Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

ITE > Hematological/Oncologic > Flashcards

Hematological/Oncologic Flashcards

(69 cards)

Start Studying
1
Q

Transfusion + Fever + Otherwise
well

A

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

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

Transfusion + Urticaria +
Otherwise well

A

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

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

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

Transfusion + Shock +
Angioedema + Normal CXR

A

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What is the most common
infection transmitted by blood
transfusion?

A

Hepatitis B

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Elderly with chronic back pain, lytic lesions on XR
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.
26
What symptoms suggest aggressive Lymphoma?
"B symptoms": fever, night sweats, lymphadenopathy
27
What distinguishes Non- Hodgkins from Hodgkins Lymphoma?
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
28
What are the two most common types of Non-Hodgkins Lymphoma and what distinguishes them?
Follicular Lymphoma: indolent, slow growing, widespread at dx, no cure; Diffuse Large B cell Lymphoma: aggressive and symptomatic, rapid spread, 50% cured
29
What are the two types of Burkitt's (non-Hodgkin's) lymphoma?
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
Dx and Tx of Hodgkins lymphoma
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
What is the difference between Acute and Chronic Leukemia?
Acute: rapid increase in blasts, most common in children; Chronic: mature abnormal WBCs, slow growing, most common in elderly
32
What is the difference between Lymphocytic and Myelogenous Leukemia?
Lymphocytic: B & T cells; Myelogenous: RBCs, platelets & other WBCs
33
What is the difference between the presentation of ALL vs AML?
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
What is the difference between CLL and CML?
BOTH: slow onset, elevated WBCs; CLL: most common adult leukemia, smudge cell, worst prognosis; CML: mostly adults, Philadelphia chromosome, high platelets, good prognosis
35
Dx and Tx of neutropenic fever
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
Dx and Tx of Hyperviscosity syndrome
↑ 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
Leukostasis syndrome
Pretty specific to AML or CML in blast crisis, WBC >100k.
38
Dx and Tx of Tumor Lysis Syndrome
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
Name the criteria for emergent HD in tumor lysis syndrome
K ≥ 6, uric acid ≥ 10, Cr ≥ 10, phosphorus ≥ 10, volume overload, symptomatic hypoCa
40
Thrombocytopenia, otherwise normal labs, well patient
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
Thrombocytopenia, Hemolytic Anemia, Neuro symptoms
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
What types of patients are at higher risk for developing TTP?
African-American females, Lupus, HIV, drugs (Clopidogrel, Quinine)
43
Kid with thrombocytopenia, hemolytic anemia, renal failure
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
What defines Heparin Induced Thrombocytopenia (HIT) and what is the treatment?
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
Dx and Tx of Disseminated Intravascular Coagulation (DIC)
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
In what thrombocytopenic disorders are platelets contraindicated?
TTP, HIT, HUS
47
What are the 3 main causes of microangiopathic hemolytic anemia?
TTP, HUS, DIC
48
Diseases with thrombocytopenia
TTP, HUS, DIC, SLE
49
What are classic causes of microcytic and macrocytic anemias?
Microcytic (MCV < 80): iron deficiency, thalassemia, anemia of chronic disease; Macrocytic (MCV > 100): B12 or Folate deficiency
50
Anemia + low retic, low ferritin, low iron, high TIBC
Iron Deficiency Anemia
51
Anemia + high retic, nl/high ferritin, nl/high iron + target cells (smear)
Thalassemia- deffective Hb chains (A- Africa, B- India)
52
Anemia + Headache, abdominal pain, basophilic stippling (smear)
Chronic Lead Poisoning, may also see Burton's line (blue line on gums)
53
Anemia + low retic, low iron, normal ferritin, normal TIBC
Anemia of Chronic Disease: microcytic or normocytic
54
Anemia + Hypersegmented neutrophils + Neurologic changes
B12 deficiency, hypersegmented neutrophils (on periperal smear)
55
What patients are at higher risk for B12 deficiency?
Crohns, on PPI, vegan diet
56
Anemia + Hypersegmented neutrophils + NO neurologic changes
Folate Deficiency (also consider in alcoholicswith anemia)
57
What pateints are at higher risk for Folate deficiency?
Alcoholics, tea and toast elderly
58
What are the most common causes of pancytopenia?
Malignancy (leukemias), nutritional deficiency (B12 or folate deficiency), infection, toxin exposure, aplastic anemia (complication of hepatitis)
59
Most common initial presentation of sickle cell in infants?
Acute Dactylitis: pain and swelling of hands and feet 2/2 vasoocclusive crisis, 2/2 infarction NOT infection; Rx: supportive
60
Treatment of Sickle Cell pt with Priapism?
Low-flow (venous/ischemic) causes erect penis with soft glans; Rx: aspirate corpus, intra-cavernous phenylephrine, surgical drainage prn
61
Treatment of Sickle Cell pt with Stroke?
Emergent exchange transfusion
62
Dx and Tx of Acute Chest Syndrome
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
Kid with sickle cell + nontraumatic rapid drop in Hb
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
Kid with sickle cell, abdominal pain + rapid drop in Hb
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
What infections are more common in sickle cell patients?
Encapsulated organisms: S. pneumoniae, H. influenzae, N. meningitides
66
African American +HIV + anemia after starting on dapsone
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
What are potential G6PD triggers?
Fava beans, Infections, Meds: dapsone, TMP-SMX, phenazopyridine, nitrofurantoin, antimalarials, rasburicase, and methylene blue
68
Old person, gradual face swelling, perioribital edema, cough, and cyanosis. Hx of smoking.
Think superior vena cava syndrome. order: CT chest w/ contrast.
69
Thresholds for platelet transfusions in adults
Trauma or active bleeding, ITP: less than 50,000k / coagulation disorder: 20,000k / everyone else: 5,000-10,000k

ITE (18 decks)

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