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STEP 6: HemeOnc PATHOMA > Thrombosis > Flashcards

Thrombosis Flashcards

1
Q

How does one distinguish between a thrombus (pre-death clot) and a post-mortem clot (clot that forms after death due to blood stasis)? 2 FEATURES

A
  1. LINES OF ZAHN (alternating lines of RBC and platelets/fibrin)
  2. Attachment to vessel wall
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2
Q

What is the Virchow triad (risk factors for thrombosis)?

A
  1. Disruption to blood flow
  2. Endothelial cell damage
  3. Hypercoagulable state
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3
Q

What molecules are released by the endothelium that make it inherently anti-thrombogenic?

A

Mnemonic: ‘PHTT’

  1. PGI2 + NO - Block platelet aggregation, vasodilation
  2. HEPARIN-LIKE MOLECULE - Increases Anti-thrombin III (ATIII) production, which inactivates thrombin and other coag factors
  3. THOMBOMODULIN - Modulates thrombin by redirecting it to activate Protein C, which inactivates FV and FVIII
  4. tPA - Increases plasminogen conversion to plasmin
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4
Q

Where is the most common location of THROMBOSIS (Intravascular blood clot)?

A

DEEP VEIN OF LEG below knee = DVT (DEEP VEIN THROMBOSIS)

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5
Q

What are 3 causes of stasis (VIRCHOW TRIAD #1) and thus increasing risk of thrombosis?

A
  1. IMMOBILIZATION - Surgery or flight on plane
  2. ARRHYTHMIA, VENTRICULAR WALL DYSFUNCTION - No atrial contraction or stasis of blood flow ejection
  3. ANEURYSM (Dilatation of BV wall allows for greater turbulent flow)
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6
Q

What are 3 causes of endothelial damage (VIRCHOW TRIAD #2) and thus increasing risk of thrombosis?

A
  1. ATHEROSCLEROSIS
  2. VASCULITIS
  3. INCREASED SERUM HOMOCYSTEINE
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7
Q

What are two ways a pt can have INCREASED SERUM HOMOCYSTEINE, resulting in endothelial damage and increased risk of thrombosis?
(Hint: Nutrient deficiency, Genetic disease)

A
  1. VitB12 or FOLATE DEFICIENCY - FOLATE transfers methyl group to VitB12, VitB12 transfers methyl group to Homocys to form Methionine. Without VitB12 or Folate, SERUM HOMOCYS will INCREASE
  2. CYSTATHIONINE BETA SYNTHASE DEFICIENCY - Cystathione beta synthase converts HOMOCYS to CYSTATHIONINE. Results in INCREASED SERUM HOMOCYS and HOMOCYSTINURIA
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8
Q

Which lab finding makes CYSTATHIONE BETA SYNTHASE DEFICIENCY highly likely?

A

HOMOCYSTINURIA

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9
Q

Vessel thrombosis + Mental Retardation + Lens dislocation + Long, slender fingers
What am I signs of? What genetic disease could I be?

A

Signs of HOMOCYSTINURIA
Vessel thrombosis - Due to elevated homocys levels -> Endothelial damage -> Virchow triad of thrombosis #2

CYSTATHIONE BETA SYNTHASE DEFICIENCY

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10
Q

What are 3 possible etiologies of DISRUPTION IN BLOOD FLOW (VIRCHOW TRIAD #1) increasing the risk of THROMBOSIS?

A
  1. IMMOBILIZATION - Blood stasis activating coagulation cascade
  2. CARDIAC WALL DYSFUNCTION - Arrhythmia (e.g. Afib) or MI -> Blood stasis
  3. ANEURYSM - Balloon-like dilatation of the BV -> Turbulent blood flow -> Activation of coag cascade
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11
Q

What are the 4 inherited diseases that result in a HYPERCOAGULABLE STATE? (VIRCHOW TRIAD #3)

A

‘2 involving Factor V, 2 involving thrombin’

  1. PROTEIN C/S DEFICIENCY - Too much Factor V and VIII
  2. FACTOR V LEIDEN MUTATION - Mutation that affects the cleavage site for deactivation by Protein C/S
  3. PROTHROMBIN20210A - Point mutation that results in INCREASED PROTHROMBIN -> Increased thrombin
  4. ATIII DEFICIENCY - DECREASED ATIII that can bind to endothelium protective factor (HLM) -> Decreased inactivation of thrombin and other coag factors -> Increased thrombin
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12
Q

How do pts with a PROTEIN C/PROTEIN S DEFICIENCY have an INCREASED RISK of WARFARIN-INDUCED SKIN NECROSIS?

A

Warfarin -> Inhibits HEPATIC EXPOXIDE REDUCTASE -> Inhibits VitK activation -> Inhibits activation of factors 2,7,9,10, C,S

Proteins C and S have a shorter half-life -> 2,7,9,10 (PRO-COAGULANT factors) will be around longer -> Increased THROMBOSIS in skin -> Necrosis

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13
Q

In a pt with a HYPERCOAGULABLE STATE, how come WARFARIN + HEPARIN need to be administered simultaneously for a particular window?

A

WARFARIN -> Inhibits epoxide reductase -> Inhibits VitK -> Inhibits PROTEIN C and PROTEIN S first (shorter half-lives) -> FACTORS 2,7,9,10 are lying around longer (EVEN MORE HYPERCOAGULABLE -> SKIN NECROSIS)

Need to administer HEPARIN during this window to avoid HYPERCOAGULABLE STATE-MEDIATED SKIN NECROSIS

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14
Q

What is the MOST COMMON inherited cause of hypercoagulable state?

A

FACTOR V LEIDEN

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15
Q

Normally what lab value is used to measure the effect of HEPARIN? Will this value increase in standard dosing of HEP in pts with ATIII DEFICIENCY with recurrent DVTs?

A

PTT
ATIII deficiency will NOT show an INCREASED PTT because standard dose of HEP doesn’t have the ATIII to bind to. ATIII can not act to block thrombin and other coagulation factors

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16
Q

What is the treatment plan for ATIII DEFICIENT PTS with a recurrent DVT?

A
  1. HIGH DOSES OF HEP - Will bind to and activate the limited ATIII
    2 COUMADIN - For maintenance of anti-coagulated state once the safety window of coumadin/warfarin skin necrosis is passed
17
Q

Which medication is associated with a hypercoagulable state? How?

A

ORAL CONTRACEPTIVES

ER - Induces INCREASED production of coagulation factors -> Increases risk of thrombosis

18
Q

MOIST mneumonic of HYPERCOAGULABLE STATE (VIRCHOW TRIAD #3) for increased risk of thrombosis

A 
M - malignancy, motherhood/pregnancy 
O - oral contraceptives
I - immobilization 
S - surgery 
T - trauma, thrombophilic disorder (Protein C/S Def, Factor V Leiden Mut, Prothrombin20210, ATIII Def), thrombophilic event (MI, Afib, aneurysm)
19
Q

What are the 5 types of EMBOLI? Which is the most common?

A
  1. THROMBOEMBOLUS ***- MOST COMMON
  2. ATHEROSCLEROTIC EMBOLUS
  3. FAT EMBOLUS
  4. GAS EMBOLUS
  5. AMNIOTIC FLUID EMBOLUS
20
Q

Cholesterol clefts in embolus

What am I?

A

ATHEROSCLEROTIC EMBOLUS

21
Q

What events can elicit a FAT EMBOLUS dislodging into pulm vessels, which explains why DYSPNEA is a common presenting Sx?

A
  1. LONG BONE FRACTURES

2. SOFT TISSUE TRAUMA

22
Q

Name two etiologies of GAS EMBOLUS formation?

A
  1. DECOMPRESSION SICKNESS - When a diver rapidly ascends from depths, N2 gas precipitates out of blood
  2. LAPARASCOPIC SUGERY - Air is pumped into the abdomen during laparascopic surgery -> Air bubbles precipitate out of the blood
23
Q

What are the Sx of decompression sickness and subsequent gas embolus formation? What is the chronic form of decompression sickness, and what is the CP of this form? BE

A

BENDS (Joint and muscle pain - N2 precipitation onto joints and muscle tissue) and CHOKES (Dyspnea - N2 precipitation onto pulm circulation)

CAISSON = Chronic form of decompression sickness
MULTIFOCAL ISCHEMIC NECROSIS of bones - chronic N2 precipitation onto bones

24
Q

Pregnant mother with DYSPNEA + NEUROLOGICAL Sx + DIC (unstoppable bleeding)
What is pathophysiologically going on?

A

During labor or delivery, pregnant mother had an AMNIOTIC FLUID EMBOLUS dislodging in the lungs (DYSPNEA), brain (NEURO SX).

TISSUE FACTOR/THROMBOPLASTIN from the amniotic fluid activated the coag cascade -> DIC

25
Q

Squamous cells + Keratin debris in BV

What am I?

A

AMNIOTIC FLUID EMBOLUS

Sloughed fetal skin in the amniotic fluid

26
Q

What are the 2 requirements of a HEMORRHAGIC INFARCT?

A
  1. Blood needs to RE-ENTER the dead tissue

2. Dead tissue needs LOOSE CONSISTENCY to hold the blood in and reveal “HEMORRHAGE”

27
Q

What is the most common source of systemic embolus? What is the most common location of lodging of that systemic embolus?

A

LEFT HEART

Lodging onto BV that supply LOWER EXTREMITIES (popliteal, femoral, iliac vein)

STEP 6: HemeOnc PATHOMA (8 decks)

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