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General Pathology - NEETMDS- courses
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General Pathology

Fanconi’s syndrome

Characterized by the failure of the proximal renal tubules to resorb amino acids, glucose, and phosphates.
May be inherited or acquired.

Clinical manifestations include 

glycosuria, hyperphosphaturia, hypophosphatemia, aminoaciduria, and systemic acidosis.

STREPTOCOCCAL INFECTIONS

Most streptococci are normal flora of oropharynx

Group A streptococci:  Str. pyogenes

Group B streptococci:  Str. agalactiae

Str. pneumoniae

Strep viridans group

Group D: Enterococcus (lately Strep. Fecalis and E. fecium), causes urinary tract infections,

Pulmonary edema

Pulmonary edema is swelling and/or fluid accumulation in the lungs. It leads to impaired gas exchange and may cause respiratory failure.

Signs and symptoms

Symptoms of pulmonary edema include difficulty breathing, coughing up blood, excessive sweating, anxiety and pale skin. If left untreated, it can lead to death, generally due to its main complication of acute respiratory distress syndrome.

Diagnosis

physical examination: end-inspiratory crackles during auscultation (listening to the breathing through a stethoscope) can be due to pulmonary edema. The diagnosis is confirmed on X-ray of the lungs, which shows increased vascular filling and fluid in the alveolar walls.

Low oxygen saturation and disturbed arterial blood gas readings may strengthen the diagnosis

Causes

Cardiogenic causes:

  1. Heart failure
  2. Tachy- or bradyarrhythmias
  3. Severe heart attack
  4. Hypertensive crisis
  5. Excess body fluids, e.g. from kidney failure
  6. Pericardial effusion with tamponade

Non-cardiogenic causes, or ARDS (acute respiratory distress syndrome):

  1. Inhalation of toxic gases
  2. Multiple blood transfusions
  3. Severe infection
  4. Pulmonary contusion, i.e. high-energy trauma
  5. Multitrauma, i.e. severe car accident
  6. Neurogenic, i.e. cerebrovascular accident (CVA)
  7. Aspiration, i.e. gastric fluid or in case of drowning
  8. Certain types of medication
  9. Upper airway obstruction
  10. Reexpansion, i.e. postpneumonectomy or large volume thoracentesis
  11. Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
  12. Lack of proper altitude acclimatization.

Treatment

When circulatory causes have led to pulmonary edema, treatment with loop diuretics, such as furosemide or bumetanide, is the mainstay of therapy. Secondly, one can start with noninvasive ventilation. Other useful treatments include glyceryl trinitrate, CPAP and oxygen.

Salivary gland pathology

Inflammation 

a. Sialolithiasis produces a secondary inflammatory reaction  to obstruction and the resultant enlargement of ducts by stones. It may be complicated by actual infection with mouth flora. 

b. Sialadenitis is a primary inflammatory reaction, but it is not always infectious. It may be part of an autoimmune disease  (e.g., Sjogren's syndrome), or the result of bacterial or virals (e.g., mumps) infection. 

Sjögren’s syndrome

a. An autoimmune disease of the salivary and lacrimal glands.
b. Autonuclear antibodies (ANAs) against salivary ducts may be seen.
c. Triad of symptoms include:
(1) Xerostomia—from decreased saliva production.
(2) Keratoconjunctivitis sicca (dry eyes)—from decreased tear production.
(3) Rheumatoid arthritis.
(4) Enlargement of the salivary or lacrimal glands, known as Mikulicz syndrome, may also be observed. 

d. Histologically, a dense infiltration of the gland by lymphocytes is observed.

Tumors

The parotid gland accounts for more than three-quarters of these tumors, most of which are benign. Of the remainder, more occur in the submandibular gland than in the sublingual, and most of these are malignant. Many are surgically, cured, but local recurrence is common. 

a. Pleomorphic adenoma is generally benign and accounts for approximately three-quarters of all salivary gland tumors. If  is composed of multiple epithelial and mesenchymal cell types. Complications may arise due to involvement of cranial nerve VII. 

(a) The most common salivary gland tumor.
(b) Is benign.
(c) Prognosis is good after proper surgical excision.

b. Warthin's tumor (adenolymphoma) is also benign, occuring almost exclusively in the parotid gland. It is grossly cystic.

Microscopic examination reveals cell types suggestive of branchial cleft origin embedded in a lymphoid matrix. 

c. Mucoepidermoid tumors also occur primarily in the parotid and have a high rate of malignant transformation.The malignant component is usually squamous cell.  Prognosis of tumor depends on grade and stage of disease.

d. Cylindroma (adenoid cysticc. Mucoepidermoid tumors carcinoma) is more common in the minor salivary glands found in the oral mucosa, and metastases are more common than in other tumors of the salivary glands. Facial nerve complications are frequent. 
(1) Grossly, the tumor forms multiple lobules surrounded by a capsule. 
(2) Microscopically, small cells form glands containin mucoid material 

Psoriasis
1. Characterized by skin lesions that appear as scaly, white plaques.
2. Caused by rapid proliferation of the epidermis.
3. Autoimmune pathogenesis; exact mechanism is unclear.

Urticaria (hives) refers to the presence of edema within the dermis and itchy elevations of the skin which may relate to either a Type I (MC) or Type III hypersensitivity reaction.

Type III hypersensitivity reaction.

 - exaggerated venular permeability MC related to IgE mediated disease and release of histamine from mast cells.

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)

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