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Year 5 Pathology > Hematology > Flashcards

Hematology Flashcards

1
Q

Factors in extrinsic pathway

A

TF, VII

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2
Q

Factors in intrinsic pathway

A

VIII, IX, XI, XII

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3
Q

Sxs of platelet disorders

A

Bleeding from skin, mucous membranes, petechiae, small superficial ecchymoses.
Immediate bleeding after sx

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4
Q

Sxs coagulation disorders

A

Bleeding into soft tissues, joints, and muscles. Large deep ecchymoses. Delayed bleeding after sx.

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5
Q

Platelet disorders resulting from increased consumption

A

Immune: ITP, drugs

Non-immune: TTp-HUS, DIC

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6
Q

Platelet disorders resulting from decreased platelet fn

A

Inherited: gp Ib mutation; gpIIb/IIIa mutation; storage pool disease
Acquired: Aspirin, uremia

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7
Q

Type I VWD

A

AD. Partial VWF deficiency

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8
Q

Type II VWD

A

AD. Loss multimers-altered quality

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9
Q

Type III VWD

A

AR. Complete deficiency VWF

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10
Q

Presentation VWD

A

Decreased platelet adhesion–>presents as platelet problem.

Increased bleeding time, normal PT, aPTT

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11
Q

Tx-VWD

A

Desmopressin, VIII, VWF concentrates

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12
Q

Clotting derangements in Vit K defic

A

Increased PT and aPTT

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13
Q

Clotting derangements in liver disease

A

Increased PT, aPTT

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14
Q

Protein C or S deficiency

A

AD. Early thrombosis (<40 years)

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15
Q

Prothrombin mutation

A

Increases transcription, therefore more likely to clot

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16
Q

Factor V Lieden

A

Cannot be degraded by protein C

-> Thrombophilia

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17
Q

Causes of acquired thrombophilia

A

Immobility/stasis, tissue trauma (sx), malig, anti-phospholipid syndrome, high estrogen states

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18
Q

Classic signs anemia

A

Sxs hypoxia

Conjunctival pallor, koilonychia, glossitis, angular stomatits, post-cricoid webs, high flow murmur

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19
Q

Causes of cellular bone marrow infiltration

A

Myeloproliferation, myelofibrosis, malignant spread

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20
Q

Causes of hypocellular bone marrow infiltration

A

Idiopathic, cytotoxic drugs +radiation, infxns, AI

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21
Q

Elliptocytosis

A

AD. Mild. No tx

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22
Q

ALL presentation

A

Bone marrow failure, LAD, HSM, testicular infiltration

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23
Q

AML presentation

A

Bone marrow failure, bleeding tendency, GUM/skin/CNS infxns

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24
Q

CLL

A 
Mostly B cell
Elderly
Indolent course with good prognosis
Increased lymphocytes
Smudge cells
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25
Q

Polycythemia rubra vera-presentation and defect

A

Elderly
Non-specific sxs: tired, depressed, vertigo, visual disturbances, HTN, angina, intermittent claudication

JAK2 mutation

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26
Q

Polycythemia rubra vera-tx

A

Venesection, hydroxyurea, radioactive 32P

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27
Q

Essential thrombocythemia

A 
Benign hx
Decreased quality platelets so actually bleed
Hypercellular marrow
JAK2 mutation
Tx w/ hydroxyurea
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28
Q

MGUS

A

Elderly

Paraprotein present

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29
Q

AIP

A

Psychosis, seizures, abdo pain, polyneuropathy, port wine urine.
AD. Precipitated by stress.
Tx-analgesia, CHO

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30
Q

Bacterial infxn transfusion rxn

  • Sxs
  • Tx
A

Sxs: Sudden onset fever, v unwell.
Tx: Stop transfusion, broad spectrum abx

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31
Q

Viral infxns possible from blood transfusions

A

Hep B/C, HIV, CMV, HTLV

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32
Q

Graft v host disease-sxs

A

Skin rashes, organ failure, marrow failure, diarrhea

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33
Q

Acanthocytosis

A

Abetalipoproteinemia, liver disease, hyposplenism

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34
Q

basophilic stippling

A 
Lead poisoning
Megaloblastic anemia
Myelodysplasia
Liver disease
Hemoglobinopathy
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35
Q

Burr cells (echinocytes)

A

Uremia, GI bleeidng, stomach carcinoma

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36
Q

Heinz bodies

A

G6PD def, chronic liver disease

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37
Q

Leukoerythroblastic anemia

A

Marrow infiltration, i.e. myelofibrosis, malignancy

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38
Q

Pelger Huet cells

A

Hyposegmented neutrophils

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39
Q

Polychromasia

A

Sign of reticulocytes: premature release from BM

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40
Q

Right shift

A

Megaloblastic anemia, uremia, liver disease

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41
Q

Rouleaux formation

A

Chronic inflamm, paraproteinemia, MYELOMA

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42
Q

Schistocytes

A

MIHA e.g. DIC, HUS, TTP, pre-eclampsia

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43
Q

Stomatocytes

A

“Smiling faces” or “fish mouth” RBCs

Hereditary stomatocytosis, high alcohol intake, liver disease

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44
Q

Target cells

A 
"HALT"
HbC disease
Asplenia
Liver disease 
Thalassemia
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45
Q

Hb components

A

Heme + globin

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46
Q

Heme components

A

Fe + protoporphyrin

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47
Q

Microcytosis

A

MCV

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48
Q

Normocytic anemia

A 
MCV 80-100
ACUTE blood loss--first stage IDA
Bone marrow failure
Renal failure
Hypothyroidism
Hemolysis
Pregnancy
F
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49
Q

Macrocytic anemia

A 
MCV>100
Alcohol excess
Liver disease
B12 defic, folate defic
Hypothyroidism (can also be normocytic)
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50
Q

Anisocytosis

A

Blood cells of varying size

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51
Q

Plummer Vinson syndrome

A

Anemia
Dysphagia (esoph webs)
Beefy red tongue

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52
Q

Common causes IDA

A 
Menorrhagia
Peptic ulcers/gastritis
Polyps/CRC
Meckel's
Hookworm infestation
Dietary deficiency
Malabsorption
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53
Q

ACD

A

Fe sequestered by hepcidin in macrophage
Increased ferritin, decreased TIBC
Decreased Fe, decreased % saturation

Causes:

  • Chronic infection (TB, osteomyelitis)
  • Vasculitis
  • RA
  • Malignancy
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54
Q

Sideroblastic anemia

A

Iron loading causing hemosiderosis
Same lab findings as hemochromatosis

Causes: Pb poisoning, B6 deficiency (ALAS cofactor), ALAS defect, myeloprolif or myelodysplastic syndromes

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55
Q

In which two causes of anemia is Fe low?

A

IDA, ACD

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56
Q

TIBC and ferritin relationship

A

Oppose each other, i.e. if TIBC high then ferritin low

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57
Q

Ferritin

A

Only low in IDA

Acute phase protein; increases with inflamm e.g. infection, malignancy

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58
Q

Megaloblastic blood film

A

Hypersegmented (>5) neutrophils, leukopenia, macrocytosis, anemia, thrombocytopenia

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59
Q

B12 deficiency

A

Takes years to develop (large liver stores)
Diet: Strict vegans, boozers
Malabsorption: pernicious anemia, gastrectomy, probs with termina ileum (Crohns, bacterial overgrowth, tropical sprue, diphyllobothrium latum)
Pancreatic insufficiency

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60
Q

Lab findings ih hemolytic anemias

A

Increased: unconj bili, urobilinogen, LDH, reticulocytosis/RDW

Intravascular types have decreased haptoglobin

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61
Q

RBC membrane defect disorders resulting in hemolysis

A

Hereditary spherocytosis

Hereditary elliptocytosis

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62
Q

RBC enzyme defect conditions resulting in hemolytic anemias

A

G6PD def

PK def

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63
Q

Non-immune causes hemolytic anemias

A

Mechanical heart valves
PNH, MAHA
Infections (malaria)
Drugs

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64
Q

Hereditary spherocytosis

A 
AD
Spectrin, ankyrin, band 3 defect
Osmotic fragility test
Parvo B19 susceptibility
Pigmented gallstones
Splenomegaly
Tx: splenectomy.  Howell-Jolly bodies post-splenectomy
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65
Q

Hereditary elliptocytosis

A

AD

Spectrin or band 4.1 mutations

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66
Q

G6PD deficiency

A

X linked
African, Mediterranean, Middle Eastern
No G6PD=no NADPH (HMP shunt)=reduced glutathione=oxidative injury by H2O2=intravasc hemolysis
Oxidants (drugs-malaria drugs, sulfonamides, aspirin; fava beans; stress) cause rapid anemia and jaundice
Bite cells and Heinz bodies
Enzyme assay 2-3 months after attack
Intarvasc hemolysis: dark urine

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67
Q

Pyruvate kinase deficiency

A

AR

Severe neonatal jaundice, splenomegaly, hemolytic anemia

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68
Q

Sickle cell

A

AR
Glu ->valine position 6 of beta chain
Trait usu asymptomatic (except kidneys)
Manifests around 6mo (HbF as newborn)
Decreased O2 tension causes polymerization and sickling
Get vaso-occlusion and infarction: dactylitis, stroke, acute chest syndrome, renal papillary necrosis
Tx: analgesia, hydration, SHiN vaccines, hydroxyurea

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69
Q

Beta thal minor

A

Asymptomatic carrier, mild anemia

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70
Q

Beta thal intermedia

A

Moderate anemia, splenomegaly, bony deformity, gallstones

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71
Q

Beta thal major

A

Severe anemia, FTT, HSM (extramedullary hematopoiesis), bony deformity.
May have heart failure

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72
Q

2 alpha gene deletion

A

Alpha thal trait

Asymptomatic, mild anemia

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73
Q

3 alpha gene deletion

A

HbH disease

Moderate anemia, splenomegaly

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74
Q

4 alpha gene deletion

A

Hb Barts

Incompatible with life

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75
Q

Warm Agglutinin Autoimmune Hemolytic Anemia

A

IgG
Coombs positive
Cause: mainly idiopathic, may be lymphoma, CLL, SLE, methydopa
Tx: steroids, splenectomy, immunosuppression

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76
Q

Cold Agglutinin-Autoimmune Hemolytic Anemia

A

IgM
Positive Coombs test
Oft has Raynauds
Causes: primarily idiopathic. may be lymphoma, infections (EBV, mycoplasma pneumoniae)
Tx: treat underlying condition, avoid cold, chlorambucil

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77
Q

Paroxysmal cold hemoglobinuria

A

Hb-uria after viral infection (e.g. measles)

Donath-Landsteiner abs attach to RBCs in cold; complement-mediated hemolysis on rewarming

78
Q

Paroxysmal Nocturnal Hemoglobinuria

A

Acquired loss GPI on RBC
GPI anchors DAF which protects against complement in blood. If you lose GPI, you lose DAF, therefore complement-mediated lysis
Dx: Hamm’s test or immunophenotype showing altered GPI

79
Q

Where in gut is iron absorbed?

80
Q

Transferrin

A

Transports iron in blood.

81
Q

Ferritin

A

Binds iron in storage

Note that Fe on its own causes ROS damage via Fenton reaction

82
Q

TIBC

A

Measure of transferrin molecules in blood

83
Q

% saturation

A

Percentage of transferrin molecules that are bound by Fe (normal is 33%)

84
Q

Most common type of anemia in hospitalized patients

85
Q

Hepcidin

A

Sequesters Fe in storage sites by:

  1. Limiting transfer of Fe from macros to erythroid precursors
  2. Suppressing EPO
86
Q

lab findings in ACD

A

Increased ferritin, decreased TIBC
Decreased serum Fe and % saturation
Increased FEP

87
Q

Lab findings in IDA

A

Decreased ferritin, increased TIBC
Decreased serum iron, decreased % saturation
Increased FEP

88
Q

HbF

89
Q

HbA

90
Q

HbA2

91
Q

Causes macrocytic anemia without megaloblastic change

A

Booze
Liver disease
Drugs (e.g. 5-FU)

92
Q

Where is folate absorbed?

93
Q

Difference in labs between folate and B12 deficiency

A

Folate: normal methylmalonic acid
B12: increased methylmalonic acid

Both have high homocysteine (increases risk thrombosis)

94
Q

Corrected retic count

A

(Retic count falsely elevated in anemia, as normal RBCs gone so retics are overall higher percentage)

Retic count * Hct/45

95
Q

Extravascular hemolysis

A

Destruction by reticuloendothelial system (macros of spleen, liver, LNs)

Findings:
Anemia, splenomegaly, unconj jaundice, risk bili gallstones
Marrow hyperplasia if corrected retic count >3%

96
Q

Intravascular hemolysis

A

Hb-emia
Hb-uria
Hemosiderinuria (renal tubular cells pick up Hb and break down to Fe, accumulates and shed with tubular cells)
Decreased haptoglobin

97
Q

Microangiopathic hemolytic anemia (MIHA)

A

Intravasc hemolysis from VASCULAR cause…RBCs destroyed as pass through circulation.
Caused by microthrombi (TTP-HUS, HIC, HELLP), prosthetic heart valves, aortic stenosis
Schistocytes

98
Q

Fever patterns:

  • Falciparum
  • Vivax
  • Ovale
  • malariae
A

Falcip: every day
Vivax, ovale: tertian (every other day)
Malariae: quartan (every third day)

99
Q

Aplastic anemia

A

Damage to hematopoietic stem cells (CD34+) cauing pancytopenia with low retic count

Causes: drugs/chemicals, viral infections, AI damage

Biopsy: empty, fatty marrow

100
Q

Primary hemostasis

A

Formation of platelet plug

101
Q

Secondary hemostasis

A

Stabilization platelet plug

Coag cascade mediated

102
Q

Mucosal bleeding

A

Epistaxis (most comm), hemoptysis, GI bleeding, hematuria, menorrhagia
Symptom of platelet abnormality

103
Q

Petechiae vs purpura vs ecchymoses

A

Petechia: 1-2mm
Purpura: >3mm
Ecchymoses: >1cm

NB petechiae are a sign of thrombocytopenia, not usu seen with qualitative platelet defects (just quantitative)

104
Q

ITP

A

AI production IgG against platelet antigens, e.g. GpIIb/IIIa
MCC thrombocytopenia in adults
Ab-bound platelets consumed by splenic macros causing thrombocytopenia

Acute: post viral infection or immunization. Kids. Self-limiting
Chronic: primary or secondary. Women of child bearing age

105
Q

TTP-HUS

A

TTP: ADAMTS13 deficiency
HUS: E. coli O157:H7 verotoxin destroys endothelial cells resulting in platelet microthrombi

"FATRN"
Fever
Anemia (MIHA)
Thrombocytopenia
Renal failure
Neuro sxs
106
Q

Bernard-Soulier

A

GpIb deficiency–impaired platelet adhesion

Mild thrombocytopenia with enlarged platelets

107
Q

Glanzmann thrombasthenia

A

GpIIb/IIIa deficiency–impaired platelet aggregation

108
Q

Uremia’s effect on platelets

A

Disrupts adhesion and aggregation of platelets

109
Q

Clinical difference between hemophilia A and B

A

There is none, you numpty

110
Q

Vitamin K deficiency–causes

A

Newborn (lack GI colonization)
Long term antibiotic therapy
Malabsorption of fat-soluble vitamins

111
Q

Heparin-Induced Thrombocytopenia

A

Platelet destruction.

Fragments destroyed platelets may activate others, causing thrombosis

112
Q

DIC

A

Widespread microthrombi result in ischemia and infarction
Consumption factors and platelets result in bleeding, esp from IV sites and mucosal surfaces

Causes:
Obstetric complications--tissue thromboplastin in amniotic fluid activates coag
Sepsis, esp E. coli and N men
Adenocarcinoma (mucin activates coag)
APML
Rattlesnake bites
113
Q

Lab findings in DIC

A

Decreased: platelets, fibrinogen, D-dimer
Increased: PT, PTT

114
Q

tPA

A

Converts plasminogen to plasmin

115
Q

Plasmin

A

Cleaves fibrin and serum fibrinogen, destroys coag factors, blocks platelet activation

116
Q

How do you distinguish thrombosis from postmortem clot?

A

Lines of Zahn
Attachment to vessel wall
(Both these found in thrombosis)

117
Q

Mechanisms by which intact endothelium prevents thrombosis

A

Block exposure subendothelial collagen and underlying tissue factor
Produce PGI2 and NO (vasodilation and inhibition platelet agg)
Secrete heparin-like molecules
Secrete tPA
Secrete thrombomodulin

118
Q

Causes endothelial cell damage :(

A

Atherosclerosis
Vasculitis
High levels homocysteine

119
Q

Cystathionine beta synthase deficiency

A

Results in high levels homocysteine and homocystinuria.

Findings: vessel thrombosis, mental retardation, lens dislocation, long slender fingers

120
Q

Protein C or S deficiency

A

AD

Increased risk warfarin skin necrosis

121
Q

Most common cause inherited hypercoagulable state

A

Factor V Lieden

122
Q

Prothrombin mutation

A

Point mutation in thrombin that causes increased gene expresion, therefore more thrombi (pro-thrombin…)

123
Q

ATIII deficiency

A

Decreases protective effect of heparin-like molecules produced by endothelium

124
Q

Why does estrogen (e.g. OCP) cause increased thrombosis risk?

A

Increased production coag factors

125
Q

Types of emboli

A

Thrombo-embolism (MCC)
Fat embolism
Gas embolism
Amniotic fluid embolism

126
Q

Fat embolus

A

BONE FRACTURES, esp long bones, and soft tissue trauma

Dyspnea and petechiae on skin over chest

127
Q

Gas embolus

A

Decompression sickness–rapid ascent while diving
Nitrogen gas precipitates out during rapid ascent
Joint and muscle pains (the bends) and resp sxs (the chokes)
Chronic form=Caisson disease. Multifocal ischemic necrosis of bone

May also occur during laparoscopic surgery

128
Q

Amniotic fluid embolism

A

Amniotic fluid enters maternal circulation during labor/delivery
SOB, neuro sxs, DIC
Squamous cell and keratin debris from fetal skin found in thrombus

Extremely high mortality: only 10% survive

129
Q

Pulmonary embolism

A

Most often clinically silent due to dual blood supply of lung
Usually small and self-resolves

10% cause infarction: SOB, hemoptysis, pleuritic CP, pleural effusion
Sudden death if saddle embolus
Pulm HTN if chronic emboli that are reorganized over time

130
Q

Systemic embolism

A

Usu due to thromboembolus

Most commonly arise in L heart

131
Q

factor II

A

Aka thrombin

132
Q

JAK 2

A

Non-receptor tyrosine kinase

Mutations found in:
PV
ET
Myelofibrosis
Other Myeloproliferative disorders
133
Q

Acquired causes sideroblastic anemia

A

Alcoholism, Pb poisoning, B6 deficiency

134
Q

Disorders with increased MCHC

A

Hereditary spherocytosis

AI anemia

135
Q

Metabisulfite test

A

Detects both sickle cell and sickle cell trait, i.e. any presence of HbS

136
Q

HbC disse

A

LYSINE instead glutamic acid HbC crystals

137
Q

PNH-cause

A

ACQUIRED deficiency GPI

138
Q

GPI

A

Anchors DAF and MIRL which degrade complement getting too close to RBCs

139
Q

Test for PNH

A

Look for presence CD55 (aka DAF) on cells. If no CD55, then can assume no GPI

140
Q

MCC death in PNH

A

Thrombosis, e.g. portal vein

10% go on to develop AML

141
Q

HIT

A

Heparin destroys platelets. Some of destroyed platelets go on to activate other platelets causing THROMBOSIS
Do not use warfarin–increased incidence skin necrosis

142
Q

Secondary causes DIC

A

Obstetric complications (amniotic fluid activates tissue thromboplastin), sepsis, adenocarcinoma, APML (Auer rods), rattlesnake bite

143
Q

GpIb-function

144
Q

GpIIb/IIIa

A

Platelet AGGREGATION. Uses fibrinogen as linker

145
Q

Petechiae are a sign of what problem?

A

QUANTITATIVE platelet problem, i. thrombocytopenia. Not seen in qualitative disorders

146
Q

ITP

A

AI: IgG against platelet antigens (eg. GpIIb/IIIa).
Most common cause thrombocytopenia in kids and adults
Ab-bound platelets consumed by splenic macrophages
Spleen also one making antibody
Acute-kids. Usu post-viral infxn or immunization
Chronic-adult women (may be secondary to SLE)
Tx: steroids (esp if acute), IVIG, splenectomy

147
Q

MIHA

A

Pathological formation microthrombi in small vessels, which shears RBCs. Use up platelets making microthrombi
TTP-HUS is a major cause

148
Q

TTP-mechanism

A

Deficiency ADAMTS13–can’t degrade vWF multimers. Pile up vWF multimers causes abn platelet adhesion thus microthrombi

149
Q

HUS-mechanism

A

E. coli O157:H7 vertotoxin damages endotherlial cells causing platelet microthrombi. Also decreases ADAMTS13
Kids + undercooked beef –>dysentery

150
Q

Signs and sxs TTP-HUS

A 
Fever
MIHA
Thrombocytopenia
Renal insufficiency (esp HUS)
CNS abnormalities (esp TTP)

Increased bleeding time, normal PT/PTTtX-ttp-hus

151
Q

Tx-TTP-HUS

A

Plasmapheresis, ‘roids

152
Q

Bernard-Soulier

A

Genetic gpIb deficiency
Impaired platelet adhesion
Mild thrombocytopenia with enlarged platelets (“Big Suckers”)

153
Q

Glanzmann’s thrombasthenia

A

Deficienct gpIIb/IIIa

Impaired platelet aggregation

154
Q

Indications for transfusion

A

Acute blood loss >30% blood volume

Peri-op/critical care, when Hb

155
Q

Intra operative cell salvage

A

Collect blood lost during surgery and reinfuse into pt.

NB-washed/filtered so lose coagulation factors and platelets

156
Q

Type of blood used in transfusions for highly immunosuppressed individuals

A

Irradiated

157
Q

Reaction when use the wrong blood in transfusion

A

Signs/sxs Intravascular hemolysis

Restless, chest/loin pain, fever, vomiting, flushing, collapse, later–hemoglobinuria

158
Q

Febrile non-hemolytic transfusion reaction

A

Increase in temp by 1 degree C, chills, rigors
Common before blood leukodepleted, now rare
Stop/slow transfusion, give paracetamol. Can re-start

159
Q

Allergic transfusion reaction

A

Usually with plasma
Common
Mild urticarial or itchy rash +/- wheeze
Tx with antihistamines

160
Q

Delayed hemolytic transfusion reaction

A

1-3% pts who have received transfusion
Develop Sb to one of foreign RBC antigens
Complement-mediated phagocytosis
Extravascular hemolysis

161
Q

Anaphylactic reaction to blood transfusion

A

Hypotensive shock, very breathless, wheeze, laryngeal and facial edema
E.g. Donor eaten peanuts (antigen) and pt has IgE Ab to this antigen already

162
Q

TACO

A

Transfusion Associated Circulatory Overload
Within 6 hrs
Acute resp distress, tachycardia, increased BP, acute or worsening pulm edema, positive fluid balance

163
Q

TRALI

A

Transfusion Related Acute Lung INjury
Dry cough, dyspnea, fever, not due to fluid overload or other causes
Donor anti-leukocytic Abs interact with pt’s leukocyte antigens causing aggregation. These aggregations get stuck in pulm caps. Neutrophils in aggregates release proteolytic enzymes that cause lung damage

Can prevent by giving virally-activated plasma, and plasma from men

164
Q

Cabot rings

A

Looped structures in RBCs. Found in megaloblastic anemia

165
Q

Pappenheimer bodies

A

Iron granules. Foud in sideroblastic anemia, Pb poisoning, hemolytic anemias

166
Q

Prothrombin 20210A mutation

A

Substitution G to A at position 20210 of prothrombin gene. Increases transcription thus more clotting after vessel damage
5% Caucasian population

167
Q

Post-transfusion purpura

A

5-9 days after transfusion
Severe thrombocytopenia with bleeding
Tx with IVIG

168
Q

Pencil bodies

A

Type of elliptocyte

Seen in IDA, thal, PK deficiency

169
Q

Cooley’s anemia

A

Old name for beta thal major

170
Q

Cabot rings

A

Looped structures in RBCs

Caused by megaloblastic anemia

171
Q

Pappenheimer bodies

A

Iron granules. Pb poisoning, sideroblastic anemia, hemolytic anemia

172
Q

Buerger’s disease

A

Aka thromboangitis obliterans
Strong relation to smoking
Recurrent arterial and venous thromboses
Corkscrew arteries in upper and lower limbs

173
Q

Protein S

A

Degrades Factors Va, VIIIa

174
Q

Antithrombin

A

Inhibits thrombin, factor Xa

175
Q

C-myc

176
Q

Lymphoma with centrocytes, centroblasts

A

Follicular

177
Q

Bcl-2 associated lymphoma

A

Follicular

178
Q

Donath-Landsteiner Abs

A

Paroxysmal cold Hb-uria

179
Q

Non-megaloblastic causes of macrocytic anemia

A 
"RALPH"
Reticulocytosis
Alcohol
Liver disease
Pregnancy?
Hypothyroidism
180
Q

Hemochromatosis-sxs

A 
Hepatomegaly/deranged LFTs
Arthralgia and chondrocalcinosis
Diabetes
DCM
Hypogonadism/impotence
Adrenal insufficiency
Skin color changes (slate grey or bronze)
181
Q

MM-lab findings

A

Normal ALP
Increased ESP
Increased Ca

182
Q

MGUS

183
Q

Waldenstroms

A

High IgM

Hyperviscosity and vascular complications

184
Q

Combined polycythemia

A

Aka “smoker’s polycythemia”
Combination decreased plasma volume and decreased O2 (CO displaces) causing an increase in EPO

Be very suspicious if smoker + COPD picture

185
Q

Secondary polycythemia

A

Increase in EPO or testosterone (anabolic roids)

Ectopic EPO from HCC, RCC, hemangioblastoma, pheo, uterine myomata

186
Q

Primary polycythemia

A

LOW EPO

E.g. polycythemia vera

187
Q

Non-classical subtype of Hodgkins

A

Nodular lymphocytic

188
Q

Ann Arbor Staging for Hodgkins

A

I: Single LN region
II: 2+ LN on SAME SIDE of diaphragm
III: LN on both sides diaphragm
IV: extranodal spread

Add “a” if no B sxs, add “B” if there are B sxs

189
Q

B sxs

A

Significant unexplained fever
Night sweats
Weight loss >10% in preceding 6/12

190
Q

Imantinib

A

Tyrosine kinase inhibitor.

Used in CML

191
Q

Absence LONG arm chromo 5

A

Subtype of myelodysplastic syndrome

192
Q

Absence SHORT arm chromo 5

A

Cri-du-chat

They will try to trick you with long v short arm

Year 5 Pathology (6 decks)

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