NEET MDS Lessons
General Pathology
Posterior Pituitary Syndromes
The posterior pituitary, or neurohypophysis, is composed of modified glial cells (termed pituicytes) and axonal processes extending from nerve cell bodies in the hypothalamus. The hypothalamic neurons produce two peptides: antidiuretic hormone (ADH) and oxytocin that are stored in axon terminals in the neurohypophysis.
The clinically important posterior pituitary syndromes involve ADH production and include
1. Diabetes insipidus and
2. Inappropriate secretion of high levels of ADH.
- ADH is released into the general circulation in response to increased plasma oncotic pressure & left atrial distention.
- It acts on the renal collecting tubules to increase the resorption of free water.
- ADH deficiency causes diabetes insipidus, a condition characterized by polyuria. If the cause is related to ADH Diabetes insipidus from - - ADH deficiency is designated as central, to differentiate it from nephrogenic diabetes insipidus due to renal tubular unresponsiveness to circulating ADH.
- The clinical manifestations of both diseases are similar and include the excretion of large volumes of dilute urine with low specific gravity. Serum sodium and osmolality are increased as a result of excessive renal loss of free water, resulting in thirst and polydipsia.
- ADH excess causes resorption of excessive amounts of free water, with resultant hyponatremia.
- The most common causes of the syndrome include the secretion of ectopic ADH by malignant neoplasms (particularly small-cell carcinomas of the lung), and local injury to the hypothalamus and/or neurohypophysis.
- The clinical manifestations are dominated by hyponatremia, cerebral edema, and resultant neurologic dysfunction.
1. Human papillomavirus types 6 and 11 → condyloma acuminta (venereal warts).
2. Molluscum contagiosum is characterized by a bowl shaped lesion filled with keratin, the latter containing the viral inclusions (molluscum bodies) in the squamous cells.
German measles (rubella)
- sometimes called "three day measles".
- incubation 14-21 days; infectious 7 days before the rash and 14 days after the onset of the rash.
- in adults, rubella present with fever, headache, and painful postauricular Lymphadenopathy 1 to 2 days prior to the onset of rash, while in children, the rash is usually the first sign.
- rash (vasculitis) consists of tiny red to pink macules (not raised) that begins on the head and spreads downwards and disappears over the ensuing 1-3 days; rash tends to become confluent.
- 1/3rd of young women develop arthritis due to immune-complexes.
- splenomegaly (50%)
Lymphocytosis:
Causes
-Infections in children and the neutropenic infections in adults.
-Lymphocytic leukaemia.
-Infectious mononucleosis.
-Toxdplasmosis.
-Myast'henia gravis.
Urinary tract infection
Most often caused by gram-negative, rod-shaped bacteria that are normal residents of the enteric tract, especially Escherichia coli.
Clinical manifestations:
frequent urination, dysuria, pyuria (increased PMNs), hematuria, and bacteriuria.
May lead to infection of the urinary bladder (cystitis) or kidney (pyelonephritis).
Herpes simplex is subdivided into type 1 and 2, the former usually developing lesions around the lips and mouth and the latter producing vesicular lesions in the genital region
- contracted by physical contact; incubation 2-10 days.
- primary HSV I usually is accompanied by systemic signs of fever and Lymphadenopathy, while recurrent herpes is not associate with systemic signs.
- dentists often become infected by contact with patient saliva and often develop extremely painful infections on the fingers (herpetic whitlow).
- Herpes viruses remain dormant in sensory ganglia and are reactivated by stress, sunlight, menses, etc.
- Herpes gingivostomatitis is MC primary HSV 1 infectionÆpainful, vesicular eruptions that may extend for the tongue to the retropharynx.
- Herpes keratoconjunctivitis (HSV 1)
- Kaposi's varicelliform eruption refers to an HSV 1 infection superimposed on a previous dermatitis, usually in an immunodeficient person.
- laboratory: culture; ELISA test on vesicle fluid; intranuclear inclusions within multinucleated squamous cells in scrapings (Tzanck preps) of vesicular lesions.
Connective tissue diseases
Marfan’s syndrome
a. Genetic transmission: autosomal dominant.
b. Characterized by a defective microfibril glycoprotein, fibrillin.
c. Clinical findings include tall stature, joints that can be hyperextended, and cardiovascular defects, including mitral valve prolapse and dilation of the ascending aorta.
Ehlers-Danlos syndrome
a. Genetic transmission: autosomal dominant or recessive.
b. This group of diseases is characterized by defects in collagen.
c. Clinical findings include hypermobile joints and highly stretchable skin. The skin also bruises easily. Oral findings include Gorlin’s sign and possible temporomandibular joint (TMJ) subluxation.
The oral mucosa may also appear more fragile and vulnerable to trauma.