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Sem3: PATH30030 Hematology/Immunosupression > L2 Anemia I > Flashcards

L2 Anemia I Flashcards

1
Q

Requirements for Erythropoiesis?

A

oIron - necesary for formation of hemoglobin

oFolic acid

oVitamin B12

oErythropoietin (EPO) – colony stimulating factor, growth factor that induces the synthesis of RBCs

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2
Q

How long does the production of new red blood cell take?

A

~ 7 days

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3
Q

Where is Erythropoietin (EPO) Made?

A

Kidneys produce in response to low O2- disease can disrupt

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4
Q

Stages of Erythropoiesis and requirements of each?

A

Pro-Erythroblast (EPO) → Erythroblast (Iron, Folate, B12)→ Reticulocyte (NO NUCLEUS)

Ribosome synthesis → Hemoglobin Accumulation → Ejection of Nucleus

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5
Q

What does an increase in number of Reticulocytes indicate?

A

Indicate increased RBC synthesis/turnover → Implying increased peripheral RBC destruction

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6
Q

Reticulocyte Characteristics?

A

Reticulocytes constitute ~ 1 % of normal RBC count

Recently released from marrow, ‘young/immature’ larger RBCs

NO nucleus

Blue tinge to cytoplasm (normally pink) as contain ribosomal RNA

Reticulocyte maturation to a mature erythrocyte: ~ 1 day

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7
Q

Erythrocyte Characteristics

A

Biconcave discs with NO nucleus

No protein synthesis

Cytoplasm contains haemoglobin (Hb)

Primary function: to deliver oxygen

Metabolically active (Glycolysis → ATP; Pentose phosphate pathway → counteract oxidative stress)

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8
Q

What leads to a shift toward HIGHER Hemoglobin O2 Affinity?

Direction of dissociation curve shift?

A

LEFT shift

Lower CO2

Lower Temp

Higher pH

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9
Q

What leads to a shift toward LOWER Hemoglobin O2 Affinity?

Direction of dissociation curve shift?

A

RIGHT shift

Higher CO2

Higher Temperatures

Lower pH

Higher Altitude

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10
Q

Proteins in RBC membrane that contribute to shape/felxibility?

What do mutations with these lead to?

A

Ankyrin, Spectrin, Band 3

Mutations → Hemolytic Anemia

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11
Q

Lifespan/Removal of RBC?

A

Live for 120 Days in circulation

Removed by macrophages in the spleen

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12
Q

Process of RBC Breakdown?

Side Effect of Excess?

A

Macrophages Breaks blood into Heme and Globin

Globin further broken into AA

Heme

=> iron extracted

=> stored as ferritin in liver

=> Iron transferred to Bone marrow for new RBC

=> Biliverdin

=> Bilirubin

=> Excessive buildup of Bilirubin => Jaundice

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13
Q

The threshold for diagnosis of Anemia?

A

Measured as FALL IN HAEMOGLOBIN LEVEL

  • Hb<13 g/dL in men
  • Hb<11.5 g/dL in women
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14
Q

Symptoms of Anemia?

A

Symptoms:

  • Weakness, fatigue, dyspnoea
  • Pale conjunctiva and skin
  • Headache, dizziness, angina
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15
Q

Clinical Manifestation of Acute Anemia?

A

Volume depletion

o Shortness of breath

o Tachycardia

o Decreased blood pressure

o Loss of consciousness

o Organ failure

o Shock

LIFE THREATENING
Casued by Traumatic injury, massive GI hemorrhage, ruptured ectopic pregnancy, ruptured aneurysm

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16
Q

Clinical Manfiestation of Chronic Anemia

A
  • Pallor
  • Fatigue, lassitude
  • With haemolysis:
    • Jaundice
    • Gallstones
  • With ineffective erythropoiesis
    • Iron overload
    • Heart failure (myocardial iron overload)
    • Endocrine failure
      • If severe and congenital:
        • Growth retardation
        • Bone deformities
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17
Q

Most useful Classification for diagnosing Anemia?

A

Morphological Classification of Anaemia

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18
Q

Morphological Classification of Anemia?

A

Microcytic Hypochromic (MCV <80 fL)

Normocytic normochromic (MCV: 80 - 100 fL)

Macrocytic (MCV > 100 fL)

19
Q

Classification of Anemia by Cause

A
20
Q

Causes of Microcytic Hypochromia? (MCV <80)

A

▪ Iron deficiency (due to chronic blood loss)

▪ Anaemia of chronic disease (~20%)

▪ Thalassaemia

21
Q

Causes of Normocytic Normochromatic Anemia? (MCV 80-100)

A

▪ Hyperproliferative Anemia:

Acute blood loss

Haemolytic anaemia

▪ Anaemia of chronic disease (~80%)

▪ Renal disease

▪ Leukaemia

22
Q

Causes of Macrocytic Anemia (MCV >100)

A
  • Megaloblastic Anemia:
    • B12 Deficiency
    • Folate Deficiency
    • Chemotherapy
  • Non-Megoblastic Anemia:
    • LIver Disease
    • Chronic Alcholoism
    • Increased Reticulocytes
23
Q

Most Common Types of Anemia?

A

Iron deficiency anemia (microcytic hypochromic)

Anemia of chronic disease (normocytic OR microcytic)

24
Q

Absorption of Iron from Diet

A
  • Heme and ferrous Fe2+ absorbed in small intestine
  • Iron transported in the plasma bound to TRANSFERRIN
  • Stored as Ferrtin
25
Q

Causes of Iron Deficiency Anemia?

A

Deficient iron stores:

Poor dietary intake

Impaired iron absorption (Celiac disease, Small intestine removal

Chronic blood loss (Gastrointestinal/ Gynaecologic problems)

Increased Demand:

Pregnancy

Growth

26
Q

The most common cause of blood loss and iron deficiency anemia in males and post-menopausal females?

A

GI BLEEDING is the most common cause of blood loss and iron deficiency anaemia in males and post-menopausal females!!!

GI workup is mandatory if the source of bleeding has not been identified!!!

Failure to evaluate the GI tract →failing to diagnose potentially resectable colon cancers before they metastasize and become incurable!!!

27
Q

Clinical Presentations Characteristic of Iron Deficiency Anemia?

A

➢Angular cheilitis

➢Koilonychia–“spoon nail”

28
Q

-Cytic versus -chromic with regard to anemia Morphilocal Classification?

A

TERMS:

-cytic→refers to cell size (MCV –Mean Corpuscular Volume)

-chromic→refers to hemoglobin content (MCHC –Mean Corpuscular Haemoglobin Conc.)

28
Q

Treatment for Iron Deficiency Anemia

A

Iron replacement:

  1. Oral iron is preferable to parenteral iron
  2. Ferrous (Fe2+) sulphate therapy
  • For several months to restore iron stores
  • Significant increase in Hb within 3 weeks of therapy

Inappropriate iron therapy can lead to haemosiderosis

Transfusions: only to avoid life-threatening complications of anaemia

29
Q

Pathogenesis of Anemia of Chronic Disease

A

Pathogenesis:

o Abnormality in iron utilization: Inflammatory cytokines (IL-6)

→ increased hepcidin levels

→ iron sequestered in macrophages

→ Decreased utilization of endogenous iron stores

o Relative deficiency of EPO (decrease in EPO production and marrow responsiveness to EPO)

→ Inhibition of erythropoiesis

o Reduced proliferation of erythroid precursors in response to EPO and decreased lifespan of erythrocytes

30
Q

Chronic Diseases that can lead to Anemia?

A

o Chronic infections (tuberculosis)

o Chronic inflammatory conditions (Crohn’s Disease)

o Rheumatologic disorders

o Malignancy

o Chronic kidney disease

31
Q

Investigations/Management for Anemia of Chronic Disease?

A

Investigations:

o Low serum iron

o Low serum iron binding capacity

o Normal or increased serum ferritin

Management: Treatment of underlying cause. DON’t GIVE IRON!!

32
Q

_____________ regulates iron levels in criculation

A

Hepcidin: regulates iron level in circulation

Inflammation

→ HIGH hepcidin level

→ serum iron level falls (due to iron trapping in macrophages)

→ anemia

Hemochromatosis

→ hepcidin is low

→ Iron Overload

33
Q

Etiology of Aplastic Anemia?

A

Bone marrow failure → Marrow hypoplasia and peripheral pancytopenia

Anaemia is often NORMOCYTIC, mild macrocytosis can also be observed in association with stress erythropoiesis

Aetiology:

  • -Alkylating agents, insecticides*
  • -Radiation*
  • -Viruses (parvovirus, EBV, CMV)*
  • -Idiosyncratic reactions to drugs*
  • -Inherited defects in telomerase and DNA repair (e.g., Fanconi anaemia)*
  • -Immune-mediated or acquired stem cell defects*
34
Q

Types of Macrolytic Anemia?

A

Megaloblastic anemia (Defective DNA synthesis)

Non-megaloblastic anemia (NO impairment of DNA synthesis)

  • Liver disease (RBCs become stuffed with cholesterol and are larger)
  • Alcoholism
  • Hypothyroidism
  • Myelodysplastic syndromes (MDS)
35
Q

Common Causes of Megaloblastic Anemia?

A

Vitamin B12 Defciency

Folate Deficiency

Drugs interfering with DNA synthesis (e.g., methotrexate given for chemotherapy/rheumatology. Folate given to avoid deficiency)

36
Q

Megaloblastic Anemia Pathogenesis?

Presentation?

A
  • Defective DNA synthesis leading to unbalanced growth and delayed cell division without impairment of RNA synthesis

→ Nuclear-cytoplasmic asynchrony (affects all rapidly growing cells)

→ Unusally large erythroid precursor cells: ‘megaloblasts’

→ Mature into unusually large RBCs: ‘macro-ovalocytes

  • Macro-ovalocytes are removed prematurely in the circulation
  • Autohaemolysis of affected megaloblasts in bone marrow (ineffective erythropoiesis)

→ Low reticulocyte count

→ increased bilirubin and increased LDH

→ pancytopaenia

37
Q

Testing for Megaloblastic Anemia

A

BLOOD FILM

Raised MCV →macro-ovalocytes (MCHC normal)

Anisocytosis (variation in size), poikilocytosis (variation in shape)

Neutrophils are larger than normal, platelets are not increased in size

Hypersegmentation of neutrophils (> 5 lobes)

BONE MARROW: Hypercellular with large forms of precursor cells

38
Q

Dietary Origin of B12/ Cobalalim

A

Fish, animal muscle, milk products, egg yolks

39
Q

B12 Deficiency Etiology

A

DECREASED ABSORPTION OF B12

  1. Loss of gastric parietal cells that produce Intrinsic Factor and hydrochloric acid
    1. Gastrectomy
    2. Atrophy
    3. Lye injury to gastric mucosa
    4. PERNICIOUS ANAEMIA -Autoimmune: anti-parietal cell, anti-IF antibodies (B12 used to create Intrinsic factor)
  2. Ileal Disorders
  3. Defects in B12 Transpoert
  4. Metabolic Disorders

DIETARY DEFICIENCY: RARE only in strict vegetarians (Stored in liver takes years to develop deficiency)

40
Q

What causes PERNICIOUS ANAEMIA?

A

PERNICIOUS ANAEMIA -Autoimmune Disorder: anti-parietal cell, anti-IF antibodies created => loss of gastric parietal cells that produce Intrinsic Factor and Hydrochloric Acid

41
Q

Clinical Consequences/Treatment of B12 Deficiency?

A

Macrocytic Anemia with hypersegmented neutrophils (>5 Lobes)

Glossitis- Smooth tongue, beefy red appearance

Neurological symptoms

Polyneuropathy →Paraesthesia (abnormal burning senstation)

Subacute combined degeneration of the spinal cord → progressive weakness, ataxia

TREATMENT: Vitamin B12 replacement (intramuscular hydroxocobalamin injections)

42
Q

Clinical Consequences/Treatment of Folate Deficiency

A

Folate Normally absorbed via passive diffusion in small intestine

Deficiency Etiology:

oDecreased intake (alcoholics, older adults)

oIncreased requirements (pregnancy, infancy)

oMalabsorption

oDrugs (methotrexate)

NO neurologic symptoms (As opposed to B12 Deficiency)

Treatment: folate replacement

Sem3: PATH30030 Hematology/Immunosupression (11 decks)

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