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ITE > Hematological/Oncologic > Flashcards

Hematological/Oncologic Flashcards

1
Q

Transfusion + Fever + Otherwise
well

A

Febrile non-hemolytic transfusion reaction. Most common reaction. Rx:
tylenol, hold for 30min, likely restart

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2
Q

Transfusion + Urticaria +
Otherwise well

A

Simple Allergic (Urticarial) Reaction. Rx: benadryl (premedicate in future)
but don’t need to stop transfusion

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3
Q

Transfusion + Shock + AKI

A

Acute Hemolytic Transfusion Reaction. Often 2/2 ABO incompatability.
SSx: fever, flank pain, shock; Labs: +Coombs; Rx: stop transfusion,
IVF, diuretics, treat hyperK; Alternate Dx SEPSIS

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4
Q

Transfusion + Shock +
Angioedema + Normal CXR

A

Severe Allergic Reaction (Anaphylactic). Associated with hereditary IgA
deficiency. Rx: stop transfusion, epinephrine, supportive care

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5
Q

Transfusion + Pulmonary Edema
without other signs of heart
failure

A

Transfusion Related Acute Lung Injury (TRALI). ARDS after transfusion.
SSx: HIGH fever, hypoxemia, hypotension. CXR: pulmonary infiltrates.
Rx: stop transfusion, supportive, NO furosemide. Most common cause
of death following blood transfusion.

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6
Q

Transfusion + Pulmonary Edema
WITH other signs of heart failure

A

Transfusion-Associated Circulatory Overload (TACO). Presentation
similar to TRALI BUT….HTN, + sx of overload (e..g JVD, peripheral
edema, high bnp), NO Fever; Rx: stop transfusion, supoprtive care,
furosemide OK

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7
Q

What patients are higher risk for
developing TRALI?

A

Those with existing systemic inflammation (e.g. sepsis, trauma); linked to
platelet and FFP transfusions

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8
Q

What is the most common
infection transmitted by blood
transfusion?

A

Hepatitis B

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9
Q

What is the underlying pathology
in Hemophilia A and B

A

Bleeding disorder due to lack of Factor 8 (A; 85%) or Factor 9 (B); both
X-linked recessive and clinically indistinguishable; Dx: factor activity
levels, normal PT BUT abnormal PTT

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10
Q

What are the common clinical
features of Hemophilia A&B?

A

Minor trauma causing large amounts of bleeding or hemarthrosis
(hallmark sign); Children: ankle (most common joint); Adults: knee (most
common) > elbow & ankle. CNS bleeding = leading cause of death in
hemophilia. In CNS bleeding, factor replacement should precede
diagnostic imaging.

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11
Q

What is the appropriate dosage
of factor replacement for a pt
with Hemophilia A and Minor,
Moderate and Severe Bleeding?

A

# Factor VIII units = wt (kg) x (desired % increase in factor activity)
x 0.5. Minor (hemarthrosis): 20-30% factor desired (10-15U/kg of Factor
VIII); Moderate (epistaxis, GI bleed): 50% factor desired (25U/kg of
Factor VIII); Severe (CNS, RBP): 100% factor required (50U/kg of
Factor VIII)**

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12
Q

What is the appropriate dosage
of factor replacement for a pt
with Hemophilia B and Minor,
Moderate and Severe Bleeding?

A

# Factor units = wt (kg) x (desired % increase in factor acitivty).
Minor (hemarthrosis): 20-30% factor required (25U/kg of Factor IX);
Moderate (epistaxis, GI bleed): 50% factor required (50U/kg of Factor
IX); Severe (CNS, RBP): 100% factor required (100U/kg of Factor IX)

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13
Q

What are alternative treatments if
Factor is not available for
bleeding hemophiliac patient?

A

FFP (1cc FFP = 1U F8); Cryo (1 bag = 100U F8), DDAVP: 0.3 mcg/kg
IV/SQ, 150 vs 300mcg nasally, increases F8 activity & vWF (carries F8);
PCC

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14
Q

What does Von Willebrand
Factor (vWF) do during
hemostasis

A

1° hemostasis: attaches subendothelium to platelets (platelet
aggregation); 2° hemostasis: protects F8 from degradation + delivers
FV8 to site of injury (Factor VIII carrier protein)

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15
Q

Dx and Tx of Von Willebrand’s
Disese

A

Most common inherited bleeding disorder.

SSx: easy bruising, skin bleeding, prolonged bleeding from mucosal surfaces (mouth, GI/GU);

Labs: platelet count normal, normal PT/INR, prolonged bleeding time;

Rx: DDAVP (first-line Rx, increases release of vWF), non-recombinant F8, Cryo NOT recommended (risk of viral transmission), no FFP (very little F8); ± Antifibrinolytics (Amicar, Tranexamic acid) which inhibit clot
breakdown

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16
Q

Dx and Tx of Polycythemia Vera

A

Clonal proliferation of RBCs/increased RBC mass. SSx: pruritis
(aquagenic, plethora (facial), HTN, engorged retinal veins, thrombosis,
erythromelalgia (burning of hands/feet), splenomegaly; Labs: all cell
lines inc (esp. RBC). Rx serial phlebotomy, hydroxyurea, ASA

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17
Q

How does heparin work and how
can it be reversed?

A

Activates antithrombin III (inactivates F10 & thrombin), monitored with
PTT; Reversal: Protamine Sulfate 1mg per 100U heparin, give slowly to
avoid anaphylactoid reaction

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18
Q

How does LMWH work and how
can it be reversed?

A

Activates antithrombin III (inactivates ONLY F10), monitored with Xa
level; 60% reversal with Protamine Sulfate (dose based on timing since
last LMWH injection)

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19
Q

How does coumadin work and
how can it be reversed?

A

Inhibits vitamin K clotting factors (2, 7, 9, 10, proteins C & S), monitored
with INR; Reversal: FFP/VitK (alternate PCC), dosage based on type of
bleeding and INR

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20
Q

Review appropriate treatment to
reverse coumadin based on
severity of bleeding and INR

A

INR < 5 & NO bleeding: lower or skip 1 dose; INR ≥5 but ≤10 & NO
bleeding: skip next 1-2 doses, alt: skip 1 dose + Vit K 2.5-5mg PO; INR
≥10 & NO serious bleeding: hold med until INR is therapeutic + Vit K
5mg PO; ANY serious bleeding regardless of INR: hold med + Vit K
10mg IV + FFP or PCC; Life Threatening bleeding: hold med + Vit K
10mg IV + FFP or PCC or F7a

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21
Q

How does tPA work and how can
it be reversed?

A

Converts plasminogen to plasmin to breakdown clots; Nothing specific
reversal agent. Can give large amount of everything (pRBCs, cryo, FFP,
platelets, PCC, amicar, transexamic acid)

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22
Q

How does clopidogrel work and
how can it be reversed?

A

Blocks glycoprotein 2b/3a & prevents platelet activation (crosslinking
with fibrin); nothing specifically reverses, can give platelets

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23
Q

How does Dabigatran (Pradaxa)
work and how can it be
reversed?

A

Direct thrombin inhibitor, associated with GIB; Reversal agent:
Idarucizumab, PCC/pRBCs/platelets, can also do HD

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24
Q

How does Rivaraxaban (Xarelto)
work and how can it be
reversed?

A

Factor 10a inhibitor; no specific reversal, NOT dialyzable, can try
thrombin activation with PCC, FFP, cryo

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25
Q

Elderly with chronic back pain,
lytic lesions on XR

A

Multiple myeloma (“CRAB”): hyperCalcemia, Renal failure, Anemia, Bone lesions/Back pain.

Dx: abnormal SPEP (M-spike) & UPEP (Bence-
Jones protein), peripheral smear: rouleaux formation,
XR skull: “punched out lesions.”
Complications: hypogammaglobulinemia (leads to sepsis), hyperviscosity syndrome.

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26
Q

What symptoms suggest
aggressive Lymphoma?

A

“B symptoms”: fever, night sweats, lymphadenopathy

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27
Q

What distinguishes Non-
Hodgkins from Hodgkins
Lymphoma?

A

NHL: more common, more widespread, less curable, leading cause of
non-solid organ cancer-related death; HL: less common, related to viral
infection; often presents with B symptoms and local spread, high cure
rates

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28
Q

What are the two most common
types of Non-Hodgkins
Lymphoma and what
distinguishes them?

A

Follicular Lymphoma: indolent, slow growing, widespread at dx, no cure;
Diffuse Large B cell Lymphoma: aggressive and symptomatic, rapid
spread, 50% cured

29
Q

What are the two types of
Burkitt’s (non-Hodgkin’s)
lymphoma?

A

Associated with EBV. Endemic (African) Burkitt lymphoma (eBL): most
common; jaw and facial bone including the orbit (> 50%); Sporadic
Burkitt lymphoma (sBL): less common; abdominal tumors with bone
marrow involvement

30
Q

Dx and Tx of Hodgkins
lymphoma

A

Bimodal age (teens/young adults, older adults). SSx: nontender cervical
LAD, mediastinal mass on CXR, B symptoms; Labs: Reed-Sternberg cell
(“owls eye”); Rx: chemo, radiation

31
Q

What is the difference between
Acute and Chronic Leukemia?

A

Acute: rapid increase in blasts, most common in children; Chronic:
mature abnormal WBCs, slow growing, most common in elderly

32
Q

What is the difference between
Lymphocytic and Myelogenous
Leukemia?

A

Lymphocytic: B & T cells; Myelogenous: RBCs, platelets & other WBCs

33
Q

What is the difference between
the presentation of ALL vs AML?

A

BOTH: bony pain, big liver/spleen, anemia, bleeding, thrombocytopenia,
infection and blasts in blood; ALL: most common childhood leukemia,
+LAD; AML: more common in adults, no LAD, + gingival infiltration, Auer
rods on blood smear

34
Q

What is the difference between
CLL and CML?

A

BOTH: slow onset, elevated WBCs; CLL: most common adult leukemia,
smudge cell, worst prognosis; CML: mostly adults, Philadelphia
chromosome, high platelets, good prognosis

35
Q

Dx and Tx of neutropenic fever

A

1 oral temp ≥ 38.3°C or ≥ 38°C for ≥ 1 hour + ANC < 500. Leading
cause of cancer death: infection. Obtain cultures (gram pos. most
common). Rx: admission, empiric ABX

36
Q

Dx and Tx of Hyperviscosity
syndrome

A

↑ serum viscosity that causes sludging & vascular stasis. Cause:
Leukemias (AML or CML in blast crisis, WBC > 100k), multiple myeloma
Waldenstrom macroglobulinemia (most common cause), polycythemia
vera. SSx: mucosal bleeding (epistaxis), CNS sx (blurred vision,
headache, AMS, stroke), end-organ ischemia; Labs: Rouleaux
formation; Rx: phlebotomy (polycythemia) + IVF, plasmapheresis (high
proteins), leukapheresis for blast transformations (induction
chemotherapy = definitive tx)

37
Q

Leukostasis syndrome

A

Pretty specific to AML or CML in blast crisis, WBC >100k.

38
Q

Dx and Tx of Tumor Lysis
Syndrome

A

Massive cytolysis + release of the intracellular contents, can occur with
aggressive heme malignancies, large solid tumors/steroids after start of
tx. Metabolic derangements: HIGH uric acid, phosphate, potassium &
LOW calcium. Tx: aggressive IVF, correct lytes (hyperUA: Allopurinol,
Rasburicase; hyperPhos: aluminum hydroxide, Renagel, HD; hyperK:
calcium, insulin/glucose, biarb, kayexalate, HD; hypoCa: 2/2 high phos,
treat phos first, only treat if symptomatic). Complications: cardiac
arrhythmias, renal failure

39
Q

Name the criteria for emergent
HD in tumor lysis syndrome

A

K ≥ 6, uric acid ≥ 10, Cr ≥ 10, phosphorus ≥ 10, volume overload,
symptomatic hypoCa

40
Q

Thrombocytopenia, otherwise
normal labs, well patient

A

Idiopathic Thrombocytopenic Purpura (ITP), results from rapid
destruction of plts (fxn is normal). Types: children (2-6yo): acute, postinfectious;
adults (20-50). SSx: petechiae (most common), pupura,
gingival bleeding, epistaxis, menorrhagia; Dx: thrombocytopenia; Rx:
observation (only if asymptomatic + plt <50k), supportive (kids), steroids
(plt<50k) & IVIG, platelets (only for severe bleeding, VERY low plt),
others: splenectomy (refractory cases)

41
Q

Thrombocytopenia, Hemolytic
Anemia, Neuro symptoms

A

Thrombotic Thrombocytopenic Purpura (TTP): enzyme defect leads to unstable platelet plugs & hemolytic anemia.
SSx (PENTAD): Fever, Anemia (MAHA, schistocytes; HIGH indirect bili, LDH, retic count; LOW haptoglobin), Thrombocytopenia (10-50k), Renal failure, Neuro sx.
Dx: decreased ADAMTS-13 activity, schistocytes, normal: PT/INR,
fibrinogen, dimer;
Rx: supportive, plasmapheresis (Rx of choice);
others: plasma exchange transfusion, steroids, DMARDs, IVIG, splenectomy; DO NOT GIVE PLATELETS

42
Q

What types of patients are at
higher risk for developing TTP?

A

African-American females, Lupus, HIV, drugs (Clopidogrel, Quinine)

43
Q

Kid with thrombocytopenia,
hemolytic anemia, renal failure

A

Hemolytic Uremic Syndrome (HUS)- often after diarrheal illness
(O157:H7- shiga-like toxin), labs with eo hemolysis (schistocytes, high
unconj bili, high LDH), supportive care, transfuse prbcs Hb <6, DO NOT
GIVE PLATELETS OR ANTIBIOTICS

44
Q

What defines Heparin Induced
Thrombocytopenia (HIT) and
what is the treatment?

A

Antibodies that inactivate platelets usually at 5d if naive and only
min/hours if prior exposure. Dx (4 T’s): Thrombocytopenia (platelets
<150K or >50% drop after starting heparin [less often LMWH]), Time of
onset (5-10d), THROMBOSIS (thrombosis, skin reactions, PE, CVA, MI),
no oTher cause. Labs: +HIT antibody. Rx: STOP heparin or LMWH
(dont cont while waiting for tests), can change to DTI (Argatroban,
Dabigatran), NO platelets, change to direct thrombin inhibitor (DTI)

45
Q

Dx and Tx of Disseminated
Intravascular Coagulation (DIC)

A

Microvascular thrombosis AND consumptive coagulopathy causing multi
organ failure. Related to underlying severe illness (sepsis = most
common cause) & massive inflammation (trauma, pregnancy
complications, cancers); Labs: LOW: platelets (most common) &
fibrinogen; HIGH: PT/INR, fibrinogen degradation, dimer; Rx underlying
cause, Rx (primarily bleeding): FFP, plts, RBCs; Rx (primarily
thrombosis): heparin, LMWH

46
Q

In what thrombocytopenic
disorders are platelets
contraindicated?

A

TTP, HIT, HUS

47
Q

What are the 3 main causes of
microangiopathic hemolytic
anemia?

A

TTP, HUS, DIC

48
Q

Diseases with thrombocytopenia

A

TTP, HUS, DIC, SLE

49
Q

What are classic causes of
microcytic and macrocytic
anemias?

A

Microcytic (MCV < 80): iron deficiency, thalassemia, anemia of chronic
disease; Macrocytic (MCV > 100): B12 or Folate deficiency

50
Q

Anemia + low retic, low ferritin,
low iron, high TIBC

A

Iron Deficiency Anemia

51
Q

Anemia + high retic, nl/high
ferritin, nl/high iron + target cells
(smear)

A

Thalassemia- deffective Hb chains (A- Africa, B- India)

52
Q

Anemia + Headache, abdominal
pain, basophilic stippling (smear)

A

Chronic Lead Poisoning, may also see Burton’s line (blue line on gums)

53
Q

Anemia + low retic, low iron,
normal ferritin, normal TIBC

A

Anemia of Chronic Disease: microcytic or normocytic

54
Q

Anemia + Hypersegmented
neutrophils + Neurologic
changes

A

B12 deficiency, hypersegmented neutrophils (on periperal smear)

55
Q

What patients are at higher risk
for B12 deficiency?

A

Crohns, on PPI, vegan diet

56
Q

Anemia + Hypersegmented
neutrophils + NO neurologic
changes

A

Folate Deficiency (also consider in alcoholicswith anemia)

57
Q

What pateints are at higher risk
for Folate deficiency?

A

Alcoholics, tea and toast elderly

58
Q

What are the most common
causes of pancytopenia?

A

Malignancy (leukemias), nutritional deficiency (B12 or folate deficiency), infection, toxin exposure, aplastic anemia (complication of hepatitis)

59
Q

Most common initial presentation
of sickle cell in infants?

A

Acute Dactylitis: pain and swelling of hands and feet 2/2 vasoocclusive crisis, 2/2 infarction NOT infection; Rx: supportive

60
Q

Treatment of Sickle Cell pt with
Priapism?

A

Low-flow (venous/ischemic) causes erect penis with soft glans; Rx: aspirate corpus, intra-cavernous phenylephrine, surgical drainage prn

61
Q

Treatment of Sickle Cell pt with
Stroke?

A

Emergent exchange transfusion

62
Q

Dx and Tx of Acute Chest
Syndrome

A

Sickle cell pt with fever, SOB and infiltrate on CXR, HIGH mortality (most common cause of death in sickle cell pts). Causes: infection, VOC, fat embolism; Rx: ICU admit, supportive (incentive spirometer, IVF, O2, pain control) antibiotics for CAP, pRBCs vs. exchange transfusion (severe crises marked by PaO2 < 60 mm Hg, not first line)

63
Q

Kid with sickle cell + nontraumatic
rapid drop in Hb

A

Aplastic Crisis. SSx: pallor, weakness/lethargy, shock; arthralgias,
arthritis (adults). Dx: Hgb drop by at least 2 points from their baseline, LOW retic <2%; associated with Parvovirus B19. Rx: pRBCs, IVIG

64
Q

Kid with sickle cell, abdominal
pain + rapid drop in Hb

A

Splenic Sequestration: rapid sequestration of RBCs in the spleen
causing splenomegaly and severe anemia. SSx: pallor, splenomegaly.
Dx: low Hgb, high retic. Rx: IVF, transfuse prn, splenectomy

65
Q

What infections are more
common in sickle cell patients?

A

Encapsulated organisms: S. pneumoniae, H. influenzae, N. meningitides

66
Q

African American +HIV + anemia
after starting on dapsone

A

G6PD deficiency. X-linked recessive. Most common disease-producing enzympathy in humans. Found in African, Asian, and Mediterranean ancestry. Oxidative stress causes hemlytic anemia. Potective aganst malaria. Dx: neg. Coombs, Heinz bodies on smear. Rx:

67
Q

What are potential G6PD
triggers?

A

Fava beans, Infections, Meds: dapsone, TMP-SMX, phenazopyridine, nitrofurantoin, antimalarials, rasburicase, and methylene blue

68
Q

Old person, gradual face
swelling, perioribital edema,
cough, and cyanosis. Hx of
smoking.

A

Think superior vena cava syndrome. order: CT chest w/ contrast.

69
Q

Thresholds for platelet
transfusions in adults

A

Trauma or active bleeding, ITP: less than 50,000k / coagulation
disorder: 20,000k / everyone else: 5,000-10,000k

ITE (18 decks)

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