Pathoma - Hematology

Front 1

Steps of Primary Hemostasis
(5)

Back 1

1) Enodthelin induced vasospasm
2) vWF binds exposed collagen
3) Plts bind vWF via Gp1b
4) Plts release ADP -->exposes GPIIb/IIIa; and TXA2
5) Fibrinogen links plts together via GPIIb/IIIa

Front 2

Where does vWF come from?

Back 2

Weibel-Pallade body of enodthelial cells and plts

Front 3

What do plt mediators do?
1) ADP
2) GPIIb/IIIa
3) TXA2

Back 3

1) ADP promotes exposure of GPIIb/IIIa
2) GPIIb/IIIa links plts via fibrinogen
3) TXA2 promotes plt aggregation

Front 4

Petechiae indicates what re plts?

Back 4

Decreased plt NUMBER, not quality.

Front 5

Etiology
ITP Idiopathic Thrombocytopenic Purpura

Back 5

IgG Autoimmune destruction of plts

Front 6

Dx
Thrombocytopenia in CHILD, after viral INFXN, self limited

Back 6

Acute ITP

Front 7

Dx
Women of childbearing age, low plts, transient low plts in newborn

Back 7

Chronic ITP

Front 8

Tx
ITP
(3)

Back 8

1st) Corticosteroids
2nd) IVIG (temporary)
Refractory) Splenectomy (spleen is where plts destroyed in ITP)

Front 9

Etiology
Microangiopathic Hemolytic Anemia

Back 9

-Pathologic formation of MICROTHROMBI shear RBCs as they flow past in small vessels --> hemolytic anemia

Front 10

Dx
Schistocyte

Back 10

MAHA
Microangiopathic hemolytic anemia

Front 11

Causes of Microhemolytic anemia

Back 11

1) TTP (Thrombocytopenic Purpura)
2) HUS (Hemolytic Uremic Sx)

Front 12

Etiology
TTP
Thrombocytopenic purpura

Back 12

DECREASED ADAMS 13 leading to inability to breakdown vWF multimers --> build up --> abnormal plt adhension --> inappopriate microthrombi --> MAHA

Front 13

Etiology
HUS
Hemolytic uremic sx

Back 13

E.coli O157 infxn --> verotoxin --> damages endothelial cells --> plt microthrombi --> MAHA

Front 14

HUS exposure

Back 14

CHILDREN to undercooked beef with E. coli O157

Front 15

Dx
Skin and mucosal bleeding, hemolytic anemia, fever, renal insufficiency, CNS abnormalities

Back 15

MAHA from either TTP or HUS

TTP = primarily CNS
HUS = primarily renal (uremia)

Front 16

Dx
Low plts, hi BT, NORMAL PT/PTT, anemia with schistocytes

Back 16

MAHA from TTP or HUS

(normal PT/PTT bc coag cascade never activated so not depleted)

Front 17

Etiology
Bernard-Soulier Sx

Back 17

GPIb deficiency --> can't bind vWF --> no plt adhesion to injury

Front 18

Dx
Enlarged plts on smear

Back 18

Bernard Soulier sx

Front 19

Etiology
Glanzmann Thrombasthenia

Back 19

GIIb/IIIa def. --> plts cannot stick together

Front 20

MOA
ASA anti-plt

Back 20

ASA inhibits COX --> no TXA2 --> NO plt aggregation

Front 21

Steps of Secondary Hemostasis

Back 21

1) Coag cascade makes THROMBIN
2) Thrombin converts fibrinogen to FIBRIN
3) Fibrin cross links with itself to stabilized plug

Front 22

Dx
1) Skin and mucosal surface bleeding
2) Deep tissue (muscle and joint) bleeding

Back 22

1) Primary hemostasis disorder (plt problem)
2) Secondary hemostasis disorder (coag problem like hemophilia)

Front 23

Coag cascade memorize now

Back 23

12, 11, 9, 8 |X| 7
5,2,1
SEC, PTT, HEP v

Front 24

Etiology
Hemophilia A

Back 24

FVIII (Aeight) deficiency

Front 25

Dx
1) Hi PTT, nl PT, lo FVIII, nl plts, nl BT
2) if Hi VIII, lo IX
3) If doesn't fix with blood mixing

Back 25

1) Hemophilia A
2) Hemophila B
3) Coagulation factor inhibitor

Front 26

Etiology
Hemophilia B

Back 26

FIX deficiency (Be Mine/nine)

Front 27

Dx
Hi BT, hi PTT, nl PT, abnormal ristocetin test

Back 27

vWF deficiency
(vWF stabilized FVIII so increases PTT)

Front 28

Tx, MOA
vWF disease

Back 28

Desmopressin
MOA) Desmopressin increases vWF release from Weibel-Pallade bodies of endothelial cells

Front 29

MOA
Warfarin

Back 29

Blocks Vitamin K Epoxide Reductase preventing reuse of vit K

Front 30

Liver failure increases what coag number

Back 30

PT

Front 31

Etiology
HIT
Heparin induced Thrombocytopenia

Back 31

Heparin induces plt destruction --> sometimes activates other plts -->thrombosis

Front 32

Etiology DIC
(2)

Back 32

1) Inappropriate activation of coag cascade --> microthrombi everywhere --> ischemia/infarction
2) Also consumes plts and coag factors --> bleeding

Front 33

Causes of DIC

Back 33

1) Obstetric complication
2) Sepsis
3) Adenocarcinoma
4) Acute promyelocytic leukemia
5) Rattlesnake bite

Front 34

Dx
Lo Plts, Hi PT/PTT, lo fibrinogen, elevated D-dimer, MAHA

Back 34

DIC

Front 35

Dx
Hi PT/PTT, hi BT, nl Plts, Increased fibrinogen split products without D-dimers

Back 35

Plasmin Overactivity
(no D-dimer bc no thrombus was ever made, just overactive plasin cleaving fibriogen not fibrin)

Front 36

MOA
tPA (so really plasmin)
(3)

Back 36

Activates Plasmin which does:
1) Cleaves FIBRIN and FIBRINOGEN
3) Destroys Coag Factors
4) Blocks plt aggregation

Front 37

Causes of
Plasmin overactivity

Back 37

1) Radical prostatectomy (release of urokinase activates plasmin)
2) Liver cirrhosis (decreased anti-plasmin production)

Front 38

Dx
No Lines of Zahn

Back 38

Postmortem clot

Front 39

Causes of High homocysteine
(3)

Back 39

1) Vit B12 def
2) Folate def
3) CBS def (cystathionine beta synthase)

Front 40

Dx
Vessel thrombosis, mental retardation, lens disolcation, long slender fingers

Back 40

Homocystinuria due to CBS def

Front 41

Etiology
Protein C or S def

Back 41

Protein C and S normally inactivate FV and FVIII, KO --> hypercoagulable state

Front 42

Vitamin K dependent factors

Back 42

10,9,7,2, C and S

Front 43

Etiology
Warfarin skin necrosis

Tx?

Back 43

Initial warfarin knocks out new production 10,9,7,2 and C/S but C/S decrease first so hypercoagulable.

Bridge with HEPARIN for 3 days

Front 44

Etiology
Factor V Leiden

Back 44

Mutated FV cannot be deactivated by Proteins C or S --> hypercoagulable

Front 45

Etiology
ATIII deficiency

Back 45

Heparin like molecules activate ATIII normally, but if ATIII KO can't inactivate thrombin --> hypercoagulable

Front 46

MOA
Heparin

Back 46

Activates ATIII which inactivates thrombin

Front 47

Initial anti-coag for ATIII def patients

Back 47

Give HIGH DOSE HEPARIN (bc not much ATIII to activate) to bridge to nL warfarin dose.

Front 48

What happens to PTT with heparin if pt ATIII def?

Back 48

Nothing

Front 49

Dx
Dyspnea, petechiae over chest

Back 49

Fat embolism

Front 50

Dx
SOB, neurologic sx, DIC, keratin debris in embolus,

Back 50

Amniotic emboli

Front 51

Dx
SOB, hemoptysis, pleuritic CP, pleural effusion, D-dimer

Back 51

Pulmonary embolus

Front 52

Complication of chronic pulmonary emboli

Back 52

Pulmonary HTN

Front 53

Normocytic range

Back 53

80-100

Front 54

What causes microcytosis?

Back 54

An extra division after erythroblast stage 2/2 decreased total Hb (attempt to maintain correct Hb concentration inside cell)

Front 55

Hemoglobin has what components that lead to microcytosis?

Back 55

Heme = Fe + protoporphyrin
Globin

Front 56

All causes of Microcytic anemia

Back 56

1) Iron def
2) Anemia of chronic disease (sequester iron problem)
3) Sideroblastic (porphoryin problem)
4) Thalassemias (globin problem)

Front 57

Where is Fe absorbed?

Back 57

Duodenum absorbs and puts into blood via Ferroportin

Front 58

What does Transferrin do?

Back 58

Transports Fe to liver and bone marrow macros for storage

Front 59

What does Ferritin do?

Back 59

Stores intracellular Fe (to avoid free radicals)

Front 60

What do Fe studies tell us?
Serum Fe
TIBC
% Saturation
Serum Ferritin

Back 60

Serum Fe - Total Fe on transferrin in blood
TIBC - Total Transferrin in blood
% Saturation - Percent of Transferrin with Fe (about 1/3)
Serum Ferritin - Total Fe in cells

Front 61

Stages of Iron Def

Back 61

1) Stored Fe is depleted (Ferritin goes down, TIBC goes up)
2) Serum Fe is depleted (Serum Fe goes down, % sat goes down,
3) Normocytic anemia
4) Micocytic, hypochromic anemia

Front 62

Relationship between Ferritin and TIBC

Back 62

Inversely proportional

Front 63

Dx
High Free Erythyrocyte Protoporphyrin

Back 63

Iron def anemia

(Normal porphyrin production outpaces lack of Iron in heme production)

Front 64

What size are RBCs

Back 64

The size of lymphocyte nucleus

Front 65

Mechanism Chronic disease anemia
(2)

Back 65

Chronic disease --> Hepcidin binding of Ferroportin on Enterocytes and Marcophages --| Fe transport
1) Sequesters Fe preventing macrophagic transport to erythroid precursors
2) Also suppresses FEP

Front 66

Fe studies in Anemia of Chronic Disease
ferritin, TIBC,
Serum iron, Saturation
FEP (Free erythrocyts protoporphyrin)

Back 66

Hi ferritin, lo TIBC,
Lo serum iron, lo saturation
Hi FEP

Front 67

Where is heme made in the cell?

Back 67

Mitochondria

Ring Sideroblast: Hence sideroblastic anemia is ring of Iron in Mito around nucleus

Front 68

Congenital sideroblastic anemia defect

Back 68

delta-ALA Synthase (1st step in protoporphyrin synth)

Front 69

Acquired causes of Sideroblastic anemia

Back 69

1) EtOH
2) Pb
3) Vit B 6 def (needed for ALAS in protoporphyrin synth)

Front 70

Fe studies in Sideroblastic Anemia
ferritin, TIBC,
Serum iron, Saturation

Back 70

Iron overloaded state:
Hi ferritin, Lo TIBC
Hi Serum Fe, Hi %sat

Front 71

Etio of Alpha Thalassemia

Back 71

Gene DELETION of alpha globin copy(ies) (1-4)

Front 72

Alpha thalassemia 2 losses:
Cis:
Trans:

Back 72

Cis: Asians (worse for offspring)
Trans: Africans

Front 73

What is HbA
What is HbA2
What is HbH
What is HbF
What is Hb Barts?

Back 73

HbA: normal, A2B2
HbA2: normal, A2D2
HbH: In alpha thal, B4
Hb Barts: Complete alpha thal (fatal), Gamma4

Front 74

Etiology of Beta thalassemia

Back 74

Gene MUTATIONS of 1-2 beta copies
Beta 0 = KO
Beta + = Decreased production

Front 75

Dx
Target cell

Back 75

Beta thalassemia
Minor or major
OR
Sickle cell anemia

Front 76

Dx
Expansion of hematopoesis into marrow and facial bones (if skull = crew cut appearance), liver, spleen

Back 76

Beta thal major

Front 77

Tx
Beta thal major

Back 77

Chronic transfusions

Front 78

Mech of Macrocytic anemia

Back 78

1 Less division occurs of erythroblast lineage 2/2 to lack of DNA precursors bc of lack of THF (Folate) or VitB12

Front 79

How many lobes in a Neutro is normal

Back 79

Up to 5
(Hypersegmented is like 7)

Front 80

Causes of Macrocyctic Anemia
Hyperseg Neutros (2)
Normal Neutros (3)

Back 80

Hyper: Folate or VitB12 def

Normal:
1) EtOH
2) Liver Disease
3) Drugs (5-FU)

Front 81

Where is Folate absorbed

Back 81

Jejunum

Front 82

Dx
Glossitis, Inc serum Homocysteine, nL Methylmalonic acid

Dx
" " except Hi Methylmalonic acid causing degeneration of spinal cord

Back 82

1) Folate def

2) VitB12 def

Front 83

How is B12 absorbed

Back 83

Binds to R binder, cleaved in small bowel, binds to IF and travels to Ileum where absorbed

Front 84

Etio Pernicious Anemia?

Back 84

Autoimmune destruction of Parietal cells of stomach so can't make IF for VitB12 absorption

Front 85

Causes of B12 def?

Back 85

1) Pancreatic insufficiency (can't release from R binder)
2) Damage to terminal ileum (e.g. Crohn's)
3) Long term veganism
4) Pernicious anemia

Front 86

Why are reticulocytes bluish?

Back 86

The RNA stains blue

Front 87

Retic correction Eq

And cutoff

Back 87

Retic count x Hct/45 = corrected retic count

If anemic, normal is over 3%

Front 88

How are RBCs degraded?
(3)

Back 88

Macros digest engulfed RBCs
1) Globin --> a. acids
2) Heme --> Fe (recycled) and
3) Protoporphyrin --> Unconj bilirubin

Front 89

Dx
Decreased haptoglobin, hemosiderinuria

Back 89

Intravascular hemolysis

When haptoglobin is overwhelmed Hb deposits into cells of renal tubules, sloughing off later as hemosiderin

Front 90

Etio of
Hereditary Spherocytosis

Back 90

Deficiency of Spectrin, Ankyrin, or Band 3.1
(proteins that tether cytoskeleton to membrane for disc shape)

Front 91

Dx
Inc RDW, and Inc MCHC

Back 91

Hereditary spherocytosis

Blebs are removed form membrane leading to different sizes.
Reduction of membrane without losing contents concentrates the Hgb.

Front 92

Increased risk for all hemolytic anemias

Back 92

Bilirubin gallstones

Front 93

Increased risk for all anemias with limited RBC reserves

Back 93

Parvovirus induced Aplastic Anemia

Front 94

How to diagnose
Hereditary Spherocytosis

Back 94

Osmotic fragility test

Front 95

Tx
Hereditary Spherocytosis

Back 95

Splenectomy

Front 96

Sickle cell is on what gene

Back 96

Beta globin gene

Front 97

Mechanism of
Sickle cell pathology
(1+2)

Back 97

HbS polymerize when deoxygenated -->
1) Needles prick the membrane
2) Irreversible sickling vasoocclusive crises --> swollen hands and feet, and Autosplenectomy

Front 98

MOA
Hydroxyurea in sickle cell

Back 98

Increases HbF by uknown mechanism
HbF doesn't sickle (no Beta globin involved)

Front 99

Sickle cell has increased risk of what infxn?

Back 99

Salmonella paratyphi osteomyelitis

Front 100

Etio of
Acute Chest Sx in sickle cell

Back 100

Vaso-occlusion in pulmonary microcirculation --> increased transit time --> ischemic feeling

Front 101

Renal manifestation of sickle cell

Back 101

Renal papillary necrosis (vaso-occlusive) --> hematuria and proteinuria

Front 102

Why don't sickle cell trait have sx?

Back 102

Hbs is made less than HbA (only about 45%) and 50% needed to sickle --> asymptomatic

EXCEPT in renal medulla

Front 103

Only complication of sickle cell trait

Back 103

Renal medulla's EXTREME hypoxia and hypertonicity cause even sickle trait to sickle --> microinfarctions --> microscopic hematuria --> eventual inability to concentrate urine

Front 104

Dx
Metasulbite screen

Back 104

Both Sickle disease and Trait will sickle

Front 105

Mech
Hemoglobin C

Back 105

Glu --> Lysine point replacement in Beta globin --> HbC crystals on blood smear

Front 106

What protects RBC from Complement?
(2)

Back 106

DAF and MIRL

Front 107

Mech
Paroxysmal nocturanal hematuria
(2)

Back 107

1) Deficiency of GPI which attaches DAF and MIRL to RBC

2) At night shallow breathing --> slight acidosis --> activates complement a little --> no GPI so no DAF --> complement destroys RBCs, WBCs, and plts

Front 108

Dx study
Paroxysmal Nocturnal Hematuria

Back 108

CD55 lacked in PNH

Front 109

Cause of death in
Paroxysmal Nocturnal Hematuria

Back 109

Plt destruction --> thrombosis of Hepatic or Cerebral veins

Front 110

High risk in PNH

Back 110

AML develops in 10% due to pre-existing mutation in myeloid precursor

Front 111

Mech
G6PD def

Back 111

G6PD cannot reduce Glutathione back --> Hgb gets oxidized --> splenic macros turn them into BITE CELLS --> Intravascular Hemolysis

Front 112

Variants of G6PD

Back 112

African: Mild, G6PD 1/2 life mildly shorter, only old RBCs have damage
Mediterranean: Severe, G6PD 1/2 markedly shorter, wide RBC damage

Front 113

Dx
Hemoglobinuria, back pain

Back 113

G6PD def
Hgb is nephrotoxic --> back pain

Front 114

Mech
Warm (IgG mediated) Autoimmune Hemolytic Anemia

Back 114

IgG binds RBCs --> splenic macros eat membrane ---> spherocytes --> Extravascular Hemolysis in spleen

Front 115

Mech
IgM

Back 115

IgM fixes complement on RBCs in cold extremities

Front 116

Associated with IgM Autoimmune Hemolytic Anemia (AIHA)

Back 116

1) Mycoplasma pneumoniae
2) EBV

Front 117

How does Direct Coomb's test work

What does it answer?

Back 117

If RBC is ALREADY coated with Ig, the ADDED IgG will bind --> Agglutination

Answers: Do RBCs already have Ig on them?
Tests for Autoimmune Hemolytic Anemia (AIHA)

Front 118

How does Indirect Coomb's test work

What does it answer?

Back 118

Add IgG and fresh RBCs to Pt's serum. If Abs to RBCs present, IgG will bind --> Agglutination

Answers: Are Abs to RBC in BLOOD?

Front 119

What mosquito spreads Malaria?

Back 119

Anopheles

Front 120

What is a myelophthisic process?

Back 120

A pathologic process that replaces bone marrow --> Pancytopenia

Front 121

Cortisol causes lymphocyte destruction

Back 121

!

Front 122

Causes of neutrophilic leukocytosis
(3)

Back 122

1) Bacterial infxn
2) Tissue necrosis
3) Hi Cortisol (disrupts neutro storage marginilaztion)

Front 123

What CD marker marks Left shift in Neutros

Back 123

Lo CD16 (i.e. lack of Fc receptor on immature neutros)

Front 124

Causes of Eosinophilia
(3)

Back 124

1) Allergic rxn
2) Parasitic infxn
3) Hodgkin lymphoma

Front 125

Associated with Basophilia

Back 125

CML

Front 126

Causes of Lymphoctyic Leukocytosis

Back 126

1) Viral infxns (not bacterial!!)
2) Bordetella pertussis (1 bacterial exception)

Front 127

How monospot works

Back 127

If EBV infxn --> Herterophile Abs will cause xenogenous RBCs to agglutinate

Will NOT be positive if CMV is causing infectious mononucleosis

Front 128

Complications of Infectious mononucleosis
(3)

Back 128

1) Splenic rupture
2) PCN induced rash
3) Dormany in B cells --> Lymphoma

Front 129

Markers for Acute Leukemia
tDt
Myeloperoxidase

Back 129

tDt = ALL (Acute leukemia of Lymphoblasts)
Myeloperoxidase = AML (Acute leukemia of Myeloblasts)
*MPO becomes Auer Rods

Front 130

Dx
CD10, Cd19, and CD20

CD2-8, no CD10

Back 130

B-ALL

T-ALL

Front 131

Tx
B-ALL

Back 131

Chemotherapy + to Scrotum and CSF

(Can't cross those specialized blood barriers)

Front 132

B-ALL translocations and prognoses
Children
Adults

Back 132

Children - t(12,21) good
Adults - t(9,22) (Ph+ ALL) bad

Front 133

Dx
Lymphoblastic Leukemia in teenager

Back 133

T-ALL

Front 134

Associated with Acute Promyelocytic Leukemia
(3)

Back 134

1) t(15;17)
2) RAR receptor disruption prevents maturation
3) Auer rods cause DIC

Front 135

Tx
Acute Promyelocytic Leukemia

Back 135

ATRA

Front 136

Dx
Blasts infiltrate gums, MPO (-)

Back 136

Acute Monocytic Leukemia

Front 137

Dx
Down sx Leukemia
Less than 5 yo
More than 5 yo

Back 137

Less than 5: Acute Megakaryoblastic Leukemia
More than 5: ALL

Front 138

Dx
Hypercellular bone marrow with Cytopenia, blasts in bone marrow
Less than 20% blasts
More than 20% blasts

Back 138

Less than 20% blasts = Myelodysplastic sx (from previous chemo/rad)
More than 20% blasts = Leukemia proper

Front 139

Dx
Neoplasm of naive B cels, CD5 and CD20

Back 139

CLL

Front 140

Dx
Smudge cells

Back 140

CLL

Front 141

Complications of
CLL
(3)

Back 141

1) Lo Ig
2) AIHA
3) Transformation to Large B Cell Lymphoma

Front 142

Dx
Neoplasm of mature B cells, TRAP positive

Back 142

Hairy Cell Leukemia

Front 143

Dx
Splenomegaly of red pulp, dry bone marrow tap, lymphadenopathy is absent

Back 143

Hairy Cell Leukemia

TRAP(ped) in Red pulp so not in bone or lymph nodes

Front 144

Tx
Hairy Cell Leukemia

Back 144

2-CDA

Front 145

Dx
Lytic bone lesions, rash

Back 145

ATLL (Adult T cell leukemia lymphoma)
NOT Multiple myeloma

Front 146

Complication of Chronic Myeloid proliferative disorders
(3)

Back 146

1) Hyperuricemia and gout (high nuclear turnover and degradation --> uric acid)
2) Hypercellular marrow --> Marrow fibrosis
3) Chronic leukemia --> Acute leukemia

Front 147

Neoplasm in CML

Back 147

ALL myeloid cells, but mostly granulocytes especially Basophils

Front 148

Mech of CML

Back 148

BCR-ABL fusion with t(9;22) translocation

Front 149

CML progresses to what?

Back 149

AML or ALL

*ALL bc mutation can be in Hematopoetic stem cell not necessarily in myeloblast

Front 150

How to prove CML over physiologic Leukocytosis
(3)

Back 150

1) LAP neg
2) Hi Basophils
3) t(9;22)

Front 151

Mutation in
Polycythemia vera

Back 151

Jak2 kinase mutation

Front 152

Dx
Blurry vision, HA, flushed face, itching after shower

Back 152

Polycythemia vera

Front 153

Neoplasm of Platelets

Neoplasm of Megakaryocytes

Back 153

Plts = Essential Thrombocythemia

Megakaryocytes = Myelofibrosis

Front 154

Which myeloproliferative disorder RARELY progresses?

Back 154

Essential Thrombocythemia (plts don't have nuclear material)

Front 155

Dx
Follicle hyperlasia
(2)

Back 155

1) Rheumatoid arthritis
2) Early HIV infxn

Front 156

Dx
Sinus histiocytes in lymph node

Back 156

Lymph node is draining a cancer (not necessarily metastatic)

Front 157

Dx, Etio
Adult, t(14;18)

Back 157

Follicular Lymphoma
(a type of Non-Hodgkin's Lymphoma)
Bcl2 to Ig Heavy chain

Front 158

Tx
Follicular lymphoma

Back 158

Rituximab (CD20 MAb)

Front 159

Dx, Etio
t(11;14)

Back 159

Mantle Cell Lymphoma
(a type of Non-Hodgkin's Lymphoma)
CDK1 to Ig Heavy chain

Front 160

Dx
Lyphoma in setting of chronic inflammatory state

Back 160

Marginal Zone Lymphoma
(a type of Non-Hodgkin's Lyphoma)

Front 161

Dx, Etio
t(8;14)
Jaw mass -
Abdominal mass -

Back 161

Burkitt's Lymphoma
c-myc to Ig Heavy chain
Jaw = African
Abdomen = sporadic

Front 162

Dx
Neoplasm of B cells making sheets in lymph node or OUTSIDE a lymph node

Back 162

Diffuse Large B cell Lymphoma
(a type of Non-Hodgkin's Lymphoma)

Front 163

Almost All Lymphomas are what cell

Back 163

B cell

Front 164

Dx
Hodgkin's Lymphoma
1) Lacunar cells
2) Best prognosis
3) Abundant Eos (IL-5)
4) Worst prognosis (HIV pts)

Back 164

1) Nodular scleroris
2) Lymphocyte rich
3) Mixed cellularity
4) Lymphocyte depleted

Front 165

Dx
High IL-6 in blood

Back 165

Multiple Myeloma

Front 166

Most common Ig's in MM

Back 166

IgG > IgA

Front 167

Dx
Rouleaux formation

Back 167

Multiple myeloma

RBC electrical charge of membrane disrupted by Ig's so stack up into rolls of poker chips

Front 168

Amyloid in Multiple Myeloma

Back 168

Ig Light chain overproduced --> Primary AL amyloidosis

Front 169

Dx
High serum monoclonal IgM, LAD, no lytic bone lesions

Back 169

Waldenstrom Macroglobulinemia

Front 170

Dx
Tennis racket on EM (Birbeck granules)

Back 170

Langerhan cell Histiocytosis

Front 171

Rules for Langerhans cell Histiocytosis:
(3)

Back 171

1) If eponym = malignant = skin rash + bone problems
2) If 2 names, presents in 2 yo or younger
3) If 3 names, 3 yo or older

Front 172

Dx
Pathologic bone fracture in adolescent, Langerhans cells with Eos on biopsy

Back 172

Eosinophilic Granuloma
( a Benign Langerhans Histiocytosis)

Front 173

What is the other thing Pathoma teaches us helps us discriminate between Megaloblastic and Nonmegaloblastic Macrocytosis?

Back 173

Megaloblastic anemia = Hypersegmented neutros

Nonmegaloblastic = Normal neutros (EtOH, Liver disease, and Reticulocytosis)

Front 174

HbSC phenotype?

Back 174

Milder than HbSS