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OSI (CAMELITA) > Hemodynamic Derangements > Flashcards

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
Q

Von Willebrand Disease

A
  • 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
Q

_________ normally stabilizies FVIII.

A

vWF

27
Q

Ristocetin test

A
  • Ristocetin incudes platelet agglutination by causing vWF to bind platelet GPIb
    • Lack of vWF, leads to impaired agglutination and an abnormal test
28
Q

Vitamin K is activated by ________ in the liver.

A

Epoxide reductase

29
Q

Vitamin K is important for which factors function?

A

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
Q

In what cases does Vitamin K deficiency occur?

A
  • 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
Q

Disseminated intravascular coagulation (DIC)

A
  • 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
Q

DIC is almost always secondary to another disease process. What are some examples?

A
  • 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
Q

Laboratory findings of DIC

A
  • Decreased platelet count
  • increase PTT/PT
  • Decreased fibrinogen
  • Microangiopathic hemolytic anemia
  • Elevated fibrin slit products, particular D-dimer
34
Q

Fibrinolysis

A

Normal fibrinolysis removes thrombus after famged vessel heals

35
Q

_____________ coverts plasminogen to plasmin.

A

Tissue plasminogen activator (tPA)

NOTE: plasmin cleaves fibrin and serum fibrinogen, destroys coagulation factors, and blocks platelet aggregation

36
Q

________________ inactivates plasmin.

A

a2- antiplasmin

37
Q

Plasmin overactivity can result in disorders of fibrolysis. In what disorders is overactivity of plasmin seen?

A
  • Radical prostatectomy- Release of urokinase activates plasmin
  • Cirrhosis of liver- reduced production of a2-antiplasmin
38
Q

What are the laboratory finds of disorders of fibrolysis?

A
  • Increased PT/PTT- Plasmin destroys coagulation factors
  • Increased bleeding time with normal platelet count
  • Increased fibrinogen split products without D-dimers
39
Q

treatment for disorders of fibrinolysis

A

Aminocarproic acid, which blocks activation of plasminogen

40
Q

What are the characteristics of pre-mortem thrombi?

A
  • Lines of Zahn
  • Attachment to vessel wall
41
Q

Risk factors for disruption in normal blood flow

A
  • Immobilization
  • Cardiac wall dystfunction
  • Aneurysm

NOTE: All of these factors can lead to thrombosis

42
Q

How do endothelial cells prevent thrombosis?

A
  • 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
Q

Causes of endothelial cell damage

A
  • Atherosclerosis
  • Vasculitis
  • High levels of homocysteine
44
Q

Cystathonine beta synthase deficiency

A
  • Results in high levels of homocysteine
    • Cystathonine converts homocystein to cystathonine
  • Characterized by: Vessel thrombosis, mental retardation, lens dislocation, and long slender fingers
45
Q

Initial stage of __________therapy results in a terporary deficiency of proteins C and S relative to facrtors II, VII, IX, and X.

A

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
Q

___________ is a mutated form of factor V that lacks the cleavage site for deactivation by proteins C and S.

A

Factor V Leiden

NOTE: This is the most common inherited cause of hypercoagulable state

47
Q

Oral contraceptives are associated with a hypercoagulable state. Why?

A

Estrogen induces increased productopn of coagulation factors

48
Q

Atherosclerotic embolus

A
  • Due to an athersclerotic plaque that dislodges
  • Characterized by the presence of cholesterol clefts in the embolus
49
Q

Fat embolus

A
  • 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
Q

Gas embolus

A
  • 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
Q

Amniotic fluid embolus

A
  • 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
Q

Veins usually involved in DVT

A

Femoral, iliac, and popliteal veins

53
Q

Characteristics of a pulmonary infarction

A
  • 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
Q

Damage to what three organs are most likely to cause edema?

A

Heart

Liver

Kidney

55
Q

What is the most common site of turbelent blood flow?

A

Dilated left atrium

Other causes: Hyperviscocity, sickle cell anemia

56
Q

Where do superficial venous thombosis normally occur?

A

Saphenous vein

NOTE: Superficial venous thrombosis predisposes to skin infections and ulcers. Rarely embolize

57
Q

Paradoxical embolus

A
  • DVT to system
  • Congenital heart defect (atrial septal or ventricular septal defect)
58
Q

What are the neurologic symptoms of ft and marrow embolism?

A

Irritable, Restless, Delirium and Coma

59
Q

With cardiogenic and hypovolemic shock, what happens to cardiac output and peripheral resistance?

A

Decrease in CO

Increase in Peripheral resistance

60
Q

With anaphylatic, septic, and neurogenic shock, what happens to cardiac output and peripheral resistance?

A

Increase in CO

Decrease in peripheral resistance

OSI (CAMELITA) (38 decks)

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