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Hemodynamic Derangements Flashcards

1
Q

What are the steps to primary hemastasis?

A
  1. Transient vasoconstriction of damaged vessel
    * Mediated by reflex neural stimulation and endothelin release from endothelial cell
  2. Platelet adhesion
  • vWF binds to exposed subendothelial collagen
  • Platelets bind vWF using the GPIb receptor
  1. Platelet degranulation
    * Release of ADP and TX2
  2. Platelet aggregation
    * Via GPIIb/IIIa using fibrinogen as a linking molecule
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2
Q

Where is vWF released from?

A

Weibel-Palade bodies of endothelial cells and alpha-granules of platelets

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3
Q

Role of ADP in primary hemostasis

A

Promotes exposure of GPIIb/IIIa receptor on platelets

NOTE: ADP is released from platelet dense granules

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4
Q

Role of TX2 in primary hemastasis

A
  • Promotes platelet aggregation

NOTE: TX2 is synthesized by platele cyclooxygenase

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5
Q

Immune Thrombocytopenic Purpura (ITP)

A
  • IgG against platelet antigens
    • Antibodies are produced by plasma cells in the spleen
    • Antibody-bound platelets are consumed by splenic macrophages; resulting in thrombocytopenia
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6
Q

Laboratory findings of ITP

A
  • Decreased platelet count
  • Normal PT/PTT
  • Increased megakaryocytes on bone marrow biopsy
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7
Q

Treatment of ITP

A
  • Corticosteroids (initial)
    • Children respond well. Adults may show early response but often relapse
  • IVIG (gives antibodies something else to bind to for a moment)
  • Splenectomy
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8
Q

Microangiopathic Hemolytic Anemia

A
  • Pathologic formation of platelet microthrombi in small vessels
  • Hemolytic anemia with schistocytes
  • Seen in thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic syndrome (HUS)
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9
Q

TTP is due to decreased __________.

A

ADAMTS13

NOTE: This is an enxzyme that normally cleaves vWF multimers into smaller monomers for eventual degradation

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10
Q

HUS

A
  • Due to damage by drugs or infection
  • Seen in children with E. coli O157:H7 dysentery, which results from exposure to undercooked beef
  • E.coli verotoxin damges endothelial cells resulting in platelet microthrombi
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11
Q

What are the clinical findings of HUS and TTP?

A
  • Skin and mucousal bleeding
  • Microangiopathic hemolytic anemia
  • Fever
  • Renal insufficiency (more common in HUS)
  • CNS abnormalities (more common in TTP)
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12
Q

Treatment for microangiopathic hemolytic anemia

A

Plasmapheresis and corticosteriods, particularly in TTP

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13
Q

What are the laboratory findings of microangiopathic hemolytic anemia?

A
  • Thrombocytopenia with increased bleeding time
  • Normal PT/PTT
  • Anemia with schistocytes
  • Increased megakaryocytes on bone marrow biopsy
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14
Q

Bernard-Soulier syndrome

A
  • Genetic GPIb defiency
  • Qualitative
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15
Q

Glanzmann thromboasthenia

A
  • Genetic GPIIb/IIIa deficiency
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16
Q

Role of thrombin

A

Converts fibrinogen to fibrin

NOTE: Thrombin is produced through the coagulation cascade

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17
Q

Factors of the coagulation cascade are produced by the _________ in an inactive state.

A

Liver

Activation requires:

  • Exposure to an activating substance
  • Phospolipid surface of platelets
  • Calcium
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18
Q

___________ activates factor VII.

A

Tissue thromboplastin

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19
Q

_________ activates factor XII.

A

Subendothelial collagen

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20
Q

PT measures…

A

Extrinsic (VII) and common (II, V, X, and fribrinogen) pathways

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21
Q

PTT measures…

A

Instrinsic (XII, XI, IX, VIII) and common (II,V,X, and fibrinogen) pathways

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22
Q

Hemophilia A

A
  • Factor VIII deficiency
  • X-linked recessive
  • Increased PTT; normal PT
  • Decreased VIII
  • Normal platelet count and bleeding time
  • Treatment: Recombinant FVIII

NOTE: PTT corrects with treatment

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23
Q

Hemophilia B

A
  • Genetic factor IX deficiency
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24
Q

Coagulation factor Inhibitor

A
  • Acquired antibody against a coagulation factor resulting in imparied factor function; anti-FVIII is most common
  • PTT does not correct upon mixing normal plasma with patient’s plasma
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25
Von Willebrand Disease
* Genetic vWF defiency * presents with mild mucousal and skin bleeding * Increased bleeding time * Increased PTT; normal PT * Abnormal ristocetin test * Treatment: Desmopressin (ADH analog), which increases vWF release from Weibel-Palade bodies of endothelial cells
26
\_\_\_\_\_\_\_\_\_ normally stabilizies FVIII.
vWF
27
Ristocetin test
* Ristocetin incudes platelet agglutination by causing vWF to bind platelet GPIb * Lack of vWF, leads to impaired agglutination and an abnormal test
28
Vitamin K is activated by ________ in the liver.
Epoxide reductase
29
Vitamin K is important for which factors function?
II, VII, IX, and X, and protein C and S **NOTE:** Activated vitamin K gamma carboxylates the above factors. Gamma carboxylation is necessary for factor function
30
In what cases does Vitamin K deficiency occur?
* Newborns (due to lack of GI colonization by bacteri that normally synthesize Vitamin K) * Long-term antibiotic therapy * Malabsorption * Liver failure * Decreased activation of vitamin K (due decreased production of epoxide reductase)
31
Disseminated intravascular coagulation (DIC)
* pathologic activation of the coagulation cascade * Widespread microthrombi result in ischemia and infarcation * Consumption of platelets and factors results in bleeding, especially from IV sites and mucosal surfaces
32
DIC is almost always secondary to another disease process. What are some examples?
* OB complications- Tissue thromboplastin in the amniotic fluid activates coagulation * Sepsis- Endotoxins from the bacterial wall and cytokines induce endothelial cells to make tissue factor * Adenocarcinoma- Mucin activates coagulation * Acute promyelocytic leukemia- primary ganulaes activate coagulation * Rattlesnale bite- Venom activates coagulation
33
Laboratory findings of DIC
* Decreased platelet count * increase PTT/PT * Decreased fibrinogen * Microangiopathic hemolytic anemia * Elevated fibrin slit products, **particular D-dimer**
34
Fibrinolysis
Normal fibrinolysis removes thrombus after famged vessel heals
35
\_\_\_\_\_\_\_\_\_\_\_\_\_ coverts plasminogen to plasmin.
Tissue plasminogen activator (tPA) **NOTE:** plasmin cleaves fibrin and serum fibrinogen, destroys coagulation factors, and blocks platelet aggregation
36
\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_\_ inactivates plasmin.
a2- antiplasmin
37
Plasmin overactivity can result in disorders of fibrolysis. In what disorders is overactivity of plasmin seen?
* Radical prostatectomy- Release of urokinase activates plasmin * Cirrhosis of liver- reduced production of a2-antiplasmin
38
What are the laboratory finds of disorders of fibrolysis?
* Increased PT/PTT- Plasmin destroys coagulation factors * Increased bleeding time with normal platelet count * Increased fibrinogen split products **without D-dimers**
39
treatment for disorders of fibrinolysis
Aminocarproic acid, which blocks activation of plasminogen
40
What are the characteristics of pre-mortem thrombi?
* Lines of Zahn * Attachment to vessel wall
41
Risk factors for disruption in normal blood flow
* Immobilization * Cardiac wall dystfunction * Aneurysm **NOTE:** All of these factors can lead to thrombosis
42
How do endothelial cells prevent thrombosis?
* Block exposure to subendothelial collage and underlying tissue factor * Produce PGI2 and NO (vasodilation and inhibition of platelet aggregation) * Secrete heparin like molecules * Augment antithrombin III (ATIII), which inactivates thrombin and coagulation factors * Secrete tPA * Secrete thrombomodulin * Redirects thrombin to activate protein C, which inactivates factors V and VIII
43
Causes of endothelial cell damage
* Atherosclerosis * Vasculitis * High levels of homocysteine
44
Cystathonine beta synthase deficiency
* Results in high levels of homocysteine * Cystathonine converts homocystein to cystathonine * Characterized by: Vessel thrombosis, mental retardation, lens dislocation, and long slender fingers
45
Initial stage of **\_\_\_\_\_\_\_\_\_\_**therapy results in a terporary deficiency of proteins C and S relative to facrtors II, VII, IX, and X.
Warfarin **NOTE:** In preexisting C or S deficiency, a severe deficiency is seen at the onset of warfarin therapy increasing rsik for thrombosis, especially in the skin.
46
\_\_\_\_\_\_\_\_\_\_\_ is a mutated form of factor V that lacks the cleavage site for deactivation by proteins C and S.
Factor V Leiden **NOTE:** This is the most common inherited cause of hypercoagulable state
47
Oral contraceptives are associated with a hypercoagulable state. Why?
Estrogen induces increased productopn of coagulation factors
48
Atherosclerotic embolus
* Due to an athersclerotic plaque that dislodges * Characterized by the presence of cholesterol clefts in the embolus
49
Fat embolus
* Associated with bone fractures, particularly long bones, and soft tissue trauma * Develops while fracture is still present or shortly after repair * Characterized by dyspnea, and petechiae on the skin overlying the chest
50
Gas embolus
* Classically seen in decompression sickness * Presents with joint and muscle pain (bends) and respiratory symptoms (chokes) * Chronic form: Caisson disease * Multifocal ischemic necrosis of bone * May occur during laparoscopic surgery
51
Amniotic fluid embolus
* Enters materanl circulation during labor or delivery * Presents with shortness of breath, neurologic symptoms, and DIC * Characterizedby squamous cells and keratin debris, from fetal skin, in embolus
52
Veins usually involved in DVT
Femoral, iliac, and popliteal veins
53
Characteristics of a pulmonary infarction
* Hemorrhagic, wedge-shaped infarct * D-dimer * Lower extremity doppler sound * Sudden death occurs with a **large saddle embolus** that blocks both left and right pulmonary arteries or with significant occlusion of a large pulmonary artery
54
Damage to what three organs are most likely to cause edema?
Heart Liver Kidney
55
What is the most common site of turbelent blood flow?
Dilated left atrium **Other causes:** Hyperviscocity, sickle cell anemia
56
Where do superficial venous thombosis normally occur?
Saphenous vein **NOTE:** Superficial venous thrombosis predisposes to skin infections and ulcers. Rarely embolize
57
Paradoxical embolus
* DVT to system * Congenital heart defect (atrial septal or ventricular septal defect)
58
What are the neurologic symptoms of ft and marrow embolism?
Irritable, Restless, Delirium and Coma
59
With cardiogenic and hypovolemic shock, what happens to cardiac output and peripheral resistance?
Decrease in CO Increase in Peripheral resistance
60
With anaphylatic, septic, and neurogenic shock, what happens to cardiac output and peripheral resistance?
Increase in CO Decrease in peripheral resistance

OSI (CAMELITA) (38 decks)

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