Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Tintinalli Section 18 - Hematologic and Oncologic Emergencies > S18C229 - Clotting disorders > Flashcards

S18C229 - Clotting disorders Flashcards

1
Q

Virchow’s triad of thrombus

A
  • venous stasis
  • hypercoagulability
  • endothelial injury
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Hypercoagulable states: inherited

A
  • activated protein C resistance due to factor V leiden mutation
  • prothrombin gene mutation 20210A
  • protein c deficiency
  • protein s deficiency
  • antithrombin deficiency
  • hyperhomocysteinemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Hypercoagulable states: acquired

A
  • antiphospholipid syndrome
  • pregnancy
  • OCP/HRT
  • malignancy
  • HIT
  • warfarin induced skin necrosis
  • hyperviscosity syndrome
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Antithrombin

A
  • inhibits thrombin, factor Xa, factor IXa

- UFH/LMWH cause anticoagulation by increasing the rate at which antithrombin inhibits these factors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

what does it mean if a behind factor? eg. Xa

A

that it is activated

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Protein C

A
  • vit K dependent protein that binds to endothelial cells
  • activated by thrombin
  • cleaves factor Va and factor VIIIa, and therefore inhibits the common and intrinsic pathway
  • homozygous is rare, presents as neonatal purpura fulminans
  • higher risk for warfarin-induced skin necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Protein S

A
  • cofactor for protein C
  • also vit K dependent
  • increases the inhibitory action of activated protein C
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Features suggestive of Thrombophilia

A

-early thrombosis (age

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Management of Inherited/Acquired thrombophilias (hypercoagulable)

A
  • first episode: UFH/LMWH x5d until warfarin therapeutic
  • continue AC tx for 6mo-2y, possibly life
  • can just go straight onto a DOAC

-2nd episode : life long AC

  • pregnancy: begin UFH or LMWH at diagnosis of pregnancy
  • may use warfarin in post-partum period
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Factor V Leiden mutation - activated protein C resistancw

A
  • most prevalent hypercoagulable d/o
  • mutation in factor Va makes it resistant to inhibition by activated protein C and therefore there is an increase in conversion of prothrombin to thrombin` and more fibrin and excessive thrombus
  • most are heterozygous
  • have a 7x increase in DVT (homozygotes 20x)
  • 21% of pts with first time DVT will have FVL deficiency/mutation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Prothrombin gene mutation 20210A

A
  • mutation leads to increased prothrombin biosynthesis with 30% increase in circulating prothrombin levels
  • causes a hypercoagulable state
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Antithrombin Deficiency

A

-can be deficient in patients due to mutations
-2 main groups:
type 1: measured level of antithrombin is decreased
type 2: normal level of antithrombin but fxn diminished

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Hyperhomocysteinemia

A
  • 3 enzymes involved in metabolism of homocysteine
  • deficiency in 2 of the enzymes causes incr arterial/venous thrombosis and atherosclerosis
  • if incr homocysteine in the blood this is a sign of functional enzyme deficiency
  • can have mental retardation, dvpt delay as well
  • unknown mechanism
  • tx: folate, pyridoxine, vit B12
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Antiphospholipid Syndrome

A
  • antibodies assoc with APS: beta2-glycoprotein I and Lupus anticoagulant
  • procoagulant, causes thrombosis (clots)
  • acquired
  • occurs in 1 in 5 patients
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Clinical signs of APS

A
  • venous: DVT
  • arterial: premature atherosclerosis, ACS, CVA
  • obstetric: fetal loss after 10w GA, preterm labor, low BW, preeclampsia
  • neuro: stroke, migraine, seddon syndrome (Stroke, HTN, livedo reticularis), cognitive dysfxn, dementia, chorea, dysphagea, GBS, Sz, optic neuritis
  • skin: livedo reticularis
  • cardiac: syndrome X, valvular dz
  • skeletal: osteonecrosis
  • renal: microangiopathy, renal artery/vein thrombosis, stenosis with HTN
  • pulmonary: PE, HTN
  • GI: budd chiari syndrome, mesenteric ischemia, hepatic infarction, cholecystitis with gallbladder necrosis
  • hematologic: bleeding deathesis (Rare), thrombocytopenia, hemolytic anemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

APS Dx

A
  • one or more thrombotic events or pregnancy losses and repeated positive results for one or more AP antibodes at least 6w apart
  • presence of antibodies can be transient, therefore absence of lab findings should not dissuade the dx
17
Q

APS Tx

A
  • IV heparin - keeping in mind that the activate thromboplastin time may not be useful for determining efficacy as this test is abnormal in APS
  • if known hx but no thrombotic hx then do not treat prophylactically unless pregnant
18
Q

Pregnancy and hypercoagulability

A
  • occurs to prevent excess hemorrhage during delivery
  • increased estrogen is part of what increases coagulability (increases factors 7,8,10, prothrombin and fibrinogen) and decreases antigoagulant proteins (antithrombin, protein S, C)
  • OCP also causes protein C resistance
  • factors making pregnancy hypercoagulable: venous occlusion from uterus, increased thrombin and procoagulants, decreased protein C
19
Q

Malignancy and hypercoagulability

A
  • pts with 1st time episode of VTE 10-20% will have new dx of cancer in previous 6mo or following year
  • risk of VTE is highest in 1st 3mo after dx
  • the following have increased risk of VTE: brain, pancreatic, AML, gastric, espophageal, gyne, kidney, lung
  • cancer also increases risk of arterial clot (MI, CVA)
20
Q

HIT

A
  • consumptive coagulopathy similar to TTP and DIC but in DIC coag factors are consumed and in HIT there is activation and consuption of platelets
  • pts develop IgG Abs against the heparin-PF4 complex
  • do not need to have been exposed to heparin to develop antibody
  • heparin-Ab complex binds and activates platelets fomring clot and setting off cascade
  • can be caused by unfractionated and LMWH
  • occurs in 0.5-5% of pts
21
Q

HIT: Dx

A
  • usually have low platelets (50) w/in 5-15d of starting heparin
  • 10% will need amputation and 20-30% will die w/in 1mo
  • lab dx, not clinical
  • suspect if platelets have dropped by 50% in pt on or recently on heparin
  • can have rapid onset w/in hours of initiating heparin
  • platelets normalize 1w after stopping heparin
22
Q

HIT: Tx

A
  • stop all heparin products
  • will still need AC b/c risk of thrombosis highest in 1st wk after dx (argatroban) don’t use warfarin b/c this can increase microvascular thrombosis b/c transient protein C deficiency
23
Q

Warfarin induced skin necrosis

A
  • inhibits production of vit K coag factors (1972, C)
  • transient C deficiency can lead to hypercoagulability
  • painful red lesions over extremities, breasts, trunk, penis
  • initial central erythenatous macule then edema, then central purpuric zones then necrosis
  • therefore bridge with heparin and avoid high loading doses of warfarin

Tintinalli Section 18 - Hematologic and Oncologic Emergencies (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions