NEET MDS Lessons
General Pathology
Psoriasis is a chronic disorder characterized by scaly, erythematous plaques, which histologically are secondary to epidermal proliferation.
- genetic factors (HLA relationships), environmental (physical injury, infection, drugs, photosensitivity), abnormal cellular proliferation (deregulation of epidermal proliferation) and microcirculatory changes in the papillary dermis (diapedesis of neutrophils into the epidermis) are all interrelated.
- the plaques of psoriasis are characteristically well-demarcated pink or salmon colored lesions covered by a loosely-adherent silver-white scale which, when picked off, reveals pinpoint bleeding sites (Auspitz sign).
- the nail changes in psoriasis include pitting, dimpling, thickening and crumbling with a yellowish-brown discoloration of the nail plate.
- the characteristic histologic features of psoriasis include:
- hyperkeratosis
- absence of the granulosa cells (present in lichen planus).
- parakeratosis
- regular, club-shaped elongation of the rete pegs (irregular and saw toothed in lichen planus) with vessel proliferation in the papillary dermis (reason for the bleeding associated with Auspitz sign).
- characteristic subcorneal collection of neutrophils called a Munro's microabscess (diapedesis from vessels in papillary dermi).
- 7% develop HLA B27 positive psoriatic arthritis
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
Bacterial endocarditis
Endocarditis is an infection of the endocardium of the heart, most often affecting the heart valves.
A. Acute endocarditis
1. Most commonly caused by Staphylococcus aureus.
2. It occurs most frequently in intravenous drug users, where it usually affects the tricuspid valve.
B. Subacute endocarditis
1. Most commonly caused by less virulent organisms, such as intraoral Streptococcus viridans that can be introduced systemically via dental procedures.
2. Pathogenesis: occurs when a thrombus or vegetation forms on a previously damaged or congenitally abnormal valve. These vegetations contain bacteria and inflammatory cells. Complications can arise if the thrombus embolizes, causing septic infarcts.
Other complications include valvular dysfunction or abscess formation.
3. Symptoms can remain hidden for months.
4. Valves affected (listed most to least common):
a. Mitral valve (most frequent).
b. Aortic valve.
c. Tricuspid (except in IV drug users, where the tricuspid valve is most often affected).
Rheumatic fever
Before antibiotic therapy, this was the most common cause of valvular disease.
1. Usually preceded by a group A streptococci respiratory infection; for example, strep throat.
2. All three layers of the heart may be affected. The pathologic findings include Aschoff bodies, which are areas of focal necrosis surrounded by a dense inflammatory infiltration.
3. Most commonly affects the mitral valve, resulting in mitral valve stenosis, regurgitation, or both.
Bullous and Vesicular Disease
1. There are many diseases characterized by the presence of vesicles and bullae filled fluid.
2. In pemphigus vulgaris, large, flaccid bullae filled with fluid occur on the skin and within the oral mucosa.
- immunologic disease with IgG antibodies against the intercellular attachment sites between keratinocytes (type II hypersensitivity).
- the vesicle in pemphigus vulgaris has a suprabasal location (just above the basal cell layer and resembling "tombstones")
- scattered keratinocytes in the fluid as a result of acantholysis.
- Nikolsky's sign is where the epidermis slips when touched with the finger.
- fatal disease if left untreated (systemic corticosteroids)
3. Bullous pemphigoid is an immunologic vesicular disease whose vesicle are in a subepidermal location.
- circulating IgG antibody against antigens in the basement membrane (type II hypersensitivity).
4. Dermatitis herpetiformis is an immunologic vesicular lesion characterized by the presence of IgA immune complexes (type III hypersensitivity) at the tips of the dermal papilla at the dermal/epidermal junction producing a subepidermal vesicle filled with neutrophils.
- strong association with gluten-sensitive enteropathy, or celiac disease.
SHOCK
Definition. It is a clinical state of acute inadequacy of perfusion to tissues due to fall in effective circulating blood volume.
This inadequacy can be caused by :
- Increased vascular capacity
- Decreased blood volume
- Altered distribution of available blood
- Defective pumping system
Causes:
(1) Hypovolemic
- Massive hamorrhage (external or internal).
- Loss of plasma as in bums.
- Dehydration due to severe vomiting, diarrhea diabetic coma.
- Generalized capillary permeability as in anaphylaxis.
(2) Cardiogenic
- Myocardial infarction.
- Pulmonary embolism.
- Cardiac tamponade
(3) Peripheral pooling:
- Endotoxic shock.
- Disseminated intravascular coagulation (DIC).
(4) Neurogenic:
- Syncope.
- Contributory factor in trauma, bums etc.
Metabolic changes in shock
- Hyperglycaemia due to glycogenolysis.
- Increased blood lactate and pyruvate due to anaerobic glycolysis. This results in metabolic acidosis.
- Protein catabolism and increased blood urea.
- Interference with enzyme systems.
Organs involved in shock
(1) Kidneys:
- Renal tubular necrosis.
- Cortical necrosis.
(2) Lungs:
- Oedema, congestion and haemorrhage.
- Microthrombi.
(3) G.I.T. :
- Mucosal oedema.
- Ulceration and haemorrhage
(4) Degeneration and focal necrosis in:
- Heart.
- Liver.
- Adrenals
(5) Anoxic encephalopathy
Keratoses (Horny Growth)
1. Seborrheic keratosis is a common benign epidermal tumor composed of basaloid (basal cell-like) cells with increased pigmentation that produce a raised, pigmented, "stuck-on" appearance on the skin of middle-aged individuals.
- they can easily be scraped from the skin's surface.
- frequently enlarge of multiply following hormonal therapy.
- sudden appearance of large numbers of Seborrheic keratosis is a possible indication of a malignancy of the gastrointestinal tract (Leser-Trelat sign).
2. An actinic keratosis is a pre-malignant skin lesion induced by ultraviolet light damage.
- sun exposed areas.
- parakeratosis and atypia (dysplasia) of the keratinocytes.
- solar damage to underlying elastic and collagen tissue (solar elastosis).
- may progress to squamous carcinoma in situ (Bowen's disease) or invasive cancer.
3. A keratoacanthoma is characterized by the rapid growth of a crateriform lesion in 3 to 6
weeks usually on the face or upper extremity.
- it eventually regresses and involutes with scarring.
- commonly confused with a well-differentiated squamous cell carcinoma.