya there
    • as tumor invades/metastasizes, ends up with more thrombosis formation throughout body
  • often present with deep vein thrombosis or migratory superficial thrombophlebitis
  • release pro-coagulant factors by the tumor that can directly activate factor X
  • endothelial damage by tumor invasion
  • blood stasis
53
Q

How does pregnancy and oral contraceptive use contribute to hypercoagulability?

A
  • increase the risk of thrombosis
  • approximately 1 in 1500 pregnancies
  • higher in women who have an inherited hypercoagulable state, a history of deep vein thrombosis or pulmonary embolism, or a family history of thromboembolic disease
  • The association of oral contraceptive use with thrombosis and thromboembolism appears to be multifactorial
54
Q

How does nephrotic syndrome cause hyperocagulability?

A
  • risk of thromboembolic disease, including renal vein thrombosis
  • losing proteins, including lcotting factors
  • lose plasminogen, anticlotting factors as well
  • end up with coagulapathies, start clotting slower and stop clotting slower
55
Q

How do antiphospholipid antibodies cause hypercoaguability?

A
  • not necessarily correlate with thrombosis
  • hepatitis C, mononucleosis, syphilis, Lyme disease, multiple sclerosis, or HIV infection can have circulating antiphospholipid antibodies, do not have a propensity for thrombosis
  • Patients with lupus anticoagulants have an increased propensity for thrombosis
56
Q

How does heart disease cause hypercoaguability?

A
  • hemostasis increases risk of clot formation
  • atrial fibrillation- atria aren’t contracting properly, allowing blood to sit still and clot
  • ventricular wall motion abnormality
57
Q

What does venous hypercoagulability cause? arterial hypercoagulability?

A
  • Venous hypercoagulability
    • Slow moving blood with excess thrombin
  • Arterial hypercoagulability
    • Fast moving blood (which can damage endothelial cells, causing basement membrane/collagne to be exposre, activating plt )–> excess platelet function

Patho Test 3 (4 decks)

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