NEET MDS Synopsis
Fibrous and Fibro-Osseous Tumors
General Pathology
Fibrous and Fibro-Osseous Tumors
Fibrous tumors of bone are common and comprise several morphological variants.
1. Fibrous Cortical Defect and Nonossifying Fibroma
Fibrous cortical defects occur in 30% to 50% of all children older than 2 years of age; they are probably developmental rather than true neoplasms. The vast majority are smaller than 0.5 cm and arise in the metaphysis of the distal femur or proximal tibia; almost half are bilateral or multiple. They may enlarge in size (5-6 cm) to form nonossifying fibromas. Both lesions present as sharply demarcated radiolucencies surrounded by a thin zone of sclerosis. Microscopically are cellular and composed of benign fibroblasts and macrophages, including multinucleated forms. The fibroblasts classically exhibit a storiform pattern. Fibrous cortical defects are asymptomatic and are usually only detected as incidental radiographic lesions. Most undergo spontaneous differentiation into normal cortical bone. The few that enlarge into nonossifying fibromas can present with pathologic fracture; in such cases biopsy is necessary to rule out other tumors.
2. Fibrous Dysplasia
is a benign mass lesion in which all components of normal bone are present, but they fail to differentiate into mature structures. Fibrous dysplasia occurs as one of three clinical patterns:
A. Involvement of a single bone (monostotic)
B. nvolvement of multiple bones (polyostotic)
C. Polyostotic disease, associated with café au lait skin pigmentations and endocrine abnormalities, especially precocious puberty (Albright syndrome).
Monostotic fibrous dysplasia accounts for 70% of cases. It usually begins in early adolescence, and ceases with epiphyseal closure. It frequently involves ribs, femur, tibia & jawbones. Lesions are asymptomatic and usually discovered incidentally. However, fibrous dysplasia can cause marked enlargement and distortion of bone, so that if the face or skull is involved, disfigurement can occur.
Polyostotic fibrous dysplasia without endocrine dysfunction accounts for the majority of the remaining cases.
It tends to involve the shoulder and pelvic girdles, resulting in severe deformities and spontaneous fractures.
Albright syndrome accounts for 3% of all cases. The bone lesions are often unilateral, and the skin pigmentation is usually limited to the same side of the body. The cutaneous macules are classically large, dark to light brown (café au lait), and irregular.
Gross features
• The lesion is well-circumscribed, intramedullary; large masses expand and distort the bone.
On section it is tan-white and gritty.
Microscopic features
• There are curved trabeculae of woven bone (mimicking Chinese characters), without osteoblastic rimming
• The above are set within fibroblastic proliferation
Individuals with monostotic disease usually have minimal symptoms. By x-ray, lesions exhibit a characteristic ground-glass appearance with well-defined margins. Polyostotic involvement is frequently associated with progressive disease, and more severe skeletal complications (e.g., fractures, long bone deformities, and craniofacial distortion). Rarely, polyostotic disease can transform into osteosarcoma, especially following radiotherapy.
Mucosal protective agents
Pharmacology
Mucosal protective agents.
These are locally active agents that help heal gastric and duodenal ulcers by forming a protective barrier between the ulcers and gastric acid, pepsin, and bile salts. They do not alter the secretion of gastric acid. These drugs include sucralfate and colloid bismuth compounds. (e.g. tripotassium, dicitratobismuthate). Colloidal bismuth compounds additionally exert bactericidal action against H.pylori. Also, Prostaglandins have both antisecretory and mucosal protective effects.
Example: Misoprostol- used for prevention of NSAID – induced ulcer.
- Drugs that exert antimicrobial action against H.pylori such as amoxicillin, metronidazole, clarithromycin and tetracycline are included in the anti-ulcer treatment regimens.
Aspirin
Pharmacology
Aspirin
Mechanism of Action
ASA covalently and irreversibly modifies both COX-1 and COX-2 by acetylating serine-530 in the active site Acetylation results in a steric block, preventing arachidonic acid from binding
Uses of Aspirin
Dose-Dependent Effects:
Low: < 300mg blocks platelet aggregation
Intermediate: 300-2400mg/day antipyretic and analgesic effects
High: 2400-4000mg/day anti-inflammatory effects
Often used as an analgesic (against minor pains and aches), antipyretic (against fever), and anti-inflammatory. It has also an anticoagulant (blood thinning) effect and is used in long-term low-doses to prevent heart attacks
Low-dose long-term aspirin irreversibly blocks formation of thromboxane A2 in platelets, producing an inhibitory affect on platelet aggregation, and this blood thinning property makes it useful for reducing the incidence of heart attacks
Its primary undesirable side effects, especially in stronger doses, are gastrointestinal distress (including ulcers and stomach bleeding) and tinnitus. Another side effect, due to its anticoagulant properties, is increased bleeding in menstruating women.
HYPERPLASIA
General Pathology
HYPERPLASIA
It is the increase in the size of an organ or tissue due to increase in the number of its constituent cells. This is seen in organs made up of labile and stable cells.
Causes
I. Increased demand:
- Bone marrow in hypoxia and haemolytic states.
- Thyroid gland in puberty
2. Persistant Trauma:
- Acanthosis of the epidermis in chronic inflammations and in warts.
- Hyperplasia of oral mucosa due tooth and denture trauma.
- Mucosa at the edges of a gastric ulcer.
3. Endocrine target organ:
- Pregnancy hyperplasia of breast.
- Prostatic hyperplasia.
4. Compensatory:
Hyperplasia of kidney when the other kidney has been removed.
5. Idiopathic:
Endocrine organs like thyroid, adrenals, pituitary etc. can undergo hyperplasia with no detectable stimulus. .
Emergency conditions in Dental Clinics p2
Oral Medicine
Emergency conditions in Dental Clinics
Hypoadrenalism - Usually the patient is known to have Addison's disease or to be taking steroids long term and has forgotten to take the tablets.
Signs and symptoms
• Pallor
• Confusion
• Rapid weak pulse.
Treatment:
Give oxygen
Give 200 mg hydrocortisone sodium succinate by slow i.v. injection.
Give steroid replacement
Determining and managing underlying cause once the crisis over.
If required:
• Transfer to Emergeny hostpital
• Fluids and further hydrocortisone, both i.v.
Acute asthma - Exposure to antigen but precipitated by many factors including anxiety.
Signs and symptoms
• Persistent shortness of breath poorly relieved by bronchodilators
• Restlessness and exhaustion
• Tachycardia greater than 110 beats/min and low peak expiratory flow
• Respirations may be so shallow in severe cases that wheezing is absent.
Treatment
Excluded respiratory obstruction
Sit the patient up
Give oxygen
Salbutamol (Ventolin) via a nebuliser (2.5-5 mg of 1 mg/ml nebuliser solution) or via a large-volume spacer (two puffs of a metered dose inhaler 10-20 times: one puff every 30 seconds up to 10 puffs for a child)
Reassure and allow home if recovered.
• Bronchodilatation.
If Major Problem recommend to hospital Emergeny
• Hydrocortisone sodium succinate i.v.: adults 200 mg; child 100 mg
• Add ipratropium 0.5 mg to nebulised salbutamol
• Aminophylline slow i.v. injection of 250 mg in 10 ml over at least 20 minutes: monitor or keep finger on pulse during injection.
Caution in epilepsy: rapid injection of aminophylline may cause arrhythmias and convulsions.
Caution in patients already receiving theophylline: arrhythmias or convulsions may occur.
Anaphylactic shock
Signs and symptoms
• Paraesthesia, flushing and swelling of face, especially eyelids and lips (Fig. 13)
• generalised urticaria, especially hands and feet
• wheezing and difficulty in breathing
• rapid weak pulse.
These may develop over 15 to 30 minutes following the oral administration of a drug or rapidly over a few minutes following i.v. drug administration.
Treatment
Lay patient flat and raise feet
Give oxygen
Give 0.5 ml epinephrine (adrenaline) 1 mg/ml (1 in
1000) intramuscular
— 0.25 ml for 6-12 years
— 0.12 ml for 6 months to 6 years
repeated every 10 min until improvement.
Requires prompt energetic treatment of
• laryngeal oedema
• bronchospasm
• hypotension.
• Chlorphenamine (chlorpheniramine) 10 mg in 1 ml intramuscular or slow i.v. injection
• Hydrocortisone sodium succinate 200 mg by slow i.v. injection: valuable as action persists after that of adrenaline has worn off
• Fluids i.v. (colloids) infused rapidly if shock not responding quickly to adrenaline.
Stroke - Stroke results from either cerebral haemorrhage or cerebral ischaemia.
Signs and symptoms
• Confusion followed by signs and symptoms of focal brain damage
• Hemiplegia or quadriplegia
• Sensory loss
• Dysphasia
• Locked-in syndrome (aware, but unable to respond).
Treatment
Maintain and transfer for further investigation.
Benzodiazepine overdose - Overdose can result from a large or a fast dose of benzodiazepine or can occur in a sensitive patient.
Signs and symptoms
• Deeply sedated
• Severe respiratory depression.
Treatment
Flumazenil (Annexate) 200 mg over 15 seconds as 100 mg/ml i.v. followed by 100 mg every 1 minute up to maximum of 1 mg Maintain airway with head tilt/chin lift
Give oxygen.
Treatment
The action of the benzodiazepine is reversed with the specific antagonist.
Angina and myocardial infarction
Signs and symptoms
• Sudden onset of severe crushing pain across front of chest, which may radiate towards the shoulder and down the left arm or into the neck and jaw; pain from angina usually radiates down left arm
Skin pale and clammy
Shallow respirations
Nausea
Weak pulse and hypotension
If the pain not relieved by glyceryl trinitrate (GTN) then cause is myocardial infarction rather than angina.
First-line treatment of angina and myocardial infarction
Allow patient to rest in position that feels most comfortable:
• in presence of breathlessness this is likely to be the sitting position, whereas syncopal patients will want to lie flat
• often an intermediate position will be most appropriate.
Angina -
Angina results from reduced coronary artery lumen diameter because of atheromatous plaques
Myocardial infarction is usually the result of thrombosis in a coronary artery.
Angina is relieved by rest and nitrates:
• Glyceryl trinitrate spray 400 mg metered dose (sprayed on oral mucosa or under tongue and mouth then closed)
• Give oxygen
• Allow home if attack is mild and the patient recovers rapidly.
Myocardial infarction
If a myocardial infarction is suspected:
• give oxygen
• aspirin tablet 300 mg chewed.
• Pain control
• Vasodilatation of blood vessels to reduce load on heart.
Further management for severe angina or myocardial infarction
• Transfer to Emergency
• Diamorphine 5 mg (2.5 mg in older people) by slow i.v. injection (1 mg/min)
• Early thrombolytic therapy reduces mortality.
Cardiac arrest
• Most cardiac arrests result from arrhythmias associated with acute myocardial infarction or chronic ischaemic heart disease
• The heart arrests in one of three rhythms
— VF (ventricular fibrillation) or pulseless VT (ventricular tachycardia)
— asystole
— PEA (pulseless electrical activity) or EMD (electromechanical dissociation).
Signs and symptoms
• Unconscious
• No breathing
• Absent carotid pulse.
Treatment
• Circulation failure for 4 minutes, or less if the patient is already hypoxaemic, will lead to irreversible brain damage
• Institute early basic life support as holding procedure until early advanced life support is available.
• Transfer to Emergency
• Advanced life support.
Advanced life support for cardiac arrest
Advanced airway management techniques and specific treatment of the underlying cause of cardiac arrest constitute advanced life support (ALS).
Drugs Used in Diabetes -SGLT-2 Inhibitors
Pharmacology
SGLT-2 Inhibitors
canagliflozin
empagliflozin
Mechanism
glucose is reabsorbed in the proximal tubule of the nephron by the sodium-glucose cotransporter 2 (SGLT2)
SGLT2-inhibitors lower serum glucose by increasing urinary glucose excretion
the mechanism of action is independent of insulin secretion or action
Clinical use
type II DM
Lichen planus
General Pathology
Lichen planus is an itchy, violaceous, flat-topped papule highlighted by white dots or lines called Wickham's striae.
- lichen planus may occur in the oral mucosa, where it has a fine white net-like appearance.
- increased epidermal proliferation; ? immunologic; initiated by epidermal injury from drugs, viruses, or topical agents.
- characteristic histologic features include:
- hyperkeratosis
- absence of parakeratosis
- prominent stratum granulosum
- an irregular "saw toothed" accentuation of the rete pegs.
- dermal-epidermal junction obscured by a band-like infiltrate of lymphocytes.
- It is generally self-limiting and resolves spontaneously 1 to 2 years after onset; however, the oral lesions may persist for years.
Types of Expansion
OrthodonticsExpansion in orthodontics refers to the process of widening the dental arch
to create more space for teeth, improve occlusion, and enhance facial
aesthetics. This procedure is particularly useful in treating dental crowding,
crossbites, and other malocclusions. The expansion can be achieved through
various appliances and techniques, and it can target either the maxillary
(upper) or mandibular (lower) arch.
Types of Expansion
Maxillary Expansion:
Rapid Palatal Expansion (RPE):
Description: A common method used to widen the
upper jaw quickly. It typically involves a fixed appliance that is
cemented to the molars and has a screw mechanism in the middle.
Mechanism: The patient or orthodontist turns
the screw daily, applying pressure to the palatine suture, which
separates the two halves of the maxilla, allowing for expansion.
Indications: Used for treating crossbites,
creating space for crowded teeth, and improving the overall arch
form.
Duration: The active expansion phase usually
lasts about 2-4 weeks, followed by a retention phase to stabilize
the new position.
Slow Palatal Expansion:
Description: Similar to RPE but involves slower,
more gradual expansion.
Mechanism: A fixed appliance is used, but the screw
is activated less frequently (e.g., once a week).
Indications: Suitable for patients with less severe
crowding or those who may not tolerate rapid expansion.
Mandibular Expansion:
Description: Less common than maxillary expansion,
but it can be achieved using specific appliances.
Mechanism: Appliances such as the mandibular
expansion appliance can be used to widen the lower arch.
Indications: Used in cases of dental crowding or to
correct certain types of crossbites.
Mechanisms of Expansion
Skeletal Expansion: Involves the actual widening of the
bone structure (e.g., the maxilla) through the separation of the midpalatine
suture. This is more common in growing patients, as their bones are more
malleable.
Dental Expansion: Involves the movement of teeth within
the alveolar bone. This can be achieved through the application of forces
that move the teeth laterally.
Indications for Expansion
Crossbites: To correct a situation where the upper
teeth bite inside the lower teeth.
Crowding: To create additional space for teeth that are
misaligned or crowded.
Improving Arch Form: To enhance the overall shape and
aesthetics of the dental arch.
Facial Aesthetics: To improve the balance and symmetry
of the face, particularly in growing patients.
Advantages of Expansion
Increased Space: Creates additional space for teeth,
reducing crowding and improving alignment.
Improved Function: Corrects functional issues related
to occlusion, such as crossbites, which can lead to better chewing and
speaking.
Enhanced Aesthetics: Improves the overall appearance of
the smile and facial profile.
Facilitates Orthodontic Treatment: Provides a better
foundation for subsequent orthodontic procedures.
Limitations and Considerations
Age Factor: Expansion is generally more effective in
growing children and adolescents due to the flexibility of their bones. In
adults, expansion may require surgical intervention (surgical-assisted rapid
palatal expansion) due to the fusion of the midpalatine suture.
Discomfort: Patients may experience discomfort or
pressure during the expansion process, especially with rapid expansion.
Retention: After expansion, a retention phase is
necessary to stabilize the new arch width and prevent relapse.
Potential for Relapse: Without proper retention, there
is a risk that the teeth may shift back to their original positions.