NEET MDS Synopsis
Structure and function of skeletal muscle
PhysiologyStructure and function of skeletal muscle.
Skeletal muscles have a belly which contains the cells and which attaches by means of tendons or aponeuroses to a bone or other tissue. An aponeurosis is a broad, flat, tendinous attachment, usually along the edge of a muscle. A muscle attaches to an origin and an insertion. The origin is the more fixed attachment, the insertion is the more movable attachment. A muscle acts to shorten, pulling the insertion toward the origin. A muscle can only pull, it cannot push.
Muscles usually come in pairs of antagonistic muscles. The muscle performing the prime movement is the agonist, the opposite acting muscle is the antagonist. When the movement reverses, the names reverse. For example, in flexing the elbow the biceps brachii is the agonist, the triceps brachii is the antagonist. When the movement changes to extension of the elbow, the triceps becomes the agonist and the biceps the antagonist. An antagonist is never totally relaxed. Its function is to provide control and damping of movement by maintaining tone against the agonist. This is called eccentric movement.
Muscles can also act as synergists, working together to perform a movement. This movement can be different from that performed when the muscles work independently. For example, the sternocleidomastoid muscles each rotate the head in a different direction. But as synergists they flex the neck.
Fixators act to keep a part from moving. For example fixators act as postural muscles to keep the spine erect and the leg and vertebral column extended when standing. Fixators such as the rhomboids and levator scapulae keep the scapula from moving during actions such as lifting with the arms.
Malnutrition
General Pathology
Malnutrition
A. Marasmus - calorie malnutrition
A child with marasmus suffers growth retardation and loss of muscle. The loss of muscle mass results from catabolism and depletion of the somatic protein compartment.
With such losses of muscle and subcutaneous fat, the extremities are emaciated; by comparison, the head appears too large for the body. Anemia and manifestations of multivitamin deficiencies are present, and there is evidence of immune deficiency, particularly of T cell-mediated immunity.
B. Kwashiorkor - protein malnutrition - importance of protein quality as well as quantity
Marked protein deprivation is associated with severe loss of the visceral protein compartment, and the resultant hypoalbuminemia gives rise to generalized, or dependent, edema.
The weight of children with severe kwashiorkor is typically 60% to 80% of normal.
However, the true loss of weight is masked by the increased fluid retention (edema).
Children with kwashiorkor have characteristic skin lesions, with alternating zones of hyperpigmentation, areas of desquamation, and hypopigmentation, giving a "flaky paint" appearance.
Hair changes include overall loss of color or alternating bands of pale and darker hair, straightening, line texture, and loss of firm attachment to the scalp.
An enlarged, fatty liver (resulting from reduced synthesis of carrier proteins) and a tendency to develop early apathy, listlessness, and loss of appetite.
The bone marrow in both kwashiorkor and marasmus may be hypoplastic, mainly because of decreased numbers of red cell precursors. How much of this derangement is due to a deficiency of protein and folates or to reduced synthesis of transferrin and ceruloplasmin is uncertain. Thus, anemia is usually present, most often hypochromic microcytic anemia, but a concurrent deficiency of folates may lead to a mixed microcytic-macrocytic anemia.
C. Most cases of severe malnutrition are a combination of A and B usually characterized by:
• Failure of growth
• Behavioral changes
• Edema (kwashiorkor)
• Dermatosis
• Changes in hair
• Loss of appetite
• Liver enlargement
• Anemia
• Osteoporosis
MECHANISM OF HORMONE ACTION
Physiology
Hormones are carried by the blood throughout the entire body, yet they affect only certain cells. The specific cells that respond to a given hormone have receptor sites for that hormone.
This is sort of a lock and key mechanism. If the key fits the lock, then the door will open. If a hormone fits the receptor site, then there will be an effect. If a hormone and a receptor site do not match, then there is no reaction. All of the cells that have receptor sites for a given hormone make up the target tissue for that hormone. In some cases, the target tissue is localized in a single gland or organ. In other cases, the target tissue is diffuse and scattered throughout the body so that many areas are affected.
Hormones bring about their characteristic effects on target cells by modifying cellular activity. Cells in a target tissue have receptor sites for specific hormones. Receptor sites may be located on the surface of the cell membrane or in the interior of the cell.
In general those protein hormones are unable to diffuse through the cell membrane and react with receptor sites on the surface of the cell. The hormone receptor reaction on the cell membrane activates an enzyme within the membrane, called adenyl cyclase, which diffuses into the cytoplasm. Within the cell, adenyl cyclase catalyzes or starts the process of removal of phosphates from ATP to produce cyclic adenosine monophosphate or c AMP. This c AMP activates enzymes within the cytoplasm that alter or change the cellular activity. The protein hormone, which reacts at the cell membrane, is called the first messenger. c Amp that brings about the action attributed to the hormone is called the second messenger. This type of action is relatively rapid because the precursors are already present and they just needed to be activated in some way.
Fungal Skin Disease
General Pathology
Fungal
Superficial mycoses
1. Superficial mycoses→outermost layers of the skin or its appendages; skin, nails and/or hair.
2. Dermatophytoses transmitted by contact with man (anthropophilic; weak inflammatory response), animals (zoophilic; brisk inflammatory response), or contact with soil (geophilic; strongest inflammatory response).
3. Trichophyton→hair, skin, or nails; Microsporum → hair and skin; and Epidermophyton→skin alone.
4. The diagnosis is best made by culture of skin scrapings secured from the leading edge of the lesion.
- use Wood's light to check for fluorescing metabolites.
- direct KOH preparations of the scraped material
Subcutaneous Mycoses
1. Subcutaneous mycoses are usually related to traumatic implantation into the skin.
2. Chromoblastomycosis, or verrucous (wart-like) dermatitis, is a chronic skin lesion associated with several pigmented fungi (Fonsecaea, Phialophora, and Cladosporium).
- granulomatous reaction in subcutaneous tissue are pigmented, thick walled bodies are visible in tissue section.
3. Mycetomas (maduromycosis) are characterized by a localized, tumorous nodule (usually foot) that occurs in response to chronic progressive destruction of skin, subcutaneous tissue, fascia, muscle and bone
4. Sporotrichosis is caused by the dimorphous fungus, Sporothrix schenckii.
- traumatic implantation of the fungus growing in soil, thus the association with "rose gardeners disease".
- MC lymphocutaneous disease → painless nodule at inoculation site → chain of suppurating subcutaneous nodules that drain to the skin surface along the course of the lymphatics.
- cigar shaped yeast forms are seen in the suppurative nodules and asteroid bodies (Splendore-Hoeppi phenomenon) are noted within granulomatous microabscesses.
- treatment: oral potassium iodide
Esophagus pathology
General Pathology
ESOPHAGUS Pathology
Congenital malformations
1. A tracheoesophageal fistula (the most prevalent esophageal anomaly) occurs most commonly as an upper esophageal blind pouch with a fistula between the lower segment of the esophagus and the trachea. It is associated with hydramnios, congenital heart disease, and other gastrointestinal malformation.
2. Esophageal atresia is associated with VATER syndrome (vertebra1 defects, anal atresia, tracheoesophageal fistula, and renal dysplasia)
3. Stenosis refers to a narrowed esophagus with a small lumen. lt may be congenital or acquired, e.g., through trauma or inflammation.
Inflammatory disorders
Esophagitis
most often involves the lower half of the esophagus. Caused by the reflux of gastric contents (juices) into the lower esophagus. One of the most common GI disorders.
Clinical features.
Patients experience substernal burning associated with regurgitation, mild anemia, dysphagia, hematemesis, and melena. Esophagitis may predispose to esophageal cancer.
Etiology
- Reflux esophagitis is due to an incompetent lower esophageal sphincter that permits reflux of gastric juice into the lower esophagus.
- Irritants such as citric acid, hot liquids, alcohol, smoking, corrosive chemicals, and certain drugs, such as tetracycline, may provoke inflammation.
- Infectious etiologies include herpes, CMV, and C. albicans. The immunocompromised host is particularly susceptible to infectious esophagitis.
Although chronic or severe reflux disease is uncommon, consequences of these conditions can lead to Barrett’s esophagus, development of a stricture, or hemorrhage.
Pathology
-Grossly, there is hyperemia, edema, inflammation, and superficial necrosis.
Complications include ulceration, bleeding, stenosis, and squamous carcinoma.
Treatment: diet control, antacids, and medications that decrease the production of gastric acid (e.g., H blockers).
Barrett's esophagus,
gastric or intestinal columnar epithelium replaces normal squamous epithelium in response to chronic reflux.- A complication of chronic gastroesophageal reflux disease.
- Histologic findings include the replacement of squamous epithelium with metaplastic columnar epithelium.
- Complications include increased incidence of esophageal adenocarcinoma, stricture formation, or hemorrhage (ulceration).
Motor disorders.
Normal motor function requires effective peristalsis and relaxation of the lower esophageal sphincter.
Achalasia is a lack of relaxation of the lower esophageal sphincter (LES), which may be associated with aperistalsis of the esophagus and increased basal tone of the LES.
Clinical features. Achalasia occurs most commonly between the ages of 30 and 50. Typical symptoms are dysphagia, regurgitation, aspiration, and chest pain. The lack of motility promotes stagnation and predisposes to carcinoma.
Hiatal hernia is the herniation of the abdominal esophagus, the stomach, or both, through the esophageal hiatus in the diaphragm.
Scleroderma is a collagen vascular disease, seen primarily in women, that causes subcutaneous fibrosis and widespread degenerative changes. (A mild variant is known as CREST syndrome which stands for calcinosis. raynaud's phenomenon , esophageal dysfunction, sclerodactyly and telengectseia. esophagus is the most frequently involved region of the gastrointestinal tract.
Clinical features are mainly dysphagia and heartburn due to reflux oesophagitis caused by aperlistalsis and incompetent LES.
Rings and webs
1. Webs are mucosal folds in the upper esophagus above the aortic arch.
2. Schatzki rings are mucosal rings at the squamocolumnarjunction below the aortic arch.
3. Plummer Vinson Syndrome consist of triad of dysphagia, atrophic glossitis, and anemia. Webs are found in the upper esophagus. The syndrome is associated specifically with iron deficiency anemia and sometimes hypochlorhydria. Patients are at increased risk for carcinoma of the pharynx or esophagus.
Mallory-Weiss syndrome
Mallory-Weiss tears refers to small mucosal tears at the gastroesophageal junction secondary to recurrent forceful vomiting. The tears occur along the long axis an result in hematemesis (sometimes massive).
- Characterized by lacerations (tears) in the esophagus.
- Most commonly occurs from vomiting (alcoholics).
- A related condition, known as Boerhaave syndrome, occurs when the esophagus ruptures, causing massive upper GI hemorrhage.
Esophageal varices
- The formation of varices (collateral channels) occurs from portal hypertension.
Causes of portal hypertension include blockage of the portal vein or liver disease (cirrhosis).
- Rupture of esophageal varices results in massive hemorrhage into the esophagus and hematemesis.
- Common in patients with liver cirrhosis.
Diverticula
are sac-like protrusions of one or more layers of pharyngeal or esophageal wall.
Tumors
- Benign tumors are rare.
- Carcinoma of the esophagus most commonly occurs after 50 and has a male:female ratio of 4.1.
Etiology: alcohal ingestion, smoking, nitrosamines in food, achalasia , web ring, Barrettes esophagus, and deficiencies of vitamins A and C , riboflavin, and some trace minerals
Clinical features include dysphagia (first to solids), retrosternal pain, anorexia, weight loss, melena, and symptoms secondary to metastases.
Pathology
- 50% occur in the middle third of the esophagus, 30% in the lower third, and 20% in the upper third. Most esophageal cancers are squamous cell carcinomas.
Adenocarcinomas arise mostly out of Barrett's esophagus.
Prognosis
is poor. Fewer than 10% of patients survive 5 years, usually because diagnosis is made at a late stage. The most common sites of metastasis are the liver and lung. The combination of cigarette smoking and alcohol is particularly causative for esophageal cancer (over l00% risk compared to nondrinkers/nonsmokers).
Phases of cardiac cycle
Physiology
Phases of cardiac cycle :
1. Early diastole ( also called the atrial diastole , or complete heart diastole) : During this phase :
- Atria are relaxed
- Ventricles are relaxed
- Semilunar valves are closed
- Atrioventricular valves are open
During this phase the blood moves passively from the venous system into the ventricles ( about 80 % of blood fills the ventricles during this phase.
2. Atrial systole : During this phase :
- Atria are contracting
- Ventricles are relaxed
- AV valves are open
- Semilunar valves are closed
- Atrial pressure increases.the a wave of atrial pressure appears here.
- P wave of ECG starts here
- intraventricular pressure increases due to the rush of blood then decrease due to continuous relaxation of ventricles.
The remaining 20% of blood is moved to fill the ventricles during this phase , due to atrial contraction.
3. Isovolumetric contraction : During this phase :
- Atria are relaxed
- Ventricles are contracting
- AV valves are closed
- Semilunar valves are closed
- First heart sound
- QRS complex.
The ventricular fibers start to contract during this phase , and the intraventricular pressure increases. This result in closing the AV valves , but the pressure is not yet enough to open the semilunar valves , so the blood volume remain unchanged , and the muscle fibers length also remain unchanged , so we call this phase as isovolumetric contraction ( iso : the same , volu= volume , metric= length).
4. Ejection phase : Blood is ejected from the ventricles into the aorta and pulmonary artery .
During this phase :
- Ventricles are contracting
- Atria are relaxed
- AV valves are closed
- Semilunar valves are open
- First heart sound
- Intraventricular pressure is increased , due to continuous contraction
- increased aortic pressure .
- T wave starts.
5. Isovolumetric relaxation: This phase due to backflow of blood in aorta and pulmonary system after the ventricular contraction is up and the ventricles relax . This backflow closes the semilunar valves .
During this phase :
- Ventricles are relaxed
- Atrial are relaxed
- Semilunar valves are closed .
- AV valves are closed.
- Ventricular pressure fails rapidly
- Atrial pressure increases due to to continuous venous return. the v wave appears here.
- Aortic pressure : initial sharp decrease due to sudden closure of the semilunar valve ( diacrotic notch) , followed by secondary rise in pressure , due to elastic recoil of the aorta ( diacrotic wave) .
- T wave ends in this phase
CHRONIC INFLAMMATlON
General Pathology
CHRONIC INFLAMMATlON
When the inflammatory reaction instead of subsiding after the acute phase (or without entering an acute phase), persists as a smouldering lesion, it is called chronic inflammation. .
Characteristics
Predominantly mononuclear response.
Inflamation.and..repair going on simultaneously.
Usually results in more prominent-scarring.
Causes:
Chronicity may be due to :
- Defective defence mechanisms.
- Persistence of injurious agent.
(a) Certain organisms resist phagocytosis and destruction e.g tubercle bacillus, fungi
(b) insoluble particulate matter e.g., crystals. fibres suture materials.
(c) Constants supply of causative agent as in autoimmune disease where body reacts against its own tissues.
- Defective healing.
Granulomatous inflammation
It is a type of chronic inflammation characterised by localised collections of histiocytes.
These cells are usually accompanied by lymphocytes, fibroblasts and giant cells also.
Granulomas are characteristically seen in diseases like tuberculosis. syphilis, leprosy, sarcoidosis, fungal infections etc. In some of these, the lesion is morphologically distinct enough to point to the type of underlying disease. These are sometimes called' specific' granulomas. Granulomas can also be elicited by particulate, insoluble foreign material e.g. granuloma, suture granuloma, cholesterol granuloma (organising haemorrhages).
Polycystic kidney disease
General Pathology
Polycystic kidney disease
Characterized by the formation of cysts and partial replacement of renal parenchyma.
Genetic transmission: autosomal dominant.
Clinical manifestations:
hypertension, hematuria, palpable renal masses, and progression to renal failure. Commonly associated with berry
aneurysms.