Hyperparathyroidism 

Abnormally high levels of parathyroid hormone (PTH) cause hypercalcemia. This can result from either primary or secondary causes. Primary hyperparathyroidism is caused usually by a parathyroid adenoma, which is associated with autonomous PTH secretion. Secondary  hyperparathyroidism, on the other hand, can occur in the setting of chronic renal failure. In either situation, the presence of excessive amounts of this hormone leads to significant skeletal changes related to a persistently exuberant osteoclast activity that is associated with increased bone resorption and calcium mobilization. The entire skeleton is affected. PTH is directly responsible for the bone changes seen in primary hyperparathyroidism, but in secondary hyperparathyroidism additional influences also contribute. In chronic renal failure there is inadequate 1,25- (OH)2-D synthesis that ultimately affects gastrointestinal calcium absorption. The hyperphosphatemia of renal
failure also suppresses renal α1-hydroxylase, which further impair vitamin D synthesis; all these eventuate in hypocalcemia, which stimulates excessive secretion of PTH by the parathyroid glands, & hence elevation in PTH serum levels. 

Gross features
• There is increased osteoclastic activity, with bone resorption. Cortical and trabecular bone are lost and replaced by loose connective tissue. 
• Bone resorption is especially pronounced in the subperiosteal regions and produces characteristic radiographic changes, best seen along the radial aspect of the middle phalanges of the second and third fingers.

Microscopical features

• There is increased numbers of osteoclasts and accompanying erosion of bone surfaces.
• The marrow space contains increased amounts of loose fibrovascular tissue.
• Hemosiderin deposits are present, reflecting episodes of hemorrhage resulting from microfractures of the weakened bone.
• In some instances, collections of osteoclasts, reactive giant cells, and hemorrhagic debris form a distinct mass, termed "brown tumor of hyperparathyroidism". Cystic change is common in such lesions (hence the name osteitis fibrosa cystica). Patients with hyperparathyroidism have reduced bone mass, and hence are increasingly susceptible to fractures and bone deformities.

Enterococci

Most common are E. fecalis and E. fecium.  Cause inflammation at site of colonization.

Serious resistance to antibiotics.  E. fecium is now a vancomycin resistant enterococcus (VRE)

Chickenpox (varicella)
 - primarily a childhood disease (70%)
 - incubation period 14-16 days; highly contagious; infectious 2 days before the vesicles until the last one dries.
 - present with generalized, intensely pruritic skin lesions starting as macules vesicles pustules (MVP-most valuable player) usually traveling centrifugally to the face and out to the extremities; unlike smallpox vesicles, chickenpox vesicles appear in varying stages of development as successive crops of lesions appear; intranuclear inclusions similar to HSV.
 - pneumonia develops in 1/3 of adults; MCC death in chickenpox.
 - association with Reye's syndrome if child takes aspirin. 

Diseases from Str. pyogenes (Group A strep)

1.  Streptococcal pharyngitis.  Most frequent Group A infection.  Throat has gray-white exudate.  Infection may become systemic into blood, sinuses, jugular vein, meninges.  In less than a week the M-protein and capsule production decrease, and transmission declines.

2.  Skin infections, such as impetigo.  Especially in children.  Different M-proteins than in pharyngitis.  Skin infections associated with edema and red streaking (characteristic).

3.  Necrotizing fasciitis/myositis.  Infection of deeper tissue advances despite antibiotics.

4. Scarlet fever.  Caused by phage-associated erythrogenic toxin-producing strains.  Toxins cause cardiac, renal, and other systemic failures.  Rash is very red with a sand-papery feel and shedding of superficial skin.

5.  Toxic Shock Syndrome.  Parallels the toxic shock caused by TSST-carrying Staph. aureus.

6.  Non-suppurative, post-infection diseases. 

Rheumatic fever (myocarditis, cardiac valve disease, polyarthralgia, rashes.  Occurs two  weeks after a pharyngeal infection)

Glomerulonephritis (Occurs two weeks after pharyngeal or skin infections.  Often due to immunologic reaction to M-protein type 12)

ATROPHY
It is the acquired decrease in the size of an organ due to decrease in the size and/or number of its constituent cells.
Causes:
(1) Physiological

- Foetal involution.
    o    Branchial clefts.
    o    Ductus arterious.
- Involution of thymus and other lymphoid organs in childhood and adolescence.
- In adults:
    o    Post-partum uterus.
    o    Post-menopausal ovaries and uterus
    o    Post-lactational breast
    o    Thymus.
(2) Pathological:
- Generalised as in

    o    Ageing.
    o    Severe starvation and cachexia
- Localised :
    o    Disuse atropy of bone and muscle.
    o    Ischaemic atrophy as in arteriosclerotic kidney. .
    o    Pressure atrophy due  to tumours and of kidney in hydronephrosis.
    o    Lack of trophic stimulus to endocrines and gonads.
 

Chronic myelocytic leukaemia
Commoner in adults (except the Juvenile type)

Features:

- Anaemia.
- Massive splenomegaly
- Bleeding tendencies.
- Sternal tenderness.
- Gout and skin manifestations

Blood picture:

- Marked leucocytosis of 50,-1000,000 cu.mm, often more
- Immature cells of the series with 20-50 % myelocytes
- Blasts form upto 5-10% of cells
- Basophils may be increased
- Leuocyte alkaline phosphate is reduced
- Anaemia with reticutosis and nucleated RBC
- Platelets initially high levels may fall later if patient goes into blast crisis.

Bone marrow:
- Hyper cellular marrow.
- Myeloid hyperplasia with more of immature forms, persominatly myelocytes.

Chromosomal finding. Philadelphia (Phi) chromosome is positive adult cases .It is a short chromosome due to deletion  of long arm of chromosome 22 (translocated to no.9),

Juvenile type :- This is Ph1 negative  has more nodal enlargement and has a worse prognosis, with a greater proneness to infections and haemorrhage