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Pathoma > Hemostasis and Related DIsorders > Flashcards

Hemostasis and Related DIsorders Flashcards

1
Q

What is hemostasis?

Why is it important?

A
  • Literally, the “arrest” of bleeding
  • Integrity of the blood vessel is necessary to carry blood to tissues.
  • Damage to the wall is repaired by hemostasis, which involves formation of a
    thrombus (clot) at the site of vessel injury
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2
Q

Whatre the stages of hemostasis? Describe each stage.

A

Hemostasis occurs in two stages: primary and secondary.

  • Primary hemostasis forms a weak platelet plug and is mediated by interaction between platelets and the vessel wall.
  • Secondary hemostasis stabilizes the platelet plug and is mediated by the
  • *coagulation cascade**.
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3
Q

What are the steps of primary hemostasis? Briefly describe each stage.

A
  1. Transient vasoconstriction of damaged vessel
  2. Platelet adhesion to the surface of disrupted vessel - vWF binds subendothelial collegen, platelets bind using GPIb receptor.
  3. platelet degranulation - ADP and TXA2
  4. Platelet aggregation - ADP helps make GPIIb/IIIa and allows platelets to aggregate via fibrinogen linker molecules.
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4
Q

**$ What is the first step in primary hemostasis? **

$$ How is this step mediated?

A

Step 1- Transient vasoconstriction of damaged vessel

Mediated by reflex neural stimulation and endothelin release from endothelial cells

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5
Q

Where does vWF come from?

How does it bind platelets?

A

vWF is derived from the Weibel-Palade bodies of endothelial cells (majority) and alpha-granules of platelets.

GPIb receptor

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6
Q

Name 2 major products produced by W-P bodies.

A

Weibel-Palade bodies of endothelial cells produce:

  1. vWf
  2. P-selectins (speed bumps)
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7
Q

$ How is TXA2 synthesized?

A

TXA2 is synthesized by platelet cyclooxygenase (COX) and released; promotes platelet aggregation

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8
Q

Describe the degranulation process of platelet and the mediators involved.

A

Adhesion induces shape change in platelets and degranulation with release of multiple mediators.

  • ADP is released from platelet dense granules; promotes exposure of GPIIb/
    IIIa     receptor on platelets –> aggregation occurs via a FIBRINOGEN linker molecule connecting the GPIIb/IIIa receptors!
  • TXA2 is synthesized by platelet cyclooxygenase (COX) and released;
    promotes platelet aggregation.
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9
Q

How do platelets aggregate?

What happens after aggregation?

A
  • Platelets aggregate at the site of injury via GPIIb/IIIa using fibrinogen (from plasma) as a linking molecule –> results in formation of platelet plug
  • Platelet plug is weak as shit –> coagulation cascade (secondary hemostasis) stabilizes it.
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10
Q

How can disorders of primary hemostasis be divided?

A

Usually due to abnormalities in platelets; divided into **quantitative (bleeding! Not enough platelets!) **or **qualitative **disorders

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11
Q

$ What is the primary feature of individuals with disorders of primary hemostasis?

A

Clinical features include mucosal and skin bleeding.

Symptoms of mucosal bleeding include epistaxis (most common overall symptom), hemoptysis, GI bleeding, hematuria, and menorrhagia.

Intracranial bleeding occurs with severe thrombocytopenia.

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12
Q

What are some signs of thrombocytopenia?

A

**petechiae (1-2 mm) **are a sign of thrombocytopenia and are not usually seen with qualitative disorders.

  • ecchymoses (> 1 cm)
  • purpura (> 3 mm)
  • easy bruising

Qualitative disorders usually do not have petechiae

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13
Q

Useful laboratory studies in Disorders of primary hemostasis?

A
  1. Platelet count-normal 150-400 K/uL; < 50 K/uL leads to symptoms.
  2. Bleeding time-normal 2-7 minutes; prolonged with quantitative and qualitative platelet disorders
  3. Blood smear- used to assess number and size of platelets
  4. Bone marrow biopsy-used to assess megakaryocytes, which produce platelets
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14
Q

Most common cause of thrombocytopenia in children and adults?

A

**IMMUNE THROMBOCYTOPENIC PURPURA (ITP) - **Autoimmune production of IgG against platelet antigens (e.g., GPII b/IIIa)

IgG Autoantibodies are produced by plasma cells in the spleen.

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15
Q

Why does thrombocytopenia result in ITP?

A

Antibody-bound platelets are consumed** by **splenic macrophages, resulting in thrombocytopenia.

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16
Q

Types of ITP?

A

Divided into acute and chronic forms

  1. Acute form arises in children weeks after a viral infection or immunization; selflimited,
    usually resolving within weeks of presentation
  2. Chronic form arises in adults, usually women of childbearing age. May be_ primary or secondary (e.g., SLE)._ May cause short-lived thrombocytopenia in
    offspring since antiplatelet IgG can cross the placenta.
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17
Q

Lab findings in ITP?

A
  1. Decreased platelet count, often < 50 K/uL
  2. Normal PT/PTT-Coagulation factors are not affected.
  3. Increased megakaryocytes on bone marrow biopsy
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18
Q

Treatment for ITP

A

Initial treatment is corticosteroids. Children respond well; adults may show early response, but often relapse.

  1. IVIG is used to raise the platelet count in symptomatic bleeding, but its effect is short -lived.
  2. Splenectomy eliminates the primary source of antibody and the site of platelet destruction (performed in refractory cases).
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19
Q

What is MICROANGIOPATHIC HEMOLYTIC ANEMIA?

How does it happen?

A
  • Pathologic formation of platelet microthrombi in small vessels
  • 2 Classic disorders: Seen in thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS)
  1. Platelets are consumed in the formation of microthrombi.
  2. RBCs are “sheared” as they cross microthrombi, resulting in hemolytic anemia with schistocytes

Holy SCHISTOCYTE! look at the 2 points ont he “helment cell”

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20
Q

$$$ What causes thrombotic thrombocytopenic purpura (TTP)?

A

TTP is due to decreased ADAMTS13, an enzyme that normally cleaves vWF multimers into smaller monomers for eventual degradation

  • Large, uncleaved multimers lead to abnormal platelet adhesion, resulting in microthrombi.
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21
Q

Why does ADAMTS13 usually decrease and cause TTP?

A

Decreased ADAMTS13 is usually due to an acquired autoantibody; most commonly seen in adult females

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22
Q

What causes HUS?

A

HUS is due to endothelial damage by drugs or infection.

  • Classically seen in children with E coli Ol57:H7 dysentery, which results from exposure to undercooked beef
  • E coli verotoxin damages endothelial cells resulting in platelet microthrombi in the kidney and brain.
  • Verotoxin also causes a reduction in ADAMTS13!
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23
Q

Clinical findings (HUS and TTP)

A
  1. Skin and mucosal bleeding
  2. Microangiopathic hemolytic anemia
  3. Fever
  4. Renal insufficiency (more common in HUS)- Thrombi involve vessels of the kidney.
  5. CNS abnormalities (more common in TTP) - Thrombi involve vessels of the CNS.
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24
Q

Laboratory findings expected in microangiopathic hemolytic anemias (HUS and TTP) include:

What is the treatment for Microangiopathic hemolytic anemia?

A
  • Thrombocytopenia with ↑ bleeding time
  • $$$ 2. Normal PT/PTT (coagulation cascade is not activated)
  • Anemia with schistocytes
  • ↑ megakaryocytes on bone marrow biopsy
  • Treatment involves **plasmapheresis (removes autoantibodies against ADAMTS13) **and corticosteroids (reduces production of autoantibodies against ADAMTS13), particularly in TTP.
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25
Q

Name the Qualitative platelet disorders

A
  • Bernard-Soulier syndrome
  • Glanzmann thrombasthenia
  • Aspirin
  • Uremia

Remember, you don’t see petechiae in qualitative disorders (do you ever see petechiae if you take too much aspirin? I didn’t think so)

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26
Q

Bernard-Soulier syndrome

A

Qualitative platelet disorder due to a genetic GPIb deficiency –> ** platelet adhesion is impaired**.

Blood smear shows mild thrombocytopenia (platelets don’t live as long so they get destroyed) with $enlarged platelets (more immature).

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27
Q

Glanzmann thrombasthenia

A

A qualitative platelet disorder in which there is a genetic GPIIb/IIIa deficiency –> platelet aggregation is impaired.

Remember: ADP causes the GpIIb/IIIa receptor to flip out and allow platelets to aggregate with fibrinogen linker molecules.

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28
Q

Aspirin impairs which aspect of hemostasis?

A

Aspirin irreversibly inactivates cyclooxygenase; lack of TXA2 impairs aggregation

Remember: it is thromboxane A2 from COX that calls in platelets and says “lets aggregate!”

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29
Q

What is secondary hemostasis? What is the end-product?

A
  • Stabilizes the weak platelet plug via the coagulation cascade
  • Coagulation cascade generates thrombin, which converts fibrinogen in the platelet plug to fibrin.
  • Fibrin is then cross-linked, yielding a stable platelet-fibrin thrombus
30
Q

Where are coagulation factors produced?

How are they activated?

A

Factors of the coagulation cascade are produced by the liver in an inactive state. Circulate in blood in the inactive form.

Activation requires:

  1. Exposure to an activating substance
  • Tissue thromboplastin activates factor VII (extrinsic pathway).
  • Subendothelial collagen activates factor XII (intrinsic pathway).
  1. Phospholipid surface of platelets
  2. Calcium (derived from platelet dense granules)
31
Q

What is the usual cause of disorders of secondary hemostasis?

What are the clinical features?

A
  • Usually due to factor abnormalities
  • Clinical features include deep tissue bleeding into muscles and joints (hemarthrosis) and rebleeding after surgical procedures (e.g., circumcision and wisdom tooth extraction)
32
Q

Extrinsic factor

What activates it?

A

Factor VII

Activated by tissue thromboplastin

33
Q

Intrinsic factors

A

factors 12, 11, 9, 8

subendothelial collagen activates 12

34
Q

Common pathway of the coagulation cascade

A

10, 5, 2, fibrinogen

35
Q

Laboratory studies to evaluate disorders of secondary hemostasis include?

A

Prothrombin time (PT)-measures extrinsic (factor VI I) and common (factors II, V, X, and fibrinogen) pathways of the coagulation cascade

Partial thromboplastin time (PTT) - measures intrinsic (factors XII, Xl, IX, VIII) and common (factors Il, V, X, and fibrinogen) pathways of the coagulation cascade

36
Q

HEMOPHILIA A

A

Genetic factor VIII (FV Ill) deficiency

  • X-linked recessive (predominantly affects males)
  • Can arise from a new mutation (de novo) without any family history
37
Q

Presentation and Lab findings in Hemophilia A?

Treatment?

A

**Presents with deep tissue, joint, and postsurgical bleeding - **Clinical severity depends on the degree of deficiency.

Laboratory findings include

  • *1. ↑ PTT; normal PT (PT may be elevated according to Goljian)
    2. ↓ FVIII
    3. Normal platelet count and bleeding time**

Treatment involves recombinant FVIII

38
Q

HEMOPHILIA B (CHRISTMAS DISEASE)

A

**Genetic factor IX deficiency - **Resembles hemophilia A, except FIX levels are decreased instead ofFVIII

39
Q

COAGULATION FACTOR INHIBITOR

Clinical and lab findings?

$$$$$ How do you differentiate a coagulation factor inhibitor disorder from the hemophilias?

A

Acquired antibody against a coagulation factor resulting in impaired factor function; anti-FVIII is most common.

  1. Clinical and lab findings are similar to hemophilia A.
    $ 2. **MIXING STUDY! **PTT does not correct upon mixing normal plasma with patient’s plasma (mixing study) due to inhibitor;

PTT does correct in hemophilia A because you are replacing factor with the addition of normal plasma that contains factor 8.

Factor 8 is KILLED immediately by the antibody to factor 8 (the INHIBITOR) and you still have a prolonged PTT even after adding normal plasma to the patients blood!!!!

40
Q

$$$ What is the most common inherited coagulation disorder?

A

VON WILLEBRAND DISEASE

  • Genetic vWF deficiency - Multiple subtypes exist, causing quantitative and qualitative defects
  • the most common type is autosomal dominant with decreased vWF levels.
41
Q

Clinical presentation and labs seen in Von Willebrand disease?

A

Clinical features

  • Presents with mild mucosal and skin bleeding
  • low vWr impairs platelet adhesion

Labs

  • ↑ bleeding time
  • $ ↑ PTT
  • $ normal PT - Decreased FVIll half-life (vWF normally stabilizes FVIII);
    however, deep tissue, joint, and postsurgical bleeding are usually not seen.
  • **$ Abnormal ristocetin test **- Ristocetin induces platelet aggregation by causing vWF to bind platelet GPIb; lack of vWF -> impaired aggregation -> abnormal test.
42
Q

Treatment for Von Willebrand disease?

MOA?

A

Treatment is desmopressin (ADH analog), which increases vWF release from Weibei-Palade bodies of endothelial cells.

43
Q

VITAMIN K DEFICIENCY

$$$$$ Why is Vitamin K important? Explain.

A

Disrupts function of multiple coagulation factors

  • Vitamin K is activated by epoxide reductase in the liver.
  • $ Activated vitamin K gamma carboxylates factors II, VII, IX, X, and proteins C and S -> gamma carboxylation is necessary for factor function.
44
Q

When does vitamin K deficiency occur?

A
  • Newborns- due to lack of GI coloni:tation by bacteria that normally synthesize
    vitamin K; vitamin K injection is given prophylactically to all newborns at birth
    to prevent hemorrhagic disease of the newborn.
  • Long-term antibiotic therapy- disrupts vitamin K-producing bacteria in the GI
    tract
  • Malabsorption - leads to deficiency of fat-soluble vitamins, including vitamin K - leads to deficiency of fat-soluble vitamins, including vitamin K
45
Q

In addition to Hemophilia A and B, Coagulation factor inhibitor, Von willebrand disease, and vitamin K deficiency, what are some other causes of abnormal secondary hemostasis?

A

Liver failure - decreased production of coagulation factors and decreased activation of vitamin K by epoxide reductase

Large-volume transfusion - dilutes coagulation factors, resulting in a relative deficiency

46
Q

How do you follow the effect of liver failure on coagulation?

A
  • effect of liver failure on coagulation is followed using PT (Liver synthesis of factor 7 good indicator)
  • Liver failure - decreased production of coagulation factors and decreased activation of vitamin K by epoxide reductase
47
Q

HEPARIN-INDUCED THROMBOCYTOPENIA

$ Mechanism?

A
  • Platelet destruction that arises secondary to heparin therapy
  • $ Platelet factor 4 combines with heparin to make HEP-PF4 complex -> IgG antibodies are developed to this complex
  • Fragments of destroyed platelets may activate remaining platelets, leading to
    thrombosis.
48
Q

DISSEMINATED INTRAVASCULAR COAGULATION

A

Pathologic activation of the coagulation cascade

  • Widespread microthrombi result in ischemia and infarction.
  • Consumption of platelets and factors results in bleeding, especially from **IV sites **and mucosal surfaces (bleeding from body orifices).
49
Q

Causes of DIC?

A
  1. **Obstetric complications **- Tissue thromboplastin in the amniotic fluid activates coagulation.
  2. Sepsis (especially with E Coli or N meningitidis)- Endotoxins from the bacterial wall and cytokines from macrophages (e.g., TNF and IL-1) induce endothelial cells to make tissue factor.
  3. Adenocarcinoma - Mucin activates coagulation.
  4. Acute promyelocytic leukemia - Primary granules activate coagulation.
  5. Rattlesnake bite - Venom activates coagulation.
50
Q

$$$ What is the best screening test for DIC?

What other laboratory findings would be observed in DIC?

A
  • ↓ platelet count (activating all platelets)
  • ↑ PT/PTT (consume coagulation factos)
  • ↓ fibrinogen
  • Microangiopathic hemolytic anemia
  • $ ↑ fibrin split products, particularly ↑ D-dimer
    • ↑ D-dimer is the best screening test for DIC
    • Derived from splitting of cross-linked fibrin; D-dimer is not produced from splitting of fibrinogen.
51
Q

Treatment for DIC?

A
  • Treatment involves addressing the underlying cause and transfusing blood products
  • cryoprecipitate (contains coagulation factors), as necessary.
52
Q

Describe the normal fibrinolysis process.

(What are the 3 important steps of this cycle including how it is shut off)

A

Normal fibrinolysis removes thrombus after damaged vessel heals.

  1. Tissue plasminogen activator (tPA) converts plasminogen to plasmin.
  2. Plasmin cleaves fibrin and serum fibrinogen, destroys coagulation factors, and
    blocks platelet aggregation.
    $ 3. alpha2-antiplasmin inactivates plasmin.
53
Q

What cause disorders of fibrinolysis?

What are some examples?

A

Disorders of fibrinolysis are due to plasmin overactivity resulting in excessive cleavage of serum fibrinogen.

  • Radical prostatectomy - Release of urokinase activates plasmin
  • Cirrhosis of liver - reduced production of alpha2-antiplasmin
54
Q

$ A patient presents with bleeding from body orifices, mucosal surfaces, and IV sites. What do you think is wrong?

A

Primary differential dx is DIC, disorder of fibrinolysis (presents like DIC!), or finbinolytic drug OD.

55
Q

$ Lab findings in a disorder of fibrinolysis? How is it different from labs in DIC?

A
  1. ↑ PT/PTT- Plasmin destroys coagulation factors.
  2. **↑ bleeding time **
  3. _$ normal platelet count _- Plasmin blocks platelet aggregation. *(platelet count reduced in DIC b/c platelets are activated)*
  4. ↑ fibrinogen split products $ without D-dimers - Serum fibrinogen is
    Lysed (↑ fibrinogen split products); however, D-dimers are not formed because fibrin thrombi are absent, never had any thrombi formed, no fibrin to cleave!.
56
Q

Treatment for disorders of fibrinolysis?

A

Treatment is aminocaproic acid, which blocks activation of plasminogen. Plasmin can’t be formed without plasminogen, (and plasmin is the culprit that (1) fucks up fibrin and serum fibrinogen, (2) knocks the shit out of coagulation factors, and (3) blocks platelet aggregation)

57
Q

$ What are the actions of plasmin?

$What inactivates plasmin?

A
  1. Cleaves fibrin and serum fibrinogen
  2. Destroys coagulation factors
  3. $ Blocks platelet aggregation

Inactivated by alpha2-antiplasmin (produced by the liver)

58
Q

What is thrombosis?

How is it characterized? Why is this important?

A

Pathologic formation of an intravascular blood clot (thrombus)

  1. Can occur in an artery or vein
  2. Most common location is the deep veins (DVT) of the leg below the knee.

Characterized by (I) lines of Zahn (alternating layers of platelets/fibrin and RBCs,
Fig. 4.3) and (2) attachment to vessel wall
1. Both features distinguish thrombus from postmortem clot.

59
Q

3 major risk factorsfor thombosis?

A
  • disruption in blood flow
  • endothelial cell damage
  • hypercoagulable state (Virchow triad).
60
Q

Why does stasis increase the risk for thrombosis?

Give 3 examples of stasis.

A

A. Stasis and turbulence of blood flow increases risk for thrombosis.
1. Blood flow is normally continuous and laminar; keeps platelets and factors dispersed and inactivated

B. Examples include

  1. Immobilization- increased risk for deep venous thrombosis
  2. Cardiac wall dysfunction (e.g., arrhythmia or myocardial infarct ion)
  3. Aneurysm
61
Q

Why does endothelial cell damage cause thrombosis?

A

Endothelial damage disrupts the protective function of endothelial cells, increasing the risk for thrombosis.

  1. Block exposure to subendothelial collagen and underlying tissue factor
  2. Produce prostacyclin (PGI2) and NO-vasodilation and inhibition of platelet aggregation
  3. Secrete heparin-like molecules-augment antithrombin III (ATIII), which inactivates thrombin and coagulation factors
  4. Secrete tissue plasminogen activator (tPA)- converts plasminogen to plasmin,
    which (l) cleaves fibrin and serum fibrinogen, (2) destroys coagulation factors,
    and (3) blocks platelet aggregation
  5. Secrete thrombomodulin- redirects thrombin to activate protein C, which inactivates factors V and VIII
62
Q

What are some causes of endothelial damage?

A

Causes of endothelial cell damage include atherosclerosis, vasculitis, and high levels
of homocysteine.

63
Q

Why can high levels of homocysteine result?

A

$ 1. Vitamin B12 and folate deficiency result in mildly elevated homocysteine levels,
increasing the risk for thrombosis.

  • i. Folic acid (tetrahydrofolate, THF) circulates as methyl-THF in the serum.
  • ii. Methyl is transferred to cobalamin (vitamin Bl2), allowing THF to participate in the synthesis of DNA precursors.
  • iii. Cobalamin transfers methyl to homocysteine resulting in methionine.
  • iv. Lack of vitamin Bl2 or folate leads to decreased conversion of homocysteine to methionine resulting in buildup of homocysteine.

2.$ Cystathionine beta synthase (CBS) deficiency results in high homocysteine levels with homocystinuria.

  • i. CBS converts homocysteine to cystathionine; enzyme deficiency leads to
  • homocysteine buildup.
  • ii. Characterized by vessel thrombosis, mental retardation, lens dislocation, and
  • long slender fingers.
64
Q

What causes a hypercoagulable state?

A

Due to excessive procoagulant proteins or defective anticoagulant proteins; may be inherited or acquired

65
Q

Classic presentation of hypercoagulable state?

A

Classic presentation is **recurrent DVTs or DVT at a young age. **Usually occurs in the deep veins of the leg; other sites include hepatic and cerebral veins.

66
Q

Protein C or S deficiency

A
  • *Protein C or S deficiency (autosomal dominant) decreases negative feedback on the coagulation cascade.**
    1. Proteins C and S normally inactivate factors V and VIII.
  • *$ 2. Increased risk for warfarin skin necrosis**
  • i. Initial stage of warfarin therapy results in a temporary deficiency of proteins C and S (due to shorter half-life) relative to factors II, VIT, TX, and X
  • ii. In preexisting C or S deficiency, a severe deficiency is seen at the onset of warfarin therapy increasing risk for thrombosis, especially in the skin.
67
Q

Most common inherited cause of hypercoagulable state

A

factor V Leiden is a mutated form of factor V that lacks the cleavage site for deactivation by proteins C and S. C+S shut it down by cleaving it.

68
Q

Prothrombin 202l0A

A

Prothrombin 202lOA is an inherited point mutation in prothrombin that results in increased gene expression.
1. Increased prothrombin results in increased thrombin, promoting thrombus formation.

69
Q

ATIll deficiency

A

A TIll deficiency decreases the protective effect of heparin-like molecules produced by the endothelium, increasing the risk for thrombus.

  1. Heparin-like molecules normally activate ATIII, which inactivates thrombin and coagulation factors.
  2. In ATIll deficiency, PTT does not rise with standard heparin dosing.
  • i. Pharmacologic heparin works by binding and activating ATlll.
  • ii. High doses of heparin activate limited ATIII; coumadin is then given to maintain an anticoagulated state.
70
Q

MOA of OCP increasing risk for thrombosis?

A

Estrogen induces increased production of coagulation factors, thereby increasing the risk for thrombosis.

71
Q

Amniotic fluid embolus

A

Amniotic fluid embolus enters maternal circulation during labor or delivery

$ 1. Presents with shortness of breath, neurologic symptoms, and DIC (due to the thrombogenic nature of amniotic fluid - loaded with tissue thromboplastin)
2. Characterized by squamous cells and keratin debris, from fetal skin, in embolus

Pathoma (8 decks)

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