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My step 1 mnemonics > Hematology > Flashcards

Hematology Flashcards

1
Q 
Fetal erythropoiesis occurs in:
• Yolk sac (?-?)
• Liver (?- ?)
• Spleen (?- ?)
• Bone marrow (?-?)
A

Fetal erythropoiesis occurs in:
• Yolk sac (3- 8 weeks) - yolk opens from 8-3pm
• Liver (6 weeks- birth) 6iver - living
• Spleen (10- 28 weeks) spleen in between
• Bone marrow (18 weeks to adult) 18 y.o.-adult

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2
Q

ABO classification

AB -?
O -?

A

AB -Universal recipient of RBCs; universal donor of plasma.

O - Receive any non-O -> hemolytic reaction.
Universal donor of RBCs; universal recipient of plasma.

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3
Q

Neutrophils - Specific granules contain:

A

Mafia bullies: “Break, Burn, take money and get lap dances.”

leukocyte alkaline phosphatase (LAP) -“Lap dances”
Collagenase - Break
Lysozyme - Burn
Lactoferrin - “take money (Iron)”

Azurophilic granules (lysosomes) contain: Break, break burn and take
proteinases - break
acid phosphatase - take
myeloperoxidase - burn
beta-glucuronidase break
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4
Q

Important neutrophil chemotactic agents:

A 
P - platelet-activating factor.
L - LTB4
I - IL-8 
C - C5a
K - kallikrein
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5
Q

Anisocytosis = ?
Poikilocytosis =?
Reticulocyte = ?

A

Anisocytosis = varying sizes.
Poikilocytosis =varying shapes.
Reticulocyte = immature RBC; reflects erythroidproIiferation.

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6
Q

Thrombocytes dense granules contain:

A

ADP, Ca2+

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7
Q

Thrombocytes alfa granules contain:

A

4 F’s:

vWF
fibrinogen
fibronectin
platelet factor 4

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8
Q

Eosinophils - Causes of eosinophilia

A

PACA-MAN:

Parasites
Asthma
Churg-Strauss syndrome
Adrenal insufficiency (Chronic)
Myeloproliferative disorders
Allergic processes
Neoplasia (eg, Hodgkin lymphoma)
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9
Q

Eosinophils - Produce

A 
N - neurotoxin
y
M - major basic protein (MBP, a helminthotoxin)
P - peroxidase
H - histaminase 
i
C - cationic protein
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10
Q

Basophils - Densely basophilic granules contain:

A

heparin (anticoagulant)

histamine (vasodilator)

Leukotrienes synthesized and released on demand.

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11
Q

Mast cells Activated by

A

Activated by TEC

T - tissue trauma

E - surface IgE cross-linking by antigen (IgE receptor aggregation)

C - C3a and C5a

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12
Q

Mast cells degranulation ->

A 
release of 
histamine
heparin
tryptase
eosinophil chemotactic factors.
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13
Q

Plasma cells Found in_________ and

normally do not______.

A

Plasma cells Found in the bone marrow and

normally do not circulate in peripheral blood.

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14
Q

Coagulation factors that require Ca+ and phospholipid

A

Activation of 7,9 -> 2

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15
Q

factor IIa activates

A

XIa, VIIIa, Va, XIIIa

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16
Q

factor XIII purpose

A

crosslinks fibrin

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17
Q

Anticoagulation pathways:

A 
Antithrombin pathway (heparin-like molecule - enhances ATlll activity)
Inhibits IIa, VIIa, IXa. Xa, XIa, Xlla

Protein C pathway - C->S
Inhibits Va, VIIIa

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18
Q

Shortest and Longest factor half lives

A

Seven - Shortest

Two - Tallest (longest)

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19
Q

Basophilic stippling

A

Aggregation of ribosomal precipitates.

Do not contain iron.

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20
Q

Heinz bodies

A

Hb denatures and precipitates

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21
Q

Howell-Jolly bodies

A

Basophilic nuclear remnants found in RBCs.

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22
Q

Pappenheimer bodies

A

Siderocytes containing basophilic granules of iron in sideroblastic anemias.

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23
Q

Ringed sideroblasts

A

Excess iron in mitochondria - Seen inside bone marrow smear with special staining

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24
Q

Microcytic anemia

A 
Hemoglobin affected (TAIL):
Defective globin chain:
• Thalassemias
Defective heme synthesis:
•Anemia of chronic disease
•lron deficiency
•lead poisoning
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25
Q

Normocytic - Nonhemolytic anemia

A
  • Iron deficiency (early)
  • Anemia of chronic disease
  • Aplastic anemia
  • Chronic kidney disease
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26
Q

Normocytic - Hemolytic - Intrinsic anemia

A

INSIDE the cell you have (enzymes, Hb, membrane)

Membrane defects:
Hereditary spherocytosis
Paroxysmal nocturnal hemoglobinuria

Enzyme deficiencies:
G6PD deficiency
Pyruvate kinase deficiency

Hemoglobinopathies:
Sickle cell anemia
HbC disease

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27
Q

Normocytic - Hemolytic - Extrinsic anemia

A
  • Autoimmune
  • Microangiopathic
  • Macroangiopathic
  • Infections
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28
Q

Macrocytic - Megaloblastic anemia

A 
DNA affected:
Defective DNA synthesis
•Folate deficiency
•Vitamin B12 deficiency
•Orotic aciduria

Defective DNA repair:
•fanconi anemia

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29
Q

Macrocytic - Nonmegaloblastic anemia

A

Diamond-Blackfan anemia
Liver disease
Alcoholism

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30
Q

Iron-deficiency anemia progression:

A
  1. dec ferritin. inc TIBC
  2. dec. serum iron, dec saturation.
  3. Normocytic anemia
  4. Microcytic anemia
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31
Q

Iron-deficiency anemia Causes:

A

Losing - chronic bleeding
Not getting - malnutrition, absorption disorders, GI surgery
Need more - inc demand (eg, pregnancy)

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32
Q

alfa thalassemia types

A

a -thalassemia minima

a -thalassemia minor

Hemoglobin H disease (HbH);

Hemoglobin Barts disease;

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33
Q

Beta -thalassemia types

A

beta - thalassemia minor - HbA2 (> 3.5%) on electrophoresis.

beta - thalassemia major

HbS/beta-thalassemia heterozygote

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34
Q

beta-thalassemia major results in

A

H - hemochromatosis (2° to blood transfusion)
E - Extramedullary hematopoiesis -> hepatosplenomegaly.
P - Parvovirus Bl9-induced aplastic crisis risk.
A - anemia (severe microcytic, hypochromic)
T - target cells
o
M - Marrow expansion: “crew cut” skull x-ray, “chipmunk” facies
A - anisopoikilocytos (increased)

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35
Q

Sideroblastic anemia causes

A

R - reversible
A - acquired (myelodysplastic syndromes)
G - genetic (eg, X-linked defect in ALA synthase gene),

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36
Q

Reversible Sideroblastic anemia causes

A

C - copper deficiency
A - alcohol, is the most common
L - lead
B - B6 deficiency

D - drugs: isoniazid, linezolid
o
g

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37
Q

Symptoms of LEAD poisoning:

A
  • Lead Lines on gingivae (Burton lines) and on metaphyses of long bones on x-ray.
  • Encephalopathy and Erythrocyte basophilic stippling.
  • Abdominal colic and sideroblastic Anemia.
  • Drops- wrist and foot drop.
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38
Q

Anemia of chronic disease associations

A

A - autoimmune diseases (eg, SLE, rheumatoid arthritis).
I - infections
N - neoplastic disorders
K - kidney disease

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39
Q

Aplastic anemia

A

Fan DRIVe
F - Fanconi anemia

D - drugs (ABC eg, alkylating agents/antimetabolites, benzene, chloramphenicol)
R - Radiation
I - Idiopathic (immune-mediated, primary stem cell defect)
V - Viral agents (EBV, HIV, hepatitis viruses)
e

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40
Q

Fanconi anemia vs. Diamond-Blackfan anemia

A

Both have Short stature and limb defects.

Diamond-Blackfan anemia - defect in erythroid progenitor cells.
Fanconi anemia - DNA repair defect causing bone marrow failure.

Fanconi anemia also presents with tumors/ leukemia, cafe-au-lait spots

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41
Q

Aplastic anemia vs aplastic crisis

A

Dec. reticulocyte count, Inc. EPO.
Normal cell morphology, but hypocellular bone marrow with fatty infiltration

Pancytopenia characterized by anemia, leukopenia, and thrombocytopenia.

aplastic crisis - causes anemia only.

42
Q

Hereditary spherocytosis

A

defect in proteins interacting with RBC membrane skeleton and plasma membrane (eg, ankyrin, band 3, protein 4.2, spectrin).

Mostly autosomal dominant inheritance.

43
Q

Hereditary spherocytosis Labs:

A

Labs:

Dec. mean fluorescence of RBCs in eosin 5-maleimide (EMA) binding test

Inc. fragility in osmotic fragility test.

Normal to dec. MCV with an abundance of RBCs.

Small, round RBCs with less surface area and no central pallor (inc MCHC) -

premature removal by the spleen.

44
Q

Paroxysmal nocturnal hemoglobinuria Triad:

A

Triad:

Coombs (-) hemolytic anemia

pancytopenia,

venous thrombosis (eg, Budd Chiari syndrome).

45
Q

Sickle cell anemia - Vaso-occlusion:

A

Complications in sickle cell disease:

Vaso-occlusion:
1.dactilits/priapism
2.Autosplenectomy (Howell-Jolly bodies) - risk of infection by encapsulated
organisms (eg, S pneumoniae, Salmonella osteomyelitis)
3.Acute chest syndrome
4.Sickling in renal medulla (dec Po2) -> renal papillary necrosis -> hematuria.
5. avascular necrosis, stroke.

46
Q

Sickle cell anemia other complications:

A

Intravascular -> dec. haptoglobin, Target cells
Extravascular -> anemia, jaundice, gallstones.

  • Aplastic crisis (transient arrest of erythropoiesis due to parvovirus Bl9).
  • Splenic infarct/sequestration crisis.
47
Q

Sickle cell anemia Dx

A

Metabisulphite screen -> Sickels with any amount.
Disease - 90% HbS, 8% HbF, 2% HbA2 (no HbA)
Trait - 55% HbA, 43% HbS, 2% HbA2

Hemoglobin electrophoresis

48
Q

Autoimmune hemolytic anemia - IgM vs. IgG

A

Warm (lgG)- chronic anemia seen in SLE and CLL and with certain drugs (eg, alfa-methyldopa)

Cold (lgM AND COMPLIMENT)- acute anemia triggered by cold; seen in CLL, Mycoplasma pneumoniae infections, and infectious Mononucleosis.

Many warm and cold All IAs are idiopathic.

Both have CLL.

49
Q

Direct vs Indirect Coombs test.

A

Direct Coombs test - anti-lg antibody (Coombs reagent) added to the patient’s RBCs.
RBCs agglutinate if RBCs are coated with lg.

Indirect Coombs test - normal RBCs added to the patient’s SERUM. If serum has anti-RBC surface lg, RBCs agglutinate when Coombs reagent added.

50
Q

Lead poisoning

AFFECTED ENZYME

ACCUMULATED SUBSTRATE

A

AFFECTED ENZYME: Ferrochelatase and ALA dehydratase

ACCUMULATED SUBSTRATE: PORTOporphyrin, ALA

51
Q

Acute intermittent porphyria

AFFECTED ENZYME

ACCUMULATED SUBSTRATE

A

AFFECTED ENZYME: Porphobilinogen Deaminase

ACCUMULATED SUBSTRATE: PorphoBILInogen, ALA

Autosomal dominant

“call the P.D (Porphobilinogen Deaminase), because of Billi Domino, that like sweet ham”

52
Q

Porphyria cutanea tarda

AFFECTED ENZYME

ACCUMULATED SUBSTRATE

A

AFFECTED ENZYME: Uroporphyrinogen decarboxylase

ACCUMULATED SUBSTRATE: Uroporphyrin (teacolored urine)

Autosomal dominant

Uri D Carbi is an alcoholic vampire with Hep C”

53
Q

Acute intermittent porphyria Symptoms

A 
(5 P's):
• Painful abdomen
• Port wine-colored urine
• Polyneuropathy
• Psychological disturbances
• Precipitated by drugs (eg, cytochrome P-450 inducers), alcohol, starvation
Treatment: hemin and glucose.

“call the P.D (Porphobilinogen Deaminase), because of Billi Domino, that like sweet ham”

54
Q

Porphyria cutanea tarda Symptoms

A

Blistering cutaneous photosensitivity and hyperpigmentation

Most common porphyria. Exacerbated with alcohol consumption.

Associated with hepatitis C.

Treatment: phlebotomy, sun avoidance, antimalarials (eg, hydroxychloroquine).

Uri D Carbi is an alcoholic vampire (phlebotomy, sun avoidance, antimalarials) with Hep C”

55
Q

Heme and ALA synthase activity

A

Dec heme ->Inc ALA synthase activity

Inc heme -> Dec. ALA synthase activity

56
Q

Coagulation disorders can be due to…

A

clotting factor deficiencies or acquired inhibitors.

57
Q

Coagulation disorders - mixing study

A

Diagnosed with a mixing study, in which normal plasma is added to the patient’s plasma. Clotting factor deficiencies should correct whereas factor inhibitors will not correct.

58
Q

Bernard-Soulier
syndrome
Defect

A

Defect in adhesion

59
Q

Glanzmann
thrombasthenia
Defect

A

Defect in aggregation

60
Q

Immune thrombocytopenia

A

Destruction of platelets in spleen. Anti-Gpllb/ Illa antibodies

Maybe idiopathic or 2° to autoimmune disorders (eg, SLE)

OR

D - drug reactions
M - malignancy (eg, CLL)
V - viral illness (eg, HIV, HCV)

61
Q

The atypical form of HUS (aHUS)

A

Atypical form (aHUS) is caused by complement gene mutations or autoimmune response.

(common form caused by Shiga-like toxin from EHEC- serotype 0157:H7 infection)

62
Q

Disseminated intravascular coagulation

A

S - Sepsis (gram-negative)
T - Transfusion
O - Obstetric complications
P - Pancreatitis (acute)

Making - Malignancy

New - Nephrotic syndrome

ThrombuS -Trauma and Snake bites

63
Q

Antithrombin

deficiency

A

Inherited deficiency of antithrombin: has no direct effect on the PT, PTT, or thrombin time but diminishes the increase in PTT following heparin administration.

64
Q

Factor V Leiden

A

Production of mutant factor V that is resistant to degradation by activated protein C

(guanine ->adenine DNA point mutation - >Arg506Gln mutation near the cleavage site)

“G->A make you Argue with Glen 506 times”

65
Q

Protein C or S

deficiency

A

Dec ability to inactivate factors Va and VIIIa

Risk of thrombotic skin necrosis with hemorrhage after administration of warfarin. If this occurs, think protein C deficiency

66
Q

Prothrombin gene

mutation

A

Mutation in 3’ untranslated region - inc production of prothrombin - inc plasma levels and venous clots

X3 Clots

67
Q

Cryoprecipitate Contains

A

fibrinogen, factor VIII, factor XIII, vWF, and fibronectin

68
Q

Blood transfusion risks include

A

T -transfusion reactions
H - hemochromatosis 2° iron overload
I - infection transmission (low)
C - Ca2+ - hypocalcemia (citrate is a Ca2+ chelator)
K - K+ - hyperkalemia (RBCs may lyse in old blood units).

69
Q

Fresh frozen plasma/prothrombin complex concentrate clinical use:

A

Cirrhosis, immediate anticoagulation reversal

70
Q

Hodgkin lymphoma subtypes:

A

Nodular sclerosis - Most common
Lymphocyte rich - Best prognosis
Mixed cellularity - Eosinophilia, seen in immunocompromised patients
Lymphocyte deleted - seen in immunocompromised patients

71
Q

Adult T- cell lymphoma

A

Adults present with cutaneous lesions

Lytic bone lesions, hypercalcemia.

common in Japan, West Africa, and the Caribbean.

72
Q

Mycosis fungoides/

Sezary syndrome

A

skin patches and plaques (cutaneous T-cell lymphoma),

characterized by atypical CD4+ cells with “cerebriform” nuclei and intraepidermal neoplastic cell aggregates (Pautrier microabscess).

May progress to Sezary syndrome (T-cell leukemia).

73
Q

Multiple myeloma

A

Think CRAB:1,2,2,3
C - HyperCalcemia
R - Renal involvement/ Rouleaux formation
A - Anemia/ Primary amyloidosis (AL)
B - Bone lytic lesions/Back pain/ Bence Jones protein (urine dipstick is negative)

Multiple Myeloma: Monoclonal M protein spike

74
Q

Myelodysplastic

syndromes

A

Stem cell disorders involving ineffective hematopoiesis - defects in cell maturation
of nonlymphoid lineages.

Caused by de novo mutations or environmental exposure (eg, radiation, benzene, chemotherapy).

Risk of transformation to AML.

75
Q

Pseudo-Pelger-Huet anomaly

A

Neutrophils with bilobed (“duet”) nuclei . Typically seen after chemotherapy.

76
Q

Acute lymphoblastic

leukemia/lymphoma

A

Peripheral blood and bone marrow have INC (!) lymphoblasts

T-cell ALL can present as mediastinal mass (presenting as SVC-like syndrome).

TdT+ (a marker of pre-T and pre-B cells), CDI0+ (a marker of pre-B cells).

May spread to CNS and testes.
t( l2;21) - better prognosis.

77
Q

Chronic lymphocytic
leukemia/small
lymphocytic
lymphoma

A

Age> 60 years.

CD20+, CD23+, CD5+ B-cell neoplasm.

smudge cells in peripheral blood smear;

autoimmune hemolytic anemia.

Richter transformation- CLL/SLL transformation into an aggressive lymphoma, most commonly diffuse large B-cell lymphoma (DLBCL).

78
Q

Hairy cell leukemia

A

Adult males.

Mature B-cell tumor - Cells have filamentous, hair-like projections
Peripheral lymphadenopathy is uncommon.

Causes marrow fibrosis - dry tap on aspiration. Patients usually present with massive splenomegaly and pancytopenia.

Stains TRAP - largely replaced with flow cytometry. Associated with BRAF mutations.

Treatment: cladribine, pentostatin.

79
Q

Acute myelogenous

leukemia

A

Median onset of 65 years.

Auer rods; myeloperoxidase(+) cytoplasmic inclusions seen mostly in APL (formerly M3 AML); INC circulating myeloblasts on peripheral smear.

80
Q

Chronic myelogenous

leukemia

A

Median age at diagnosis 64 years.

Defined by the Philadelphia chromosome (t[9;22), BCR-ABL) and myeloid stem cell proliferation.

Presents with dysregulated production of mature and maturing granulocytes (eg, neutrophils,
metamyelocytes, myelocytes, basophils) and splenomegaly.

May accelerate and transform to AML or ALL (“ blast crisis”).

81
Q

Acute myelogenous leukemia

Risk factors:

A 
Risk factors: DRAMa
D - Down syndrome. 
R - radiation
A - alkylating chemotherapy
M - myeloproliferative disorders,
a

APL: t(15;17), responds to all-trans retinoic acid (vitamin A) and arsenic, which induce differentiation of promyelocytes; DIC is a common presentation.

82
Q

Polycythemia vera Tx

A

Treatment: phlebotomy, hydroxyurea, ruxolitinib (JAK1/2 inhibitor).

JACK rocks a lot! - ruxolitinib (JAK1/2 inhibitor)

83
Q

erythromelalgia

A

Rare but classic symptom of Polycythemia Vera and Essential thrombocytopenia

Severe, burning pain and red-blue coloration) due to episodic blood clots in vessels of the extremities.

84
Q

Polycythemia vera presents with

A

Inc in RBC, WBC, Platlets

85
Q

JAK2 MUTATIONS are present in:

A

Polycythemia vera (+)

Essential thrombocythemia and Myelofibrosis - 30-50%

86
Q

t(9;22) (Philadelphia chromosome) ASSOCIATED DISORDER

A

CML (BCR-ABL hybrid)

ALL (less common, poor prognostic factor)

87
Q

t(11;14) ASSOCIATED DISORDER

A

Mantle cell lymphoma (cyclin D1 activation)

88
Q

t(11;18) ASSOCIATED DISORDER

A

Marginal zone lymphoma

89
Q

t(14;18) ASSOCIATED DISORDER

A

Follicular lymphoma (BCL-2 activation)

90
Q

t(8; 14) ASSOCIATED DISORDER

A

Burkitt (Burk-8) lymphoma (c-myc activation)

91
Q

t(15;17) ASSOCIATED DISORDER

A

APL (M3 type of AML; responds to all-trans retinoic acid)

92
Q

Langerhans cell histiocytosis

A

proliferative disorders of Langerhans cells

Presents in a child as lytic bone lesions and skin rash or as recurrent otitis media with a mass involving the mastoid bone.

Cells express S-100 (mesodermal origin) and CD1a. Birbeck granules (“tennis rackets”)

93
Q

The lg heavy chain genes is on

A

on chromosome 14 are constitutively expressed. When other genes (eg, c-myc and BCL-2) are trans located next to this heavy chain gene region, they are overexpressed.

94
Q

Hemophagocytic lymphohistiocytosis

A

Systemic overactivation of macrophages and cytotoxic T cells - fever, pancytopenia, hepatosplenomegaly.

Bone marrow biopsy shows macrophages phagocytosing marrow elements .

INC (!) serum ferritin levels.

95
Q

Hemophagocytic lymphohistiocytosis causes

A

Can be inherited or 2° to strong immunologic activation (eg, after EBV infection, malignancy)

96
Q

Tumor lysis syndrome - Electrolytes affected

A 
Electrolytes affected: PUKe Calcium 
P - inc Po4-
U - inc Uric acid
K - inc K+
e

Calcium - dec Ca2+

97
Q

Tumor lysis syndrome results in

A 
M - Muscle weakness (K+)
A - Arrhythmias, ECG changes (K+, Ca2+)
S - Seizures (Ca2+)
T - tetany (Ca2+)
S (x2)  - Stones (uric acid/ Calcium-phosphate)
98
Q

Procarbazine

A

Cell cycle phase- nonspecific alkylating agent, mechanism not yet defined.

Hodgkin lymphoma, brain tumors.

Bone marrow suppression, pulmonary toxicity, leukemia, disulfiram-like reaction.

99
Q

Cetuximab, panitumumab

A

Monoclonal antibodies against EGFR.

Stage IV colorectal cancer (wild-type KRAS), head and neck cancer.

Rash, elevated LFTs, diarrhea.

Earl has a C-TUX and panties for colon an head and neck

100
Q

Dabrafenib, vemurafenib

A

BRAF inhibition. Often co-administered with MEK inhibitors (eg, trametinib).

VEmuRAF-enib is for V600Emutated

Devra Vemura wants to make it to the TRAM

My step 1 mnemonics (19 decks)

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