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INTRODUCTION

ANEMIA PLURIPOTENT STEM CELL

A condition that results from different - Where wbc and rbc and platelets are derived
pathologies from.
Reduction from the normal quantity of the - Found in the bone marrow
blood
RETICULOCYTES
Males(<13mg/dL) Females (<12mg/dL)
Results in decrease in the oxygen carrying Found in the peripheral circulation for 24 hrs
capacity of the blood. before maturing to erythrocytes
Released from peripheral circulation
AETIOLOGY
prematurely during inc in erythropoesis
2 MECHANISMS OF ANEMIA
ERYTHROPOETIN
1. Inc. haemoglobin loss due to:
is a hormone produced by RENAL CORTEX. It may
o Haemorrhage(loss)
inc in response to hypoxia and anemia
o Haemolysis(destruction)
2. Dec. Haemoglobin synthesis: CLINICAL MANIFESTATIONS
o Lack of nutrient
o Bone marrow failure MILDEST ANEMIA-tiredness and lethargy

Types of anemias: SPLENOMEGALY AND SIGNS OF HEART FAILURE- are sure


signs of an increase blood volume
a. Microcytic anemias
Iron def anemia HAEMOGLOBIN CONC IN THE BLODD
Anemia of chronic dse
most important parameter in assessing anemia
Sideroblastic anemia
b. MEGALOBLASTIC ANEMIA MEAN CORPUSCULAR VOLUME
Folate def
Vit. B12 def Is a useful parameter to determine the type of
c. HAEMOLYTIC ANEMIA anemia
Autoimmune haemolytic anemia Trephine or aspiration test in bone marrow
Sickle cell dse
Thalassemia -joycedmlnta
EPIDEMIOLOGY AETIOLOGY PATHOPHYSIOLO CLINICAL INVESTIGATION TREATMENT PATIENT CARE
GY MANIFESTATIONS S

IRON Most common BLOOD Iron is mainly Koilonychia, Examination PROPHYLAXIS IN Take iron with or
DEFICIENCY form of LOSS- most absorbed from dysphagia, of upper and PREGNANT- iron + after meals
ANEMIA anemia common duodenum and and pica. lower tract folic acid
cause jejunum Darker stools
Diet deficient FULL BLOOD ORAL IRON- in
in iron, CHILDBEARI Red meat iron is COUNT is an ferrous form is
parasitic NG AGE better absorbed essential cheap, safe and
infections and due to than iron found screening test effective in most pt.
multiple menstrual in green with may be continued
pregnancies loss vegetables poikilocytes(pe to 6 months to
are one of the ncil shaped) correct and
cause ADULT ASCORBIC ACID replenish body
MALES- increases the SERUM
cause is GIT absorption of FERRITIN- main STANDARD
bleeding iron parameter to TREATMENT:
establish iron FERROUS SULPHATE
100 ml loss of TRANSFERRIN- status of pt. 200 mg 3x a day
blood transports iron good
represents around the measurement Takes between 1
40 day body(serum of iron storage and 2 weeks for
absorption protein) haemoglobin to rise.
of iron 2-3 days for
TETRACYCLINES, reticulocytes to rise
PENICILLAMINE
AND NAUSEA&ABDOMIN
FLUOROQUINOL AL PAIN- related to
ONES bind iron the dose of
in GIT and elemental iron
reduce change in bowel
absorption of habit
iron

PARENTERAL IRON-
should be reserved
for patients who fail
on oral therapy
because of poor
adherence and GIT
side effects Benefit
in preoperative
anemia in patients
undergoing
orthopaedic
surgery.
Risk of
ANAPHYLACTOID
REACTIONS.

PRODUCTS OF IV
IRON:
Iron dextran(
CosmoFer)
Iron
Sucrose(VenoFer)
Iron III
isomaltoside(MonoF
er)
Ferric
carboxymaltose(FerI
njec)
ANEMIA OF 2nd most Appears to INTERLEUKIN-6 General Serum Iron : Treat the underlying
CHRONIC common form be impaired released from symptoms of Low condition.
DISEASE of anemia response to macrophages anemia+
erythropoeiti lead to an chronic Serum Ferritin: Blood transfusions
Associated n and increase inflammation + Normal or are rarely needed
with variety of inflammator production of decrease High
inflammatory y cytokines hepcidin quality of life IV IRON +
dse lead to Serum ERYTHROPOETIN
reduction in HEPCIDIN- a Transferrin: ANALOGUE = widely
bioavailabilit peptide Normal or use in chronic
y of produced by Low kidney dse
Known as circulating hepatocytes,
ANEMIA OF iron key role in iron Total It is not
INFLAMMATIO availability. capacity iron recommended to
N PLATINUM- It causes: biding: Low use erythropoietin
BASED Increase uptake analogue for
Are anemias THERAPIES- of iron by *Opposite of cancer induce
related to cytotoxic hepatocytes, Iron def anemia
CHRONIC agents, Reduce iron anemia
KIDNEY DSE more likely absorption, Consideration for
AND HEART to cause Reduce release erythropoietin
FAILURE anemia of iron from analogue are:
macrophages. 1. Women
receiving
Inflammatory platinum
cytokines based
increase chemothera
production of py for
WBC that leads ovarian
to fewer stem cancer
cells being (8g/100Ml)
available for red
cell production 2. Patients who
cannot be
given blood
transfusions
and who
have found
cancer tx
that is
necessary for
survival

TOCILIZUMAB-
interleukin-6
antagonist
monoclonal
antibody , used in
RHEUMATOID
ARTHRITIS

OLANZEPINE AND
QUETIAPINE- down
rgualtors of
interleukin 6, not to
be used clinically
SIDEROBLASTIC Are group of MAIN RING SPLENOMEGAL Presence of PYRIDOXINE:
ANEMIA conditions DEFECT: SIDEROBLASTS- Y-may lead to sideroblasts in 100mg-400mg daily
that are dx by reduced erythroblasts that mild bone Cause: peripheral
finding ring activity of have iron thrombocytop marrow. neuropathy
sideroblasts in the enzyme granules enia
the bone 5- surrounding the SERUM IRON HAEM ARGINATE-
marrow aminolevulin cell nucleus Idiopathic or AND FERRITIN: licensed for use in
ate acquired HIGH porphyria.
BOTH synthase(AL ALAS- normal in develop at Increase rbc and
hereditary AS) which is hereditary form , middle age In acquired decrease ring
and acquired involved in involves in the 1st forms: the sideroblasts in
forms haem step of haem peripheral patients with
synthesis synthesis. It blood is acquired
requires hypochromic sideroblastic
pyridoxal , normocytic anemia.
phosphate as a or
co-factor macrocytic IRON SUPPLEMENTS
are avoided
PYRIDOXINE- becaue there is an
precursor for increase iron stores.
pyridoxal
DESFERRIOXAMINE-
ACETALDEHYDE- use in iron overload,
lowers that levels iv or sq.
of ALAS and It binds free iron and
pyridoxal. iron bound to
ferritin.
ISONIAZID- Should only be used
causes when ferritin
sideroblasts reaches 1000mcg/L.

Sideroblastic Vit. C- <200mg inc


aanemia is effectiveness of
assoc. with desferroxamine .
COPPER higher doses
DEFICIENCY reported to inc iron
cardiotoxicity.

DESFERROXAMINE +
PROCHLORPERAZINE
= prolonged
unconsciousness

2 oral agents for iron


overload:

DESFERIPRONE-
causes neutropenia,
weekly neutophils
should be count
required.

DEFERASIROX-
dispersible tablets,
taken 30 mins.
Before food.

ADR: GIT ulcers and


renal impairment,

DECREASE hearing
and lens opacities

OPTHALMIC testing
before start of tx
(every 12months)

FOLATE Marginal Folate bound in CHRONIC The Managed by Blood count rise
DEFECIENCY dietary in polyglutamic FOALTE DEF.- peripheral replacement take longer
ANEMIA folate acid. predisposes blood is large therapy
patient to oval red cells
Co-trimoxazole thrombosis, Folic acid- 100mcg
increase severity depression and Neutrophils is a day in 4 months
of megaloblastic neoplasia hypersegmen
anemia. ted Eradicate vit. B12
defeciency

Red cell
folate conc- Iron + Folate= in first
most 12 weeks of
preferable pregnancy
parameter
VIT. B12 DEF Hindus has The only INTRINSIC Similar features Determine Lifelong Sore tongue
ANEMIA low vit. B12 dietary FACTOR- protect to folate serum Vit. B12 replacement May improve in
levels source is vit b12 from deficiency. level therapy 2 days and 2
from food of breakdown. weeks
Patients with animal Macrocytosis, SCHILLING No to blood Regualr
gastrectomy origin. anisocytosis, TEST- detect transfusions injections
develops this Cooking poikilocytosis, oral vit b12
does not and often mild absorption Tx of underlying
destroy vit. thrombocytope disease
B12 nia.
If blood transfusions
SPLEEN- might is necessary packed
be enlarged cells may be given,
and slight fever DIURETICS may be
given for CHF
Mild Jaundice
& Progressive STANDARD
Neuropathy TREATMENT:
HYDROXOCOBALAM
It affects the IN 1mg IM 3x a
legs not the week for 2 weeks ----
arms , tingling Then 1mg every 3
in feet and loss months
vibration sense
, muscle Hypokalemia may
weakness develop, potassium
supplement may be
given in elderly

Feels better 24-48


hours.

Haemoglobin rise
approx. 2-3 days
each forthnight

Reticulocyte rise 3-4


days peakin at 7-8
days
Neurological
damage is
irreversible with
spinal cord even
with optimum
therapy
PERNICIOUS Found Is a specific
ANEMIA commonly in autoimmune dse TREATMENT: HIGH
northern that casues ORAL DOSE or
European malabsorption of sublingual doses of
Vit. B12 due to cyanocobalamin
Disease of the lack of intrinsic
elderly, 60 factors
years of age
AUTOIMMUNE 2 types of WAIHA- WAIHA- the WAIHA- COOMBS WAIHA: Rituximab must
HAEMOLYTIC condition: assoc with haemolysis is symptoms TEST- positive STANDARD TX: high have ncessary
ANEMIA leukemia, usually depends on direct dose of pretx of
WAIHA(warm LSE, hepa B extravascular the sevrty of indicate sthe CORTICOSTEROID paracetamol
autoimmune and mediated haemolysis presence of and
haemolytic CAD- assoc by IGg antibodies to IF NO RESPONSE: chlorphenamin
anemia with viral or CAD- acute red blood azathioprine and e
bacterial CAD- mediated haemolytic cells. cyclophosphamide
CAD( cold infections by IgM crises and
agglutinine Attaches to Raynauds RITUXIMAB- the anti
dse) present erythrocytes phenomena CD-20 monoclonal
in middle age agglutinates antibody has been
below 37C , beneficial who fail
impaired blood to anti-
flow to toes nose inflammatory.
fingers and ears
CAD- need to kept
warm with
supportive mx and
tx of underlying
cause

SICKLE CELL HEREDIATARY HbS for FORMATION OF Have chronic Electrophores High incidence of
ANEMIA condition sickle cell SICKLE CELL- anemia, is is used pneumococcal
has valine anorexia, infections.
Common in substituted fatigue and
tropical for glutamic 2 PROCESSES: splenomegaly
regions acid Intracellular TREATMENT:
Afro- develops dehydration & Destructive
Carribean many polymerization of bone and joints PROPHYLACTIC: Pen
people problems HbS can be seen V 250mg 2x a day

Sickle cell SICKLE CELLS- HYDROXYCARBAMI


trait- is the are less flexible DE- effective and
carrier of than normal that may reduce crises
gene. It lead to tissue but may cause
provides hypoxia. cytotoxicity
protection
from MAINSTAY
MALARIA. TREATMENT:
Removal of trigger
THALASSAEMI Group of Causes bone No treatment
AS inherited deformity and
autosomal growth At an early age
diseases retardation they are dependent
on BLOOD
TRANSFUSION

SPLENECTOMY &
ALLOGENIC STEM
CELL TRANSPLANT is
used in severe cases
G6PD Is recessive G6Pd an Heinz bodies- Vaccination of Avoid:
defeciency hereditary dse erythrocyte oxidized Hepa A & Hepa B Ciprofloxacin
enzyme that haemoglobin may reduce attacks Dapsone
300 different is indirectly Primaquine
g6pd forms of involved in No specific drug Nalidixc acid
deficiency production treatment Sulphonamides
of reduced
glutathione Blood transfusions SEVERE:
and Vit. E to prevent Aspirin
Glutathione- haemolysis Chloramphenic
is produced ol
in response Chloroquine
to protects Menadione
and red cells Probenecid
from, Quinidine