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8/6/2019 McLeod Heme Tovee Class
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MCCQE Hematology Review
Anne McLeod e-mail [email protected]
Office 416-340-3395
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GOALS and OUTLINE
Review MCCQE objectives and samplequestions
Few blood films
Few things not in the objectives
Practice questions
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MCCQE OBJECTIVES
www.mcc.ca/ObjectivesObjectives listed alphabetically
Practice Questions
-Exams-Mccqe1-Getting started-Practice exams
Two types of sample questions: MCQand CRS
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MCCQE OBJECTIVES
Bleeding tendency/bruising (#15-1)
Hypercoagulable state (#15-2)Anemia (#42-1)
Polycythemia/Elevated Hemoglobin (#42-2)
White blood cell abnormalities (#120)
Lymphadenopathy (#54)
Splenomegaly (#2-3)
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Bruising & Bleeding-History
Pattern - lifelong or recent, deepseated bleeds or superficial bruisingand petechiae
Bleeding challenges- circumcision,tonsils, wisdom teeth, menstruation,pregnancy, appendix
Other PMHx - cancer, renal or liverdisease
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Bruising & Bleeding-Hx and Px
Family history - bleeding or transfusion
Drugs - ASA, NSAIDS, alcohol and herbals
Check for the spleen, petechiae/purpura,
telangiectasia and evidence other systemicdisease
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HEMOSTASIS
Three steps:
1. Primary Hemostasis
Vascular response, platelets and *vWF
2. Secondary Hemostasis
Fibrin clot formation (coag cascade) *vWF*carrier for FVIII
3. Fibrinolysis
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VWF
VWF
VWF
VWF
VWF
VWF
VWF
VWF =von Willebrand Factor
Subendothelium
VWF
VWF
VWF
VWFVWFVWF
VWFVWF
PRIMARY HEMOSTASIS
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Subendothelium
HEMOSTASIS
2. Secondaryhemostasis - fibrin clot
1. Primary hemostasis-platelet plug
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Subendothelium
HEMOSTASIS
3. Fibrinolysis andwound healing
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PRIMARY HEMOSTASIS-Vessel
HEREDITARY: HHT (Osler-Rendu-Weber)
Connective tissue (Ehler-Danlos)
ACQUIRED: Drugs -Steroids
Senile purpura
Infections
Vasculitis
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PRIMARY HEMOSTASIS-Platelets
Too few platelets-thrombocytopenia
Dont work- platelet dysfunction
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PRIMARY HEMOSTASIS-Thrombocytopenia
DECREASED
PLATELETPRODUCTION
INCREASED
PLATELETDESTRUCTION
SEQUESTRATION
ie. plateletsstuck in thespleen/liver
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Accelerated Platelet Destruction
Non-immune-DIC, sepsis
Immune- TTP, ITP, SLE, drugs(heparin, quinidine,cephalosporins)
Look at the blood film/smear!!
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HIT
Platelet
Activated
Heparin-PF4
Complex
HIT Antibody
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Treatment of HIT Any heparin or LMWH contraindicated
in HIT
Need to use an alternative like a directthrombin inhibitor eg. Hirudin orargatroban
Warfarin may worsen the thrombosis ifnot overlapped with an alternativeanticoagulant until therapeutic
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Venous Limb Gangrene
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Confusing PLATELET
Problems
ITP HIT
PlateletPlatelet Platelet
UnControlled
vWF Release+
TTP
ActivatedActivatedNo activation
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Platelet Dysfunction1. Congenital-rare
2. Acquired COMMON!
Drugs - ASA, NSAIDs, Anti-Platelet agentsAlcohol, Uremia
Liver disease
Bone marrow disorders eg. MPD, MDS,MM
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Von Willebrands Disease Disorder of Primary ( Increased BT) and
Secondary hemostasis (Increased PTT)
Treatment DDAVP if mild disease, HemateP ( blood product with lots of VWF) ifsevere
Test family members usually autosomaldominant
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HEMOSTASIS SCREEN
Primary Hemostasis
CBC
Blood film/smear
Bleeding time
Platelet function tests
Tests for vWD
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HISTORY tells you :
PRIMARY SECONDARY
HEMOSTASIS HEMOSTASIS
Surface cuts Prolonged Normal
Onset after injury Immediate Delayed
Typical type / site Superficial Deep
Petechiae, purpura Subcutaneous
Mucosal bleed: Bleed into:
Nose, mouth, gums Joints, muscles,GI tract, Uterus GI /GU tracts
Post op/trauma
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CLOT
GENERATION
OF
THROMBIN
EXTRINSIC(TISSUE FACTOR)
PATHWAY
INTRINSIC
PATHWAY
Secondary Hemostasis
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Disorders of Secondary Hemostasi
Hereditary
Hemophilia A (factor VIII deficiency) andHemophilia B (factor IX deficiency) are X-linked and produce hemarthroses andhematomas and are treated withrecombinant factor concentrates or if mild
deficiency DDAVP
von Willebrands disease
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Disorders of Secondary Hemostasis
Acquired
vitamin K deficiency (factors II, VII, IX and
X)
liver disease (all factors other than VIII)
DIC
Inhibitors Drugs- warfarin, heparin
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Standard Heparin
Usually administered in hospital becausecareful monitoring required if given IV
Aim is to achieve an aPTT of 2.5-3X normalie. 60-90s
IV bolus followed by continuous infusion
Short half-life once IV infusion stoppedaPTT normalizes in ~4 hrs
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Standard Heparin
Easy to over anticoagulate patientswhich carries a very high risk ofbleeding
Standard heparin can be reversed by
protamine
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Warfarin
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Warfarin
Vitamin K antagonist
Rapidly absorbed from GI tract buttakes few days to be therapeutic
Dosing varies
Very close monitoring of INR required
in first few weeks
Dont start without heparin also!
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Treatment of Warfarin Overdose
Vitamin K -works in 6-12 hrs
Fresh frozen plasma- worksimmediately but BLOOD PRODUCTuse if life threatening bleeding only!!!
Careful monitoring of INR best way to
prevent bleeding
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Extrinsic Pathway
PROTHROMBIN TIME - PT /INR
Increased if deficiency of factor VII and also of
common pathway factors- X, V, II and fibrinogen.
Results also reported as INR - to allow for
standardization between laboratories.
Used for monitoring oral anticoagulant (Warfarin)
therapy.
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Intrinsic Pathway
ACTIVATED PARTIAL THROMBOPLASTIN TIME
- aPTT
Detects deficiencies of the intrinsic
pathway factors XII, XI, IX, VIII and also
common pathway X, V, II and fibrinogen.
Used to monitor anticoagulation therapy
with standard heparin.
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50/50 MIX
PT/INR or PTT prolonged
Rule out presence of warfarin or heparin
If corrects=factor deficiency
If doesnt correct=inhibitor
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HEMOSTASIS SCREEN
THROMBIN CLOTTING TIME - TT
A test for conversion of fibrinogen to fibrin
Detects fibrinogen deficiency
Detects abnormal fibrinogens - dysfibrinogenemia
Detects inhibitors of fibrin polymerization - FDPs
(Fibrin degradation products) or D-dimers.
Detects thrombin inhibition eg. Heparin
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Quiz-Treatment of Bleeding Platelet transfusions
Vitamin K
Antifibrinolytics
DDAVP
FFP and cryoprecipitate
Protamine sulphate
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Sample Questions-MCQ
Which of the following is true about
hemorrhagic disease of the newborn:
Results from Vit K deficiency
More common in females
More common in bottle fed infants
Requires treatment with FFP
Evident in the first 24 hrs of life
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Sample Questions-MCQ Mr H has hemophilia which is shown to be due to anti-
hemophilic globulin deficiency. There is no hemophilia
in his wifes family. He has 4 sons and 4 daughters.
Which is true?:
0 sons have H, 2 daughters carriers
4 sons H, 2 daughters carriers
0sons
H,0
daughters carriers 0 sons H, 4 daughters carriers
2 sons H, 4 daughters carriers
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Made up question- CRS A 65 year old man is admitted with loss of
consciousness a few hours after a fall. He had been
experiencing a flu-like illness for several days
according to his daughter. CT head shows a subdural
hematoma and he requires urgent surgery.
According to his daughter he takes several heart pillsand she tells you he had surgery to replace his heart
valve 6 yrs ago.
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Made up question- CRS
You are called by the lab : Hb 100
MCV 95 WBC 12 Plts 350 INR 8.0
aPTT 55 Fibrinogen N Creat LFT N.
What do you think is the most likely
cause of the elevated INR?
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Made up question- CRS
What are you going to do prior to his
surgery? Choose 3 Transfuse pRBC
Transfuse platelets
Give FFP
Give cryoprecipitate
Give Vit K
Give protamine
Cross and type forpRBC
Give DDAVP
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Made up question- CRS
After treatment the
surgeons want to
know if he can go to
the OR now what
blood tests will you
do? Choose 2 or
choose NONE:
INR and PTT
Thrombin time
CBC
INR
Heparin level
Warfarin level
Bleeding time
NONE
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MCCQE OBJECTIVESBleeding tendency/bruising (#15-1)
Hypercoagulable state (#15-2)
Anemia (#42-1)
Polycythemia/Elevated Hemoglobin (#42-2)
White blood cell abnormalities (#120)
Lymphadenopathy (#54)Splenomegaly (#2-3)
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Hereditary Causes of Thrombophilia
Antithrombin III
deficiency
Protein C deficiency
Protein S deficiency
Factor V Leiden
Prothrombin 20210
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Acquired Risk Factors for VTE Age
Previous thrombosis
Immobilization
Surgery
Malignancy
Nephrotic syndrome
APLA syndrome
Myeloproliferative
disorders
BCP / HRT
Pregnancy/postpartum
Obesity Heavy smoker
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Who should be screened?Hereditary
Age
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ThrombophiliaWorkup after H+PINITIAL
CBC
Screen forantiphospholipid antibody
Fasting homocysteine
APCR-functional screenfor Factor V Leiden
DNA testing for Factor VLeiden and Prothrombinmutations
POST HEPARIN
Antithrombin
POST WARFARIN
Protein C,S
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Diagnosis Physical exam not useful
D-dimers
Doppler ultrasound
Ventilation/Perfusion scan
CT chest with PE protocol
We dont use Impedanceplethysmography
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Treatment of VTE
Antiplatelet agents-Phlebitis only
Anticoagulants
- standard heparin
low molecular weight heparins
warfarin
new agents
Thrombolytic agents
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Sample Question-CRS 28 yr old G2P2 woman presents 5 days
post SVD with 2 day history of aching and
tenderness L inguinal region. L leg isdiscoloured and swollen. No othersymptoms she is breastfeeding.
What tests if any would you order choose
up to 3:
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Sample Question-CRS ABG
Blood culture
CBC Doppler US of leg
Ear oximetry
ECG
Endometrial culture
ESR
Fibrinogen leg scan
IPG
Pelvic US
PT, PTT Radionucleotide
phlebography of leg
Thermography of legs
Venogram L leg Vent/Perf scan
No tests
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Sample Question-CRS Pt admitted with
baby to start
treatment in 4-6hrs what orderswould you write?Choose up to 5.
Acetominophen
Aspirin daily
Antibiotics IV Bedrest
CXR
CBC
Daily IPG IVC filter
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Sample Question-CRS Heparin IM
Heparin IV bolus
Heparin by IV constantinfusion
Heparin SC
Initial PTT
PTT at 4 hrs post bolus Plt count q 3 days
Stop breastfeeding
Streptokinase
Support hose Surgery consult
Traction L leg
Tubal ligation
Vitamin K Warfarin
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Sample Question-CRS Patient treated to
prepare for
discharge whatwould you do?Choose as many aswant.
Avoid ASA Contraception
Support hose
Heparin 3-4 mons
Heparin 5-6 mons Reg PT and PTT
Reg PT
Stop breastfeeding
Vitamin K
Warfarin 3-4 mons Warfarin 5-6 weeks
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MCCQE OBJECTIVESBleeding tendency/bruising (#15-1)
Hypercoagulable state (#15-2)
Anemia (#42-1)
Polycythemia/Elevated Hemoglobin (#42-2)
White blood cell abnormalities (#120)
Lymphadenopathy (#54)Splenomegaly (#2-3)
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Approach to Anemia Focus on bleeding, drugs, family
history, diet and bowel habits
Look at MCV, WBC, diff, plts and film
New or old
MCV very helpful !!
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Approach to Anemia
Look at the blood film!!!
Micro Macro vs Normo
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Microcytic Anemia T
A
I
L
S
Look at the blood film!!!
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Iron Ferritin is the best blood test for assessing
iron stores but is increased by
inflammation, cancer and liver disease
Nail changes
Pica, blue sclerae, glossitis, angularstomatitis, sore burning mouth,esophageal web
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Iron - Clinical Points Blood film is usually diagnostic
Bone marrow examination is rarely needed
Iron deficiency is nevera final diagnosis The 10-10-1 rule
10 mg in diet
10% absorbed
1 mg absorbed and lost daily Consider Celiac disease
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Iron - Therapy Iron replacement requires normalization of
the hemoglobin and the body stores (3mons after hemoglobin normal)
Iron therapy is a balance between the doseof elemental iron and GI tolerance
Iron supplements are good forpremenopausal women and potentiallyharmful to men
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Anemia of Chronic Disease Common in patients with infection, cancer,
inflammatory and rheumatologic diseases
Iron can not be remobilized from storage Blunted production of erythropoietin and
response to erythropoietin
Usually normocytic and normochromic but
may be microcytic if severe
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Thalassemia Poikilocytosis and basophilic stippling may
be seen in the blood film
Hemoglobin electrophoresis is onlydiagnostic for beta-thalassemia and maynot be diagnostic if iron deficiency is alsopresent
Hb H prep and/or DNA analysis needed todiagnose alpha-thalassemia
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Sample Question Lead exposure can cause all of the
following except:
a) Abdo painb) porphyrinuria
c) Cirrhosis of the liver
d) Paresise) anemia
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Made up Question A woman with HB SC disease presents in
pregnancy. She asks if the baby will have
HB SC disease. Choose the correctanswer:
a) Baby can not have SC disease
b) Baby will have sickle cell trait
c) Baby will be normal
d) More information is needed
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Sideroblastic Anemia Produces a dimorphic blood film
with microcytes and macrocytes
Marrow shows ring sideroblasts
Usually acquired and associated witha myelodysplastic syndrome, drugs
or toxins Rarely due to pyridoxine deficiency
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Macrocytic AnemiaOval macrocytes (megaloblastic)
B12, folate, drugs
Round Macrocytes
Reticulocytosis
Alcohol/ Liver Disease
Myelodysplasia
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B12 Deficiency Be aware of the neurological
complications
Never treat possible B12 deficiencywith folate - the CNS lesions mayprogress
Schilling test distinguishes perniciousanemia from other causes
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Folic Acid Deficiency The peripheral blood film and bone marrow
are identical to B12 deficiency
Women of childbearing age should takesupplemental folate to prevent neural tubedefects in their children
Folate supplementation lowershomocysteine levels leading to less heartdisease and stroke
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Normocytic Anemia
Are the retics high or low?
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Normocytic AnemiaHigh Retics= making RBC butbeing lost
Bleeding
Hemolysis
MyelofibrosisTreated nutritional deficiency
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Hemolytic Anemia
Destruction of RBC leads to increasedretics, increased indirect bilirubin andincreased LDH
Hereditary or acquired
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Hemolytic AnemiaIntravascular RBCs being destroyed
in the blood vessel and hemoglobin
lostTests:
RBC fragments, decreased
haptoglobin, hemoglobinuria Become iron deficient over time
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Hemolytic AnemiaExtravascular hemolysis-RBCs being
destroyed by RE system and hemoglobinrecycled:
Autoimmune hemolytic anemia -like ITPantibody on surface of RBC destroyed tooearly by RE system
Test: Direct antiglobulin test (Coombstest),dont become iron deficient
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Hemolytic Anemia-Intra and Extra
Inherent RBC Defects
Membrane defects - hereditaryspherocytosis and hereditaryelliptocytosis
Enzyme defects - G6PD
Hemoglobinopathy - Sickle CellDisease
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Sample Question What would be the best test to confirm
the diagnosis of hereditary spherocytosis:
a) RBC enzyme studiesb) HLA studies
c) Bone marrow
d) Osmotic fragility
e) Coombs test
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Normocytic AnemiaLow Retics= not making RBC
Bone marrow problem-MDS,leukemia, cancer, aplasticanemia
EPO problem- uremia, ACDThyroid
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Anemia by ageMore common in elderly:
bone marrow problemsMDS,MM leukemias (CLL,CML, AML) Low
Kids get acute leukemias notchronic or MDS or MPD
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Made up question A 32 yr old woman presents with
few day history of easy bruising
and headache. CBC: Hb 135 MCV 95 WBC 12 Plt
3
What are you going to order? What is your diagnosis?
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Made up question A 32 yr old woman presents with
a 1 day history of petechiae andheadache.
CBC: Hb 85 MCV 99 WBC 12 Plt 3
What are you going to order?
What is your diagnosis?
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MCCQE OBJECTIVESBleeding tendency/bruising (#15-1)Hypercoagulable state (#15-2)
Anemia (#42-1)Polycythemia/Elevated Hemoglobin
(#42-2)White blood cell abnormalities (#120)
Lymphadenopathy (#54)Splenomegaly (#2-3)
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Polycythemia/ Increased Hemoglobin
Increased Hgb may be due toincreased RBC mass or decreasedplasma volume
Need to measure red cell mass(blood volume studies)
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Increased Red cell mass Independent of EPO= Polycythemia
Rubra Vera (low EPO level)
Secondary to Increased EPOAppropriate EPO elevation ie. Hypoxemia,
Hb defects, carbon monoxide
Inappropriate EPO elevation ie. EPO
secreting tumours, polycystic kidneys, postrenal transplant, androgens
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Polycythemia Rubra Vera Must be differentiated from secondary
erythrocytosis and other MPD
Arterial and venous thromboses/ Bleeding Splenomegaly often massive
Increased neutrophil count and/or plateletcount is seen frequently
Treatment is phlebotomy or hydroxyurea
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MCCQE OBJECTIVESBleeding tendency/bruising (#15-1)
Hypercoagulable state (#15-2)
Anemia (#42-1)Polycythemia/Elevated Hemoglobin (#42-2)
White blood cell abnormalities(#120)
Lymphadenopathy (#54)Splenomegaly (#2-3)
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WBC DifferentialNeutrophils (ANC)
Lymphocytes
MonocytesEosinophils
Basophils
Left shifted- bands, myelocytes,metamyelocytes
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Leukemoid Reactions CML mimicked by acute bacterial infection
inflammatory reactions, severe marrow
stress such as bleeding, underlying tumorsand treatment with G-CSF and GM-CSF
CLL mimicked by pertussis, TB and mono
CMML and acute monoblastic leukemia
mimicked by TB
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Chronic Myeloproliferative Disorders Polycythemia rubra vera
Chronic granulocytic (myelogenous)leukemia
Idiopathic Myelofibrosis
Essential thrombocythemia
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Approach to Neutropenia History - drugs, toxins, recurring mouth
sores, family history, ethnic background
Physical - splenomegaly, bone pain If the patient is asymptomatic recheck the
WBC after exercise
Blood film - are granulocytic precursors or
blasts present Bone marrow
Severity significant (ANC< 500)
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Approach to Neutropenia (ANC
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Approach to Lymphocytosis
Young people think MONO
Old people CLL
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Infectious Mononucleosis Fever, pharyngitis, generalized adenopathy
splenomegaly and hepatomegaly
Monospot and EBV antibodies are positive immune thrombocytopenia and anemia
seen
the blood film shows atypical lymphs
with granules, coarse chromatin andspreading cytoplasm with pseudopods
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Chronic Lymphocytic Leukemia Common in the elderly
the blood film shows a lymphocytosis that
may be extreme and smudge cells lymphadenopathy and splenomegaly
Often complicated by autoimmune anemiaand thrombocytopenia
treatment is observation, alkylatingagents, fludarabine, steroids or radiation
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Multiple Myeloma The blood film shows rouleaux
a monoclonal immunoglobulin can be in
serum or urine Hypercalcemia, renal failure, lytic bone are
frequent
Treat hydration, steroids,
bisphosphonates, chemotherapy or BMT Need to distinguish from MGUS
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MCCQE OBJECTIVESBleeding tendency/bruising (#15-1)
Hypercoagulable state (#15-2)
Anemia (#42-1)Polycythemia/Elevated Hemoglobin (#42-2)
White blood cell abnormalities (#120)
Lymphadenopathy (#5
4)Splenomegaly (#2-3)
8/6/2019 McLeod Heme Tovee Class
123/131
Is it LYMPHOMA?Ask about B symptoms- fever, night
sweats, weight loss
Is there evidence of infection?LNs-tender, size, consistency,
fixed/matted
Examine spleen
Always consider LN biopsy
8/6/2019 McLeod Heme Tovee Class
124/131
Made up Question-CRSA 70 yr old man presents with 6 month history of
fatigue, night sweats and weight loss. Examreveals diffuse adenopathy.
What investigations would you do first?Choose 2
a) CBC with differential
b) INR and PTT
c) Blood film/smear
d) CT thorax and abdo
e) Lymph node biopsy
8/6/2019 McLeod Heme Tovee Class
125/131
MCCQE OBJECTIVESBleeding tendency/bruising (#15-1)
Hypercoagulable state (#15-2)
Anemia (#42-1)Polycythemia/Elevated Hemoglobin (#42-2)
White blood cell abnormalities (#120)
Lymphadenopathy (#54)
Splenomegaly (#2-3)
8/6/2019 McLeod Heme Tovee Class
126/131
SplenomegalySpleen should not be palpable in adults
Ask about B symptoms and look for LNs
Spleen exam- percussion most sensitive(JAMA paper)
Causes:
Infiltrative vs. Congestive vs. Increaseddemand for splenic function
8/6/2019 McLeod Heme Tovee Class
127/131
Sample Question-MCQ22 yr old man who had splenectomy 2 yrs ago
post trauma presents with confusion, coughand fever which developed over 12 hrs.
On arrival VS T 41 RR 28 BP 90/70HR 130
Which of the following would best confirm the diagnosis?
a) Blood culture
b) CXR
c) Sputum sampled) ECG
e) Urine culture
8/6/2019 McLeod Heme Tovee Class
128/131
Sample Question-MCQA 22 yr old woman presents with iron deficiency
anemia and easy bruising. Her INR/PT isnormal and PTT is slightly prolonged.
Which of the following is the most likely diagnosis?
a) DIC
b) Liver failure
c) Von Willebrand disease
d) Hemophilia A (factor VIII def)
e) Factor XII deficiency
8/6/2019 McLeod Heme Tovee Class
129/131
Sample Question-MCQA 30 yr old woman presents with a swollen left calf. She
has no family history of blood clots.Her INR/PT isnormal and her PTT is prolonged. Investigationsdemonstrate a DVT.
Which of the following is the most likely etiology of herDVT?
a) Von Willebrand disease
b) Antithrombin deficiency
c) APLA
d) Pregnancy
e) Age
8/6/2019 McLeod Heme Tovee Class
130/131
Sample Question-MCQA 60 yr old man with prostate cancer presents
with a painful swollen right leg.
Which of the following is the most appropriateinvestigation?
a) CXR
b) venogram
c) Doppler US of leg
d) D dimer
e) PSA
8/6/2019 McLeod Heme Tovee Class
131/131
MCCQE Hematology Review
Anne McLeod
e-mail [email protected]
Office 416-340-3395