NEET MDS Synopsis
Amoxicillin
Pharmacology
Amoxicillin
a moderate-spectrum
β-lactam antibiotic used to treat bacterial infections caused by susceptible
Mode of action Amoxicillin acts by inhibiting the synthesis of bacterial cell walls. It inhibits cross-linkage between the linear peptidoglycan polymer chains that make up a major component of the cell wall of Gram-positive bacteria. microorganisms. It is usually the drug of choice within the class because it is better absorbed, following oral administration, than other beta-lactam antibiotics. Amoxicillin is susceptible to degradation by β-lactamase-producing bacteria, and so is often given clavulanic acid.
Microbiology Amoxicillin is a moderate-spectrum antibiotic active against a wide range of Gram-positive, and a limited range of Gram-negative organisms
Susceptible Gram-positive organisms : Streptococcus spp., Diplococcus pneumoniae, non β-lactamase-producing Staphylococcus spp., and Streptococcus faecalis.
Susceptible Gram-negative organisms Haemophilus influenzae, Neisseria gonorrhoeae, Neisseria meningitidis, Escherichia coli, Proteus mirabilis and Salmonella spp.
Resistant organisms Penicillinase producing organisms, particularly penicillinase producing Staphylococcus spp. Penicillinase-producing N. gonorrhoeae and H. influenzae are also resistant
All strains of Pseudomonas spp., Klebsiella spp., Enterobacter spp., indole-positive
Proteus spp., Serratia marcescens, and Citrobacter spp. are resistant.
The incidence of β-lactamase-producing resistant organisms, including E. coli, appears to be increasing.
Amoxicillin and Clavulanic acid Amoxicillin is sometimes combined with clavulanic acid, a β-lactamase inhibitor, to increase the spectrum of action against
Gram-negative organisms, and to overcome bacterial antibiotic resistance mediated through β-lactamase production.
Buffers
Biochemistry
Buffers
• Biological systems use buffers to maintain pH.
• Definition: A buffer is a solution that resists a significant change in pH upon addition of an acid or a base.
• Chemically: A buffer is a mixture of a weak acid and its conjugate base
• Example: Bicarbonate buffer is a mixture of carbonic acid (the weak acid) and the bicarbonate ion (the conjugate base): H2CO3 + HCO3 –
• All OH- or H+ ions added to a buffer are consumed and the overall [H+ ] or pH is not altered
H2CO3 + HCO3 - + H+ <- -> 2H2CO3
H2CO3 + HCO3 - + OH- <- -> 2HCO3 - + H2O
• For any weak acid / conjugate base pair, the buffering range is its pKa +1.
It should be noted that around the pKa the pH of a solution does not change appreciably even when large amounts of acid or base are added. This phenomenon is known as buffering. In most biochemical studies it is important to perform experiments, that will consume H+ or OH- equivalents, in a solution of a buffering agent that has a pKa near the pH optimum for the experiment.
Most biologic fluids are buffered near neutrality. A buffer resist a pH change and consists of a conjugate acid/base pair.
Important Physiological Buffers include carbonate (H2CO3/HCO3-),
Phosphate (H2PO-4 /HPO2-4) and various protiens
COMPOSITE RESINS -Solution Liners (Varnishes)
Dental Materials
Solution Liners (Varnishes)
Applications
o Enamel and dentin lining for amalgam restorations
o Enamel and dentin lining for cast restorations that are used with non adhesive cements
o Coating over materials that are moisture sensitive during setting
Components of copal resin varnish
o 90% solvent mixture (e.g., chloroform, acetone, and alcohol)
o 10% dissolved copal resin
Reaction
Varnish sets physically by drying Solvent loss occurs in 5 to 15 seconds (a film forms the same way as drying fingernail polish)
Manipulation
Apply thin coat over dentin. enamel. And margins of the cavity preparation Dry lightly with air for 5 seconds Apply a second thin coat Final thickness is 1 to 5 µ.m
Properties
o Physical
Electrically insulating barrier that prevents shocks. Too thin to be thermally insulating. Decreases degree of percolation attributable to thermal expansion
o Chemical
Forms temporary barrier that prevents microleakage into dentinal tubules until secondary dentin formation occurs. Decreases initial tendency for electrochemical corrosion
o Mechanical
Very weak and brittle film that has limited lifetime
Film adheres to smear layer
Chloral hydrate
Pharmacology
Chloral hydrate
1. Short-acting sleep inducer—less risk of “hangover” effect the next day.
2. Little change on REM sleep.
3. Metabolized to trichloroethanol, an active metabolite; further metabolism inactivates the drug.
4. Used for conscious sedation in dentistry.
5. Can result in serious toxicity if the dose is not controlled.
Genioglossus Muscle
AnatomyGenioglossus Muscle
Origin: Mental spine of the mandible.
Insertion: Dorsum of the tongue and hyoid bone.
Nerve Supply: Hypoglossal nerve (CN XII).
Arterial Supply: Sublingual and submental arteries.
Action: Depresses and protrudes the tongue.
Anti-Diuretic Hormone Feedback
Physiology
An anti-diruetic is a substance that decreases urine volume, and ADH is the primary example of it within the body. ADH is a hormone secreted from the posterior pituitary gland in response to increased plasma osmolarity (i.e., increased ion concentration in the blood), which is generally due to an increased concentration of ions relative to the volume of plasma, or decreased plasma volume.
The increased plasma osmolarity is sensed by osmoreceptors in the hypothalamus, which will stimulate the posterior pituitary gland to release ADH. ADH will then act on the nephrons of the kidneys to cause a decrease in plasma osmolarity and an increase in urine osmolarity.
ADH increases the permeability to water of the distal convoluted tubule and collecting duct, which are normally impermeable to water. This effect causes increased water reabsorption and retention and decreases the volume of urine produced relative to its ion content.
After ADH acts on the nephron to decrease plasma osmolarity (and leads to increased blood volume) and increase urine osmolarity, the osmoreceptors in the hypothalamus will inactivate, and ADH secretion will end. Due to this response, ADH secretion is considered to be a form of negative feedback.
PNEUMONIAS
General Pathology
PNEUMONIAS
Pneumonia is defined as acute inflammation of the lung parenchyma distal to the terminal bronchioles which consist of the respiratory bronchiole, alveolar ducts, alveolar sacs and alveoli. The terms 'pneumonia' and 'pneumonitis' are often used synonymously for inflammation of the lungs, while 'consolidation' (meaning solidification) is the term used for macroscopic and radiologic appearance of the lungs in pneumonia.
PATHOGENESIS.
The microorganisms gain entry into the lungs by one of the following four routes:
1. Inhalation of the microbes.
2. Aspiration of organisms.
3. Haematogenous spread from a distant focus.
4. Direct spread from an adjoining site of infection.
Failure of defense mechanisms and presence of certain predisposing factors result in pneumonias.
These conditions are as under:
1. Altered consciousness.
2. Depressed cough and glottic reflexes.
3. Impaired mucociliary transport.
4. Impaired alveolar macrophage function.
5. Endobronchial obstruction.
6. Leucocyte dysfunctions.
CLASSIFICATION. On the basis of the anatomic part of the lung parenchyma involved, pneumonias are traditionally classified into 3 main types:
1. Lobar pneumonia.
2. Bronchopneumonia (or Lobular pneumonia).
3. Interstitial pneumonia.
BACTERIAL PNEUMONIA
Bacterial infection of the lung parenchyma is the most common cause of pneumonia or consolidation of one or both the lungs. Two types of acute bacterial pneumonias are distinguished—lobar pneumonia and broncho-lobular pneumonia, each with distinct etiologic agent and morphologic changes.
1. Lobar Pneumonia
Lobar pneumonia is an acute bacterial infection of a part of a lobe, the entire lobe, or even two lobes of one or both the lungs.
ETIOLOGY.
Following types are described:
1. Pneumococcal pneumonia. More than 90% of all lobar pneumonias are caused by Streptococcus pneumoniae, a lancet-shaped diplococcus. Out of various types, type 3-S. pneumoniae causes particularly virulent form of lobar pneumonia.
2. Staphylococcal pneumonia. Staphylococcus aureus causes pneumonia by haematogenous spread of infection.
3. Streptococcal pneumonia, β-haemolytic streptococci may rarely cause pneumonia such as in children after measles or influenza.
4. Pneumonia by gram-negative aerobic bacteria. Less common causes of lobar pneumonia are gram-negative bacteria like Haemophilus influenzae, Klebsiella pneumoniae (Friedlander's bacillus), Pseudomonas, Proteus and Escherichia coli.
MORPHOLOGY. Laennec's original description divides lobar pneumonia into 4 sequential pathologic phases:
1. STAGE OF CONGESTION: INITIAL PHASE
The initial phase represents the early acute inflammatory response to bacterial infection and lasts for 1 to 2 days.
The affected lobe is enlarged, heavy, dark red and congested. Cut surface exudes blood-stained frothy fluid.
Microscopic Examination
i) Dilatation and congestion of the capillaries in the alveolar walls.
ii) Pale eosinophilic oedema fluid in the air spaces.
iii) A few red cells and neutrophils in the intra-alveolar fluid.
iv) Numerous bacteria demonstrated in the alveolar fluid by Gram's staining.
2. RED HEPATISATION: EARLY CONSOLIDATION
This phase lasts for2 to 4 days. The term hepatisation in pneumonia refers to liver-like consistency of the affected lobe on cut section.
The affected lobe is red, firm and consolidated. The cut surface of the involved lobe is airless, red-pink, dry, granular and has liver-like consistency.
Microscopic Examination
i) The oedema fluid of the preceding stage is replaced by strands of fibrin.
ii) There is marked cellular exudate of neutrophils and extravasation of red cells.
iii) Many neutrophils show ingested bacteria.
iv) The alveolar septa are less prominent than in the first stage due to cellular exudation.
3. GREY HEPATISATION: LATE CONSOLIDATION This phase lasts for4 to 8 days.
The affected lobe Is firm and heavy. The cut surface is dry, granular and grey in appearance with liver-like consistency. The change in colour from red to grey begins at the hilum and spreads towards the periphery. Fibrinous pleurisy is prominent.
Microscopic Examination
i) The fibrin strands are dense and more numerous.
ii) The cellular exudate of neutrophils is reduced due to disintegration of many inflammatory cells. The red cells are also fewer. The macrophages begin to appear in the exudate.
iii) The cellular exudate is often separated from the septal walls by a thin clear space.
iv) The organisms are less numerous and appear as degenerated forms.
COMPLICATIONS. Since the advent of antibiotics, serious complications of lobar pneumonia are uncommon. However, they may develop in neglected cases and in patients with impaired immunologic defenses.
These are as under:
1. Organisation. In about 3% of cases, resolution of the exudate does not occur but instead it is organised. There is ingrowth of fibroblasts from the alveolar septa resulting in fibrosed, tough, airless leathery lung tissue.
2. Pleural effusion. About 5% of treated cases of lobar pneumonia develop inflammation of the pleura with effusion.
3. Empyema. Less than 1% of treated cases of lobar pneumonia develop encysted pus in the pleural cavity termed empyema.
4. Lung abscess. A rare complication of lobar pneumonia is formation of lung abscess.
5. Metastatic infection. Occasionally, infection in the lungs and pleural cavity in lobar pneumonia may extend into the pericardium and the heart causing purulent pericarditis, bacterial endocarditis and myocarditis.
CLINICAL FEATURES. The major symptoms are: shaking chills, fever, malaise with pleuritic chest pain, dyspnoea and cough with expectoration which may be mucoid, purulent or even bloody. The common physical findings are fever, tachycardia, and tachypnoea, and sometimes cyanosis if the patient is severely hypoxaemic. There is generally a marked neutrophilic leucocytosis. Blood cultures are positive in about 30% of cases. Chest radiograph may reveal consolidation.
II. Bronchopneumonia (Lobular Pneumonia)
Bronchopneumonia or lobular pneumonia is infection of the terminal bronchioles that extends into the surrounding alveoli resulting in patchy consolidation of the lung. The condition is particularly frequent at extremes of life (i.e. in infancy and old age), as a terminal event in chronic debilitating diseases and as a secondary infection following viral respiratory infections such as influenza, measles etc,
ETIOLOGY.
The common organisms responsible for bronchopneumonia are staphylococci, streptococci, pneumococci, Klebsiella pneumoniae, Haemophilus influenzae, and gram-negative bacilli like Pseudomonas and coliform bacteria.
Bronchopneumonia is identified by patchy areas of red or grey consolidation affecting one or more lobes, frequently found bilaterally and more often involving the lower zones of the lungs due to gravitation of the secretions. On cut surface, these patchy consolidated lesions are dry, granular, firm, red or grey in colour, 3 to 4 cm in diameter, slightly elevated over the surface and are often centred around a bronchiole. These patchy areas are best picked up by passing the fingertips on the cut surface.
Microscopic Examination
i) Acute bronchiolitis, ii) Suppurative exudate, consisting chiefly of neutrophils, in the peribronchiolar alveoli, iii) Thickening of the alveolar septa by congested capillaries and leucocytic infiltration, iv) Less involved alveoli contain oedema fluid.
COMPLICATIONS.
The complications of lobar pneumonia may occur in bronchopneumonia as well. However, complete resolution of bronchopneumonia is uncommon. There is generally some degree of destruction of the bronchioles resulting in foci of bronchiolar fibrosis that may eventually cause bronchiectasis.
CLINICAL FEATURES. The patients of bronchopneumonia are generally infants or elderly individuals. There may be history of preceding bed-ridden illness, chronic debility, aspiration of gastric contents or upper respiratory infection.
VIRAL AND MYCOPLASMAL PNEUMONIA (PRIMARY ATYPICAL PNEUMONIA)
Viral and mycoplasmal pneumonia is characterised by patchy inflammatory changes, largely confined to interstitial tissue of the lungs, without any alveolar exudate. Other terms used for these respiratory tract infections are interstitial pneumonitis, reflecting the interstitial location of the inflammation, andprimary atypical pneumonia, atypicality being the absence of alveolar exudate commonly present in other pneumonias. Interstitial pneumonitis may occur in all ages.
ETIOLOGY. Interstitial pneumonitis is caused by a wide variety of agents, the most common being respiratory syncytial virus (RSV). Others are Mycoplasma pneumoniae and many viruses such as influenza and parainfluenza viruses, adenoviruses, rhinoviruses, coxsackieviruses and cytomegaloviruses (CMV).
Depending upon the severity of infection, the involvement may be patchy to massive and widespread consolidation of one or both the lungs. The lungs are heavy, congested and subcrepitant. Sectioned surface of the lung exudes small amount of frothy or bloody fluid.
Microscopic Examination
I) Interstitial Inflammation: There is thickening of alveolar walls due to congestion, oedema and mononuclear inflammatory infiltrate comprised by lymphocytes, macrophages and some plasma cells. illness, chronic debility, aspiration of gastric contents or upper respiratory infection.
ii) Necrotising bronchiolitis: This is characterised by foci of necrosis of the bronchiolar epithelium, inspissated secretions in the lumina and mononuclear infiltrate in the walls and lumina.
iii) Reactive changes: The lining epithelial cells of the bronchioles and alveoli proliferate in the presence of virus and may form multinucleate giant cells and syncytia in the bronchiolar and alveolar walls.
iv) Alveolar changes: In severe cases, the alveolar lumina may contain oedema fluid, fibrin, scanty inflammatory exudate and coating of alveolar walls by pink, hyaline membrane similar to the one seen in respiratory distress syndrome.
COMPLICATIONS.
The major complication of interstitial pneumonitis is superimposed bacterial infection and its complications. Most cases of interstitial pneumonitis recover completely.
CLINICAL FEATURES.
Majority of cases of interstitial pneumonitis initially have upper respiratory symptoms with fever, headache and muscle-aches. A few days later appears dry, hacking, non-productive cough with retrosternal burning due to tracheitis and bronchitis. Chest radiograph may show patchy or diffuse consolidation.
C. OTHERTYPES OF PNEUMONIAS
I. Pneumocystis carinii Pneumonia
Pneumocystis carinii, a protozoon widespread in the environment, causes pneumonia by inhalation of the organisms as an opportunistic infection in neonates and immunosuppressed people. Almost 100% cases of AIDS develop opportunistic infection, most commonly Pneumocystis carinii pneumonia.
II. Legionella Pneumonia
Legionella pneumonia or legionnaire's disease is an epidemic illness caused by gramnegative bacilli, Legionella pneumophila that thrives in aquatic environment. It was first recognised following investigation into high mortality among those attending American Legion Convention in Philadelphia in July 1976. The epidemic occurs in summer months by spread of organisms through contaminated drinking water or in air-conditioning cooling towers. Impaired host defenses in the form of immunodeficiency, corticosteroid therapy, old age and cigarette smoking play important roles.
III. Aspiration (Inhalation) Pneumonia
Aspiration or inhalation pneumonia results from inhaling different agents into the lungs. These substances include food, gastric contents, foreign body and infected material from oral cavity. A number of factors predispose to inhalation pneumonia which include: unconsciousness, drunkenness, neurological disorders affecting swallowing, drowning, necrotic oropharyngeal tumours, in premature infants and congenital tracheo-oesophageal fistula.
1. Aspiration of small amount of sterile foreign matter such as acidic gastric contents produce chemical pneumonitis. It is characterised by haemorrhagic pulmonary oedema with presence of particles in the bronchioles.
2. Non-sterile aspirate causes widespread bronchopneumonia with multiple areas of necrosis and suppuration.
IV. Hypostatic Pneumonia
Hypostatic pneumonia is the term used for collection of oedema fluid and secretions in the dependent parts of the lungs in severely debilitated, bedridden patients. The accumulated fluid in the basal zone and posterior part of lungs gets infected by bacteria from the upper respiratory tract and sets in bacterial pneumonia.
V. Lipid Pneumonia Another variety of noninfective pneumonia is lipid pneumonia. It is of 2 types:
1. Exogenous lipid pneumonia. This is caused by aspiration of a variety of oily materials. These are: inhalation of oily nasal drops, regurgitation of oily medicines from stomach (e.g. liquid paraffin), administration of oily vitamin preparation to reluctant children or to debilitated old patients.
2. Endogenous lipid pneumonia. Endogenous origin of lipids causing pneumonic consolidation is more common. The sources of origin are tissue breakdown following obstruction to airways e.g. obstruction by bronchogenic cancer, tuberculosis and bronchiectasis.
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.