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Hashimoto’s thyroiditis:
1. Enlargement of the thyroid gland (goitre)
2. Lack of essential substances in diet (iodine)
3. Histologically:
• Destruction of thyroid follicle epithelium
• Diffuse infiltration of the thyroid by lymphocytes
• The normally flattened thyroid epithelial cells are replaced by plump
Hurthie cells
4. Hashimoto’s thyroiditis auto – Ab:
• Anti – thyroglobulin Ab against thyroglobulin Ag
• Anti – microsomal Ab against peroxidase Ag
5. Thyroglobulin:
• T3: Tri – iodothyronine
• T4: thyroxin
6. Immunologic pathogenesis:
• Ab may cooperate with normal lymphocytes to produce tissue damage
• In test tube, normal lymphocytes of human can cooperate with thyroid
Ab to damage thyroid cells (Ag) or lyses carrier cells coated with
thyroglobulin or thyroid microsomes
• This finding support the view that Ab – dependent cell mediated
lymphocytotoxicity (ADCC) is responsible for the induction of
pathologic changes in thyroid

Graves’ disease (thyrotoxicosis):

1. Hyperactivity of thyroid gland
2. Enlargement of thyroid gland (goitre)
3. Specific auto – Ab (human – thyroid – stimulating immunoglobulin (TSI)
directed against host thyroid tissue (Ag)
4. Hyper function due to presence of auto – Ab (TSI) directed to specific
hormone receptors (Ag) on the surface of the thyroid epithelium
5. Auto – Ab reacts with hormone receptor (Ag) and accelerates the function
of the cells to produce thyroid hormone
6. Graves’ disease auto – Ab:
• Anti – thyroglobulin Ab against thyroglobulin Ag

• Anti – microsomal Ab against peroxidase Ag
• Anti – human thyroid stimulating immunoglobulin Ab (TSI)
against TSH receptor Ag
7. Laboratory diagnosis:
• Thyroid function test:
o Increase level of T3 and T4
o Lower level of TSH
8. Histologically:
• Hyper secretion of the gland with little inflammation or no
• The thyroid follicular lining cells are cuboids instead of flat
• The colloid near the epithelium has a scalloped appearance

Laboratory diagnosis of Hashimoto’s and Graves’ disease:
1. Indirect immuno-fluorescence technique to detect auto – Ab against
thyroglobulin and microsomal Ag
2. Substrate (Ag): thyroid gland from rats or mice
• Auto – Ab: patient serum (diluted)
• Fluorescence is seen in either:
o In the colloid area (thyroglobulin Ab) of thyroid epithelium
o In the cytoplasm (microsomal Ab) of thyroid epithelium
3. Agglutination reaction to detect auto – Ab against thyroglobulin and
microsomal Ag
• Latex agglutination or hemagglutination reaction
• Latex beads or erythrocytes are coated with specific Ag
• Patient’s serum: contain auto – Ab

Primary hypo – thyroidism (adult myxedema)

1. Insufficiency of circulating thyroid hormone lead to hypothyroidism
2. Laboratory finding:
• Decreased level of radio – iodine uptake
• Low T3 and T4 level
• Serum cholesterol is high
3. Thyroid failure: due to pituitary insufficiency


1. Symptoms of weakness in most used muscles (reflect a problem in

neuromuscular transmission due to auto – ab)
2. Auto – ab against ACH receptor (Ag) is present that interferes with
transmission of signal from nerve to muscle (ACH = acetylcholine)
3. The auto ab binds to acetylcholine receptor (Ag), it cause damage by
fixing complement (block neuromuscular transmission causing muscle

1. RIA for detecting anti – ACH receptor Ab:
• Place labelled 125I (α-bungarotoxin) toxin in test tube
• Add preparation of human ACH receptor (Ag) complexes
• Incubate and allow to react
• Add patient’s serum (anti – ACH receptor Ab)
• Incubate
• Add specific human anti – globulin Ab (specific second Ab against
no 4)
• Incubate
• Final link: α-bungarotoxin – human ACH receptor – serum contain
anti – ACH receptor – anti globulin Ab specific
• Precipitation of the labelled toxin – receptor Ag – Ab – anti Ab =
complexes occur
• The precipitate is counted for radioactivity to estimate the Ab
content of the sample


1. Specific auto – Ab damage two major organ: kidney and lung

2. Anti – glomerular basement membrane (kidney) cross reacts with
pulmonary basement membrane (lung) and causes lung lesions
3. Test: Ag (IgG) react with Ab conjugated FITC (anti – IgG)

1. Haemoptysis (coughing up blood from the lung)
2. Haematuria (blood in urine) developing renal failure

Laboratory diagnosis:
1. Kidney biopsy (histology) glomerulonephritis, proliferation of parietal
layer of Bowman’s capsule, crescent shape
2. Direct immunofluorescence (kidney biopsy), a diffuse linear deposition of
IgG is seen along the glomerular capillary walls
3. RIA: detection of Ab to glomerular basement membrane


1. Destruction of platelets (Ag) with specific IgG anti – platelet (Ab)

2. Low number of platelets, patients are subjected to large ecchymosis
3. In babies born to mothers with ITP, IgG anti – platelet Ab crosses placenta
and attaches to the child’s platelet

Laboratory diagnosis:
1. Stained blood smear with giemsa, immature, large platelet can be found in
peripheral blood
2. Assays for auto – Ab against platelets (Ag) in serum by RIA
3. Assay for presence of auto – Ab on surface of platelets by flow cytometry

Immature platelets – platelet in blood circulation is low, so to compensate the

low level of platelet number, bone marrow release immature platelets


1. Myeloid leukaemia cells

• Most immature counterparts (myeloblasts)
• More differentiated myeloid cells
2. Lymphoid leukaemia
• B – lymphocytic group
• T – lymphocytic group

Acute lymphocytic leukaemia

1. In children under 15 years of age
2. Diagnosis of acute lymphocytic leukaemia:
• Bone marrow aspiration and biopsy
o Morphological analysis of cells
o Histochemical analysis of cells (immunofluorescence and
flow cytometry)
• Myeloperoxidase negative
• Cell nuclei: increased level of TdT (terminal deoxyribonucleotidyl
transferase) activity
3. Markers of T-acute lymphocytic leukaemia (Ab)
• CD7
• Cytoplasmic CD3 (cCD3)
4. Markers of B – acute lymphocytic leukaemia (Ab)
• CD19
• Cytoplasmic (CD22)

Adult leukaemia lymphoma

1. Caused by human T – lymphocytotropic virus (HTLV – 1)
2. Laboratory diagnosis:
• Circulating multi lobulated T – lymphocytes
• Total white blood cells counts is elevated and can exceed 100,000 /
• Hypercalcaemia

Acute myelogenous leukaemia (AML)

1. Diagnosis of AML:
• Bone marrow aspiration and biopsy: morphological and
histochemical analysis of the cells (immuno fluorescence and flow
• Auer rods (myeloperoxidase) evident on wright – stained samples

• Myeloperoxidase positive – positive for myeloid, negative for
• TdT negative (anti – TdT)

Chronic lymphocytic leukaemia (CLL)

1. Over 50 years age (none are children)
2. Small lymphocytes (immature) accumulates in:
• Bone marrow
• Lymph nodes
• Liver, spleen

Diagnosis of CLL:
1. Examination of peripheral blood smears
• Absolute lymphocyte count always greater than (10X109 litre)
• Normal small lymphocytes later stages appearance of nucleoli
2. Bone marrow not required for diagnosis

Chronic myelogenous leukaemia (CML)

1. Diagnosis of CML:
• Examination of a peripheral blood smears
o Total white blood cells count is almost always elevated to
greater than 25X109 litre
o Myeloid series cells ranging from myeloblasts to mature
segmented forms
o Modest basophiles and eosinophiles
o Increased peripheral blood platelet count
2. To draw blood from CML patient (blood quickly clotting when drawn),
use EDTA to the syringe (add EDTA) to prevent the blood from clotting
3. Neutrophil alkaline phosphatase activity (low or absent) in liver test
4. Translocation between chromosomes 9 and 22 (Philadelphia