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
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---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.
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---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
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---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.

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---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
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---Anonymous Contributor

Hypersplenism: criteria

"Hyper Splenism Ravages Cells":

Hypercellular or normal marrow
Splenomegaly
Response to splenectomy
Cytopenias
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---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.
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---Robert O'Connor University College Dublin
Microcytic anemia: causes

"Find Those Small Cells":

Fe deficiency
Thalassemia
Sideroblastic
Chronic disease
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---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.
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---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