Genmediii Buzzwords

Front 1

• Ferritin

Back 1

• Ferritin: stores Fe3+; BEST test for IDA (Iron deficient anemia); Acute phase reactant

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IDA values vs ACD

Back 2

Transferrin Serum Fe Ferritin EPO
IDA ↑ ↓ ↓↓
ACD ↓ ↑↑ ↓

Front 3

Sickle Cell Disease Complications

Back 3

o Pulmonary- Acute Chest syndrome: Fever, rales, infiltrate w/ respiratory failure, complication of Surgery Anesthesia
o Skeletal- marrow hyperplasia  osteopenia  fractures
 Hair on end of skull- reabosorption of bone, frontal bossing (normal in infants b/c of increased blood production)
 Femoral head necrosis
 Dactylitis and bone disintegration “moth eaten”

Front 4

Direct vs Indirect Anti-Globulin test

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 (+) Direct anti-globulin test (Coomb’s):
• Antibody or complement on RBC: Diagnosis of AIHA, Hemolytic transfusion Reaction
 Indirect antiglobulin test (indirect coombs)
• Ab in SERUM not bound to RBCs “Screen”

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Hemolytic Anemia Lab values

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 INCREASE: LDH / Indirect Bilirubin
 DECREASE: Haptoglobin

Front 6

Warm vs Cold Auto ATB

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• Warm Auto-ATB: Any Age Usually IgG Variable anemia
• Cold Auto-ATB: IgM
o Etiologies: Idiopathic, Post-Mycoplasma infection, Lymphoma, Mononucleosis,
o Not Helpful: Corticosteroids / Splenectomy

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Paroxysmal Nocturnal Hemoglobinemia Cause

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PNH is an acquired clonal stem cell disease: Cell membrane anchor defect

Front 8

PNH Screen

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• Screen using: CD55 and CD59 (always a boards Q)

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Main etiology of Myelodysplasias

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• CHmeotherapies (esp w/ -5/-7 alkylating agents)

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BM in Myelodysplasias: Acute Leukemia

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• BM: Hypercellular w/ >20% blasts – dry tap common – packed marrow

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Tx for 5q- syndrome

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Treatment = Lenalidomide

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Myleoproliferative disorders and cause

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CML/AML
JAK2- Essential thrombocytopenia, Myelofibrosis, Polycythemia Rubra Vera,

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Essential thrombocythemia

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Very High platelet count
o Dx: exclusion; Reactive/Neoplastic; BM = ↑megakaryocytes; Cytogenetics = FISH-JAK2

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Myelofibrosis w/ Myeloid Metaplasia

Back 14

bone marrow is replaced with fibrous tissue
o Clinical:
 33% asymp; Sxs = fatigue/wt loss/Fever/Night sweats; anemia; bleeding from thrombocytopenia
 HSM (gets bigger as BM product’n ↓) “some of the largest spleens you will ever see”
 EMH: extramedullary hemopoiesis – not as effiecient as BM:: splenomeg

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Myelofibrosis w/ myeloid metaplasia BM biopsy

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BM Fibrosis "dry tap"

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Polycythemia Vera

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Usually JAK 2- affects all 3 cell lines
Serum EPO is not elevated
Pruritis0 person takes shower and gets itchy b/c of hot water
Renal Portal vv (IVC or upper extremity = unusual)
Tx: Phlebotomy

Front 17

PRV differential diagnosis

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 Paraneoplastic Erythrocytosis: [Renal, Hepatic, Uterine myoma, Cerebellar hemangioma]  EPO HIGH!

Front 18

ALL

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m/c childhood
CD10 B- Hypogammaglobulinemia
CD 2,3,7 T- mediastinal Mass
LDH and Uric acid are very high
TX; Induction- chemotherapy (vincrisitne)
- CNS prophylaxis- intrathecal chemo
-Consolidation- reduced induction therapy
Maintenance
-- Daily- 6 mercapt
--Wkly: Methotrex
--Monthly: Vincristine/Prenisone

Treatment can cause osteonecrosis of the LE

Front 19

AML

Back 19

Chemotherapy (Or MDS) causes -5/-7/-11q mutation
Auer Rods
DIC (increased D dimer)
Complication: tumor lysis syndrome: everything is up but Ca++

Front 20

M3 Acute Promyelocityic Leukemia

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M3 Promyelocytic: t15:17 (PML:RAR) granules (RAR = retinoic acid receptor – mutations)
-APL Tx: Induction—w/All-trans-Retinoic Acid
Consolidation  maintenance 75% cure
- ATRA complication pleural/pericardial effusion

Front 21

Chronic leukemia vs Acute Luekemia blast levels

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Chronic <20%
Acute >20%

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CML

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any age
Granulocytes with increased metas, myelos and pros
Eosinophils, basophilia
Philadelphia chromosome Ph 9:22
Tx: imatinab- tyrosine kinas inhibitor (BCR/ABL antagonist)

Front 23

Hodgkins lymphomas

Back 23

Binucleate, Giant Reed-Sternberg Cell
Adenopathy: Cervical
Dx: excision of whole node

Front 24

Nodular Sclerosing

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Higher socioeconomic status

Front 25

Mixed cellularity

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EBv

Front 26

Hodgkins lyphoma staging

Back 26

o Staging (similar to NonHodkins except add A/B...) Very important (diaphragm/organs involvement)
 I = single LN – 90% Survival rate
 II = multiple LN (same side of diaphragm) -85% survival rate
 III = LN both sides diaphragm; spleen met – 75% survivial rate
 IV = dissemination (+/-LN) – 50% survival rate – m/c to relapse – need transplant.
 A = absence of B sxs
 B = presence of B sxs (tx is different depending if A or B)

Front 27

Good vs poor hodgkins lymphoma prognosis as far as staging scenario

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• Good Px: ESR<50, <50yo, NS or LP, Stage A; <3 sites involved; No bulky adenopathy
• Poor Px: Albumin <4; anemic (Hb <10.5); Male; >45 yo; Stage IV; WBC > 15,000 (↑); Low absolute lymphocyte count.

Front 28

Hodgkins Lymphomas Treatments and effects

Back 28

Radiation: breast cancer, Thyroid disease
Chemo:
--Vincristine: neuropathy
--Doxorubicin: Cardiomyopathy
--Bleomycin: Pulmonary fibrosis

Front 29

NonHodgkins lymphma

Back 29

increased epidemiology due to iatrogenic causes
know that for t and b cell the treatments are different
Risk factor= H pylori

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H pyloir

Back 30

gastric malt non-hodgkins lymphoma

Front 31

Waldeyer's ring

Back 31

you have to examine the whole thing when working up a pt for NHL

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Cytogenics in NHL diagnosis

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Anaplastic Large Cell Lymphoma (2:5) ana is 25
Burkitt's 8:14
Follicular 14:18

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young men with isolated mediastinal mass

Back 33

alpha fetal protein
betaHCG
Non-hodgkins lymphoma

Front 34

Indolent NHLs

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CLL
FOllicular grade 1/2
marginal Zone
Lymphoblastic lymphoma

Front 35

Aggressive NHLs

Back 35

Diffuse Large B cell
Follicular grade 3
Anaplastic Large Cell Lymphoma
Mantle Cell lymphoma
Burkitt's
Mycosis Fungioides
Adult T-cel

Front 36

Marginal zone

Back 36

MALT (h pylori)
Autoimmune extranodal: Sjogrens/ hashimoto affects the eyes

Front 37

Lymphoblastic lymphoma

Back 37

Increased IgM

Front 38

Follicular Grade 3

Back 38

acts the same and tx the same as DLBC
curable with chemo

Front 39

Anaplastic

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Cutaneous
T2,5
mainly T cell

Front 40

mantle Cell

Back 40

T11:14
increase in cyclin D
Lymphomatous polyposis

Front 41

Burkitt's lymphoma

Back 41

African= endemic, EBV pediatric
Western= adults, sporadic, Mesenteric LN

Front 42

Mycosis Fungiodides

Back 42

Multiple plaques

Front 43

Adult T cell leukemia

Back 43

HTLV- japan carribean
Hypercalcemia and lytic bone lesions
CD30+

Front 44

MGUS

Back 44

Benign = MGUS –monoclonal gammopathy
increase in M protein w/ normal cbc
Bone marrow plasmacytosis <10%

Front 45

Malignant Plasma cell myeloma
Multiple Myeloma

Back 45

Blacks- IL6 osteoclastic activity
13q deletion= poor prognosis
IgG
Rouleux

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Multiple Myeloma Criteria

Back 46

• Criteria:
o *monoclonal protein serum a/o urine; *plasmacytoma or *marrow plasmacytosis >10%
o *CRAB – Calcium, Renal fail, Anemia, Bone (hypercalcemia) -- painful
--- multiple infections

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Multiple Myeloma Hyperviscosity

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• Hyperviscosity: due to IgM;
o Clinical: HA, blurred vision, mucosal bleeding (epistaxis, pharyngeal bleeds), CHF, “Sausage” retinal vv
o Tx: plasmapheresis (emergency)

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Rouleux

Back 48

Multiple Myeloma

Front 49

Involved in primary hemostasis

Back 49

platelets

Front 50

PE of Thrombocytopenia

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non-palpable petechiae

Front 51

Immune thrombocytic purpura

Back 51

Easy bruising in healthy adult
• Dx of exclusion – do BM, megas are normal (morph & #); NO splenomeg
• Tx: Prednisone (suppress immune rxn); *splenectomy (long term is better than long term on predisone)

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Non-immune thrombocytopenia DIC

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 DIC – thrombin & Plasmin; recall thrombin promotes fibrinogen  fibrin which gets stuck in sm bvs  smaller vessels ... causes schistocytes (RBS get decapitated).
• Causes thrombosis in smaller vessels that can lead to death.
• excess fibrinolysis
---D Dimer

Front 53

TTP

Back 53

lg vWF multimers – lack protease so get very lg
Clinical: neurologic
Lab: Schistocytes
TX: plasmaphereiss to get rid of large multimers

Front 54

HUS

Back 54

children, no neurological, renal problems
Prior infection fo ecoli from a brger place

Front 55

Platelet alloimmunization

Back 55

happens faster than RBCs

Front 56

Tx for a pt whose platelet count doesn't respond to other therapies

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Eltrombopag

Front 57

Direct thrombin inhibitors

Back 57

 Direct thrombin inhibitors: --effective as anticoagulation for HIT (stim ATIII) or TX of HITT
• **Lepirudin – recomb hirudin – antigenic – Ab formation; excessive anticoagulation
• Argatroban – caution in hepatic dz

Front 58

Antiphospholipid syndrome

Back 58

PTT prolonged; NO correct’n w/ mixing study

Front 59

Most important drug in the Tx of any malignancy

Back 59

 after 10 days – LMWH – 3 months (6 months optimal) – most important at any point w/ malignancies

Front 60

PNH

Back 60

CD55, 59
o hypercoagulable – thrombosis = atypical (thrombotic events in “Odd” places – upper arm, IVC, etc)
 m/c cause of death
• Other : Age, Immobile; Surgery (hip/knee/ major trauma, CA); Prior VTE; Prego; Estrogen
•

Front 61

Thrombosis prophylaxis

Back 61

Prophylaxis: 3 significant risk factors: prior VTE; Hormone replacement/OC; Obesity (consider prophylaxis if 2+ risk factors)

Front 62

hereditary protein C resistance

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Venous dz

Front 63

Hyperhomocysteinemia

Back 63

• Hyperhomocysteinemia (m/c in children who go in for surgery)
o homocystein metabolism – B6, B12, Folate
o Tx: anticoagulation; vit B6, B12, Folate

Front 64

Warfarin in chronic tx can lead to

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Warfarin necrosis

Front 65

Primary plug

Back 65

1⁰ = Platelet plug = platelets + vascular injury  requires vWF + Factor VIII  activates 2⁰

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Secondary Plug

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2⁰ = Fibrin plug b/c of the activation of coagulation cascade

Front 67

genetic bleeding disorders

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o Family hx  hemophilia A/B (sex-linked)?; vWF dz (autosomal)

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Vitamin K dependent

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• Vit K dep: VII, IX, X, II: Factors Generate Thrombin  1⁰ & 2⁰ hemostasis; activates platelets and generate fibrin which is crosslinked by factor 13 which makes the fibrin plug (purpose of factor 13)

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Extrinsic

Back 69

VII
PT time
Not Vit K dependent

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Intrinsic

Back 70

XII
PTT time

Front 71

Thrombin

Back 71

PRO coagulatn= fibrinogen
Anti coatulant= thrombin + thrombomodulin

Front 72

PT

Back 72

• PT: Prolongation: ↓ in Fs II/V/VII/X/Fibrinogen,
o Extrinsic system abnormalities
o INR(Int. Normalized Ratio) for Warfarin patients

Front 73

PTT

Back 73

• PTT: Prolongation: ↓ Fs II/V/VIII/IX/X/XI/XII  bleeding and bruising
o Intrinsic system
o Rarely affected by fibrinogen
o Hemophilia
 A = congenital def of F VIII
 B = congenital def of F IX
 von Willebrand’s disease; ↓ vWBF = ↓ FVIII = ↑ aPTT;Corrects on mixing
o F XII Deficiency
o LA: no correction with mixing
o Acquired inhibitors to coagulation proteins; Patients with Hemophilia (A>B); LPD/Plasma Cell Dyscrasias

Front 74

Antithrombin

Back 74

Antithrombin (ATIII); Heparin  in lung ** - so you don’t coag in the lung!;

Front 75

Mixing studies

Back 75

Mixing studies – Prolonged PT/PTT from deficiency? –
• correction = quantitative factor abnormal (you added to the mix something the pt didn’t have), Give FFP for surgery
• uncorrected = SLE anticoagulant, something that inhibits the coagulation cascade (no bleeding or bruising but have thromboses)
• ex TQ: what’s next after taking PT & PTT? A: mixing studies ... then see if PTT is normalized.

Front 76

Screening pt pre surgery

Back 76

Screening (TQ) – PT/PTT; Platelet count; +/- fibrinogen

Front 77

Cryoprecipitate

Back 77

fibrinogen
fibrinogen or XIII (afibrinogenemia, dysfibrinogenemia)

Front 78

Irradiated blood

Back 78

stops leukocyte proliferation
(even directly related people have to have all donated blood radiated)

Front 79

CMV

Back 79

(-) must receive (-) blood; (+) can receive (-) or (+);

Front 80

Hallmark of acute transfusion reaxtion

Back 80

 Most ABO incompatible (human error – dr’s, nurses, give to wrong pt, etc)
 fever, chills, dyspnea, chest pain; hypotensive shock
 Hallmark = intravascular hemolysis – complement fixation via IgM; Hemoglobinemia; Hemoglobinuria
 DAT (+); Indirect bilirubin  Jaundice; ATN (acute Tubular necrosis)

Front 81

Delayed hemolytic transfusion reaction labs

Back 81

 unexplained ↓Hb;
 **LABS: ↑indirectbili/LDH/Reticulocyte #; jaundice; DAT (+) – usually; ↓Haptoglobin

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TRALI

Back 82

• **TRALI – transfusion associated Lung Injury – fatality 7%
o Noncardiogenic pulm edema
o usually 2 hrs after transfusion
o acute respiratory insuffiency & hypotension
o CXR – bilateral white out