NEET MDS Lessons
General Pathology
Seborrheic keratosis
1. A round, brown-colored, flat wart.
2. Most often seen in middle-aged to older adults.
3. A benign lesion.
Cardiac tamponade
A. Caused by accumulation of fluid in the pericardium. This severe condition can quickly impair ventricular filling and rapidly lead to decreased cardiac output and death.
1. Signs and symptoms include:
a. Hypotension.
b. Jugular venous distention.
c. Distant heart sounds.
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.
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.
Chronic hepatitis
Chronic hepatitis occurs in 5%-10% of HBV infections and in well over 50% of HCV; it does not occur in HAV. Most chronic disease is due to chronic persistent hepatitis. The chronic form is more likely to occur in the very old or very young, in males, in immunocompromised hosts, in Down's syndrome, and in dialysis patients.
a. Chronic persistent hepatitis is a benign, self-limited disease with a prolonged recovery. Patients are asymptomatic except for elevated transaminases.
b. Chronic active hepatitis features chronic inflammation with hepatocyte destruction, resulting in cirrhosis and liver failure.
(1) Etiology. HBV, HCV, HDV, drug toxicity, Wilson's disease, alcohol, a,-antitrypsin deficiency, and autoimmune hepatitis are common etiologies.
(2) Clinical features may include fatigue, fever, malaise, anorexia, and elevated liver function tests.
(3) Diagnosis is made by liver biopsy.
8. Carrier state for HBV and HCV may be either asymptomatic or with liver disease; in the latter case, the patient has elevate transaminases.
a. Incidence is most common in immunodeficient, drug addicted, Down's syndrome, and dialysis patients.
b. Pathology of asymptomatic carriers shows "ground-glass"" hepatocytes with finely granular eosinophilic cytoplasm.
Staphylococcal Infection
Staphylococci, including pathogenic strains, are normal inhabitants of the nose and skin of most healthy people
Virulence factors include coagulase (which clots blood), hemolysin, and protein A (which ties up Fc portions of antibodies). Although we have antibodies against staphylococci, they are of limited usefulness.
Staphylococci (and certain other microbes) also produce catalase, which breaks down H2O2, rendering phagocytes relatively helpless against them.
The coagulase-positive staphylococcus (Staphylococcus pyogenes var. aureus) is a potent pathogen. It tends to produce localized infection
It is the chief cause of bacterial skin abscesses. Infection spreads from a single infected hair (folliculitis) or splinter to involve the surrounding skin and subcutaneous tissues
Furuncles are single pimples
carbuncles are pimple clusters linked by tracks of tissue necrosis which involve the fascia.
Impetigo is a pediatric infection limited to the stratum corneum of the skin -- look for honey-colored crusts
Staphylococcal infections of the nail-bed (paronychia) and palmar fingertips (felons) are especially painful and destructive
These staph are common causes of wound infections (including surgical wounds) and of a severe, necrotizing pneumonia. Both are serious infections in the hospitalized patient.
Staph is the most common cause of synthetic vascular graft infections. Certain sticky strains grow as a biofilm on the grafts
Staph aureus is pathogenic, β-hemolytic, and makes coagulase.
Staph epidermidis are non-pathogenic strains that don’t make coagulase. Often Antibiotics resistant, and can become opportunistic infections in hospitals.
Staph aureus is normal flora in the nose and on skin, but can also colonize moist areas such as perineum. Causes the minor infections after cuts. Major infections occur with lacerations or immune compromise, where large number of cocci are introduced.
While Staph aureus can invade the gut directly (invasive staphylococcal enterocolitis), it is much more common to encounter food poisoning due to strains which have produced enterotoxin B, a pre-formed toxin in un-refrigerated meat or milk products
Staph epidermidis (Coagulase-negative staphylococci)
Universal normal flora but few virulence factors. Often antibiotic resistant.
Major cause of foreign body infections such as prosthetic valve endocarditis and IV line sepsis.
Staph saprophyticus
Common cause of UTI in women.
Pathogenicity
Dominant features of S. aureus infections are pus, necrosis, scarring. The infections are patchy. Serious disease is rare because we are generally immune. However, foreign bodies or necrotic tissue can start an infection. Staph infections include wound infections, foreign body sepsis, pneumonia, meningitis.
Occassionally, S. aureus can persist within cells.
Major disease presentations include:
--Endocarditis
--Abscesses (due to coagulase activity)
--Toxic Shock
--Wound infections
--Nosocomial pneumonia
Prevention of Staph aureus infections
S. aureus only lives on people, so touching is the main mode of transmission. Infected patients should be isolated, but containment is easy with intense hand washing.
Bacterial meningitis (pyogenic, suppurative infections)
1. Common causes include:
a. Escherichia coli in newborns.
b. Haemophilus influenzae in infants and children.
c. Neisseria meningitides in young adults.
d. Streptococcus pneumoniae and Listeria monocytogenes in older adults.
Clinical findings include severe headache, irritability, fever, and a stiff neck.
a. A spinal tap shows CSF fluid that is cloudy or purulent and is under increased pressure. There is also an increase in protein and a decrease in glucose levels.
3. Can be fatal if left untreated.