Hematology Mnemonics
Macrocytic Anaemia
Macrocytic Anaemia Leaves Big Fat Reticulocytes
Myxoedema, Alcohol, Liver disease, B12 def., Folate def.,
Reticulocytosis
Target Cells
HOT LIPS
Haemoglobinopathy, Obs jaundice, Thallasaemia
Liver abscess, Iron def., Polycythaemia, Sideroblastic anaemia
Multiple Myeloma
BAHRAIN UV
Bone pain, Anaemia, Hyper Ca2+, Renal failure, Amyloidosis, Infection,
Neuropathy,(hyper) Uricaemia / viscosity
Suspect malignancy in melanoma
BITCHES
Bleeds, Irregular / Itch, Tender, Colour change, Halo, Enlargement,
Satellite lesions
Tumours which spread to bone
PUBLIK T
Prostate, Uterine, Breast, Lung, Intestine (stomach), Kidney, Thyroid
Macrocytic anemia: Causes
" ABCDEF "
 Alcohol (liver diseases)
 B12 deficiency
 Compensatory reticulocytosis (blood loss and hemolysis)
 Drug (cytotoxic drugs and AZT)/ Dysplasia (marrow disorders)
 Endocrine (hypothyroidism)
 Folate deficieny/ Fetus (pregnancy)
Clotting factors in Blood
" Foolish People Try Climbing Long Slopes After Christmas. Some Crazy P
eople Have Fallen "
Factor I = Fibrinogen
Factor II = Prothrombin
Factor III = Tissue factor
Factor IV = Calcium
Factor V = Labile factor
Factor VI - Does not exist as it was named initially but later on
discovered not to play a part in blood coagulation.
Factor VII = Stable factor
Factor VIII = Antihemophilic factor A
Factor IX = Antihemophilic factor B or Christmas factor (named after the
first patient in whom the factor deficiency was documented)
Factor X = Stuart Prower factor
Factor XI = Antihemophilic factor C
Factor XII = Hageman factor Factor
XIII = Fibrin stabilising factor 5
Splenomegaly: Causes
" CHINA "
 Congestion – portal hypertension
 Haematological – haemolytic anaemia, sickle cell disease
 Infection – Malaria, EBV, CMV, HIV
 Neoplasm – CML, myelofibrosis, lymphoma
 Autoimmune – RA, sarcoidosis, amyloidosis
Causes of Massive splenomegaly
" 3 M’s "
Henoch–Schönlein purpura
P's of HS Purpura:
Palpable Purpura
Pressure (Blanches on pressure)
Pruritis
Pain abdomen and joints
Positive Guaiac sign in faeces
Proteinuria
Prednisolone given in treatment
Platlet count may be raised but not low (DD: ITP)
Sickle Cell Anemia
In SICKle cell anemia (HBS), the abnormality is in the SICKsth position
of Beta chain of HB. Valine is present instead of Glutamic acid,
i.e. Glutamic acid Goes.
Or remember: Sickle cell anemia is a Genetic Variation - Glutamic is
replaced byValine
BT, CT, PT, PTT
Bleeding time gives Platlet response ( Remember BP )
Clotting time gives idea about Coagulation pathway ( Remember CC )
Also remember the following about Prothrombin Time (PT) and Partial
Thromboplastin Time (PTT):
PTT - Intrinsic and common pathway
PT - Extrinsic and common pathway
( Remember this by imagining that Peter is going to take part in a Tea
drinking contest. To be IN to the contest Peter must drink two Teas
(TT) - PTT gives idea about INtrinsic and common pathway. If Peter
drinks only one T, he is OUT = Extrinsic and common pathway
represented by PT )
Hodgkin's lymphoma classification
A: Asymptomatic
B: Bad
Show Details / Rate It
---Anonymous Contributor
Wiskott-Aldrich syndrome: symptom triad
"PET WASP":
Pyrogenic infections
Eczema
Thrombocytopenia
· WASP is the name of the causitive agent: Wiskott-Aldrich
Syndrome Protein.
· Alternatively: Wiskott=Hot, Aldrich=Itch, Syndrom=Throm.
Show Details / Rate It
---Robert O'Connor University College Dublin
Sarcoidosis summarized
SARCOIDOISIS:
Schaumann calcifications
Asteroid bodies/ [ACE] increase/ Anergy
Respiratory complications/ Renal calculi/ Restrictive lung
disease/ Restrictive cardiomyopathy
Calcium increase in serum and urine/ CD4 helper cells
Ocular lesions
Immune mediated noncaseating granulomas/ [Ig] increase
Diabetes insipidus/ [D vit.] increase/ Dyspnea
Osteopathy
Skin (Subcutaneous nodules, erythema nodosum)
Interstitial lung fibrosis/ IL-1
Seventh CN palsy
Show Details / Rate It
---Rinku Uberoi UNIBE
Apoptosis vs. necrosis
"LIFELESS" (since cells are dead):
· Differences are in:
Leaky membranes
Inflammatory response
Fate
Extent
Laddering
Energy dependent
Swell or shrink
Stimulus
· See attached table for apoptosis and necrosis properties for
each of the above.
Show Details / Rate It
---Robert O'Connor University College Dublin
Leukemias: acute vs. chronic rules of thumb
ABCDE:
Acute is:
Blasts predominate
Children
Drastic course
Elderly
Few WBC's (so Fevers)
· Chronic is all the opposites:
Mature cells predominate
Middle aged
Less debilitating course
Elevated WBC's, so not a history of fevers and infections
Show Details / Rate It
---Anonymous Contributor
Hypersplenism: criteria
"Hyper Splenism Ravages Cells":
Hypercellular or normal marrow
Splenomegaly
Response to splenectomy
Cytopenias
Show Details / Rate It
---Dr. Harsh Sharma BJMC, Pune, India
Anemia: TIBC finding to differentiate iron deficiency vs. chronic
disease
TIBC levels at the:
Top=Iron deficiency.
Bottom=Chronic disease.
Show Details / Rate It
---Robert O'Connor University College Dublin
Microcytic anemia: causes
"Find Those Small Cells":
Fe deficiency
Thalassemia
Sideroblastic
Chronic disease
Show Details / Rate It
---K. Dang University of Toronto
Megaloblastic anemia: vitamin B12 deficiency vs. folate
deficiency
Vitamin B12 deficiency also affects Brain (optic neuropathy,
subacute combined degeneration, paresthesia).
· Folate deficiency is not associated with neurological symptoms.
Show Details / Rate It
---Glen Davis Cornell University Medical College
Symptoms of TTP/HUS
"Nasty Fever Ruined My Tubes":
Neurological symptoms
Fever
Renal failure
Microangiopathic hemolytic anemia
Thrombocytopenia
Warfarin metabolism
 Pharmacology
' SLOW':
 Small lipid-soluble molecule
 Liver is the site of action
 Oral route of administration.
 Warfarin

Hematology mnemonics

  • 1.
    Hematology Mnemonics Macrocytic Anaemia MacrocyticAnaemia Leaves Big Fat Reticulocytes Myxoedema, Alcohol, Liver disease, B12 def., Folate def., Reticulocytosis Target Cells HOT LIPS Haemoglobinopathy, Obs jaundice, Thallasaemia Liver abscess, Iron def., Polycythaemia, Sideroblastic anaemia Multiple Myeloma BAHRAIN UV Bone pain, Anaemia, Hyper Ca2+, Renal failure, Amyloidosis, Infection, Neuropathy,(hyper) Uricaemia / viscosity Suspect malignancy in melanoma BITCHES Bleeds, Irregular / Itch, Tender, Colour change, Halo, Enlargement, Satellite lesions
  • 2.
    Tumours which spreadto bone PUBLIK T Prostate, Uterine, Breast, Lung, Intestine (stomach), Kidney, Thyroid Macrocytic anemia: Causes " ABCDEF "  Alcohol (liver diseases)  B12 deficiency  Compensatory reticulocytosis (blood loss and hemolysis)  Drug (cytotoxic drugs and AZT)/ Dysplasia (marrow disorders)  Endocrine (hypothyroidism)  Folate deficieny/ Fetus (pregnancy) Clotting factors in Blood " Foolish People Try Climbing Long Slopes After Christmas. Some Crazy P eople Have Fallen " Factor I = Fibrinogen Factor II = Prothrombin Factor III = Tissue factor Factor IV = Calcium Factor V = Labile factor Factor VI - Does not exist as it was named initially but later on discovered not to play a part in blood coagulation. Factor VII = Stable factor Factor VIII = Antihemophilic factor A Factor IX = Antihemophilic factor B or Christmas factor (named after the first patient in whom the factor deficiency was documented) Factor X = Stuart Prower factor Factor XI = Antihemophilic factor C Factor XII = Hageman factor Factor XIII = Fibrin stabilising factor 5
  • 3.
    Splenomegaly: Causes " CHINA"  Congestion – portal hypertension  Haematological – haemolytic anaemia, sickle cell disease  Infection – Malaria, EBV, CMV, HIV  Neoplasm – CML, myelofibrosis, lymphoma  Autoimmune – RA, sarcoidosis, amyloidosis Causes of Massive splenomegaly " 3 M’s " Henoch–Schönlein purpura P's of HS Purpura: Palpable Purpura Pressure (Blanches on pressure) Pruritis Pain abdomen and joints Positive Guaiac sign in faeces Proteinuria Prednisolone given in treatment Platlet count may be raised but not low (DD: ITP) Sickle Cell Anemia In SICKle cell anemia (HBS), the abnormality is in the SICKsth position of Beta chain of HB. Valine is present instead of Glutamic acid, i.e. Glutamic acid Goes. Or remember: Sickle cell anemia is a Genetic Variation - Glutamic is replaced byValine BT, CT, PT, PTT Bleeding time gives Platlet response ( Remember BP ) Clotting time gives idea about Coagulation pathway ( Remember CC ) Also remember the following about Prothrombin Time (PT) and Partial Thromboplastin Time (PTT): PTT - Intrinsic and common pathway
  • 4.
    PT - Extrinsicand common pathway ( Remember this by imagining that Peter is going to take part in a Tea drinking contest. To be IN to the contest Peter must drink two Teas (TT) - PTT gives idea about INtrinsic and common pathway. If Peter drinks only one T, he is OUT = Extrinsic and common pathway represented by PT ) Hodgkin's lymphoma classification A: Asymptomatic B: Bad Show Details / Rate It ---Anonymous Contributor Wiskott-Aldrich syndrome: symptom triad "PET WASP": Pyrogenic infections Eczema Thrombocytopenia · WASP is the name of the causitive agent: Wiskott-Aldrich Syndrome Protein. · Alternatively: Wiskott=Hot, Aldrich=Itch, Syndrom=Throm. Show Details / Rate It ---Robert O'Connor University College Dublin Sarcoidosis summarized SARCOIDOISIS: Schaumann calcifications Asteroid bodies/ [ACE] increase/ Anergy Respiratory complications/ Renal calculi/ Restrictive lung disease/ Restrictive cardiomyopathy Calcium increase in serum and urine/ CD4 helper cells Ocular lesions
  • 5.
    Immune mediated noncaseatinggranulomas/ [Ig] increase Diabetes insipidus/ [D vit.] increase/ Dyspnea Osteopathy Skin (Subcutaneous nodules, erythema nodosum) Interstitial lung fibrosis/ IL-1 Seventh CN palsy Show Details / Rate It ---Rinku Uberoi UNIBE Apoptosis vs. necrosis "LIFELESS" (since cells are dead): · Differences are in: Leaky membranes Inflammatory response Fate Extent Laddering Energy dependent Swell or shrink Stimulus · See attached table for apoptosis and necrosis properties for each of the above. Show Details / Rate It ---Robert O'Connor University College Dublin
  • 6.
    Leukemias: acute vs.chronic rules of thumb ABCDE: Acute is: Blasts predominate Children Drastic course Elderly Few WBC's (so Fevers) · Chronic is all the opposites: Mature cells predominate Middle aged Less debilitating course Elevated WBC's, so not a history of fevers and infections Show Details / Rate It ---Anonymous Contributor Hypersplenism: criteria "Hyper Splenism Ravages Cells": Hypercellular or normal marrow Splenomegaly Response to splenectomy Cytopenias Show Details / Rate It ---Dr. Harsh Sharma BJMC, Pune, India Anemia: TIBC finding to differentiate iron deficiency vs. chronic disease TIBC levels at the: Top=Iron deficiency. Bottom=Chronic disease. Show Details / Rate It ---Robert O'Connor University College Dublin
  • 7.
    Microcytic anemia: causes "FindThose Small Cells": Fe deficiency Thalassemia Sideroblastic Chronic disease Show Details / Rate It ---K. Dang University of Toronto Megaloblastic anemia: vitamin B12 deficiency vs. folate deficiency Vitamin B12 deficiency also affects Brain (optic neuropathy, subacute combined degeneration, paresthesia). · Folate deficiency is not associated with neurological symptoms. Show Details / Rate It ---Glen Davis Cornell University Medical College Symptoms of TTP/HUS "Nasty Fever Ruined My Tubes": Neurological symptoms Fever Renal failure Microangiopathic hemolytic anemia Thrombocytopenia
  • 8.
    Warfarin metabolism  Pharmacology 'SLOW':  Small lipid-soluble molecule  Liver is the site of action  Oral route of administration.  Warfarin