NEET MDS Synopsis
Gluconeogenesis
Biochemistry
Gluconeogenesis
It is the process by which Glucose or glycogen is formed from non carbohydrate substances.
Gluconeogenesis occurs mainly in liver.
Gluconeogenesis inputs:
The source of pyruvate and oxaloacetate for gluconeogenesis during fasting or carbohydrate starvation is mainly amino acid catabolism. Some amino acids are catabolized to pyruvate, oxaloacetate, Muscle proteins may break down to supply amino acids. These are transported to liver where they are deaminated and converted to gluconeogenesis inputs.
Glycerol, derived from hydrolysis of triacylglycerols in fat cells, is also a significant input to gluconeogenesis
Glycolysis & Gluconeogenesis pathways are both spontaneous If both pathways were simultaneously active within a cell it would constitute a "futile cycle" that would waste energy
Glycolysis yields 2~P bonds of ATP.
Gluconeogenesis expends 6~P bonds of ATP and GTP.
A futile cycle consisting of both pathways would waste 4 P.bonds per cycle.To prevent this waste, Glycolysis and Gluconeogenesis pathways are reciprocally regulated.
Monocytosis
General Pathology
Monocytosis:
Causes
-Infections causing lymphocytosis, especialy tuberculosis and typhoid.
-Monocytic leukaemia.
-Some auto immune diseases.
Errors in Null Hypothesis Testing
Public Health DentistryWhen testing a null hypothesis, two types of errors can occur:
Type I Error (False Positive):
Definition: This error occurs when the null
hypothesis is rejected when it is actually true. In other words, the
researcher concludes that there is an effect or difference when none
exists.
Consequences in Dentistry: For example, a study
might conclude that a new dental treatment is effective when it is not,
leading to the adoption of an ineffective treatment.
Type II Error (False Negative):
Definition: This error occurs when the null
hypothesis is not rejected when it is actually false. In this case, the
researcher fails to detect an effect or difference that is present.
Consequences in Dentistry: For instance, a study
might conclude that a new dental material is not superior to an existing
one when, in reality, it is more effective, potentially preventing the
adoption of a beneficial treatment.
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.
Needle selection
Pharmacology
Needle selection
Nerve blocks:
Inferior alveolar- 25 G short (LLU technique)
PSA- 25 G short
Mental/Incisive- 25 G short
Palatal- 27/30 G short/ultrashort
Gow-Gates/Akinosi- 25 G long
Infraorbital- 25 G long
Field Block:
ASA 25/27 short
Infiltration:
Infiltration/SP 25/27 short
PDL/Intraosseous
PDL 27/30 short
Intraosseous 30 short/ultrashort
Antibiotic Prophylaxis
Oral and Maxillofacial SurgeryDental/Oral/Upper Respiratory Tract Procedures: Antibiotic Prophylaxis
Guidelines
Antibiotic prophylaxis is crucial for patients at risk of infective
endocarditis or other infections during dental, oral, or upper respiratory tract
procedures. The following guidelines outline the standard and alternate regimens
for antibiotic prophylaxis based on the patient's allergy status and ability to
take oral medications.
I. Standard Regimen in Patients at Risk
For Patients Allergic to Penicillin/Ampicillin/Amoxicillin:
Erythromycin:
Dosage: Erythromycin ethyl-succinate 800 mg or
erythromycin stearate 1.0 gm orally.
Timing: Administer 2 hours before the
procedure.
Follow-up Dose: One-half of the original dose
(400 mg or 500 mg) 6 hours after the initial administration.
Clindamycin:
Dosage: Clindamycin 300 mg orally.
Timing: Administer 1 hour before the procedure.
Follow-up Dose: 150 mg 6 hours after the
initial dose.
For Non-Allergic Patients:
Amoxicillin:
Dosage: Amoxicillin 3.0 gm orally.
Timing: Administer 1 hour before the procedure.
Follow-up Dose: 1.5 gm 6 hours after the
initial dose.
II. Alternate Prophylactic Regimens in Patients at Risk
For Patients Who Cannot Take Oral Medications:
For Penicillin/Amoxicillin Allergic Patients:
Clindamycin:
Dosage: Clindamycin 300 mg IV.
Timing: Administer 30 minutes before the
procedure.
Follow-up Dose: 150 mg IV (or orally) 6
hours after the initial dose.
For Non-Allergic Patients:
Ampicillin:
Dosage: Ampicillin 2.0 gm IV or IM.
Timing: Administer 30 minutes before the
procedure.
Follow-up Dose: Ampicillin 1.0 gm IV (or
IM) or amoxicillin 1.5 gm orally 6 hours after the initial dose.
For High-Risk Patients Who Are Not Candidates for the Standard
Regimen:
For Penicillin/Amoxicillin Allergic Patients:
Vancomycin:
Dosage: Vancomycin 1.0 gm IV.
Timing: Administer over 1 hour, starting 1
hour before the procedure.
Follow-up Dose: No repeat dose is
necessary.
For Non-Allergic Patients:
Ampicillin and Gentamicin:
Dosage: Ampicillin 2.0 gm IV (or IM) plus
gentamicin 1.5 mg/kg IV (or IM) (not to exceed 80 mg).
Timing: Administer 30 minutes before the
procedure.
Follow-up Dose: Amoxicillin 1.5 gm orally 6
hours after the initial dose. Alternatively, the parenteral
regimen may be repeated 8 hours after the initial dose.
Separation-Individualization
PedodonticsCharacteristics of the Separation-Individualization Subphases
The separation-individualization phase, as described by Margaret S. Mahler,
is crucial for a child's emotional and psychological development. This phase is
divided into four subphases: Differentiation, Practicing Period, Rapprochement,
and Consolidation and Object Constancy. Each subphase has distinct
characteristics that contribute to the child's growing sense of self and
independence.
1. Differentiation (5 – 10 Months)
Cognitive and Neurological Maturation:
The infant becomes more alert as cognitive and neurological
development progresses.
Stranger Anxiety:
Characteristic anxiety during this period includes stranger anxiety,
as the infant begins to differentiate between familiar and unfamiliar
people.
Self and Other Recognition:
The infant starts to differentiate between themselves and others,
laying the groundwork for developing a sense of identity.
2. Practicing Period (10 – 16 Months)
Upright Locomotion:
The beginning of this phase is marked by the child achieving upright
locomotion, such as standing and walking.
Separation from Mother:
The child learns to separate from the mother by crawling and
exploring their environment.
Separation Anxiety:
Separation anxiety is present, as the child still relies on the
mother for safety and comfort while exploring.
3. Rapprochement (16 – 24 Months)
Awareness of Physical Separateness:
The toddler becomes more aware of their physical separateness from
the mother and seeks to demonstrate their newly acquired skills.
Temper Tantrums:
The child may experience temper tantrums when the mother’s attempts
to help are perceived as intrusive or unhelpful, leading to frustration.
Rapprochement Crisis:
A crisis develops as the child desires to be soothed by the mother
but struggles to accept her help, reflecting the tension between
independence and the need for support.
Resolution of Crisis:
This crisis is typically resolved as the child’s skills improve,
allowing them to navigate their independence more effectively.
4. Consolidation and Object Constancy (24 – 36 Months)
Sense of Individuality:
The child achieves a definite sense of individuality and can cope
with the mother’s absence without significant distress.
Comfort with Separation:
The child does not feel uncomfortable when separated from the
mother, as they understand that she will return.
Improved Sense of Time:
The child develops an improved sense of time and can tolerate
delays, indicating a more mature understanding of relationships and
separations.
Hemothorax
Medicine
Hemothorax
collection of blood within the pleural space
Etiology
Penetrating or blunt trauma
Nontraumatic: malignancy, pulmonary embolism with infarction, TB, giant bullous emphysema
Clinical features
Dyspnea and diminished/absent breath sounds
Decreased tactile fremitus, dullness on percussion
Chest pain
Flat neck veins, hemorrhagic shock and respiratory distress in severe hemorrhage
Diagnostics
Chest x-ray : similar appearance to pleural effusion
Opacity
Blunting of the costophrenic angle
Tracheal deviation (mediastinal shift)
Ultrasound: detection of smaller amounts of fluid/blood than on chest x-ray possible
Treatment
Chest tube insertion into the 5th intercostal space at the midaxillary line
Thoracotomy indicated if Chest tube output > 1000 mL immediately after placement or 150–200 mL/hour for 2–4 hours
Multiple transfusions required
Complications: pleural empyema ; fibrothorax and trapped lung
A hemothorax, however small, must always be drained because blood in the pleural cavity will clot if not evacuated, resulting in a trapped lung or an empyema