HYPERTROPHY
Increase in the size of an organ or tissue due to increase in the size of its Constituent cells.

1. Skeletal muscle due to -exercise.

2. Cardiac muscle of:
- Left ventricle in:
    o    Hypertension.
    o    Aortic valvular lesion.
    o    Severe anaemia.
- Right ventricle in :
    o    Mitral stenosis
    o    Cor pulmonale
    
3. Smooth muscle of:

- GIT proximal to strictures.
- Uterus in pregnancy.
 

Rickets and Osteomalacia 

Rickets in growing children and osteomalacia in adults are skeletal diseases with worldwide distribution. They may result from
1. Diets deficient in calcium and vitamin D
2. Limited exposure to sunlight (in heavily veiled women, and inhabitants of northern climates with scant sunlight)
3. Renal disorders causing decreased synthesis of 1,25 (OH)2-D or phosphate depletion 
4. Malabsorption disorders.

Although rickets and osteomalacia rarely occur outside high-risk groups, milder forms of vitamin D deficiency (also called vitamin D insufficiency) leading to bone loss and hip fractures are quite common in the elderly.

Whatever the basis, a deficiency of vitamin D tends to cause hypocalcemia. When hypocalcemia occurs, PTH production is increased, that ultimately leads to restoration of the serum level of calcium to near normal levels (through mobilization of Ca from bone & decrease in its tubular reabsorption) with persistent hypophosphatemia (through increase renal exretion of phosphate); so mineralization of bone is impaired or there is high bone turnover.

The basic derangement in both rickets and osteomalacia is an excess of unmineralized matrix. This complicated in rickets by derangement of endochondral bone growth.

The following sequence ensues in rickets:
1. Overgrowth of epiphyseal cartilage with distorted, irregular masses of cartilage
2. Deposition of osteoid matrix on inadequately mineralized cartilage
3. Disruption of the orderly replacement of cartilage by osteoid matrix, with enlargement and lateral expansion of the osteochondral junction
4. Microfractures and stresses of the inadequately mineralized, weak, poorly formed bone
5. Deformation of the skeleton due to the loss of structural rigidity of the developing bones 

Gross features
• The gross skeletal changes depend on the severity of the disease; its duration, & the stresses to which individual bones are subjected.
• During the nonambulatory stage of infancy, the head and chest sustain the greatest stresses. The softened occipital bones may become flattened. An excess of osteoid produces frontal bossing. Deformation of the chest results from overgrowth of cartilage or osteoid tissue at the costochondral junction, producing the "rachitic rosary." The weakened metaphyseal areas of the ribs are subject to the pull of the respiratory muscles and thus bend inward, creating anterior protrusion of the sternum (pigeon breast deformity). The pelvis may become deformed.
• When an ambulating child develops rickets, deformities are likely to affect the spine, pelvis, and long bones (e.g., tibia), causing, most notably, lumbar lordosis and bowing of the legs .
• In adults the lack of vitamin D deranges the normal bone remodeling that occurs throughout life. The newly formed osteoid matrix laid down by osteoblasts is inadequately mineralized, thus producing the excess of persistent osteoid that is characteristic of osteomalacia. Although the contours of the bone are not affected, the bone is weak and vulnerable to gross fractures or microfractures, which are most likely to affect vertebral bodies and femoral necks.

Microscopic features

• The unmineralized osteoid can be visualized as a thickened layer of matrix (which stains pink in hematoxylin and eosin preparations) arranged about the more basophilic, normally mineralized trabeculae.

Keloids
1. Characterized by a progressively enlarging scar.
2. Caused by an abnormal accumulation of collagen at the site of injury.
3. More common in African-Americans.

CONGESTION

Congestion or hyperaemia means an increase in the content of blood in an organ. It may be :

A. Active - due to increased arterial flow to the organ with dilatation of micro vessels as in

• Inflammation.
• Increased metabolic activity.
• Neurogenic blushing.

B. Passive - due to decreased venous drainage resulting in pooling of blood. There is always an associated element of oedema.

Acute leukaemia
Lympheblastic is commoner in children and myeloblastic in adults .

Features:
- Anaemia.
- Fever and infections especially oral and respiratory.
- Haemorrhagic tendencies.
- Bone pains and tenderness (sternal).
- Lymphnode enlargement especially in lymphocytic.
- Gum hypertrophy especially in monocytic.

Blood picture:

- Anaemia and thrombocytopenia.
- Leucocyte count usually 20,-50,000/cu.mm. It may be less in subleukaemic leukaemia (even leucopenic levels may be seen).
- Blast cells form 30-90% of cells. Smudge cells and basket cells are seen .The type of balst cell may be recognised  by the associated more mature forms or by special cytochemical stains
- Blasts may be few in peripheral blood in the aleukamic stage

 Bone Marrow

- May be a dry tap , necessitating a trephine biopsy 
- Hypercellular with 70-90% blasts
- Reduction in megakaryocytes and erythroid cells
 

Glomerulonephritis

Characterized by inflammation of the glomerulus.

Clinical manifestations:
Nephrotic syndrome (nephrosis) → Most often caused by glomerulonephritis.

Laboratory findings:
(i) Proteinuria (albuminuria) and lipiduria—proteins and lipids are present in urine.
(ii) Hypoalbuminemia—decreased serum albumin due to albuminuria.
(iii) Hyperlipidemia—especially an increase in plasma levels of low-density lipoproteins and cholesterol.

Symptoms

severe edema, resulting from a decrease in colloid osmotic pressure due to a decrease in serum albumin.