NEET MDS Lessons
General Pathology
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.
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)
Bronchiectasis
- Bronchiectasis is abnormal and irreversible dilatation of the bronchi and bronchioles (greater than 2 mm in diameter) secondary to inflammatory weakening of bronchial wall.
- Occur in childhood and early adult life
- Persistent cough with copious amount of foul smelling purulent sputum
Aetiopathogenesis
Bronchial wall destruction is due to:
- Endobronchial obstruction due to foreign body
- Infection due to local obstruction or impaired defence mechanism
Clinical conditions:
- Hereditary and congenital factors
- Obstruction
- Secondary complication
Hereditary and congenital factors:
- Congenital bronchiectasis due to developmental defects
- Cystic fibrosis causing defective secretion resulting in obstruction
- Hereditary immune defiency diseases
- Immotile cilia syndrome- immotile cilia of respiratory tract, sperms causing Kartagener’s syndrome (bronchiectasis, situs inversus and sinusitis) and male infertility
- Allergic bronchial asthma patients
Obstruction:
Localised variety in one part of bronchial system.
Obstruction can be due to
Foreign body
Endobronchial tumors
Hilar lymph nodes
Inflammatory scarring (TB)
Secondary complication:
Necrotizing pneumonia in Staph infection and TB
Morphologic changes
- Affects distal bronchi and bronchioles
- Lower lobes more frequently
- Lungs involved diffusely/segmentally
- Left lower lobe than right
- Pleura fibrotic & thickened adherent to chest wall
C/S lung: Honey-combed appearance
Microscopic examination:
Bronchiole-dilated
Bronchial epithelium-normal, ulcerated, squamous metaplasia
Bronchial wall-infiltration by ac & Ch inflammatory cells,
destruction of muscle, elastic tissue
Lung parenchyma-fibrosis, surrounding tissue pneumonia
Pleura-fibrotic and adherent
Rocky Mountain Spotted Fever (Spotted Fever; Tick Fever; Tick Typhus)
An acute febrile disease caused by Rickettsia rickettsii and transmitted by ixodid ticks, producing high fever, cough, and rash.
Symptoms and Signs
The incubation period averages 7 days but varies from 3 to 12 days; the shorter the incubation period, the more severe the infection. Onset is abrupt, with severe headache, chills, prostration, and muscular pains. Fever reaches 39.5 or 40° C (103 or 104° F) within several days and remains high (for 15 to 20 days in severe cases),
Between the 1st and 6th day of fever, most patients develop a rash on the wrists, ankles, palms, soles, and forearms that rapidly extends to the neck, face, axilla, buttocks, and trunk. Often, a warm water or alcohol compress brings out the rash. Initially macular and pink, it becomes maculopapular and darker. In about 4 days, the lesions become petechial and may coalesce to form large hemorrhagic areas that later ulcerate
Neurologic symptoms include headache, restlessness, insomnia, delirium, and coma, all indicative of encephalitis. Hypotension develops in severe cases. Hepatomegaly may be present, but jaundice is infrequent. Localized pneumonitis may occur. Untreated patients may develop pneumonia, tissue necrosis, and circulatory failure, with such sequelae as brain and heart damage. Cardiac arrest with sudden death occasionally occurs in fulminant cases.
Parasitic
1. Leishmania produce 3 kinds of disease in man
- visceral leishmaniasis (kala azar) due to Leishmania donovani complex,
- cutaneous leishmaniasis due to Leishmania tropica complex, and
- mucocutaneous leishmaniasis due to Leishmania braziliensis.
- cutaneous (Oriental sore) and mucocutansous leishmaniasis limit themselves to the skinalone (ulcers) in the former disease and skin plus mucous membranes in the latter variant.
- the diagnosis of cutaneous or mucocutaneous leishmaniasis is made by biopsy, culture, skin test, or serologic tests
- the laboratory diagnosis of visceral leishmaniasis is made by performing a bone marrow aspirate and finding the leishmanial forms in macrophages, by culture, by hamster inoculation, or by serology.
- recovery from the cutaneous form incurs immunity.
- treatment: stibogluconate
HERPES SIMPLEX
An infection with herpes simplex virus characterized by one or many clusters of small vesicles filled with clear fluid on slightly raised inflammatory bases.
The two types of herpes simplex virus (HSV) are HSV-1 and HSV-2. HSV-1 commonly causes herpes labialis, herpetic stomatitis, and keratitis; HSV-2 usually causes genital herpes, is transmitted primarily by direct (usually sexual) contact with lesions, and results in skin lesions
Primary infection of HSV-1 typically causes a gingivostomatitis, which is most common in infants and young children. Symptoms include irritability, anorexia, fever, gingival inflammation, and painful ulcers of the mouth.
Primary infection of HSV-2 typically occurs on the vulva and vagina or penis in young adults
Herpetic whitlow, a swollen, painful, and erythematous lesion of the distal phalanx, results from inoculation of HSV through a cutaneous break or abrasion and is most common in health care workers.
Pneumoconioses—are environmentally related lung diseases that result from chronic inhalation of various substances.
1. Silicosis (stone mason’s disease)
a. Inhalant: silica dust.
b. Associated with extensive fibrosis of the lungs.
c. Patients have a higher susceptibility to tuberculosis infections.
2. Asbestosis
a. Inhalant: asbestos fibers.
b. Associated with the presence of pleural plaques.
c. Consequences include:
(1) Mesothelioma (malignant mesothelial tumor).
(2) Bronchogenic carcinoma.
3. Anthracosis
a. Inhalant: carbon dust.
b. Usually not as harmful as silicosis or asbestosis.
c. Associated with the presence of macrophages containing carbon.