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.
Ichthyosis vulgaris is a genetic disease characterized by increased cohesiveness of the cells in the stratum corneum, resulting up in a piling up stratum corneum (scales like a fish).
Hypopituitarism
Hypopituitarism is caused by
1. Loss of the anterior pituitary parenchyma
a. congenital
b. acquired
2. Disorders of the hypothalamus e.g. tumors; these interfere with the delivery of pituitary hormone-releasing factors from the hypothalamus.
Most cases of anterior pituitary hypofunction are caused by the following:
1. Nonfunctioning pituitary adenomas
2. Ischemic necrosis of the anterior pituitary is an important cause of pituitary insufficiency. This requires destruction of 75% of the anterior pituitary.
Causes include
a. Sheehan syndrome, refers to postpartum necrosis of the anterior pituitary, and is the most cause. During pregnancy the anterior pituitary enlarges considerably because of an increase in the size and number of prolactin-secreting cells. However, this physiologic enlargement of the gland is not accompanied by an increase in blood supply. The enlarged gland is therefore vulnerable to ischemic injury, especially in women who develop significant hemorrhage and hypotension during the peripartum period. The posterior pituitary is usually not affected.
b. Disseminated intravascular coagulation
c. Sickle cell anemia
d. Elevated intracranial pressure
e. Traumatic injury
f. Shock states
3. Iatrogenic i.e. surgical removal or radiation-induced destruction
4. Inflammatory lesions such as sarcoidosis or tuberculosis
5. Metastatic neoplasms involving the pituitary.
6. Mutations affecting the pituitary transcription factor Pit-1
Children can develop growth failure (pituitary dwarfism) as a result of growth hormone deficiency.
Gonadotropin or gonadotropin-releasing hormone (GnRH) deficiency leads to amenorrhea and infertility in women and decreased libido, impotence, and loss of pubic and axillary hair in men. TSH and ACTH deficiencies result in symptoms of hypothyroidism and hypoadrenalism. Prolactin deficiency results in failure of postpartum lactation.
Joint pathology
1. Rheumatoid arthritis
a. Cause is autoimmune in nature.
b. More common in women aged 20 to 50.
c. Characterized by inflammation of the synovial membrane. Granulation tissue, known as pannus, will form in the synovium and expand over the articular cartilage. This causes the destruction of the underlying cartilage and results in fibrotic changes and ankylosis.
Scarring, contracture, and deformity of the joints may occur.
d. Clinical symptoms include swollen joints. It can affect any joint in the body.
2. Osteoarthritis
a. Most common arthritis.
b. Cause is unknown.
c. Higher incidence in women, usually after age 50.
d. Characterized by degeneration of the articular cartilage and the formation of osteophytes (bony spurs) at the margins of affected areas.
Clinical signs and symptoms include:
(1) Stiff and painful joints affecting joints in the hand (phalangeal joints) and weight-bearing joints.
(2) Heberden’s nodes—nodules at the distal interphalangeal joint.
(3) Bocard’s nodes—nodules at the proximal interphalangeal joint.
Hepatitis D virus—can only infect cells previously infected with hepatitis B.
Delta hepatitis (HDV) is associated with a 35-nm RNA virus composed of a delta antigen-bearing core surrounded by HBV's Ag coat;
HDV requires HBV for replication.
Delta hepatitis can cause quiescent HBV states to suddenly worsened . Its transmission is the same as that of HBV.
Hepatitis E virus—a high mortality rate in infected pregnant women.
Hepatitis E (HEV) is caused by a single-stranded RNA virus. The disease is typically self-limited and does not evolve into chronic hepatitis; it may, however, be cholestatic.
Pregnant women may develop fulminant disease.
Transmission is by the fecal oral route.
HEV occurs mainly in India, Nepal, Pakistan, and Southeast Asia.
Cholangitis
Cholangitis is inflammation of the bile ducts.
1. It is usually associated with biliary duct obstruction by gallstones or carcinoma, which leads to infection with enteric organisms. This results in purulent exudation within the bile ducts and bile stasis.
2. Clinically, cholangitis presents with jaundice, fever, chills. leukocytosis, and right upper quadrant pain
Nephritic syndrome
Characterized by inflammatory rupture of the glomerular capillaries, leaking blood into the urinary space.
Classic presentation: poststreptococcal glomerulonephritis. It occurs after a group A, β–hemolytic Streptococcus infection (e.g., strep throat.)
Caused by autoantibodies forming immune complexes in the glomerulus.
Clinical manifestations:
oliguria, hematuria, hypertension, edema, and azotemia (increased concentrations of serum urea nitrogen
and creatine).