NEET MDS Synopsis
Surface Tension
PhysiologySurface Tension
1. Maintains stability of alveolus, preventing collapse
2. Surfactant (Type II pneumocytes) = dipalmityl lecithin
3. Type II pneumocyte appears at 24 weeks of gestation;
1. Surfactant production, 28-32 weeks;
2. Surfactant in amniotic fluid, 35 weeks.
3. Laplace equation for thin walled spheres P = 2T
a. P = alveolar internal pressure r
b. T = tension in the walls r = radius of alveolus
4. During normal tidal respiration
1. Some alveoli do collapse (Tidal pressure can't open)
2. Higher than normal pressure needed (Coughing)
3. Deep breaths & sighs promote re-expansion
4. After surgery/Other conditions, Coughing, deep breathing, sustained maximal respiration
Formation and Eruption of Deciduous Teeth.
Dental Anatomy
Formation and Eruption of Deciduous Teeth.
-Calcification begins during the fourth month of fetal life. By the end of the sixth month, all of the deciduous teeth have begun calcification.
-By the time the deciduous teeth have fully erupted (two to two and one half years of age), cacification of the crowns of permanent teeth is under way. First permanent molars have begun cacification at the time of birth. -Here are some things to know about eruption patterns:
(1) Teeth tend to erupt in pairs.
(2) Usually, lower deciduous teeth erupt first. Congenitally missing deciduous teeth is infrequent. Usually, the lower deciduous central incisors are thefirst to erupt thus initiating the deciduous dentition. The appearance of the deciduous second molars completes the deciduous dentition by 2 to 2 1/2 years of age.
- Deciduous teeth shed earlier and permanent teeth erupt earlier in girls.
- The orderly pattern of eruption and their orderly replacement by permanent teeth is important.
- order for eruption of the deciduous teeth is as follows:
(1) Central incisor.........Lower 6 ½ months, Upper 7 ½ months
(2) Lateral incisor.........Lower 7 months, Upper 8 months
(3) First deciduous molar...Lower 12-16 months, Upper 12-16 months
(4) Deciduous canine........Lower 16-20 months, Upper 16-20 months
(5) Second deciduous molar..Lower 20-30 months, Upper 20-30 months
Molecular techniques
General Pathology
Molecular techniques
Different molecular techniques such as fluorescent in situ hybridization, Southern blot, etc... can be used to detect genetic diseases.
Antiarrhythmic Drugs-Class I Sodium Channel Blockers
Pharmacology
Class I Sodium Channel Blockers
• Block movement of sodium into cells of the cardiac conducting system
• Results in a stabilizing effect and decreased formation and conduction of electrical impulses
• Have a local anesthetic effect
• Are declining in use due to proarrhythmic effects and increased mortality rates
• Na channel blockers - Class 1 drugs are divided into 3 subgroups
• 1A. 1B, 1C based on subtle differences in their mechanism of action.
• Blockade of these channels will prevent depolarization.
• Spread of action potential across myocardium will slow and areas of pacemaker activity is suppressed.
Class IA Sodium Channel Blockers
• Treatment of: symptomatic premature ventricular contractions, supraventricular tachycardia, and ventricular tachycardia, prevention of ventricular fibrillation
– Quinidine (Cardioquin, Quinaglute)
– Procainamide (Pronestyl, Procanbid)
– Disopyramide (Norpace)
• Quinidine – prototype
• Low therapeutic index
• High incidence of adverse effects
Class IB Sodium Channel Blockers
• Treatment of: symptomatic premature ventricular contractions and ventricular tachycardia, prevention of ventricular fibrillation
– Lidocaine (Xylocaine)
– Mexiletine (Mexitil)
– Tocainide (Tonocard)
– Phenytoin (Dilantin)
Side Effects: Lidocaine
• Drowsiness • Paresthesias • Muscle twitching • Convulsions • Changes in mental status (disorientation, confusion) • Hypersensitivity reactions (edema, uticaria, anaphylaxis)
Side Effects: Phenytoin (Dilantin)
• Gingival hyperplasia
• Nystagmus
• Ataxia, slurring of speech
• Tremors
• Drowsiness
• Confusion
• Lidocaine – prototype
• Must be given by injection
• Used as a local anesthetic
• Drug of choice for treating serious ventricular arrhythmias associated with acute myocardial infarction, cardiac surgery, cardiac catheterization and electrical conversion
Class IC Sodium Channel Blockers
• Treatment of: life-threatening ventricular tachycardia or fibrillation and supraventricular tachycardia unresponsive to other drugs
– Flecainide
– Propafenone
Adverse Effects
• CNS - dizziness, drowsiness, fatigue, twitching, mouth numbness, slurred speech vision changes, and tremors that can progress to convulsions.
• GI - changes in taste, nausea, and vomiting. CV - arrhythmias including heart blocks, hypotension, vasodilation, and potential for cardiac arrest.
• Other Rash, hypersensitivity reactions loss of hair and potential bone marrow depression.
Drug-Drug Interactions
• Increased risk for arrhythmias if combined with other drugs that are know to cause arrhythmias- digoxin and beta blockers
• Increased risk of bleeding if combined with oral anticoagulants.
Drug Food Interactions
• Quinidine needs an acidic urine for excretion. Increased levels lead to toxicity
• Avoid foods that alkalinize the urine- citrus juices, vegetables, antacid, milk products
Barbiturates
Pharmacology
Barbiturates (BARBS):
were used for antianxiety, sedation but now replaced by BZs; for IV sedation & oral surgery
Advantages: effective and relatively inexpensive (common in third world countries), extensively studied so have lots of information about side effects/toxicity
Peripheral effects: respiratory depression (with ↑ dose), CV effects (↓ BP and HR at sedative-hypnotic doses), liver effects (bind CYP450 → induction of drug metabolism and other enzymes → ↑ metabolism of steroids, vitamins K/D, cholesterol, and bile salts)
General mechanisms: potently depress neuron activity in the reticular formation (pons, medulla) and cortex
o Bind barbiturate site on GABAA receptor → enhanced inhibitory effect and ↑ Cl influx; → ↓ frequency of Cl channel opening but ↑ open time of Cl channels (in presense of GABA) so more Cl enters channel (at high [ ] they directly ↑ Cl conductance in absence of GABA- act as GABA mimetics)
Metabolism: liver microsomal drug metabolizing enzymes; most are dealkylated, conjugated by glucoronidation; renal excretion
Uses: anticonvulsant, preoperative sedation, anesthesia
Side effects: sedation, confusion, weight gain, N/V, skin rash
Contraindications: pain (can ↑ sensitivity to painful situations → restlessness, excitement, and delirium) and pulmonary insufficiency (since BARBS → respiratory depression)
Drug interactions: have additive depressant affects when taken with other CNS depressants, enhance depressive effects (of antipsychotics, antihistamines, antiHTNs, ethanol, and TCAs), and accelerates metabolism (of β blockers, Ca-channel blockers, corticosteroids, estrogens, phenothiazines, valproic acid, and theophylline; occurs with chronic BARB ingestion)
Acute toxicity: lower therapeutic index; can be fatal if OD; BARB poisoning a major problem (serious toxicity at only 10x hypnotic dose; → respiratory depression, circulatory collapse, renal failure, pulmonary complications which can be life-threatening)
Symptoms: severe respiratory depression, coma, severe hypotension, hypothermia
Treatment: support respiration and BP, gastric lavage (if recent ingestion)
Tolerance: metabolic (induce hepatic metabolic enzymes, occurs within a few days), pharmacodynamic (↓ CNS response with chronic exposure occurs over several weeks; unknown mechanism), and cross tolerance (tolerance to other general CNS depressants)
Physical dependence: develops with continued use; manifest by withdrawal symptoms (mild = anxiety, insomnia, dizziness, nausea; severe = vomiting, hyperthermia, tremors, delirium, convulsions, death)
Other similar agents: meprobamate (Equanil; pharmacological properties like BZs and barbiturates but mechanism unknown) and chloral hydrate (common sedative in pediatric dentistry for diagnostic imaging; few adverse effects but low therapeutic index)
Other drugs for antianxiety: β-adrenoceptor blockers (e.g., propranolol; block autonomic effects- palpitations, sweating, shaking; used for disabling situational anxiety like stage fright), buspirone (partial agonist at serotonin 1A receptor, produces only anxiolytic effects so no CNS depression, dependence, or additive depression with ethanol but onset of action is 1-3 weeks), lodipem (not a BZ but does act at BZ receptors)
Lateral Pharyngeal Space
Oral and Maxillofacial SurgeryLateral Pharyngeal Space
The lateral pharyngeal space is an important anatomical area in the neck that
plays a significant role in various clinical conditions, particularly
infections. Here’s a detailed overview of its anatomy, divisions, clinical
significance, and potential complications.
Anatomy
Shape and Location: The lateral pharyngeal space is a
potential cone-shaped space or cleft.
Base: The base of the cone is located at the base
of the skull.
Apex: The apex extends down to the greater horn of
the hyoid bone.
Divisions: The space is divided into two compartments
by the styloid process:
Anterior Compartment: Located in front of the
styloid process.
Posterior Compartment: Located behind the styloid
process.
Boundaries
Medial Boundary: The lateral wall of the pharynx.
Lateral Boundary: The medial surface of the mandible
and the muscles of the neck.
Superior Boundary: The base of the skull.
Inferior Boundary: The greater horn of the hyoid bone.
Contents
The lateral pharyngeal space contains various important structures,
including:
Muscles: The stylopharyngeus and the superior
pharyngeal constrictor muscles.
Nerves: The glossopharyngeal nerve (CN IX) and the
vagus nerve (CN X) may be present in this space.
Vessels: The internal carotid artery and the internal
jugular vein are closely associated with this space, particularly within the
carotid sheath.
Clinical Significance
Infection Risk: Infection in the lateral pharyngeal
space can be extremely serious due to its proximity to vital structures,
particularly the carotid sheath, which contains the internal carotid artery,
internal jugular vein, and cranial nerves.
Potential Complications:
Spread of Infection: Infections can spread from the
lateral pharyngeal space to other areas, including the mediastinum,
leading to life-threatening conditions such as mediastinitis.
Airway Compromise: Swelling or abscess formation in
this space can lead to airway obstruction, necessitating urgent medical
intervention.
Vascular Complications: The close relationship with
the carotid sheath means that infections can potentially involve the
carotid artery or jugular vein, leading to complications such as
thrombosis or carotid artery rupture.
Diagnosis and Management
Diagnosis:
Clinical examination may reveal signs of infection, such as fever,
neck swelling, and difficulty swallowing.
Imaging studies, such as CT scans, are often used to assess the
extent of infection and involvement of surrounding structures.
Management:
Antibiotics: Broad-spectrum intravenous antibiotics
are typically initiated to manage the infection.
Surgical Intervention: In cases of abscess
formation or significant swelling, surgical drainage may be necessary to
relieve pressure and remove infected material.
Ridge Augmentation
Oral and Maxillofacial SurgeryRidge Augmentation Procedures
Ridge augmentation procedures are surgical techniques used to increase the
volume and density of the alveolar ridge in the maxilla and mandible. These
procedures are often necessary to prepare the site for dental implants,
especially in cases where there has been significant bone loss due to factors
such as tooth extraction, periodontal disease, or trauma. Ridge augmentation can
also be performed in conjunction with orthognathic surgery to enhance the
overall facial structure and support dental rehabilitation.
Indications for Ridge Augmentation
Insufficient Bone Volume: To provide adequate support
for dental implants.
Bone Resorption: Following tooth extraction or due to
periodontal disease.
Facial Aesthetics: To improve the contour of the jaw
and facial profile.
Orthognathic Surgery: To enhance the results of jaw
repositioning procedures.
Types of Graft Materials Used
Ridge augmentation can be performed using various graft materials, which can
be classified into the following categories:
Autografts:
Bone harvested from the patient’s own
body, typically from intraoral sites (e.g., chin, ramus) or extraoral
sites (e.g., iliac crest).
Advantages: High biocompatibility, osteogenic
potential, and lower risk of rejection or infection.
Disadvantages: Additional surgical site, potential
for increased morbidity, and limited availability.
Allografts:
Bone grafts obtained from a human donor
(cadaveric bone) that have been processed and sterilized.
Advantages: No additional surgical site required,
readily available, and can provide a scaffold for new bone growth.
Disadvantages: Risk of disease transmission and
potential for immune response.
Xenografts:
Bone grafts derived from a different
species, commonly bovine (cow) bone.
Advantages: Biocompatible and provides a scaffold
for bone regeneration.
Disadvantages: Potential for immune response and
slower resorption compared to autografts.
Alloplasts:
Synthetic materials used for bone
augmentation, such as hydroxyapatite, calcium phosphate, or bioactive
glass.
Advantages: No risk of disease transmission,
customizable, and can be designed to promote bone growth.
Disadvantages: May not integrate as well as natural
bone and can have variable resorption rates.
Surgical Techniques
Bone Grafting:
The selected graft material is placed in the deficient area of the
ridge to promote new bone formation. This can be done using various
techniques, including:
Onlay Grafting: Graft material is placed on top
of the existing ridge.
Inlay Grafting: Graft material is placed within
the ridge.
Guided Bone Regeneration (GBR):
A barrier membrane is placed over the graft material to prevent soft
tissue infiltration and promote bone healing. This technique is often
used in conjunction with grafting.
Sinus Lift:
In the maxilla, a sinus lift procedure may be performed to augment
the bone in the posterior maxilla by elevating the sinus membrane and
placing graft material.
Combination with Orthognathic Surgery:
Ridge augmentation can be performed simultaneously with orthognathic
surgery to correct skeletal discrepancies and enhance the overall facial
structure.
Cartilage-Forming Tumors
General Pathology
Cartilage-Forming Tumors
1. Osteochondroma (Exostosis) is a relatively common benign cartilage-capped outgrowth attached by a bony stalk to the underlying skeleton. Solitary osteochondromas are usually first diagnosed in late adolescence and early adulthood (male-to-female ratio of 3:1); multiple osteochondromas become apparent during childhood, occurring as multiple hereditary exostosis, an autosomal dominant disorder. Inactivation of both copies of the EXT gene (a tumor suppressor gne) in chondrocytes is implicated in both sporadic and hereditary osteochondromas. Osteochondromas develop only in bones of endochondral origin arising at the metaphysis near the growth plate of long tubular bones, especially about the knee. They tend to stop growing once the normal growth of the skeleton is completed. Occasionally they develop from flat bones (pelvis, scapula, and ribs). Rarely, exostoses involve the short tubular bones of hands and feet.
Pathological features
• Osteochondromas vary from 1-20cm in size.
• The cap is benign hyaline cartilage.
• Newly formed bone forms the inner portion of the head and stalk, with the stalk cortex merging with cortex of the host bone.
Osteochondromas are slow-growing masses that may be painful. Osteochondromas rarely progress to chondrosarcoma or other sarcoma, although patients with the multiple hereditary exostoses are at increased risk of malignant transformation.
2. Chondroma
It is a benign tumor of hyaline cartilage. When it arises within the medullary cavity, it is termed enchondroma; when on the bone surface it is called juxtacortical chondroma. Enchondromas are usually diagnosed in persons between ages 20 and 50 years; they are typically solitary and located in the metaphyseal region of tubular bones, the favored sites being the short tubular bones of the hands and feet. Ollier disease is characterized by multiple chondromas preferentially involving one side of the body. Chondromas probably develop from slowly proliferating rests of growth plate cartilage.
Pathological features
• Enchondromas are gray-blue, translucent nodules usually smaller than 3 cm.
• Microscopically, there is well-circumscribed hyaline matrix and cytologically benign chondrocytes.
Most enchondromas are detected as incidental findings; occasionally they are painful or cause pathologic fractures. Solitary chondromas rarely undergo malignant transformation, but those associated with enchondromatosis are at increased risk.
3. Chondrosarcomas are malignant tumors of cartilage forming tissues. They are divided into conventional chondrosarcomas and chondrosarcoma variants. Each of these categories comprises several distinct types, some defined on microscopic grounds & others on the basis of location within the affected bone, for e.g. they are divided into central (medullary), peripheral (cortical), and juxtacortical (periosteal). The common denominator of chondrosarcoma is the production of a cartilaginous matrix and the lack of direct bone formation by the tumor cells (cf osteosarcoma). Chondrosarcomas occur roughly half as frequently as osteosarcomas; most patients age 40 years or more, with men affected twice as frequently as women
Pathological features
Conventional chondrosarcomas arise within the medullary cavity of the bone to form an expansile glistening mass that often erodes the cortex. They exhibit malignant hyaline or myxoid stroma. Spotty calcifications are typically present. The tumor grows with broad pushing fronts into marrow spaces and the surrounding soft tissue. Tumor grade is determined by cellularity, cytologic atypia, and mitotic activity. Low-grade tumors resemble normal cartilage. Higher grade lesions contain pleomorphic chondrocytes with frequent mitotic figures with multinucleate cells and lacunae containing two or more chondrocytes. Dedifferentiated chondrosarcomas refers to the presence of a poorly differentiated sarcomatous component at the periphery of an otherwise typical low-grade chondrosarcoma. Other histologic variants include myxoid, clear-cell and mesenchymal chondrosarcomas. Chondrosarcomas commonly arise in the pelvis, shoulder, and ribs. A slowly growing lowgrade tumor causes reactive thickening of the cortex, whereas a more aggressive high-grade neoplasm destroys the cortex and forms a soft tissue mass. There is also a direct correlation between grade and biologic behavior.
Size is another prognostic feature, with tumors larger than 10 cm being significantly more aggressive than smaller tumors. High-grade Chondrosarcomas metastasize hematogenously, preferentially to the lungs and skeleton.