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STEP2 > Immunology/Hematology > Flashcards

Immunology/Hematology Flashcards

1
Q

1) Reed Sternberg cells (OO), Pel-Ebstein fevers (come & go every few weeks), and lymph node pain induced by alcohol consumption are highly specific for what lymphoma?
2) Reed Sternberg cells originate from B cells and are CD_/_ +

A

HODGKIN lymphoma

CD15/30+

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2
Q

EBV, SLE, and RA increases risk of developing what lymphoma?

A

Hodgkin lymphoma

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3
Q

GOAL and 3 drug treatment for CEREBRAL toxoplasmosis?

A

GOAL: inhibit folate (= stops toxoplasmosis parasite from spreading) + replace lost folate

1) pyrimethamine (inhibits DHF reductase)
2) sulfadiazine (sulfonamide)
3) leucovorin (folinic acid).

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4
Q

A prolonged PT is associated with a deficiency in only one factor: ____

A

Factor 7.

Factor 7 is the only one standing outside (Extrinsic); all other factors (PTT) are inside (Intrinsic)

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5
Q

Which factor is responsible for the activation of factor 7?

Which vitamin is responsible for the activation of factor 7?

A

factor 9!!!

Vitamin K

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6
Q

Which immunosuppressant causes: Hyperglycemia, CMV infection, and PML of brain

A

Mycophenolate mofetil

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7
Q

Which immunosupressants do NOT cause pancytopenia?

A

Tacrolimus

Cyclosporine

  • these are neuro & nephro toxic
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8
Q

which immunosuppressant causes :

Gingival hyperplasia!!
Hypertrichosis
hirsutism,

A

Cyclosporine

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9
Q

How do you manage a displaced vs non displaced clavicular fracture?

A

Displaced (skin puncture, nerve damage, floating/shortened bone)= clavicular plate

non displaced = simple shoulder sling (will heal on own)

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10
Q

Tx for Hepatitis B infection?

A

Supportive therapy. Hep B resolves on own. Do not immunize ppl with active HepB.

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11
Q

What is the most effective way to prevent tumor lysis syndrome?

A

IV hydration!!

rasburicase/allopurinol are second line

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12
Q

Newborn with echinocytes (burr cells), indirect bilirubinemia, and FHx of hydrops fetalis has what hereditary disorder?

A

Pyruvate kinase deficiency

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13
Q

what is Ketotifen?

what eye condition does it treat?

A

Ketotifen is a second generation antihistamine

Tx seasonal allergy conjuctivitis

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14
Q

what blood condition presents with:

  • elevated RDW (size)
  • low MCV
A

Iron deficiency anemia

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15
Q

what blood condition presents with:

  • elevated RDW (size)
  • elevated MCV
A

B12 or folate deficiency

Liver disease

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16
Q

Why is IDA so common in EXCLUSIVELY fed newborns (only breast milk or only cows milk)?

A

bc they aren’t intaking any meals high in Iron (breast milk and cows milk have no iron)

you must give them iron supplementation until they start eating iron enriched foods

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17
Q

numerous BLASTS on a blood smear is red flag for what 2 blood cancers?

what are the CBC findings in this cancers?

A 
BLASTS cells (immature cells) = LEUKEMIA 
- either lymphoid (ALL) or myeloid (AML) origin

CBC= -penia (since no cells mature, theres a decrease in cell lines)
- thrombocytopenia, neutropenia, anemia, dec B&T cells

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18
Q

which acute leukemia is ALLways in children?

A

acute lymphoblastic leukemia (ALL)

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19
Q

which acute leukemia is always in older adults?

A

acute myeloid leukemia (AML)

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20
Q

which acute leukemia stains positive for myeloperoxidase?

A

Acute MYELOID Leukemia (AML)

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21
Q

which acute leukemia stains positive for:
terminal deoxynucleotidyl transferase (TdT) and
Periodic acid-Schiff (PAS)

A

acute lymphoblastic leukemia (ALL)

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22
Q

which cells are positive on flow cytometry for acute lymphoblastic leukemia (ALL) ?

A

since its lymphoblastic = lymph origin = B and T cells.

B cells: CD10, 19, 20

T cells: CD2, 3, 8

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23
Q

which cells are positive on flow cytometry for acute myeloid leukemia (AML)?

A

CD13, CD33, CD34, CD117, and HLA-DR

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24
Q

what translocations are associated with acute myeloid leukemia?

A

t(15:17)

especially in acute promyelocytic leukemia (M3 AML)

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25
Q

what translocations are associated with acute lymphoblastic leukemia?

A

t(12:21)== in B-ALL children = POOR prognosis

hint: 21 = trisomy 21 = downs syndrome associated with ALL

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26
Q

How can you remember which trisomy is associated with acute lymphoblast leukemia & where the leukemia metastasizes to?

A

ALL children are DOWN to grow up and have BRAINS and SEX (testes)

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27
Q

what acute leukemia presents with fever and testicular enlargement?

A

Acute lymphoblastic leukemia

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28
Q

auer rods are seen in which leukemia ?

A

AML & APML

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29
Q

what leukemia presents with gingival hyperplasia?

A

acute myeloid leukemia (AML)

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30
Q

what is the immediate management for a patient with Heparin induced thrombocytopenia (HIT)?

A

stop heparin!

switch to a NON-heparin anticoag typically a direct thrombin inhibitor (e.g., argatroban, bivalirudin) or a non-coumarin factor Xa inhibitor (e.g., rivaroxaban, dabigatran, fondaparinux).

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31
Q

how does Lauryn confirm G6PD deficiency before choosing it as an answer

A

anemia

blood smear abnl : Heinz bodies

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32
Q

what are cryoglobulins?

A

regular proteins (IgG & IgM) in the blood that CLUMP together when its COLD outside

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33
Q

what are the symptoms of mixed cryoglobulinemia?

A

mixed = complement deposition = vasculitis

arthralgia
red, non blanching purpura/macules (bc vessels are extravasating blood & not filling back up)
hypocomplementemia
hematuria
and increased serum concentration of polyclonal IgG and IgM

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34
Q

Why are pts with mixed cryoglobulinemia positive for rheumatoid factor?

A

IgM has the activity of RF; the HIGH levels of serum IgM (+IgG)&raquo_space;> + RF

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35
Q

what virus precipitates mixed cryoglobulinemia?

A

Hep C for Cryoglobulinemia. also HIV

all pts with cryoglobulinemia have Hep C so make sure you do a serology

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36
Q

anti-dsDNA is associated with what connective tissue diseases?

A

SLE

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37
Q

Anti-Sm is associated with what connective tissue diseases

A

SLE

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38
Q

Anti-Ro/SSA

Anti-La/SSB is associated with what connective tissue diseases

A

Sjogrens

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39
Q

Anti-histone is associated with what connective tissue diseases

A

SLE

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40
Q

anti C1q is associated with what connective tissue diseases

A

SLE

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41
Q

anti Jo1 & anti Mi2 are anti-synthetase ABs associated with what connective tissue diseases

A

Polymyositis and dermatomyositis

Mi & Jo are synners

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42
Q

Anti-U1-RNP is a Anti-ribonucleoprotein antibodiy associated with what connective tissue diseases

A

mixed connective tissue disease

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43
Q

Anticentromere is associated with what connective tissue diseases

A

systemic sclerosis

Centromere Cyctemic Clerosis

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44
Q

Antiphospholipid antibodies is associated with

A

SLE

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45
Q

what are the 3 types of antiphospholipid antibodies that point to SLE?

which antiphospholipid AB prolongs aPTT?

A 
anti-cardiolipin (most common type)
Anti-β2-glycoprotein 1 antibodies
lupus anticoagulant (LA)

lupus anticoagulant

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46
Q

Anti-cyclical citrullinated peptide antibodies are specific for what disease?

A

RA

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47
Q

Anti-DNA topoisomerase I antibodies is associated with what connective tissue diseases

A

systemic sclerosis

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48
Q

a prolonged BLEEDING TIME will always be mnemonic for what blood disorder?

what other mnemonic symptoms are there?

A

BLEEDING TIME = vWF (regardless of what PTT/PT says!!!!)

++++ nosebleeds/tooth bleeds

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49
Q

why may you see a prolonged PTT in addition to the prolonged BT seen in vWF disease?

A

Factor 8 circulates on vWF.

so no vWF factor = low F8 = prolonged PTT

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50
Q

what bleeding disorder presents with an isolated prolonged PTT?

A

Hemophilia A (Factor 8 deficiency)

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51
Q

Bernard-SOulier Syndrome

1 Giant Bernard is Injured & cant play outside

A

1 Bernard = Gp1B
Giant= giant PLTs
is injured= decreased PLTs
& cant play Outside = no adhesion = abnl ristOcetin cofactor assay

52
Q

Prolonged BT + decreased PLTs + giant PLTs on smear (megakaryocytes) =

A

Bernard-Soulier OR Immune thrombocytopenic purpura

53
Q

prolonged BT ++ normal PTT ++ normal PLTs =

A

Glanzmann thrombasthenia

54
Q

Plts with abnormal aggregation studies =

A

Glanzmann thrombasthenia

55
Q

Plts with abnormal adherence studies (risocetin cofactor assay) =

A

Bernard- soulier

56
Q

a low serum iron and ferritin ==

A

IDA

57
Q

mnemonic for hypersensitivity reactions

A

ACID

allergy/anaphylactic/atopic = HS Type 1

cytotoxic = HS Type 2

Immune complex = HS Type 3

Delayed = HS Type 4

58
Q

patients deficiency in what immunoglobulin have anaphylactic blood transfusion reactions?

A

IgA deficiency

59
Q

pathophys of T1HS rxns

A

preformed IgE crosslinks with mast cells & basophils to release histamine > urticaria

60
Q

pathophys of T2HS rxn

A

cytotoxic = cell death

IgG/IgM ABs bind against natural antigens on cell surfaces&raquo_space; complement signal to lyse/phagocytose the cell

antibody-dependent, cell-mediated cytotoxicity <3

61
Q

The following are classified as what types of HS rxns and why?:

Graves disease
Bullous pemphigoid
Pemphigus vulgaris
Myasthenia gravis

A

Graves= ABs against TSH receptor
Bullous pemphigoid = ABs against antigens on hemidesmosomes
Pemphigus vulgaris= ABs against antigens desmoglein 1/3 on desmosomes
Myasthenia gravis= ABs against AchR>weakness

Point: T2HS rxn = ABs against an antigen/receptor aka ADCC

62
Q

The following are classified as what types of HS rxns and why?:

Goodpasture syndrome
Rheumatic fever
Hyperacute transplant rejection

A 
Goodpasture= ABs against alpha 3 antigen in Type 4 collagen > hemoptysis+hematuria
Rheumatic= ABs against strep antigens (molecular mimicry)
Hyperacute transplant rejection= ABs against class 1 MHC/HLA 1 antigens on the grafted/gifted organ

Point: T2HS rxn = ABs against an antigen/receptor aka ADCC

63
Q

timeline & clx features for hyper acute transplant rejection

A

rejection occurs w/in minutes–48hrs

INTRAOPERATIVE FINDING (observed in OR/not subjective to pt): graft swells as soon as its perfused with host blood> thrombus> graft ischemia

64
Q

how do you dx hyperacute transplant rejection?

A

MUST Biopsy: graft shows small vessel thrombosis> ischemia

65
Q

how do you prevent hyperacute transplant rejection?

A

Confirm ABO/HLA compatibility first !!!!

66
Q

The following are classified as what types of HS rxns and why?:

1) Acute hemolytic transfusion reaction
2) Autoimmune hemolytic anemia (AIHA)
3) Hemolytic disease of the fetus and newborn
4) Immune thrombocytopenic purpura (ITP)
5) Drug-induced neutropenia and agranulocytosis
6) Pernicious anemia

A

1) Hosts antiA/B ABs against donors RBC’s A/B antigens
2) ABs against antigens > warm/cold agglutinins
3) Maternal antiRh- ABs against fetal Rh+ antigens
4) anti-platelet ABs to GP2B/3A antigens on platelets
5) methimazole, sulfasalazine, & trimethoprim/sulfamethoxazole
6) autoABs against the intrinsic factor antigen

67
Q

Acute hemolytic transfusion reaction&raquo_space;> urticaria. But why is it T2HS rxn and NOT T1HS rxn

A

Acute hemolytic transfusion reaction is caused by hosts antiA/B ABs against donors RBCs A/B antigens > rxn of urticaria, fever, Gi symptoms, anemia, jaundice

T1HS rxn = IgE crosslinking with mast cells/basophils === COMPLETELY different

68
Q

what are the 2 types of autoimmune hemolytic anemia?

what antobodies are associated with each one?

A

cold agglutinin (IgM)

warm agglutinin (IgG)

69
Q

lab findings for AIHA?

  • LDH
  • haptoglobin
  • indirect bilirubin
  • urinalysis
A
  • elevated LDH
  • LOW haptoglobin (dec bc it binds to Hg thats lysed from RBCs in order to preserve Fe/Hg== less freely circulating haptoglobin)
  • elevated indirect bilirubin
  • UA: urobilinogen (excess bili excreted in urine) & hemoglobinuria (lysed RBCs excreted in urine)
70
Q

mnemonic for Cold induced AIHA

A

Malignancy (non Hodgkin, CLL)
Mono (EBV)
Mycoplasma
Macroglobulinemia Waldosterom

the Cold is M.M.M.M.Miserable

71
Q

why are the T2 HS rxns often treated with IVIG in addition to systemic steroids?

A

IVIG = new ABs that wont attack against antigens == no more ADCC

72
Q

pathophys of T3HS rxn

A

IgG-antigen COMPLEX&raquo_space; deposited in TISSUES/VESSELS> complement activation> polys initiate cell death/inflammation»»> VASCULITIS

  • with T3HS rxn there will always be:
  • tissue/blood vessel vasculitis (usually kidneys & skin) affected by complex deposition*
73
Q

The following are classified as what types of HS rxns and why?:

1) Serum sickness
2) ArThus reaction
3) Drug-induced hypersensitivity vasculitis
4) Hypersensitivity pneumonitis

A

1) human ABs form complexes w/ foreign/animal proteins > deposited in blood
2) human ABs form complexes w/ DTaP antigens > deposited in dermal vessels
3) human ABs form complexes w/ drug antigens > deposited in small vessels
4) human ABs form complexes w/ inhaled environmental antigens > lungs

74
Q

The following are classified as what types of HS rxns and why?:

1) Polyarteritis nodosa (PAN)
2) Poststreptococcal glomerulonephritis
3) IgA nephropathy
4) Membranous nephropathy
5) Systemic lupus erythematosus (SLE)

A

1) IgG-HepB antigen complexes deposited in small vessel> vasculitis
2) weeks after strep infection, IgG-antigen complexes deposited in kidneys
3) hematuria directly after URI or GI infection (IgG-antigen complexes in kidneys)
4)
5)

75
Q

what foreign/animal antigens, VACCINE, & DRUG do human ABs form complexes with in Serum sickness?

when does the serum sickness rxn occur?

A

antivenom/antitoxins (snake/bug bites)
HepB
Rutuximab

ABs take week to form so you will see pt with serum sickness (urticaria, fever, lymphadenopathy) 1-2 weeks after HepB or venom exposure

76
Q

Clx skin feature of Arthus rxn

what type of HS rxn is Arthus?

A

Skin necrosis; at the location of IM dermal vaccine/booster injection

== T3 HS rxn

77
Q

what drugs cause Cutaneous small vessel vasculitis / hypersensitivity vasculitis

it forms what kind of purpura?

A

propylthiouracil, hydralazine, or allopurinol

painful purpura

78
Q

pathophys of T4HS rxn

A

PRE-sensitized T cells recognize antigens on either APCs (activates macrophages) or somatic cells» T cell mediated cell death

79
Q

what skin conditions are caused by T4 HS rxns?

A

TEN, DRESS, Steven Johnson
TB skin test, Candida skin test
Contact dermatitis

80
Q

what transplant reactions are caused by T4 HS rxns?

A

acute (<6weeks) and chronic (>6weeks) transplant rejections; bc hyper acute = T2HS

graft vs host disease (donor T CELLS attack hosts organs)

81
Q

why is Graft vs Host disease a T4HS rxn?

what organs are affected?

How is it used therapeutically?

A

a super lymphocytic organ is transplanted into host (aka allogenic hematopoietic stem cell transplant from a SIBLING for leukemia)

ALLLLL the T cells from donor are now in host and fight the hosts organs:
skin
intestines
liver

graft vs tumor effect

82
Q

what 2 neuro diseases are T4HS rxns?

A

MS & GBS

83
Q

what 3 autoimmune diseases are T4HS rxns

A

RA, diabetes, hashimoto

84
Q

what is the cause of acute ischemic stroke in SCD pts vs average pts?

A

SCD pts have strokes bc sickled RBCs clog arteries
whereas
Average pt has stroke bc fatty thrombus clogs arteries

85
Q

considering the difference btw the pathophys of SCD stroke vs avg stroke, how do you tx SCD stroke?

what do you never give a SCD stroke pt

A

Exchange transfusion therapy (MUST exchange all sickled RBCs for healthy RBCs) = removes stroke

never give SCD stroke pt antiplatelets/anticoags drugs bc

1) coagulation isnt the cause of stroke
2) it will just make them bleed out

86
Q

what is a heterophile antibody test?

what is it used to dx?

A

This phenomenon results in the aggregation of horse erythrocytes when exposed to his serum (i.e., a positive heterophile antibody test).

EBV

87
Q

lupus anticoagulant (LA) prolongs what blood paramater?

A

aPTT

88
Q

what blood syndrome is positive for VDRL?

A

antiphospholipid syndrome

89
Q

which acute leukemia present with FEVER & PAIN ?

A

Acute lymphoblastic leukemia (ALL)

ALL CHILDREN on leukemia commercials are sad/in pain=ALL

90
Q

what is the definitive dx test for ALL?

A

bone marrow biopsy!!! (bc B & T cells come from the bone & that is where the issue is)

do not choose peripheral smear!!! this is NOT as helpful as bone marrow biopsy = origin of the ALL

91
Q

what antibody finding is classic for Primary Biliary Cholangitis?

A

anti-mitochondrial antibody

aMa. M for Mamma. PBC is in hot Mammas (females) only

92
Q

anti-smooth antibody is mnemonic for

A

autoimmune hepatitis

93
Q

what are the 2 types of Cryoglobulinemia?

A

Type 1 = monoclonal = Plasma cell dyscrasia

Type 2 = polyclonal = mixed globulins

94
Q

what diseases/conditions arise in Type 1 (monoclonal/Plasma cell dyscrasia) vs Type 2 (polyclonal/mixed) Cryoglobulinemia?

A

type 1 = MM & Waldosteron

type 2 = infections (Hep C/B, HIV) & autoimmune diseases (RA, Sjogren, SLE)

95
Q

what is the mnemonic for Cryoglobulinemia (works for both Types <3 )

A

S K I N

S= skin

  • t1 = hyperviscosity = raynauds & livedo reticularis
  • t2= vasculitis = non blanchable (no blood refill), red purpura/macules

K= kidney

  • t1= hyperviscosity = thrombosis
  • t2= vasculitis= Membranoproliferative GN (hematuria)

I+ Intra-articular JOINTS = arthralgia & weakness
- both types

N=nerve damage

  • t1= n/a
  • t2= mononeuritis multiplex (non-contiguous nerve inflammation)
96
Q

what is the main goal in treating symptomatic Cryoglobulinemia?

what drugs/therapy helps tx it?

A

you want to DECREASED the B cells!!!
(B cells> plasma cells> release cryoglobulins)

Rituximab = anti-CD20 B cells 
or 
Plasmapharesis (remove all the cryoblobulins)
97
Q

which type of cyroglobulinemia is positive for RF but LOW in C3/C4?

A

Type 2 (Polyglonal/Mixed)

98
Q

what is the mnemonic for the causes of Cold agglutinin AIHA?

A

Cold weather is MMMMMiserable

Malignancy (non-Hodgkin, CLL)
Mycoplasma
Mono
Macrogobulinemia Waldenstrom

99
Q

what is the the skin finding of cold agglutinin AIHA that differentiates it from Cryoglobulinemia?

A

cold agglutinin AIHA = Acrocyanosis (PERSISTENTTT cyanosis; DOES NOT WAX/WANE LIKE RAYNAUDS)

100
Q

what are the common causes for Warm agglutinin AIHA?

A

CLL
SLE
drugs (a-methyldopa, penicillin, phenytoin, rifampin)

101
Q

what are the dx Direct Coombs/Agglutin Test (DAT) and Peripheral Blood Smear (PBS) findings for Cold vs Warm agglutinin AIHA?

A

Cold:
DAT: positive for C3d (will be low; C3 is low in Cold)
PBS: marked agglutination of RBCs

Warm:
DAT: positive for IgG (± C3d)
PBS: ABBUNDANT Spherocytes

102
Q

what organ is enlarged in Warm agglutinin AIHA?

A

splenomegaly (due to partial phagocytosis of the spherocytic RBCs by splenic macrophages)

103
Q

what is the difference in the onset of Cold agglutinin AIHA vs Warm agglutinin AIHA?

A

Cold = acute (days) onset you want to leave the cold fast

Warm = gradual (weeks) onset you want to stay on a warm vaca for a long time

104
Q

difference in acute tx for Cold AIHA vs Warm AIHA

A

Cold = avoid the cold

Warm = STEROIDS (SLE) followed by IVIG

105
Q

Immune thrombocytopenic purpura always follows

A

Infection (bacterial, viral) or a vaccination

106
Q

what is the 1st line treatment for Immune thrombocytopenic purpura (ITP)

A

steroids +++ IVIG

107
Q

true or false:

Spleenomegaly is common in Immune thrombocytopenic purpura.

A

FALSE. If theres spleenomegaly, it is NOT ITP

108
Q

What is autosplenectomy?

what is the etiology?

A

autosplenectomy = Functional asplenia

found in SSD pts who have had recurrent splenic thrombi from vasoocculsive events>
spleen loses its macrophage function so can NO LONGER eat/kill bacteria.

109
Q

treatment for an infection in a SSD pt with functional asplenia/autosplenectomy?

A

IV ceftriaxone

110
Q

explain thrombolysis pathway

A

a CLOT/Thrombus is made up of fibrinogen.

Fibrinolytic/Thrombolytic drugs dissolve clots/thrombus from fibrinogen to plasmin (an enzyme)

Plasmin then breaksdown Fibrin into Fibrin degradation products (D-dimers)

111
Q

what is the preceptor of fibrin (ie what comes before fibrin)?

A

Thrombin > Fibrin > FDPs (via Plasmin)

112
Q

what cell line is elevated in aseptic/viral meningitis?

what cell line is elevated in bacterial meningitis?

A

aseptic/viral = elevated lymphocytes (monocytes=plasma cells= lymph origin)

bacterial= >1000 POLYS/NEUTROPHILS

113
Q

What is the most common cause of Hemolytic Uremic Syndrome (HUS)?

Pathophys?

Clx findings?

A

E coli (Shiga-toxin E Coli or STEC)

Path: STEC lays microthrombi in vessel walls> HUS

Clx:
about a week of Adb pain/BLOODY diarrhea»> dec PLTs (petechiae), microagiopathic hemolytic Anemia, SCHISTOCYTES

114
Q

what is the marker/translocation for CML?

A

t(9:22)== characteristic for CML (but can also be seen in children/adults with ALL)

115
Q

what subtype of Hodgkin Lymphoma has the BEST prognosis?

A
  • lymphocytic rich classical HL
  • nodular sclerosing classical HL
  • nodular lymphocyte predominant HL

SO
lymphocytosis & nodules are GOOD PROGNOSIS in HL :)

116
Q

what are signs of a POOR prognosis in Hodgkin Lymphoma?

A

↑↑↑↑↑ ESR
↑↑↑↑↑ LDH
Involvement of three or more lymph node areas
Large mediastinal tumor

117
Q

14:18 is the marker for what cancer?

A

NHL- Follicular lymphoma

118
Q

11:14 is the marker for what cancer?

A

NH- Mantle cell lymphoma

119
Q

8:14 is the marker for what cancer?

A

NHL- Burkitts Lymphoma

120
Q

Diffuse Large B cell lymphoma (DLBCL) is the most aggressive NHL bc its transforms into what MRI finding?

A

Primary CNS lymphoma (pts with HIV/EBV who have DLBCL)

121
Q

Fanconi anemia is caused by what genetic defect? (PS: this is why there are so many chromosomal abnormalities)

A

AR defect in DNA crosslink repair > bone marrow failure

122
Q

Fanconi anemia causes genetic/early PANCYTOPENIA & therefore has a 50% predisposition to developing what malignancies in early adulthood?

A

Acute myelogenous leukemia

Myelodysplastic syndromes

both= pancytopenia of immature/early cell lines

123
Q

Fanconi anemia is a type of ______ anemia.

what are the BM biopsy findings?

A

Aplastic anemia

  • Fanconi = defect in DNA cross link repair > BONE MARROW FAILURE
  • Hypocellular fat-filled marrow (dry bone marrow tap)
124
Q

what are the following characteristics of fanconi anemia?

  • skeletal
  • skin
  • organ
  • BLOOD
A
  • skeletal: short stature, microcephaly, developmental delay, hypoplastic thumb
  • skin: hypo/hyper pigmentation ++ cafe au lait spots
  • organ: kidney, heart, EYE (strabismus/hypertelorism), and large ears (+/- deafness)
  • blood: pancytopenia (recurrent infections & bleeding)
125
Q

Fanconi anemia has what type of MCV?

A

High (>100)

126
Q

what leukocyte alkaline phosphatase score does CML have? WHY?

A

LOW leukocyte alkaline phosphatase score!

CML might be myeloproliferative, but it is a proliferation of granulocytes in all stages (still immature leukocytes = low LAP)

127
Q

smudge cells are mnemonic for:

A

CLL

STEP2 (12 decks)

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