Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A

~ 7 days

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Where is Erythropoietin (EPO) Made?

A

Kidneys produce in response to low O2- disease can disrupt

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does an increase in number of Reticulocytes indicate?

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Lifespan/Removal of RBC?

A

Live for 120 Days in circulation

Removed by macrophages in the spleen

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Symptoms of Anemia?

A

Symptoms:

  • Weakness, fatigue, dyspnoea
  • Pale conjunctiva and skin
  • Headache, dizziness, angina
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Most useful Classification for diagnosing Anemia?

A

Morphological Classification of Anaemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

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
Causes of Iron Deficiency Anemia?
Deficient iron stores: **Poor dietary intake** **Impaired iron absorption** (Celiac disease, Small intestine removal **Chronic blood loss** (Gastrointestinal/ Gynaecologic problems) Increased Demand: **Pregnancy** **Grow**th
26
The most common cause of blood loss and iron deficiency anemia in males and post-menopausal females?
**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
Clinical Presentations Characteristic of Iron Deficiency Anemia?
**➢Angular cheilitis** ➢**Koilonychia–“spoon nail”**
28
-Cytic versus -chromic with regard to anemia Morphilocal Classification?
TERMS: ***-cytic***→refers to cell size (MCV –*Mean Corpuscular Volume*) ***-chromic***→refers to hemoglobin content (MCHC –*Mean Corpuscular Haemoglobin Conc.*)
28
Treatment for Iron Deficiency Anemia
**_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
Pathogenesis of Anemia of Chronic Disease
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
Chronic Diseases that can lead to Anemia?
o Chronic infections (tuberculosis) o Chronic inflammatory conditions (Crohn’s Disease) o Rheumatologic disorders o Malignancy o Chronic kidney disease
31
Investigations/Management for Anemia of Chronic Disease?
**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
\_\_\_\_\_\_\_\_\_\_\_\_\_ regulates iron levels in criculation
**_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
Etiology of Aplastic Anemia?
**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
Types of Macrolytic Anemia?
**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
Common Causes of Megaloblastic Anemia?
Vitamin B12 Defciency Folate Deficiency Drugs interfering with DNA synthesis (e.g., ***methotrexate*** given for chemotherapy/rheumatology. Folate given to avoid deficiency)
36
Megaloblastic Anemia Pathogenesis? Presentation?
* 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
Testing for Megaloblastic Anemia
**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
Dietary Origin of B12/ Cobalalim
Fish, animal muscle, milk products, egg yolks
39
B12 Deficiency Etiology
**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
What causes **PERNICIOUS** **ANAEMIA**?
**PERNICIOUS ANAEMIA -**Autoimmune Disorder: anti-parietal cell, anti-IF antibodies created =\> loss of gastric parietal cells that produce Intrinsic Factor and Hydrochloric Acid
41
Clinical Consequences/Treatment of B12 Deficiency?
**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
Clinical Consequences/Treatment of Folate Deficiency
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)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions