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MF2 HEMATOLOGY Flashcards

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USMLE® Step 1 flashcards
1
Q

Hematopoeisis

A

Monoblast -> monocyte
Myeloblast -> basophil,
Common -> neutrophil,
Myeloid eosinophil
Promegakaryocyte -> platelets
Preerythroblast -> RBCs
Stem cell ->

                 Common                                   B-lymphocyte
                 Lymphoid -> Lymphocyte ->  NK Cell
                                                                     T            -> Th & Tc

Basophil, neutrophil, eosinophil = 5-10 days
Platelets = 7-10 days
RBCs = 100-120 days

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2
Q

Pancytopenia

A

BM SUPPRESSION
- Drugs sequestration
> Chemo
> Radiation
> HIV meds
> Anti-seizure
> Anti-thyroid
> Sulfonamides
- Infection
> Viral (HIV, Hep B, EPV, parvovirus B19)
> Bacterial (TB)
- Illness
> MDS
> Lupus
> DIC
> Starvation, Anorexia nervosa
> Autoimmune destruction
> Aplastic anemia (acquired, inherited)
- Fanconi
> Sarcoidosis

SPLENOMEGALY

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3
Q

Microcytic Anemias

A

TAILS (thalassemia, anemia chronic disease, Fe, lead, sideroblast)

DECREASED HEME DECREASED GLOBIN

  • Fe deficiency
    > Sometimes high platelets
  • Sideroblastic
    > High hepcidin, lead
    > Buildup Fe RBC in periphery
    > Defect ih heme synthesis
  • Copper deficiency
  • Anemia chronic disease
    > Hepcidin (liver) response to inflammation
    > Feroportin in macros

DECREASED GLOBIN
- Thalassemia
> alpha
- Minima: silent
- Minor: trans v cis
- HbH: moderate, 4B
- Hb Barts: deadly

> beta
- Minor: often silent
- Intermedia: less B
- Major: no B; 3-6 months; anemia, jaundice, hemochromatosis, large forehead, cheekbones

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4
Q

Normocytic Anemia

A

—- HEMOLYTIC —-

INTRINSIC
- Membrane Issue
> Hereditary spherocytosis (no ankyrin or spectrin)
> Eliptocytosis
> Paroxysmal nocturnal hemoglobinuria (complement
mediated)
- Enzyme issue
> G6DPH anemia (ROS destroy Hb -> Heinz bodies;
common in young African Americans, post infection)
- Folic acid
> Pyruvate kinase deficiency (less ATP –> rigid)
- Hemoglobin Issue
> Sickle cell anemia (B globin point mutation; shape
change when deoxy -> aggregate -> polymers -> lyse->
free Hb -> low haptoglobin -> high unconjugated
bilirubin (jaundice, gallstones) -> increased BM to
compensate & extramedullary hematopoeisis
(hepatomegally) -> VASO-OCCLUSION -> acute chest,
stroke (Moya-Moya), pain crisis, auto-splenectomy,
renal necrosis, priapism, aplastic crisis, marrow infarct
(-> fat emboli);
**Howel-Jolly bodies
**Folic acid, hydroxyurea, supportive care for vaco-occ
> Hemoglobin C disease

EXTRINSIC
- Infection (fever, rash)
> Sepsis
> Malaria
> Babesiosis
> Disseminated C. difficile
- Autoimmune
> Cold ( - IgG, + IgM )
> Warm ( + IgG )
- Microangiopathic hemolytic anemia (MAHA)
> DIC (septic, high coagulation, low fibrinogen)
> TTP (fever, anemia, thrombocytopenia, renal, neuro)
> HUS (younger, prior GI infection, acute renal failure)
> HELLP (pregnant, elevated LFTs; preeclampsia)
> Mechanical valve (chew up RBCs)

—-NON-HEMOLYTIC —-
- Hypothyroidism
- Early Fe deficiency
- Liver failure
- Early B12/Folate deficiency
- Poor gut absorption (low Fe and B12)
- CKD (kidneys make EPO)
- Hemorrhagic (acute blood loss)

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5
Q

Macrocytic Anemia

A

MEGALOBLASTIC (DNA synthesis issue)
- B12/Folate deficiency (pancytopenia)
- Fanconi aplastic anemia (pancytopenia)
- Orotic aciduria

NON-MEGALOBLASTIC
- Liver disease
- Diamond Blackfam anemia
- Alcohol abuse

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6
Q

Ferritin vs transferrin

A

Ferritin: Fe storage
> Fe deficiency anemia low
> Anemia chronic disease high

Transferrin: Fe binding
> Fe deficiency anemia high
> Anemia chronic disease low

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7
Q

Hemostasis: regulation

A
  • Secrete NO, PGI2 –| platelets
  • Heparin sulfate binds antithrombin III –| II, IX, X
  • Thrombomodulin binds II –> protein C –| V, VIII
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8
Q

Hemostasis Steps

A
  1. Vascular spasm: endothilin, inflammation -> smooth muscle contraction
  2. Platelet plug formation: vMF by endothelial cells –> platelets bind via GpIa –> bind eachother by GpIIb/IIIa & fibrinogen –> secrete ADP, thromboxane A2, serotonin –> stimulate platelets & vasocontriction

***Aspirin inhibits TXA2

  1. Coagulation:
    > Extrinsic: III –> VII –> IX
    > Intrinsic: XII –> XI –> IX
    > Common: Ix + VIII –> X + V –> prothrombin activator
    –> II + I –> Fibrin + XIII –> FIBRIN MESH

**Not made by liver: III, VIII
**Shortest half-life: VII
**Longest half-life: II
**Made with vitamin K: X, IX, VII, II (1972)
> Warfarin inhibits VK

  1. Clot retraction: platelet-derived growth factor (collagen, endo repair)
  2. Fibrinolysis: plasminogen eats clot
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9
Q

Coagulation Tests

A
  • INR: problem with extrinsic and/or common pathway
    (ratio measures time to clot)
  • aPTT: problem with intrinsic and/or common pathway
    (activation partial thromboplastin time)
  • TCT: activity of fibrinogen (I; thrombin clotting time)
  • Factor deficiency vs inhibitor: mix with normal blood
    > Corrects: deficiency
    > Does not correct: inhibitor (auto-Ab; if delayed often
    for VII, VIII b/c delayed activation)
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10
Q

Primary hemostasis vs secondary hemostasis bleeding disorders

A

PRIMARY
- Instant onset bleeding
- Mucosal bleeding (superficial)
> Nose
> Gums
> Periods
> GI
- Petichae (won’t disappear when you press)
- Vascular or Platelet issue

SECONDARY
- Delayed onset bleeding
- Joint bleeding
- Bleed into muscle -> compartment syndrome (*electrolytes, myoglobin, lactic acid, hyperK)
- Affecting intrinsic, extrinsic, or common pathway

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11
Q

Bleeding disorders

A

PRIMARY

  • Vascular
    > Amyloidosis
    > HHT/Osler Webber Rendu (bad vessels)
    > Ehlers Danlos (bad collagen)
    > Scurvy (low vitC → bad collagen)
    > Cushings (thin walls)
    > Vasculitis, infection
  • Platelets
    > Quantitiative
    - Low production: aplastic anemia
    - Increased destruction: ITP, TTP/HUS, HIT
    - Sequestration: splenomegaly
    > Qualitative
    - Bernard soulier syndrome (Gp1b deficiency)
    - Glanzmans syndrome (GpIIb/IIIa)
    - Drugs (ASA, EtOH, NSAIDs)
    - Renal failure
    - Myeloproliferative disorder
    > vWD: most common inherited bleeding disorder
    - VIII broken down faster, eventual deficiency
    - Type 1: 3/4 cases; mild quantitative defect, non-severe
    - Type 2: qualitative, moderate-severe
    > A = reduced platelet adhesion b/c multimer
    > B = increased GPIb affinity (**don’t use DDAVP)
    > M = reduced platelet adhesion
    > N = decreased FVIII affinity (recessive)
    - Type 3: quantitative, near/total absence, severe (rec)
    - Epistaxis, oral cavity bleeding, menorrhagia
    - Normal PT, n/low platelet, n/prolonged aPTT, vWD
    testing, VIII activity
    - TREATMENT: estrogen contraceptives for
    mennhoragia, DDAVP for mild (1, 2A); if
    active bleeding, surgery desmopressin
    (DDAVP), vWF:VIII, antifibrinolytics
    (tranexamic acid)

SECONDARY
- Intrinsic
> Hemophilia: X-linked recessive, 50% severe
- Easy bruising, hemarthrosis, epistaxis, hematomas
- Prolonged aPTT, PT/INR, vWF:Ag, platelets normal
- Hemophilia A: VIII deficiency, most common
- Hemophilia B: factor IX deficiency, “Christmas”
- TREATMENT: desmopressin (DDAVP), VIII concentrate,
antifinrinolytics (tranexamic acid)
> vWD
> Factor IX deficiency: common in Ashkenazi Jewish, mild

  • Extrinsic
    > Factor VII (acquired factor inhibitor; malignancy,
    autoimmune disorders, post-partum)
  • Common
    > Vitamin K deficiency (needed for some factors; 1972)
    - Drugs: warfarin, antibiotics
    - Poor diet
    - Biliary obstruction
    > Liver disease (makes factors)
    - Thrombocytopenia, deficiency in factors (but VIII), less
    II, less anticoagulants and altered fibrinolysis
    > DIC (use up factors)
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12
Q

Thrombocytopenia

A

**mucocutaneous bleeding, epistaxis, perioperative bleeding, heavy period, bruising, petichiae, ecchymoses, purpura (non-palpable, wet)

INCREASED DESTRUCTION
- Immune
> ITP
> Viral: HIV
> Systemic: SLE, RA
> Alloimmune
> Drug-induced
- HIT
- Quinine
- Sulfonamides, ampicillin, vancomycin
- Acetaminophen, ibuprofen, naproxen (aleve)
- Non-immune
> HELLP, preeclampsia
> Thrombotic microangiopathies: hemolytic anemia, low
platelets, organ damage from microthrombi
- TTP
- HUS
> DIC

DECREASED PRODUCTION
- B12/Folate deficiency
- Marrow damage
> Chemo, radiation
> Aplastic anemia
> Malignancy
> Myelodysplastic
> Drug-induced
- Valproic acid
- Daptomycin
- Linezolid
> Congenital
- Alport (kidney disease, TPO)
- Fanconi syndrome (kidney disease, TPO)

SEQUESTRATION
- Splenomegaly
> Liver failure
> Portal HTN
> Infection (HIV, mono, Hep C, Tb, endocarditis)
> Amyloidosis, sarcoidosis, hemochromatosis
- Malignancy
> Lymphoma
> Leukemia

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13
Q

HIT

A

Heparin-induced thrombocytopenia (HIT)

  • Type I HIT: also known as heparin-associated thrombocytopenia (HAT), non-immune mediated reaction.
    > More common than type II
    > Mild reaction, not associated with complications,
    platelet counts spontaneously normalize (even if
    heparin continued)
  • Type II HIT: immune, antibody-mediated reaction (PF4-heparin + IgG –> activates more platelets)
    > Time for Abs, 5 to 14 days after heparin
    > If exposed to heparin w/in 100 days, Abc may remain
    > Serious rxn -> hypercoagulable state ->
    venous/arterial thrombosis –> DVT, PE, skin necrosis
    > Macros eat IgG coated platelets
  • 4T SCORE
    > Thrombocytopenia (30-50% drop)
    > Thrombosis (DVT, MI, gangrene, etc)
    > Timing (5-14 days)
    > Thrombocytopenia (other causes)
  • ELISA: antibodies test
  • SRA: confirm IgG
  • TREATMENT
    > Stop heparin
    > Anti-thrombins: argatroban
    > Anti-X: rivoroxaban (take with food!!), apixaban, edoxapan
    > If on warfarin, stop and five vitK
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14
Q

TTP

A

Thrombotic thrombocytopenic purpura (TTP)

  • Decreased ADAMTS-13 (cleaves vWF)
  • Congenital (5%) or acquired (95%; auto-Abs)
    > Congenital: kids
    > Acquired: adults; cancer, meds, HIV, BM transplant, SLE
  • PRESENTATION: Fever, Anemia, Thrombocytopenia, Renal failure, Neurological deficits ; can be mild and non-specific symptoms
  • INVESTIGATION: ADAMTS13 activity, inhibitor, platelets, hemolysis (cooms, haptoglobin, LDH), MCV, INR, creatining
  • TREATMENT: plasma exchange, corticosteroids, FFP, caplacizumab (prevents platelet vWF interaction, so stop thrombi formation)
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15
Q

Blood film interpretation (size, colour, shape)

A

SIZE
- Microcytic <80
- Normocytic 80-100
- Macrocytic >100
- Anisocytosis: variability in size
> low Fe, hemolytic, myelofibrosis, myelodysplastic

COLOUR
- Hypochromic: central pallor
> low Fe, anemia chronic disease, sideroblastic
- Polychromasia: increased reticulocytes (pinkish-blue)
> Increased RBC production by BM

SHAPE
- Poikilocytosis: increased proportion of abnormal shape
> Fe low, Hb-opathies, severe low B12, myelofibrosis

**myelofibrosis = bone marrow cancer (uncommon)
**myelodysplastic synromes = cancers where blood cells in the bone marrow do not mature

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16
Q

RBC inclusions

A
  • Nucleus: erythroblast → hemolytic anemia, BM infiltration
  • Heinz bodies: Thalassemia, G6PD, unstable Hb
  • Howell-Jolly bodies: megaloblastic, hyposplenism
  • Basophilic stippling: blue granulations → thalassemia, heavy
    metal, megaloblastic, myelodysplastic
  • Sideroblast: late erythrocyte → drugs, ethanol, hypothyroid,
    idiopathic
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17
Q

Hypersegmented neutrophils

A

> 5 lobes suggests megaloblastic process
- B12 deficiency
- Folate deficiency

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18
Q

Bone marrow aspiration and biopsy

A
  • Posterior iliac crest/spine, sternum (apsiration only)
  • Aspiration: takes fluid marrow for cell morphology
  • Biopsy: takes intact BM for histology and
    immunohistochemistry
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19
Q

Causes of splenomegally

A

CHINA

Cirrhosis, congestion (portal HTN)
Hematological
> Nutritional anemias
> Hb-opathies
> Hemolysis
> Spherocytosis
> Sequestration crisis
Infectious
> Viral: EBV, HIV
> Bacterial: TB, endocarditis
> Parasitic: malaria, histoplasmosis, leishmaniasis
Neoplasm
> Leukemia
> Lymphoproliferative disease
Autoimmune
> SLE
> Sarcoidosis

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20
Q

Microcytic anemia iron tests (ferritin, serum Fe, TIBC, % sat, RDW)

A

Ferritin Serum Fe TIBC % sat RDW
Fe deficiency: low low high low high
Chronic disease: n/high low low n n
Sideroblastic: n/high high n n/high high
Thalassemia: n/high n/high n n/high n/h

21
Q

Organs affected by vaso-occlusive crisis

A

Brain = ischemic or hemorrhagic stroke
Eye = hemorrhage, blindness
Liver = infarcts
Lung = acute chest syndrome, long-term pulmonary HTN
Gallbladder = stones
Heart = hyperdynamic flow murmurs
Spleen = enlarged (child), atrophied (adult)
Kidney = hematuria, proteinuria
Intestines = acute abdomen
Placenta = stillbirths
Penis = priapism
Digits = dactylitis
Bone = infarction, infection, avascular necrosis
Skin = leg ulcers (ankle)

22
Q

Drugs associated with thrombocytopenia

A

trimethoprim/sulfamethoxazole
heaprin
NSAIDs
Vancomycin
Digoxin (increased myocardial contractility, reduce HR)
Acetominaphen
Ethanol
H2-antagonists (for duodenal ulcers)

23
Q

Thrombocytopenia treatment

A

EMERGENCY
- Corticosteroids (prednisone)
- Antifibrinolytic if mucosal bleeding
- Platelet transfusion for major bleeding or urgent surgery

NON-URGENT
- 1st line: corticosteroids
- 2nd line: splenectomy, rituximab
- 3rd line: TPO receptor agonsist

24
Q

Affects of alcohol on hemostasis

A
  • Harm liver → TPO synthesis
  • Bone marrow suppression
  • Decrease lifespan of platelet
  • Directly toxic to platelets in blood
  • Impair platelet response to activators
  • Rebound effect: acute platelet drop when drinking then
    when stop → thrombocytosis → can lead to stroke
25
Q

HUS (causes, clinical features, treatment)

A

Hemolytic Uremic Syndrome

  • Predominantly children and elderly
  • RBC lysis → kidney failure
  • Shiga toxin (E.coli) 90%
  • Clinical features
    > Severe thrombocytopenia
    > MAHA (non-immune hemolysis) /thrombotic
    microangiopathy
    > AKI
    > Bloody diarrhea
    > GI prodrome
  • Treatment
    > Supportive therapy: fluids, RBC transfusion, nutrition
    > Plasma exchange (some evidence)
26
Q

DIC (causes, clinical features, treatment)

A

Disseminated Intravascular Coagulation

  • Excessive, dysregulated release of plasmin and thrombin → intravascular coagulation and depletion of platelets, coagulation factors, fibrinogen
  • Causes
    > Intravascular hemolysis: incompatible blood, malaria
    > Tissue injury: trauma, burns, crush injuries
    > Malignancy: solid tumors, hematologic malignancies
    > Snake venom (viper), fat embolism, heat stroke
    > Endothelial injury: infection, vasculitis
    > Liver disease
    > Splenectomy
    > Vascular stasis: hypotension, hypovolemia, PE, shock
    > Acute hypoxia/acidosis
  • Clinical features
    > Neuro: multifocal infarcts, delirium, coma, seizures
    > Skin: focal ischemia, gangrene, purpura fulminans
    > Renal: oliguria, azotemia, cortical necrosis
    > Pulmonary: ARDS
    > GI: acute ulceration, liver dysfunction
    > Adrenal: hemorrhage or infarct
    > RBC: microangiopathic hemolysis
  • Treatment
    > Underlying condition
    > Transfuse platelets if active bleeding
    > Fibrinogen concentrate if severe hypofibrinogenemia
27
Q

Hypercoagulability Indications

A
  • Patients with multiple recurrent thromboses
  • Warfarin-induced skin necrosis or neonatal purpura fulminanas (protein C or S deficiency)
  • Thrombosis at an unusual venous site
  • If abnormal blood work, constitutional symptoms, or physical exam suggestive of cancer → workup for malignancy
28
Q

Pathophysiologic causes of hypercoagulability

A

ACTIVATED PROTEIN C RESISTANCE
- Factor V Leiden
- Most common cause of hereditary thrombophilia
- Point mutationn in factor V → C cannot inactivate V

PROTHROMBIN GENE MUTATION (PT) G20210A
- Transposition of prothrombin promoter → increased
prothrombin → increased thrombin

PROTEIN C DEFICIENCY
- C inactivates V and VIII using S as cofactor
- Homozygous: neonatal purpura fulminans
- Heterozygous:
> Type I: decreased C levels
> Type II: decreased C activity
- Acquired: liver disease, sepsis, DIC, warfarin, some chemo

PROTEIN C S DEFICIENCY
- Type I: decreased free and total S
- Type II: decreased S activity
- Type III: decreased free S
- Acquired: liver disease, DIC, pregnancy, nephrotic
syndrome, infammatory conditions, warfarin

ANTITHROMBIN DEFICIENCY
- In absence of heparin, antithrombin inactivates thrombin,
quickly with heparin
- Causes:
> Autosomal inheritance
> Urinary losses in nephrotic syndrome
> Reduced liver synthesis
- May have heparin resistance

ELEVATED FACTOR VIII LEVELS

CONGENITAL DYSFIBRINOGENEMIA
- May predispose to thromboembolic disease, bleeding, or
both

DISORDERS OF FIBRINOLYSOS
- Includes congenital plasminogen deficiency, tissue
plasminogen activator deficiency, association with VTE risk
not clear

29
Q

Venous Thromboembolism (definition, features, investigation)

A
  • Thrombus formation and subsequent inflammatory response in superficial or deep vein
    > Superficial thrombophlebitis
    > DVT
    > PE
    **Most severe sequela of PE is chronic
    thromboembolic pulmonary HTN (CTEPH)
  • Clinical features
    > Unilateral leg edema, erythema, warmth, tenderness
    > Palpable cord (thrombosed vein)
    > Phlegmasia alba dolens (white appearance) and
    phlegmasia cerula dolens (acute pain and edema)
    with massive thrombosis
    > Homan’s sign (pain or resistance with foot
    dorsiflexion); unreliable
  • Investigation
    > D-dimer test (rule out DVT; protein made when clot
    dissolves)
    > Doppler ultrasound
    > Venography (gold standard but expensive, invasive,
    higher risk)
    > CT pulmonary angiogram, V/Q scan
30
Q

Virchow’s Triad

A
  • Endothelial damage
    > Exposes endothelium to prompt hemostasis
    > Decreased inhibition of coagulation and local
    fibrinolysis
  • Venous stasis
    > Immobilization inhibits clearance and dilution of
    factors
    > Post-MI, CHF, stroke, postoperative
  • Hypercoagulability
    > Inherited
    > Acquired
    > Age
    > Surgery (especially orthopaedic, thoracic, GI, GU)
    > Trauma (especially spine, pelvis, femur, tibia)
    > Neoplasms (especially pancreas, stomach, bladder,
    lymphoma, lung, testicular, colorectal, gynaecologic)
    > Blood dyscrasias, hyperviscosity (multiplemyeloma,
    polycythemia, leukemia, and SCD), hemolytic anemia
    > Prolonged immobilization (CHF, stroke, MI, leg injury)
    > Hormone (OCP, HRT, selective estrogen rec
    modulators)
    > Pregnancy
    > Heart failure
31
Q

Venous thromboembolism treatment (initial, long-term, in hospital prophylaxis)

A

INITIAL TREATMENT
- LMWH subcutaneous, lower bleeding risk
> Predictable dose response
> Lab monitoring not required
> <1% HIT
> Long term use associated with osteoporosis, $$
> Renally cleared (adjustment if renal dysfunction)
- UFH if high risk of bleeds or surgery
> Rapidly reversible by protamine
> Must monitor aPPT or heparin levels to reach
therapeutic level, higher risk of HIT
- Direct thrombin inhibitors and Xa inhibitors as alternatives
> II: Hirudin, lepirudin, argatroban, dabigatran
> X: Apixaban, rivaroxaban

LONG-TERM TREATMENT
- Anticoagulation therapy
> Warfarin: with heparin overlap for at least 48hr with
INR>2, then discontinue heparin
LMWH more effective than warfarin at
preventing recurrence of venous thrombosis in
cancer patients
> DOACs:
- Apixaban or rivaroxaban (no lab monitoring)
- Dabigatran (LMWH or IV heparin for 5d before)
> If provoked VTE with transient risk factor: 3 months
> If provoked VTE with ongoing risk factor: indefinite
> First unprovoked DVT/PE: >/= 3 months, indefinite
> Second unprovoked VTE: indefinite
> Cancer-associated DVT: 3-6 months, longer if
continued evidence of cancer
*Annual reassessment
- IVC filters
> Temporary if acute DVT (<4wk) with
contraindications to anticoagulant therapy (active
bleeding, surgery)
> Pro-thrombic in long term, so retrieve once safe
- Special considerations
> Pregnancy: LMWH during, then LMWH or warfarin
6wk post partum
**avoid warfarin and DOAC in pregnancy, DOAC in
breastfeeding
> Surgery:
- Preoperatively: IV heparin up to 4-6hr prior
- Perioperatively: warfarin or DOACs discontinued
at least 2-5 days prior
- Postoperatively: IV heparin, MWH, DOAC
- High risk: IV heparin or LMWH may be
considered before & after while INR<2

IN HOSPITAL PROPHYLAXIS
- Early ambulation, elastic compression stockings, intermittent pneumatic compression
- LMWH
- DOACs for orthopaedic surgery thromboprophylaxis

32
Q

LMWH vs UFH

A

Low molecular weight heparin differs from unfractionated heparin:
- The average molecular weight
- It is more expensive
- Greater effect on X, less on II
- Only once or twice daily dosing (lasts longer)
- The absence of monitoring the aPTT
- The lower risk of bleeding, osteoporosis, and HIT

33
Q

Pulmonary embolism treatment

A
  • Admit for observation and stratify risk
  • Supplemental oxygen
  • Pain relief (narcotics, acetaminophen)
  • Acute anticoagulation
    > LMWH or
    > Rivaroxaban, apixaban, edoxaban or
    > Dabigatran
  • Long term anticoagulation
    > DOACs (rivaroxaban, dabigatran)
    > or warfarin
    **LMWH instead of warfarin if pregnant, cancer, high
    risk bleeding
  • IV thrombolytic therapy
    > If massive PE and no contraindications
34
Q

What should be used in place of warfarin to prevent VTE in cancer patients

A

LMWH more effective than warfarin at preventing recurrence of venous thrombosis in cancer patients

35
Q

What anticoagulants should be avoided in pregnancy? What instead?

A

Avoid warfarin and DOAC in pregnancy, DOAC in
breastfeeding
Use LMWH instead

36
Q

Most common hereditary thrombophilia

A

Factor V Leiden (Activated protein C resistance)
Resistance to activation of Factor V by activated protein C

37
Q

Hemoglobins

A

HbA: 95-98% 2a2b
HbA2b: 2-3% 2a2d
HbF: fetal (higher O2 affinity for placenta) 0.8-2% 2a2g
- 50-80% newborn

38
Q

Lymphoma general presentations

A

GENERAL
> Mediastinal mass
> Splenomegaly
> Fatigue
> B symptoms (fever, night sweats, weight loss >10% in 6mo)

HODGKINS LYMPHOMA
> Contiguous spread, rarely extranodal
> Reed-Sternberg cells (B-derived)
> 50% connected to EBV
> Better prognosis; often bimodal (20s then >50s)
> Abnormal lymph nodes (enlarged, immobile, non-tender [unless fast growing], hard/rubbery) cervical > axilla > inguinal
> Alcohol-induced pain
> More likely classical

NON- HODGKINS LYMPHOMA (90%)
> Non-contiguous, often extranodal (GI, brain, skin), usually genetic mutation
> HIV, EBV, HepB, HILV, autoimmunity risk factors
> Spinal involvement (compression; decreased sensation)
> CNS symptoms (focal neuro deficits)
> GI symptoms (pain, bleeding, satiety, obstruction, nausea/vomit)
> Recurrent infection, frequent bruising, fatigue (cytopenia)
> 85% b cell

39
Q

Hodgkin’s Lymphoma (presentation, types)

A

CLASSICAL
> More common
> No CD45 or CD20, yes CD15 and CD30

> Nodular Sclerosis (most common; surround by collagen)
Lymphocyte-depleted (least common; lack reactive lymphos)
Lymphocyte-rich (best prognosis; mostly lymphos)
Mixed cellularity (2nd most common; neuts, eos, lymphos, plasma, histocytes surround)

40
Q

Lymphoma diagnostic approach

A
  1. Labs:
    > CBC (differential, blasts, peripheral smear, retic count)
    > HIV/Hep (risk factors)
    > Electrolytes
    > LDH (tumor lysis, cell death/turnover)
    > Uric Acid
    > Liver enzymes (liver involvement
    > Calcium (iodized or corrected for albumin; bone involvement)
    > Renal tests (before chemo)
    > PTT/PT (before biopsy)
  2. Imaging
    > PET/CT (whole body)
    > CXR (mediastinal mass)
  3. Biopsy
    > Excisional
    > Core needle
    > Bone marrow
41
Q

Tumor Lysis Syndrome (cause, complications, treatment)

A

> Oncologic emergency triggered by tumor cell lysis
Seen most often in lymphomas/leukemias (rare solid tumors)
Caused by treatment or spontaneous (fast-growing)

> K release: hyperkalemia (**arrhythmias, muscle weak)
SOLUTION: insulin (&glucose), ventilin, K oxalate or diuretics (remove), calcium gluconate (stabilize heart)

> PO4 release: hypocalcemia due to sequestration (**tetany, ECG changes, seizures)

> Nucleic acid breakdown: hyperuricemia (**AKI)
………>Crystals: precipitate in tubules, minimal change; intrinsic
………>Stones: uric acid, calcium phosphate; post-renal

> Rasburicase: chemotoxicity amelioration; recombinant uricase that breaks down uric acid
………>Side effects: anaphylaxis, methemoglobinemia (G6DPH low)
Allopurinol: prevents production, renally dosed
………>Side effects: dress syndrome (rare, more common in Asian)
Aggressive hydration, dialysis (for kidneys [crystals], for hyperK)

42
Q

Non-Hodgkins Lymphoma (presentation, types)

A

B-CELL (85%)
> Usually CD20
> Indulent (slow), aggressive, highly aggressive

> Follicular: most common indulent; death prevention
Diffuse large B cell: aggressive; most common in adults
Mantle cell lymphoma: aggressive; more growth
Marginal zone lymphoma: indulent; most common type is MALT
Burkit lymphoma: highly aggressive; more division

T-CELL
> Adult T-cell lymphoma: HTLV (Japan, Carribbean)
> Mycosis Furigosis: patches look like fungal infection, erythrodema

43
Q

Lymphoma treatment approach

A

Cyclophosphamide: alkylating agent (damage DNA; cycle indep)
Hydroxy doxorubicin (adriamycin): anthracycline (cell cycle independent alkylating agent)
Oncovin (vincristine): vinca alkaloid (inhibit microtubules; cycle-dependent)
Prednisone: immunosupressant, feel better

Radiation

44
Q

Leukemia classification

A
  • By how immature the originative cell is:
    >Acute: grow fast, acute onset; origin cells most immature
    >Chronic: grow fast, chronic onset; origin cell more developed
  • By cell type
    >Acute lymphocytic leukemia (ALL)
    –> B cell (more common)
    –> T cell
    >Acute myeloid leukemias (AML)
    –> Megakaryoblastic
    –> Myeloblastic
    –> Monoblastic
    –> Erythroblastic
    >Chronic lymphoid leukemia (CLL)
    –> B cell
45
Q

Acute lymphocytic leukemia (ALL): Dx, Sx, prognosis

A
  • Most common in kids, associated with Down Syndrome
  • INVESTIGATIONS:
    >CBC (small blasts, low RBCs & platelets)
    >peripheral blood smear (blasts, glycogen granules, fewer nuclei), flow cytometry (CD markers)
    >BM biopsy (to confirm diagnosis; Tdt protein)
    >Lumbar puncture (additional test to see spread to CSF)
    >HIV/Hep B screens (prior to treatment)
  • PRESENTATION:
    >Pancytopenia (increased infection, fatigue, bruising)
    >Bone pain (sternal pain common)
    >B Symptoms
    >Hepatosplenomegally
    >Lymphadenopathy
    >T CELL: thymus mass (can compress airway/esophagus), teenagers
    >B CELL: translocations (t12;21 kids, t9;22 adults), better prognosis in kids
  • PROGNOSIS:
    >60-70% 5 year survival adults
    >80% 5 year survival kids
46
Q

Acute myeloid leukemias (AML)

A
  • Most common leukemia among older adults (80%), median 65 years old
  • Most common risk factor is myelodysplastic syndrome, Down Syndrome, male
  • Environmental risk factors: benzene, radiation, chemo drugs
  • INVETIGATIONS:
    >CBC (big blasts, auer rods, more nuclei)**
    >Peripheral blood smear, flow cytometry (CD markers)
    >BM biopsy (to confirm diagnosis; Tdt protein)
    >Lumbar puncture (additional test to see spread to CSF)
    >HIV/Hep B screens (prior to treatment)
  • PRESENTATION:
    >Pancytopenia (increased infection, fatigue, bruising)
    >Bone pain (sternal pain common)
    >B Symptoms (fever less likely)
    >Hepatosplenomegaly
    >Lymphadenopathy
    >Swollen gums
    >DIC**
    >Tumor lysis syndrome**
  • PROGNOSIS
    >Worse than ALL; variable if respond to chemo

** = different from ALL

47
Q

Chemotherapy Drug classes

A
  1. Alkylating agents: unstable alkyl groups inhibit rep/trans
    > Cyclophosphamide
    > Platinum containing compounds
    **Myelosuppression, mucositis, nausea/vomiting, neurotoxicity, alopecia
  2. Antimetabolites: immitate DNA ingredients
    >Cytidine analogs
    >Folate antagonists (methotrexate)
    >Purine analogs
    >Pyrimidine analogs
  3. Antimicrotubular: target cytoskeleton (M phase)
    >Taxanes: disrupts eq of po/depol of microtubules
    >Vinca alkyloids: inhibit formation (vincristine)
  4. Topoisomerase inhibitors: inhibit unwinding
    >Topoisomerase I inhibitors: prevent relegation
    >Topoisomerase II inhibitors: inhibit DNA synthesis/repair
  5. Antibiotics: inhibit RNA/DNA synthesis
    >Release ROS, inhibit topoisomerase, intercalating agents
    >Actinomycin D
    >Doxorubicin (anthracycline)
  6. Protein kinase inhibitors
    >Tyrosine kinase inhibitors (ex. t9;22 = BCR-ABL mutation)
  7. Antibodies + Immunotherapy (more targeted)
    > Antibodies: Rituximab (CD20)
    > Immunotherapy: CAR-T cell therapy, checkpoint inhibitors
  8. Miscellaneous:
    >Hydroxyurea
    >Tretinoin
    >Arsenic trioxide
    >Proteasome inhibitors
48
Q

Febril Neutropenia

A
  • Fever + neutrophil count (ANC) less than 1500cells/mL
  • Most common serious and common complication of cancer therapy
  • Infectious etiology usually unable to be determined (30%)
  • INVESTIGATION:
    > Complete blood count, 2 blood cultures, urinalysis, throat cultures
  • TREATMENT:
    >Low risk: oral fluoroquilolone + amoxicillin
    > High risk: IV antibiotics

medical school (9 decks)

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