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CHEST SEEK Library > Hematology and Oncology Disorders > Flashcards

Hematology and Oncology Disorders Flashcards

1
Q

recent RCTs comparing the use of fresh or “young” RBC transfusion w/ “older” units w/ longer storage time in critically ill adults have shown what?

A

more febrile, nonhemolytic transfusion reactions in patients receiving younger units

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2
Q

systemic autoimmune d/o characterized by the presence of antiphospholipid Abs

A

APS (antiphospholipid syndrome)

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3
Q

one of the most commonly acquired thrombophilias and is unique from most genetic thrombophilias because of it a/w BOTH arterial AND venous thromboses

A

APS (antiphospholipid syndrome)

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4
Q

what are the most common venous and arterial sites of involvement of thrombosis in APS (antiphospholipid syndrome)?

A
  • DVT of the lower extremities
  • cerebral arterial circulation
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5
Q

thrombosis in unusual sites such as, hepatic veins, visceral veins, cerebral venous circulation, should prompt consideration for

A

APS (antiphospholipid syndrome)

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6
Q

is a/w significant obstetric morbidity
- should be considered in the setting of an unexplained death of ≥ 1 morphologically normal fetuses ≥ 10 weeks of gestation
- premature birth of ≥ 1 neonates before 34 weeks of gestation because of eclampsia or severe preeclampsia
- or ≥ 3 unexplained, consecutive spontaneous abortions before the tenth week of gestation

A

APS (antiphospholipid syndrome)

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7
Q

other manifestations of APS (antiphospholipid syndrome)

A
  • thrombocytopenia
  • autoimmune hemolytic anemia
  • nonbacterial cardiac valve thickening or vegetations
  • livedo reticularis
  • skin ulcers
  • TIAs
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8
Q

aPTT and mixing study in APS (antiphospholipid syndrome)

A
  • often prolonged
  • does NOT correct w/ mixing study
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9
Q

clinical criteria for diagnosis of APS (antiphospholipid syndrome)

A
  • confirmed thrombotic event, or
  • confirmed obstetric morbidity
  • combined w/ presence of a lupus anticoagulant (IgM or IgG isotype anticardiolipin Abs (medium-high titer), or IgM or IgG subtype anti-β2-glycoprotein I antibodies (titer >99th percentile))
  • confirmed on ≥ 2 occasions at least 12 weeks apart
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10
Q

rare complication of APS defined as small vessel thrombosis in ≥ 3 organs in < 1 week

A

catastrophic APS (CAPS)

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11
Q

catastrophic APS (CAPS) is often triggered by

A
  • infection
  • malignancy
  • another acute precipitating event
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12
Q
  • most commonly affects women in their 30s
  • a/w mortality rates of 40-50% d/t cerebral and cardiac thrombosis, infection a/w treatment, and multiorgan failure
A

catastrophic APS (CAPS)

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13
Q

diagnosis of catastrophic APS (CAPS)

A

requires objective demonstration of microvascular thrombosis w/o vessel inflammation to suggest an underlying vasculitis

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14
Q

PBS of catastrophic APS (CAPS) often demonstrates

A
  • microangiopathic hemolytic anemia (MAHA)
  • schistocytes
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15
Q

current guidelines for management of catastrophic APS (CAPS)

A
  • heparin gtt
  • corticosteroids to reduce proinflammatory cytokine production
  • IVIG or plasma exchange in severe cases
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16
Q

treatment of catastrophic APS (CAPS) a/w SLE

A
  • cyclophosphamide
  • rituximab or eculizumab in refractory cases
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17
Q

long-term AC for catastrophic APS (CAPS) in patients who respond to initial treatment

A

warfarin

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18
Q

what conditions are a/w higher mortality in catastrophic APS (CAPS)?

A
  • older patients
  • underlying SLE
  • higher Charlson Comorbidity Index (CCI)
  • higher day 0 Simplified Acute Physiology Score II (SAPS)
  • higher SOFA score
  • renal and neurological involvement
  • hemorrhagic events
  • macrovascular arterial thrombosis
  • low hb
  • persistently low thrombocytopenia (likely indicating diffuse, ongoing microangiopathy)
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19
Q

what is the Charlson Comorbidity Index (CCI)?

A

predicts 10-year survival in patients w/ multiple comorbidities

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20
Q

what is the Simplified Acute Physiology Score (SAPS)?

A

estimates mortality in ICU patients; comparable to APACHE II

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21
Q

what is the Sequential Organ Failure Assessment (SOFA) score?

A

predicts ICU mortality based on lab results and clinical data

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22
Q
  • mild, transient drop in platelet count
  • typically occurs w/i the first 2 days of heparin exposure
A

heparin-induced thrombocytopenia type 1 (HIT 1)

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23
Q

mechanism of HIT 1

A

direct effect of heparin on platelets, causing non-immune platelet aggregation

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24
Q

clinically significant syndrome d/t Abs to platelet factor 4 (PF4) complexed to heparin, referred to as “HIT Abs” or “PF4/heparin Abs”

A

heparin-induced thrombocytopenia type 2 (HIT 2)

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25
Q

HIT 2 is aka

A

heparin-induced thrombocytopenia and thrombosis (HITT)

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26
Q

the risk of thrombosis, including life-threatening limb gangrene, from HIT 2 persists until what measures are taken?

A
  • heparin is eliminated, AND
  • non-heparin anticoagulant is initiated
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27
Q

what are HIT variants?

A

clinical HIT d/t HIT Abs that activate platelets in the ABSENCE of heparin

  • delayed-onset HIT
  • refractory (persistent) HIT
  • spontaneous HIT
  • VITT (vaccine-induced immune thrombotic thrombocytopenia)
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28
Q

delayed-onset HIT is defined by

A

thrombocytopenia and/or thrombosis occurring ≥ 5 days after heparin has been withdrawn

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29
Q

why might delayed-onset HIT occur?

A

high-titer Abs to PF4/heparin

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30
Q

refractory (persistent) HIT is defined as

A
  • persistent thrombocytopenia and/or thrombosis that last for weeks AFTER stopping heparin
  • the presence of HIT Abs alone does NOT define this condition
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31
Q

spontaneous HIT is described as

A
  • RARELY, HIT has been described in the absence of recent heparin exposure
  • most affected patients have a preceding infection or have undergone a major surgical procedure
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32
Q

what diagnostic criteria have been proposed for spontaneous HIT?

A
  • otherwise UNEXPLAINED thrombocytopenia and/or thrombosis w/o recent heparin exposure
  • demonstration of anti-PF4 Abs of IgG subclass that cause strong in vitro platelet activation in the absence of heparin
  • occurring in the setting of exposure to minimal amount of heparin
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33
Q

VITT (vaccine-induced immune thrombotic thrombocytopenia) is described as

A

a condition that may occur in individuals vaccinated w/ certain covid-19 vaccines (AstraZeneca, University of Oxford, and Serum Institute of India, and Janssen; Johnson & Johnson)

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34
Q

some patients produce Abs that react in laboratory assays for HIT but do NOT cause thrombocytopenia or thrombosis

A

heparin-induced Abs (HIA)

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35
Q

although there are similarities in clinical presentation between TMA (thrombotic microangiopathies) and CAPS, what are some key differences that may help differentiate them?

A
  • no schistocytes seen on PBS w/ TMA
  • likely underlying diagnosis of APS makes CAPS much more likely
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36
Q
  • aka typhlitis
  • necrotizing enterocolitis
  • typically develops in neutropenic patients, < 500 cells/µL
  • most commonly occurs following chemotherapy for acute hematologic malignancies (leukemia, lymphoma, MM), or immunosuppressive therapy for solid tumor malignancies and transplants
A

neutropenic enterocolitis

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37
Q

initial management of neutropenic enterocolitis

A
  • abx
  • supportive care
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38
Q

neutropenic enterocolitis has been reported in what infection?

A

HIV

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39
Q

pathophysiology of neutropenic enterocolitis

A

damage of gut mucosal barrier, necrosis, and hemorrhagic transmural inflammation of multiple layers of the bowel wall, resulting in impaired host defenses, and bacterial translocation

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40
Q

sepsis, bacteremia, and fungemia often develop in neutropenic enterocolitis; what are the organisms typically isolated?

A
  • Pseudomonas aeruginosa
  • Escherichia coli
  • Klebsiella spp
  • Bacteroides spp
  • Clostridium spp
  • Candida
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41
Q

clinical diagnosis of neutropenic enterocolitis

A
  • neutropenic host
  • fever (93%)
  • abdominal pain
  • characteristic abdominal CT findings
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42
Q

what are the characteristic CT abdominal findings in neutropenic enterocolitis?

A

bowel wall thickening; > 4 mm of the cecum and terminal ileum
- mesenteric fat stranding
- bowel dilation
- mucosal enhancement
- pneumatosis

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43
Q

ddx for neutropenic enterocolitis

A
  • CDI
  • colonic pseudo-obstruction (aka Ogilvie syndrome)
  • CMV colitis
  • GVHD in the setting of BMT
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44
Q

GVHD presentation

A
  • rash
  • diarrhea
  • abnormal liver function
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45
Q

treatment for colonic pseudo-obstruction (Ogilvie syndrome)

A
  • conservative; decompression w/ NGT
  • neostigmine if cecal diameter > 12 cm or 48-72 hours of conservative therapy has failed
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46
Q

subtype of acute myeloid leukemia (AML) that differs from other forms of AML because of its propensity to cause coagulopathy w/ DIC

A

acute promyelocytic leukemia (APL)

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47
Q

subtype of leukemia that mimics DIC w/ the following clotting tests abnormalities;

  • low fibrinogen level
  • thrombocytopenia
  • elevated PT
  • elevated thrombin time
  • elevated PTT
  • elevated fibrinogen degradation products
A

acute promyelocytic leukemia (APL)

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48
Q

what is a distinguishing feature in the diagnosis of acute promyelocytic leukemia (APL)?

A

Auer rods on PBS

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49
Q

leukemia subtype w/ translocation between chromosomes 15 and 17

A

acute promyelocytic leukemia (APL)

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50
Q

targeted therapy for acute promyelocytic leukemia (APL)

A

all-trans retinoic acid (ATRA)

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51
Q

what activates endothelial cells in CAPS?

A

anti-β2-glycoprotein

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52
Q

rare d/o characterized by overstimulation of the immune system, leading to systemic inflammation and multisystem organ failure

A

hemophagocytic syndromes (HPSs)

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53
Q

what are the poor prognostic factors of hemophagocytic syndromes (HPSs)?

A
  • a/w lymphoma
  • > 30 yoa
  • higher ferritin elevation
  • marked thrombocytopenia
  • male sex
  • low albumin
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54
Q
  • d/o infancy and childhood
  • caused by genetic mutations that impair the cytotoxic function of NK and cytotoxic T cells
A

primary hemophagocytic lymphohistiocytosis (HLH)

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55
Q
  • often a/w predisposing condition, malignancy (lymphoma), immunodeficiency, or infection (EBV)
  • can be referred to as macrophage activation syndrome when it occurs in a/w AI disease, such as juvenile idiopathic arthritis, adult-onset Still’s disease, and SLE
A

secondary hemophagocytic syndrome (HPS)

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56
Q

the diagnostic HLH guidelines proposed by the Histiocyte Society remain the most widely used criteria, but are poorly validated and exclude a number of manifestations, which are?

A
  • neurological involvement
  • rash
  • coagulopathy
  • hyponatremia
  • elevated transaminases
  • elevated LDH
  • low CRP
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57
Q

treatment for hemophagocytic syndromes (HPSs) is extrapolated from the pediatric literature which includes what?

A
  • dexamethasone
  • etoposide w/ or w/o cyclosporine A
  • doxorubicin
  • IVIG
  • ruxolitinib
  • anakinra
  • allogeneic SCT
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58
Q

treatment that be used for HLH when a/w lymphoma and EBV

A
  • cyclophosphamide, adriamycin, vincristine, prednisone (CHOP), and rituximab
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59
Q

what treatment can be considered in patients w/ HLH that have marked elevations in ferritin and LDH?

A

plasma exchange

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60
Q

treatment consideration for relapsed cases of HLH

A

splenectomy

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61
Q

a fall in platelet count after cardiopulmonary bypass (CPB) is expected to drop by how much and for how long?

A
  • 1/2
  • can persist for 4 to 6 days following surgery
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62
Q

anti-PF4 heparin ELISA testing is positive in what percentage of patient between post-op days 3 to 10 of CPB? and what percentage are confirmed to have HIT?

A
  • 25-50%
  • 1-4%
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63
Q

the risk-benefit ratio and timing of initiation of DVT chemoprophylaxis following cardiac surgery and CPB is controversial, but chemoprophylaxis can be safely initiated once post-op bleeding risk has declined which is usually by post-op day?

A

1 or 2

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64
Q

treatment of HIT consists of what?

A
  • d/c heparin
  • removal of heparin-coated intravascular devices (important! and easy to forget)
  • avoidance of warfarin (d/t enhanced prothrombotic activity early in warfarin therapy)
  • AC w/ alternative agents
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65
Q

what is the only AC agent currently approved by the FDA for HIT?

A

argatroban

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66
Q

what adjunct therapy may be used for refractory HIT, but w/ limited evidence to support its use?

A

IVIG

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67
Q

TEG (thromboelastometry) has been proposed to assist in guidance of factor replacement in patients w/ hemorrhage; RCTs in which patient populations have supported the utility of TEG?

A
  • traumatic hemorrhagic shock
  • liver transplant
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68
Q

a visual guide depicted as a graph that helps answer questions about the components of clot formation, stability, and lysis

A

TEG (thromboelastometry)

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69
Q

in TEG, the clotting time (R, or activated clotting time, ACT) is what?

A

the time from reagent addition to the sample until FIBRIN forms

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70
Q

what is the most common cause of a prolonged R or ACT time?

A

coagulation factor deficiency

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71
Q

in TEG, clot kinetics are measured by the K time, which is?

A

the time to achieve a clot amplitude of 20 mm; a measure of clot STRENGTH

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72
Q

in TEG, clot kinetics are also measured by the α angle, which is?

A

the rate of clot formation d/t fibrin accumulation and cross-linking

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73
Q

in TEG, maximum amplitude (MA) is what?

A

a measure of the maximum dynamic properties of fibrin and platelet bonding through glycoprotein 2b/3a receptors

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74
Q

the maximum amplitude (MA) reflects what?

A

the OVERALL strength of the fibrin clot and is most impacted by platelet numbers and function

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75
Q

in TEG, LY30 and LY60 are what?

A

a measure of clot stability and breakdown by the percentage decrease at 30 and 60 minutes after MA

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76
Q

LY30 and LY60, basically, provides what information?

A

the degree of fibrinolysis

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77
Q

an increase in LY30 and/or LY60 might prompt consideration of treatment w/ what?

A

tranexamic acid (TXA)

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78
Q

when administered w/i the first 8 hours (especially the first 3 hours), what treatment has been shown to decrease all-cause mortality in patients p/w or at risk for traumatic hemorrhage?

A

tranexamic acid (TXA)

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79
Q

the 4T scoring system is best studied in the ICU population to help stratify the risk of HIT; what are the citeria?

A
  • degree of thrombocytopenia
  • change and timing of platelet count from baseline
  • presence of thrombosis
  • other possible causes of thrombocytopenia
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80
Q

HIT Ab testing should ONLY be performed in patients at what risk?

A

intermediate or high risk

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81
Q

the initial screening ELISA for HIT has what test characteristics?

A

very sensitive but not specific

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82
Q

an intermediate or high 4T score and positive ELISA should prompt what management?

A
  • d/c heparin
  • remove heparin-bound devices
  • confirmatory testing w/ a functional assay (either 14C-serotonin release assay or heparin-induced platelet activation assay)
  • initiation of an alternate form of AC
  • lower extremity doppler US
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83
Q

what is the most common complication of HIT?

A

lower extremity DVT

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84
Q

in patients w/ HIT, current guidelines support treatment w/ what agents?

A
  • direct thrombin inhibitors; argatroban or bivalirudin
  • indirect factor Xa inhibitors; danaparoid or fondaparinux
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85
Q

current guidelines recommend the use of what AC agent ONLY for HIT in pregnant patients when danaparoid is NOT available?

A

fondaparinux

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86
Q

what AC agent has a long half-life making it less preferred in critically ill patients, the elderly, AKI or CKD, or significant bleeding risk?

A

fondaparinux

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87
Q

there is emerging evidence suggesting that non-vitamin K antagonists, such as what AC agent, may be effective in treating critically ill patients w/ HIT?

A

rivaroxaban

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88
Q

what are the only IV direct thrombin inhibitors available for use in HIT?

A
  • argatroban
  • bivalirudin
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89
Q

argatroban is the recommended first-line agent and only drug approved by the FDA for HIT, but should be used w/ caution in which patients?

A
  • HF
  • liver disease
  • severe anasarca
  • after cardiac surgery
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90
Q

which medication is recommended for patients w/ HIT requiring emergent cardiac surgery or PCI, but requires significant dose adjustments in both hepatic and renal dysfunction?

A

bivalirudin

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91
Q

tranexamic acid, a lysine analogue that acts as an inhibitor of fibrinolysis, has been shown to reduce mortality in patient populations?

A
  • postpartum hemorrhage
  • trauma
  • selected patients w/ traumatic brain injury (TBI)
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92
Q

the use of tranexamic acid in what patient population has NOT been shown to reduce mortality?

A

patients undergoing coronary artery bypass grafting (CABG)

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93
Q

what is another practical use of TEG (thromboelastometry)?

A

can measure functional impact of hypothermia and acidosis

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94
Q

trauma-induced coagulopathy following massive hemorrhage is multifactorial; what are these factors?

A
  • consumption of platelets and coagulation factors during clot formation in damaged blood vessels
  • plasma dilution from ivf or excessive prbc administration
  • dysregulated activation of the thrombomodulin-protein C system d/t tissue injury and hypoperfusion
  • hypoxemia
  • acidosis
  • hypothermia
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95
Q

what are the concerns surrounding the 1:1:1 ratio (1 unit of pooled platelets approximating 6 units, followed by alternating units of prbcs and plasma) approach based on the PROPPR trial fallen out of favor to a more targeted approach as w/ the use of TEG?

A
  • TRALI
  • transfusion-associated circulatory overload
  • infection
  • immunomodulation risk
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96
Q

preferred initial therapeutic option for splenic rupture

A

embolization; either proximal splenic artery or selective distal embolization

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97
Q

dasatinib, a second-generation tyrosine kinase inhibitor, is a/w adverse effects?

A
  • cytopenias
  • pleural effusions
  • bleeding (decreases platelet function)
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98
Q

criteria for hyperleukocytosis

A

total leukemic blood count of 50,000-100,000/μL

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99
Q

leukostasis, when WBCs coalesce in the microvasculature, typically occurs in AML and CML during a myeloid blast crisis w/ very blast counts, and most commonly p/w

A

respiratory distress and/or neurological symptoms

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100
Q

pulmonary signs/symptoms of leukostasis

A
  • dyspnea
  • hypoxia
  • variable interstitial or alveolar infiltrates on cxr
  • decreased PO2 on abg measurement d/t increased O2 uptake by the large numbers of blast cells (hallmark sign)
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101
Q

since a hallmark sign of leukostasis is a decreased PO2 on abg measurement d/t increased O2 uptake by the large numbers of blast cells, how should O2 levels be monitored?

A

pulse oximetry

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102
Q

neurological signs/symptoms of leukostasis

A
  • visual changes
  • headache
  • dizziness
  • tinnitus
  • gait instability
  • decreased levels of consciousness
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103
Q

patients w/ hyperleukocytosis have an increased risk of what? and that risk may persist for at least a week after reduction of the WBC count, possibly from reperfusion injury

A

intracranial hemorrhage

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104
Q

what is the initial therapy for leukostasis?

A

leukapheresis

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105
Q

specificity of US for the detection of splenic rupture

A

> 90%

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106
Q
  • h/o blood product transfusion
  • skin rash
  • diarrhea
  • elevated bilirubin
A

transfusion-associated graft-vs-host disease (TA-GVHD)

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107
Q

classic skin lesion a/w GVHD

A

erythematous maculopapular morbilliform eruption that starts on the face, ears, palms, and soles

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108
Q

what are the important predispositions to developing TA-GVHD?

A
  • lymphoproliferative malignancies (in particular, Hodgkin’s lymphoma)
  • prior receipt of certain chemotherapeutic medications
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109
Q

use of what may prevent TA-GVHD?

A

irradiated blood products

110
Q

PPIs have been a/w w/ what severe delayed-type hypersensitivity reactions?

A
  • SJS
  • TEN
  • drug rash w/ eosinophilia and systemic symptoms (DRESS)
111
Q

characteristic skin lesion of Pseudomonas aeruginosa

A

ecthyma gangrenosum (bullous hemorrhagic lesions)

112
Q

contamination of platelet concentrates predominantly transmit what pathogen?

A

gram-positive bacteria from skin flora

113
Q

contamination of prbc products predominantly transmit what pathogen?

A

gram-negative organisms, usually Enterobacteriaceae w/ Yersinia enterocolitica being the most characteristic organism

114
Q

contaminated blood transfusion reactions are 2/2 either the organism itself or toxin produced by the organism; the clinical result is

A

severe sepsis or septic shock

115
Q

DOAC that inhibits thrombin (factor IIa)

A

dabigatran

116
Q

DOACs that inhibit factor Xa

A

“-Xabans” –> they “ban” factor Xa

  • rivaroxaban
  • apixaban
  • edoxaban
  • betrixaban
117
Q

FDA-approved reversal agent for coagulation deficit a/w factor Xa inhibitors

A

andexanet

118
Q

what is the dosing for andexanet?

A
  • depends on dosing of factor Xa inhibitor
  • if lower dose then andexanet 400 mg iv then 4 mg/min x 120 minutes
  • if higher dose then andexanet 800 mg iv then 8 mg/min x 120 minutes
119
Q

management if andexanet is unavailable

A

4 factor prothrombin complex concentrate (PCC) 50 to 100 units/kg

120
Q

3 factor prothrombin complex concentrate includes concentrates of what?

A
  • factor II
  • factor IX
  • factor X
121
Q

4 factor prothrombin complex concentrate includes concentrates of what?

A
  • factor II
  • factor IX
  • factor X

AND

  • factor VII
122
Q

monoclonal Ab directed to dabigatran and its metabolites

A

idarucizumab

123
Q

hemophagocytic lymphohistiocytosis (HLH) mimics severe sepsis and septic shock because of

A

massive, unchecked release of inflammatory cytokines, often referred to as cytokine storm

124
Q

by consensus, the diagnostic criteria for hemophagocytic lymphohistiocytosis (HLH) are

A
  • known HLH-associated genetic mutation (usually of genes PRF I, UNC 13D, or STX 11)

OR

at least 5 of 8 criteria:

  • fever, temperature ≥ 38.5°C
  • splenomegaly
  • cytopenias of at ≥ 2 blood cell lines (hb < 9, ANC < 1,000, platelet < 100,000)
  • hypertriglyceridemia (fasting TG > 265 mg/dL), and/or hypofibrinogenemia (fibrinogen < 150 mg/dL)
  • hemophagocytosis in BM, spleen, LN, or liver
  • low or absent NK cell activity
  • ferritin > 500 ng/mL; greater specificity when > 3,000 ng/mL
  • increased soluble CD25 (soluble interleukin-2 receptor alpha)
125
Q

why might TGs be elevated and is one of the diagnostic criteria in HLH?

A

inflammatory cytokines inhibit lipoprotein lipase (LPL)

126
Q

why might ferritin be elevated and is one of the diagnostic criteria in HLH?

A

macrophages are a major repository of ferritin

127
Q

treatment of patients w/ HLH-induced acute organ dysfunction, including hypotension

A

administration of etoposide (aka VP-16), and dexamethasone

128
Q
  • tick-borne protozoan
  • in USA
  • may cause hepatosplenomegaly
A

babesiosis (Babesia microti)

129
Q

severe disease from this protozoan, Babesia microti, is a/w

A
  • abdominal pain
  • vomiting
  • diarrhea
  • hemolytic anemia
  • thrombocytopenia
130
Q

how is babesiosis diagnosed?

A
  • presence of organisms in RBCs on thick PBS
  • serologically, or
  • PCR
131
Q
  • tick-borne bacteria
  • can cause hepatic and multisystem organ failure
A

ehrlichiosis (Ehrlichia)

(genus under the Rickettsiales order)

132
Q

common laboratory features of ehrlichiosis

A
  • thrombocytopenia
  • increased liver enzymes
  • anemia
  • AKI
133
Q

how is ehrlichiosis diagnosed?

A
  • presence of inclusions, called morulae, in neutrophils or monocytes on PBS or buffy coat
  • serology, or
  • PCR
134
Q

what is the buffy coat?

A

the fraction of an anticoagulated blood sample that contains most of the WBCs and platelets following centrifugation that sits between the plasma and erythrocytes

135
Q

hematologic disease induced by acquired deficiency of von Willebrand factor cleaving protease ADAMTS13

A

thrombotic thrombocytopenic purpura (TTP)

136
Q

measure activity level of ADAMTS13 in thrombotic thrombocytopenic purpura (TTP)

A

< 10%

137
Q

thrombotic thrombocytopenic purpura (TTP) is characterized clinically by

A
  • microangiopathic hemolytic anemia (MAHA)
  • thrombocytopenia
  • purpura or bleeding
  • major or minor neurologic symptoms
138
Q
  • anti-β2 glycoprotein I antibody positive
  • histopathological evidence of vessel occlusion
A

catastrophic antiphospholipid Ab syndrome

139
Q

mainstays of treatment for catastrophic antiphospholipid Ab syndrome (CAPS)

A
  • AC (in the absence of bleeding)
  • corticosteroids
  • plasma exchange
140
Q

there is NO consensus on absolute criteria needed for the diagnosis of disseminated intravascular coagulation (DIC), but what are the common laboratory criteria?

A
  • thrombocytopenia
  • prolonged PT
  • prolonged aPTT
  • low plasma fibrinogen
  • elevated plasma D-dimer
141
Q

disseminated intravascular coagulation (DIC) can present under what circumstances?

A
  • trauma
  • sepsis
  • malignancy
142
Q

disseminated intravascular coagulation (DIC) often manifests how?

A

oozing from sites of trauma, catheters, or drains

143
Q

what is the Coombs test result in TTP and why

A
  • negative
  • the hemolytic anemia is NOT from an immune process; is d/t mechanical shear stress
144
Q

most common etiology of pulmonary-renal syndromes

A

microscopic polyangiitis

145
Q
  • fever
  • elevated ESR
  • elevated CRP
  • AKI
  • anemia
  • usually MPO-ANCA positive
A

microscopic polyangiitis

146
Q

aPTT measures activity of what?

A
  • contact activation clotting pathway (factors VIII, IX, XI, XII)

AND

  • common pathway (factors I (fibrin), II (thrombin), V, X)
147
Q

PT measures activity of what?

A
  • tissue factor clotting pathway (factor VII)

AND

  • common pathway (factors I (fibrin), II (thrombin), V, X)
148
Q

because the INR is a part of the measurement of both aPTT and PT, conditions that affect factors in the common pathway can result in both being elevated; what are those conditions?

A
  • disseminated intravascular coagulation (DIC)
  • supratherapeutic heparin
  • direct thrombin inhibitors
  • warfarin
  • vitamin K deficiency
  • hepatic insufficiency
149
Q

what might accidentally happen in an emergency situation in an ESRD patient w/ a TDC that might lead to severe coagulopathy?

A

administration of medications via the TDC w/o removing the heparin “lock” which might be as much as 20,000 units

150
Q

treatment for DIC

A
  • treat underlying condition if possible
  • cryoprecipitate if low fibrinogen levels
151
Q

protamine dosing

A
  • 1 mg per 100 units of heparin (max single dose 50 mg)
  • may repeat 0.5 mg per 100 units of heparin if aPTT remains elevated
  • but also depends on time elapsed since heparin overdose or if on gtt (heparin half-life 60-90 minutes)
152
Q

the supernatant of cryoprecipitate from pooled plasma used to purify and concentrate relevant clotting factors generates what?

A

prothrombin complex concentrates (PCC)

153
Q

what must be administered in conjunction w/ PCC and why?

A
  • vitamin K 10 mg iv
  • factors II, VII, IX, X are vitamin K dependent factors!
154
Q

generally, how long does vitamin K take to reverse supratherapeutic warfarin?

A

8-24 hours

155
Q

what are the most common adverse effects of checkpoint inhibitors (anti-PD1 and CTLA-4 Ab therapy)?

A
  • skin reactions; rash
  • GI problems; colitis
156
Q

what are the most common severe complications of checkpoint inhibitors?

A
  • myocarditis
  • pneumonitis
  • enteritis
  • neurological dysfunction
157
Q
  • rotary nystagmus on upward gaze
  • peripheral sensory neuropathy (lack of any movement to stimulation and decreased DTRs)
  • anti-Ma2 Abs against both central and peripheral neurons
  • a/w RCC
A

paraneoplastic syndrome

158
Q

what is the grading scale for complications from checkpoint inhibitors?

A
  • grade 1 = mild
  • grade 2 = moderate
  • grade 3 = severe
  • grade 4 = life-threatening
159
Q

typically, patients w/ grade 3 or 4 complications from checkpoint inhibitors should be admitted where?

A

ICU

160
Q

treatment for complications from checkpoint inhibitors grades 2 to 4

A
  • d/c checkpoint inhibitor
  • diagnosis of the syndrome
  • initiation of treatment specific for the diagnosed syndrome
161
Q

in some cases d/c’ing the checkpoint inhibitor is sufficient to improve the patient; in patients who continue to progress, what treatment options should be considered?

A
  • glucocorticoids
  • plasmapheresis
  • immunosuppressants
162
Q

it is believed that treatment w/ a checkpoint inhibitor does not initiate a paraneoplastic response, but amplifies it, and d/c’ing the checkpoint inhibitor has little effect to ameliorate symptoms; in a few isolated cases what medication has been initiated w/o d/c’ing the checkpoint inhibitor?

A

natalizumab (α4 integrin blocker that prevents the entry of immune cells into the brain)

  • has NOT been tested in a clinical trial!
163
Q
  • patient that is highly likely to have type 2 HIT
  • hypotensive

think of what?

A

adrenal insufficiency d/t adrenal vein thrombosis and hemorrhage 2/2 hypercoagulable state

164
Q

what infections are known to produce adrenal insufficiency?

A
  • disseminated TB
  • fungal disease
  • meningococcal sepsis
165
Q
  • fever
  • leukocytosis
  • pain localized to RUQ
  • CT a/p showing enlarged GB w/ intraluminal gas and/or surrounding fluid
A

acalculous cholecystitis

166
Q
  • back and flank pain
  • subsequent hypotension
  • receiving full-dose AC
  • drop in hb
A

retroperitoneal hemorrhage

167
Q

to determine if a patient should be considered for reversal of their DOAC, what are the 2 main factors?

A
  • determine if it’s a major bleed
  • assess the AC status
168
Q

when considering DOAC reversal, a major bleed is defined by

A
  • location (critical sites)
  • volume of blood loss
169
Q

when considering DOAC reversal, a AC status is based on

A
  • the specific agent
  • time of last dose
  • renal function
170
Q
  • major complication of chimeric Ag receptor (CAR)-T cell therapy
  • fever
  • hypotension
  • hypoxemic respiratory failure
A

cytokine release syndrome (CRS)

171
Q

cytokine release syndrome (CRS) is in part mediated by

A

cytokine IL-6

172
Q

treatment for cytokine release syndrome (CRS)

A
  • supportive treatment
  • empiric abx
  • corticosteroids
  • tocilizumab
173
Q

cytokine release syndrome (CRS) may affect any organ, but in some patients it can manifest as a predominant neurologic syndrome called

A

immune effector cell-associated neurotoxicity syndrome

174
Q

when do signs/symptoms of cytokine release syndrome (CRS) occur?

A

2-14 days after initiating CAR-T cell therapy

175
Q

severity of cytokine release syndrome (CRS) is graded which helps guide treatment;

  • grade 1
A
  • fever
  • no hypotension
  • no hypoxia
  • flu-like symptoms
176
Q

severity of cytokine release syndrome (CRS) is graded which helps guide treatment;

  • grade 2
A
  • fever
  • hypotension
  • no vasopressors required, and/or
  • hypoxia requiring < 6 L/min NC
177
Q

severity of cytokine release syndrome (CRS) is graded which helps guide treatment;

  • grade 3
A
  • fever
  • hypotension
  • 1 vasopressor required, and/or
  • higher supplemental O2 support required
178
Q

severity of cytokine release syndrome (CRS) is graded which helps guide treatment;

  • grade 4
A
  • fever
  • hypotension
  • multiple vasopressors required, and/or
  • positive pressure ventilation required
179
Q

treatment for grade 2 CRS

A

tocilizumab alone

180
Q

treatment for grades 3 and 4 CRS

A

both corticosteroids and tocilizumab

181
Q

mechanism of tumor lysis syndrome (TLS)

A

rapid release of intracellular K+, PO4, and NAs into the bloodstream

182
Q

TLS is most commonly seen when?

A
  • after induction cytotoxic chemotherapy for acute leukemias and lymphomas
183
Q

can TLS happen spontaneously?

A

yes

184
Q

TLS is defined as

A

≥ 2 of the following during a 24-hour period w/i 3 days before the start of cytotoxic therapy OR up to 7 days afterward:

  • hyperkalemia
  • hyperphosphatemia
  • hypocalcemia
  • hyperuricemia
  • oliguria

(nb, electrolyte disturbances are absolute values or relative to baseline)

185
Q

complications of TLS

A
  • cardiac arrhythmias
  • AKI
  • seizures
  • death
186
Q

enzyme responsible for metabolism of nucleic acids to uric acid

A

xanthine oxidase

187
Q

uric acid can crystallize and precipitate in the renal tubules; this is enhanced in the presence of what?

A

calcium phosphate

188
Q

initial treatment for TLS if oliguria is not already present

A

judicious ivf to maintain renal tubular flow

189
Q

a form of recombinant urate oxidase that metabolizes uric acid to nontoxic allantoin thus preventing uric acid nephropathy and renal failure

A

rasburicase

190
Q

xanthine oxidase inhibitor

A

allopurinol

191
Q

what are the data in support of alkalization of urine to prevent or abort TLS-induced kidney injury?

A

mixed; most experts suggest avoiding

192
Q

criteria for emergent hemodialysis for TLS

A

usual criteria

  • life-threatening hyperkalemia
  • diuretic-refractory volume overload
  • uremic symptoms
  • severe metabolic acidosis
  • intoxication w/ a dialyzable toxin
193
Q

has prophylactic HD in the absence of usual criteria shown to improve clinical outcomes of patients w/ TLS?

A

no

194
Q

tumor embolization or surgical procedures in patients w/ neuroendocrine tumors can release large amounts of what?

A

serotonin and other small-molecule neurotransmitters

195
Q

most common clinical features of carcinoid crisis

A
  • flushing
  • diarrhea
  • bronchospasm
  • tachycardia
196
Q

prevention of carcinoid crisis prior to tumor embolization or surgery

A

long-acting somatostatin analogue

197
Q

treatment for carcinoid syndrome intraoperatively

A
  • octreotide iv prn
  • should not be given preemptively if already on long-acting somatostatin analogue
198
Q

thrombotic thrombocytopenic purpura (TTP) is a medical emergency caused by

A

reduced von Willebrand factor-cleaving protease, ADAMTS13

199
Q
  • small-vessel platelet-rich thrombi
  • thrombocytopenia
  • microangiopathic hemolytic anemia (MAHA)
  • organ damage
A

thrombotic thrombocytopenic purpura (TTP)

200
Q

what are the 2 different forms of thrombotic thrombocytopenic purpura (TTP)?

A
  • autoantibodies against ADAMTS13
  • hereditary defect in the ADAMTS13 gene
201
Q
  • microangiopathic hemolytic anemia (MAHA), hb < 10 g/dL
  • thrombocytopenia, platelets < 30,000/μL
  • AMS
  • TIA or stroke
  • seizures
A

thrombotic thrombocytopenic purpura (TTP)

202
Q

should therapy be withheld or delayed while waiting for ADAMTS13 activity?

A

no!

203
Q

what is the mechanism of microangiopathic hemolytic anemia (MAHA) in thrombotic thrombocytopenic purpura (TTP)?

A

mechanical shearing (fragmentation) of RBCs as they pass through the microvasculature full of platelet-rich microthrombi

204
Q

PBS findings in thrombotic thrombocytopenic purpura (TTP)

A
  • schistocytes
  • thrombocytopenia
205
Q

standard therapy for thrombotic thrombocytopenic purpura (TTP)

A
  • therapeutic plasma exchange (TPE)
  • glucocorticoids
  • rituximab
206
Q

what medication should be added if standard therapy for thrombotic thrombocytopenic purpura (TTP) doesn’t work?

A

caplacizumab

207
Q

caplacizumab MOA

A

MAB that binds to von Willebrand factor and blocks its interaction w/ platelet glycoprotein 1b-IX-V

208
Q

what is the leading preventable cause of maternal death globally and accounts for 20% of maternal deaths in developing countries?

A

postpartum hemorrhage (PPH)

209
Q

what is the most common cause of postpartum hemorrhage (PPH) and accounts for 70% of cases?

A

uterine atony

210
Q

what is the current definition of postpartum hemorrhage (PPH)?

A

blood loss > 1,000 mL, regardless of method of delivery

211
Q

what are the “four T’s” of postpartum hemorrhage (PPH)?

A
  • tone (uterine atony)
  • trauma (lacerations and rupture)
  • tissue (retained placenta or clots), and
  • thrombin (clotting d/o’s)
212
Q

postpartum hemorrhage (PPH) d/t atony is often a/w a number of risk factors which are

A
  • chorioamnionitis
  • therapeutic use of magnesium
  • prolonged labor
  • fetal macrosomia
  • advanced maternal age
  • labor induction or augmentation
  • multiple gestation
213
Q

what agents may be used for uterine atony to restore tone?

A
  • oxytocin
  • methylergonovine
  • misoprostol
214
Q

what mechanical approaches are used for uterine atony?

A
  • uterine massage
  • uterine balloon tamponade
  • uterine compression suturing
  • uterine and vaginal packing
215
Q

if pharmacological agents and mechanical approaches fail to control PPH, what is the next best step?

A

emergent hysterectomy

216
Q
  • a rare but serious complication of bone marrow and hematopoietic SCT
  • risk factors include;
  • calcineurin inhibitors
  • mammalian target of rapamycin inhibitors
  • GVHD
  • multiple previous transplants
  • HLA mismatch
  • opportunistic infection
  • certain conditioning regimens (especially those including total body irradiation)
A

transplant-associated thrombotic microangiopathy (TMA)

217
Q

what are the clinical features of transplant-associated TMA?

A
  • new or worsening HTN
  • progressive AKI
  • worsening thrombocytopenia
  • MAHA
  • pHTN
  • progressive neurologic dysfunction
218
Q
  • a/w systemic inflammation and characterized by fever, rash, and diffuse capillary leak
  • pulmonary edema
  • end-organ dysfunction
A

engraftment syndrome

219
Q
  • pathologic lesion in arterioles and capillaries resulting in microvascular thrombosis
  • microangiopathic hemolytic anemia (MAHA)
  • schistocytes and thrombocytopenia on PBS
A

thrombotic microangiopathy (TMA)

220
Q

there are several different types of TMAs; what are they?

A
  • immune-mediated TTP (autoantibody against ADAMTS13)
  • hereditary-mediated TTP (defect in ADAMTS13 gene)
  • HUS from Shiga toxin
  • acquired, complement-mediated TMA
  • hereditary, complement-mediated TMA
  • drug-mediated TMA
  • metabolism-mediated TMA
  • coagulation-mediated TMA
221
Q

TMAs can be broadly categorized how?

A
  • hereditary d/o’s
  • acquired d/o’s
222
Q

aside from the TMAs, what are other causes of MAHA and thrombocytopenia?

A
  • DIC
  • infection
  • some malignancies
  • preeclampsia
  • HELLP syndrome
  • severe HTN
  • collagen vascular disease
  • s/p organ and hematopoietic cell transplant
223
Q

TTP treatment continues until when?

A

thrombocytopenia has resolved w/ a platelet count of ≥ 150,000/µL

224
Q
  • can occur between 2 to 24 months of administration of medication
  • main clinical symptoms include, dyspnea, cough, fever, and chest pain
  • radiographic features are nonspecific; traction bronchiectasis, consolidation, reticular opacities, GGO, centrilobular nodularity, honeycombing
A

checkpoint inhibitor pneumonitis (CIP)

225
Q

therapy w/ immune checkpoint inhibitors has been a/w what adverse effects?

A
  • enteritis
  • dermatitis
  • encephalitis
  • pneumonitis
226
Q

acute radiation pneumonitis typically occurs after what time period?

A

1-6 months after completion of external beam radiation

227
Q

checkpoint inhibitor pneumonitis (CIP) is diagnosed how?

A

diagnosis of exclusion

228
Q

histopathology of checkpoint inhibitor pneumonitis (CIP)

A

CD8+ lymphocytic alveolitis

229
Q

should a patient be on empiric abx for respiratory pathogens while investigating for checkpoint inhibitor pneumonitis (CIP)?

A

yes, if indicated

230
Q

in thromboelastography (TEG), what represents the time from reagent activation to onset of clot formation?

A

reaction time (R-time, aka ACT)

231
Q

the reaction time (R-time, aka ACT) is primary affected by what?

A

perturbation of the intrinsic clotting cascade (eg, clotting factor depletion, or administration of AC)

232
Q

what is a normal R-time?

A

varies depending on the reagents used to initiate clotting, so a control sample is used as a reference

233
Q

in thromboelastography (TEG), the K-time is what?

A

time from onset of clot formation until clot amplitude reaches 20 mm

234
Q

in thromboelastography (TEG), the α-angle is what?

A

a measure of the rate of rise of clot strength

235
Q

both the K-time and α-angle are primarily affected by what?

A

deficiencies of fibrinogen

236
Q

both the K-time and α-angle can be corrected by administering what?

A

cryoprecipitate

237
Q

in thromboelastography (TEG), the maximum amplitude (MA) is what?

A

a measure of maximal viscoelastic strength of a clot

238
Q

the maximum amplitude (MA) primary depends on what?

A

platelet number and function

239
Q

what will decrease the maximum amplitude (MA)?

A
  • thrombocytopenia
  • impaired platelet function
240
Q

what will increase the maximum amplitude (MA)?

A
  • platelet transfusions
  • desmopressin
241
Q

once clot strength has reached its maximum, what is the next step in the process?

A

counterregulatory process of thrombolysis to begin weakening the clot

242
Q

in thromboelastography (TEG), what is the lysis index (LY-30)?

A

the percentage of loss of amplitude at 30 minutes after reaching the maximum amplitude (MA)

243
Q

the lysis index (LY-30) is a measure of what?

A

intensity of fibrinolytic activity

244
Q

overly exuberant fibrinolytic activity can lead to what?

A

destabilization of fresh clot and recurrent bleeding

245
Q

what therapies can help normalize LY-30?

A
  • tranexamic acid
  • aminocaproic acid
246
Q

in the CRASH-2 trial, what reduced bleeding and mortality after major trauma?

A

tranexamic acid

247
Q

the utility of TEG has been evaluated in subsets of patients at risk of major bleeding including advanced liver disease who were undergoing invasive procedures; what were the take home points?

A
  • significantly lower transfusions of blood products w/o concomitant increase in bleeding complications
  • fewer transfusion-related adverse effects
248
Q

TEG has also been shown to reduce unnecessary blood transfusions in which patients?

A
  • patients undergoing cardiac surgery
  • perioperative or peripartum bleeding
249
Q

interpret this TEG pattern

A

normal

250
Q

interpret this TEG pattern

A

increased thrombolytic activity

251
Q

interpret this TEG pattern

A

fibrinogen deficiency

252
Q

interpret this TEG pattern

A

inadequate platelet function

253
Q

interpret this TEG pattern

A

presence of AC or depletion of clotting factors

254
Q

what are some of the number hematological abnormalities that can occur w/ covid-19 infection?

A
  • lymphopenia
  • leukocytosis
  • leukopenia
  • monocytosis
  • reactive lymphocytes
  • leukoerythrobastosis
  • thrombocytopenia
  • hyposegmented neutrophils characteristic of acquired Pelger-Huet anomaly
255
Q

a normal neutrophil has an average of 3.5 nuclei, how many nuclei are seen in Pelger-Huet anomaly (inherited or acquired) and what is the cell called?

A
  • < 3.5, usually 2
  • “pince-nez” cell
256
Q

more often, the Pelger-Huet anomaly is acquired, sometimes called “pseudo-Pelger-Huet anomaly,” and can result as a consequence of what?

A
  • leukemia
  • myelodysplasia
  • myxedema
  • viral infections
  • malaria
  • drug toxicity
257
Q

what can cause hypersegmented neutrophil nuclei?

A
  • occasionally iron deficiency
  • folate deficiency
  • B12 deficiency
258
Q

leukemias manifesting w/ acute hyperleukocytosis are a/w very high risk of early mortality, predominantly d/t what?

A
  • respiratory failure
  • intracranial bleeding
259
Q

what is a unique finding that can be seen in patients w/ leukemias manifesting w/ acute hyperleukocytosis?

A

spurious hypoxemia w/ an artificial decrease in PaO2

260
Q

symptomatic hyperleukostasis is aka

A

leukostasis

261
Q

hyperleukostasis can be seen w/ what malignancies?

A
  • AML
  • ALL
  • CLL
  • CML
262
Q

hyperleukostasis is most commonly seen in what malignancy?

A

large, poorly deformable blasts in AML

263
Q

respiratory and neurologic symptoms d/t lung and brain microvascular involvement are most common in a patient w/ symptomatic hyperluekocytosis; what are other findings?

A
  • myocardial ischemia
  • bowel ischemia
  • renal ischemia
  • limb ischemia
  • priapism
264
Q

fever is common in hyperleukocytosis, can be d/t what?

A
  • inflammation from leukostasis
  • concurrent infection
265
Q

circulating blast fragments in hyperleukocytosis can lead to what lab test result error?

A

overestimation of platelet count w/ automated blood cell counters

266
Q

use of heparinized tubes will reduce the risk of what lab error in hyperleukocytosis?

A

erroneous hyperkalemia

267
Q

what other findings can be present on presentation of hyperleukocytosis and may worsen during initial treatment?

A
  • DIC
  • TLS
268
Q

what are the treatment options for hyperluekocytosis?

A
  • leukapheresis
  • pharmacologic cytoreduction w/ hydroxyurea or chemotherapy
269
Q

what initial chemotherapy is initially started for hyperleukocytosis?

A

7+3 (cytarabine and idarubicin)

270
Q

what is transfusion strategy is used during the initial treatment of hyperleukocytosis?

A
  • limited prbc transfusion d/t risk of worsening blood viscosity
  • continued platelet support to reduce risk of hemorrhage d/t to both thrombocytopenia and DIC
271
Q

the PROPPR trial demonstrated what transfusion strategy reduced exsanguination in hemorrhagic shock patients?

A

1:1:1 (equal parts plasma, platelets, and prbcs), but this approach has fallen out of favor d/t increased r/o TRALI and TACO; more targeted approach w/ TEG is now preferred

272
Q

the most benefit of plasma-first resuscitation has been shown in which patients?

A
  • transport times > 20 minutes
  • cicilian air transports
  • blunt injury

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