NEET MDS Synopsis
The Nasal Mucosa
AnatomyThe Nasal Mucosa
Mucosa lines the entire nasal cavities except for the vestibule of the nose.
The nasal mucosa is firmly bound to the periosteum and perichondrium of the supporting structures of the nose.
It is continuous with the adjoining cavities to which the nasal cavity communicates (e.g., the nasopharynx and paranasal sinuses).
The inferior 2/3 of the nasal mucosa is called the respiratory area and air passing over this is warmed and moistened before it passes into the lungs.
The superior 1/3 is called the olfactory area.
The Olfactory Area of Nasal Mucosa
This area contains the peripheral organ of smell.
Sniffing draws air into this area
Olfactory receptor cells (from the olfactory nerve, CN I, are located in the mucosa of this area in the nose.
Nerves to the Respiratory Area of Nasal Mucosa
The inferior 2/3 of the nasal mucosa are supplied chiefly by the trigeminal nerve (CN V).
The mucous membrane of the nasal septum is supplied chiefly by the nasopalatine nerve, a branch of the maxillary nerve (CN V2).
Its anterior portion is supplied by the anterior ethmoidal nerve (a branch of the nasociliary nerve) which is derived from the ophthalmic nerve (CN V1).
The lateral walls of the nasal cavity are supplied by branches of the maxillary nerve (CN V2); the greater palatine nerve, and the anterior ethmoidal nerve.
Arteries of the Nasal Mucosa
The blood supply of the mucosa of the nasal septum is derived mainly from the maxillary artery.
The sphenopalatine artery, a branch of the maxillary, supplies most of the blood of the nasal mucosa.
It enters by the sphenopalatine foramen and sends branches to the posterior regions of the lateral wall and to the nasal septum.
The greater palatine artery, also a branch of the maxillary, passes through the incisive foramen to supply the nasal septum.
The anterior and posterior ethmoidal arteries, branches of the ophthalmic artery, supply the anterosuperior part of the mucosa of the lateral wall of the nasal cavity and nasal septum.
Three branches of the facial artery (superior labial, ascending palatine, and lateral nasal) also supply the anterior parts of the nasal mucosa.
Veins of the Nasal Mucosa
The veins of the nasal mucosa form a venous network of plexus in the connective tissue of the nasal mucosa.
Some of the veins open into the sphenopalatine vein and drain to the pterygoid plexus.
Others join the facial and infraorbital veins.
Some empty into the ophthalmic veins and drain into the cavernous sinus.
Anticonvulsant Drugs
Pharmacology
Anticonvulsant Drugs
A. Anticonvulsants: drugs to control seizures or convulsions in susceptible people
B. Seizures: abnormal neuronal discharges in the nervous system produced by focal or generalized brain disturbances
Manifestations: depend on location of seizure activity (motor cortex → motor convulsions, sensory cortex → abnormal sensations, temporal cortex → emotional disturbances)
Causes: many brain disorders such as head injury (glial scars, pH changes), anoxia (changes in pH or CSF pressure), infections (tissue damage, high T), drug withdrawal (barbiturates, ethanol, etc.), epilepsy (chronic state with repeated seizures)
C. Epilepsy: most common chronic seizure disorder, characterized by recurrent seizures of a particular pattern, many types (depending on location of dysfunction)
Characteristics: chronic CNS disorders (years to decades), involve sudden and transitory seizures (abnormal motor, autonomic, sensory, emotional, or cognitive function and abnormal EEG activity)
Etiology: hyperexcitable neurons; often originate at a site of damage (epileptogenic focus), often found at scar tissue from tumors, strokes, or trauma; abnormal discharge spreads to normal brain regions = seizure
Idiopathic (70%; may have genetic abnormalities) and symptomatic epilepsy (30%; obvious CNS trauma, neoplasm, infection, developmental abnormalities or drugs)
Neuropathophysiology: anticonvulsants act at each stage but most drugs not effective for all types of epilepsy (need specific drugs for specific types)
Seizure mechanism: enhanced excitation (glutamate) or ↓ inhibition (GABA) of epileptic focus → fire more quickly → ↑ release of K and glutamate → ↑ depolarization of surrounding neurons (=neuronal synchronization) → propagation (normal neurons activated)
Mercury Release in Dentistry
Conservative DentistryMercury Release in Dental Procedures Involving Amalgam
Mercury is a key component of dental amalgam, and its release during various
dental procedures has been a topic of concern due to potential health risks.
Understanding the amounts of mercury released during different stages of amalgam
handling is essential for dental professionals to implement safety measures and
minimize exposure.
1. Mercury Release Quantification
A. Trituration
Amount Released: 1-2 µg
Description: Trituration is the process of mixing
mercury with alloy particles to form a homogenous amalgam. During this
process, small amounts of mercury can be released into the air, which can
contribute to overall exposure.
B. Placement of Amalgam Restoration
Amount Released: 6-8 µg
Description: When placing an amalgam restoration,
additional mercury may be released due to the manipulation of the material.
This includes the handling and packing of the amalgam into the cavity
preparation.
C. Dry Polishing
Amount Released: 44 µg
Description: Dry polishing of amalgam restorations
generates the highest amount of mercury release among the listed procedures.
The friction and heat generated during dry polishing can vaporize mercury,
leading to increased exposure.
D. Wet Polishing
Amount Released: 2-4 µg
Description: Wet polishing, which involves the use of
water to cool the restoration during polishing, results in significantly
lower mercury release compared to dry polishing. The water helps to capture
and reduce the amount of mercury vapor released into the air.
Neurogenic Shock
Oral and Maxillofacial SurgeryNeurogenic Shock
Neurogenic shock is a type of distributive shock that occurs
due to the loss of vasomotor tone, leading to widespread vasodilation and a
significant decrease in systemic vascular resistance. This condition can occur
without any loss of blood volume, resulting in inadequate filling of the
circulatory system despite normal blood volume. Below is a detailed overview of
neurogenic shock, its causes, symptoms, and management.
Mechanism of Neurogenic Shock
Loss of Vasomotor Tone: Neurogenic shock is primarily
caused by the disruption of sympathetic nervous system activity, which leads
to a loss of vasomotor tone. This results in massive dilation of blood
vessels, particularly veins, causing a significant increase in vascular
capacity.
Decreased Systemic Vascular Resistance: The dilated
blood vessels cannot effectively maintain blood pressure, leading to
inadequate perfusion of vital organs, including the brain.
Causes
Spinal Cord Injury: Damage to the spinal cord,
particularly at the cervical or upper thoracic levels, can disrupt
sympathetic outflow and lead to neurogenic shock.
Severe Head Injury: Traumatic brain injury can also
affect autonomic regulation and result in neurogenic shock.
Vasovagal Syncope: A common form of neurogenic shock,
often triggered by emotional stress, pain, or prolonged standing, leading to
a sudden drop in heart rate and blood pressure.
Symptoms
Early Signs:
Pale or Ashen Gray Skin: Due to peripheral vasodilation
and reduced blood flow to the skin.
Heavy Perspiration: Increased sweating as a response to
stress or pain.
Nausea: Gastrointestinal distress may occur.
Tachycardia: Increased heart rate as the body attempts
to compensate for low blood pressure.
Feeling of Warmth: Particularly in the neck or face due
to vasodilation.
Late Symptoms:
Coldness in Hands and Feet: Peripheral vasoconstriction
may occur as the body prioritizes blood flow to vital organs.
Hypotension: Significantly low blood pressure due to
vasodilation.
Bradycardia: Decreased heart rate, particularly in
cases of vasovagal syncope.
Dizziness and Visual Disturbance: Due to decreased
cerebral perfusion.
Papillary Dilation: As a response to low light levels
in the eyes.
Hyperpnea: Increased respiratory rate as the body
attempts to compensate for low oxygen delivery.
Loss of Consciousness: Resulting from critically low
cerebral blood flow.
Duration of Syncope
Brief Duration: The duration of syncope in neurogenic
shock is typically very brief. Patients often regain consciousness almost
immediately upon being placed in a supine position.
Supine Positioning: This position is crucial as it
helps increase venous return to the heart and improves cerebral perfusion,
aiding in recovery.
Management
Positioning: The first and most important step in
managing neurogenic shock is to place the patient in a supine position. This
helps facilitate blood flow to the brain.
Fluid Resuscitation: While neurogenic shock does not
typically involve blood loss, intravenous fluids may be administered to help
restore vascular volume and improve blood pressure.
Vasopressors: In cases where hypotension persists
despite fluid resuscitation, vasopressor medications may be used to
constrict blood vessels and increase blood pressure.
Monitoring: Continuous monitoring of vital signs,
including blood pressure, heart rate, and oxygen saturation, is essential to
assess the patient's response to treatment.
Addressing Underlying Causes: If neurogenic shock is due
to a specific cause, such as spinal cord injury or vasovagal syncope,
appropriate interventions should be initiated to address the underlying
issue.
The Henderson-Hasselbalch Equation
Biochemistry
By rearranging the above equation we arrive at the Henderson-Hasselbalch equation:
pH = pKa + log[A-]/[HA]
It should be obvious now that the pH of a solution of any acid (for which the equilibrium constant is known, and there are numerous tables with this information) can be calculated knowing the concentration of the acid, HA, and its conjugate base [A-].
At the point of the dissociation where the concentration of the conjugate base [A-] = to that of the acid [HA]:
pH = pKa + log[1]
The log of 1 = 0. Thus, at the mid-point of a titration of a weak acid:
pKa = pH
In other words, the term pKa is that pH at which an equivalent distribution of acid and conjugate base (or base and conjugate acid) exists in solution.
Aplasticanaemia and pancytopenia
General Pathology
Aplasticanaemia and pancytopenia.
Aplastic anaemia is a reduction in all the formed elements of blood due to marrow hypoplasia.
Causes
- Primary or Idiopathic.
- Secondary to :
1 Drugs :
Antimetabolites and antimitotic agents.
Antiepileptics.
Phenylbutazone.
Chloramphenicol.
2 Industrial chemicals.
Benzene.
DDT and other insecticides.
TNT (used in explosives).
3 Ionising radiation
- Familial aplasia
Pancytopenia (or reduction in the formed elements of blood) can be caused by other conditions also like:
-Subleukaemic acute leukaemia.
-Megaloblastic anaemia
-S.L.E.
-hypersplenism.
-Marrow infiltration by lymphomas metastatic deposits, tuberculosis, myeloma etc
Features:
- Anaemia.
- Leucopenia upper respiratory infections.
- Thrombocytopenis :- petechiae and bruising.
Blood picture:
- Normocytic normochromic anaemia with minimal anisopoikilocytosis in aplastic anaemia. Other causes of pancytopenia may show varying degrees of anisopoikilocytosis
- Neutropenia with hypergranulation and high alkaline phosphatase.
- Low platelet counts
Bone marrow:
- Hypoplastic (may have patches of norm cellular or hyper cellular marrow) which may -> dry tap. .
- Increase in fat cells , fibroblasts , reticulum cells, lymphocytes and plasma cells
- Decrease in precursors of all three-Series.
- Underlying cause if any, of pancytopenia may be seen
Cognitive Theory
PedodonticsCognitive Theory by Jean Piaget (1952)
Overview of Piaget's Cognitive Theory
bb Jean Piaget formulated a comprehensive theory of cognitive development that
explains how children and adolescents think and acquire knowledge. His theories
were derived from direct observations of children, where he engaged them in
questioning about their thought processes. Piaget emphasized that children and
adults actively seek to understand their environment rather than being shaped by
it.
Key Concepts of Piaget's Theory
Piaget's theory of cognitive development is based on the process of
adaptation, which consists of three functional variants:
Assimilation:
This process involves observing, recognizing, and interacting with
an object and relating it to previous experiences or existing categories
in the child's mind. For example, a child who knows what a dog is may
see a cat and initially call it a dog because it has similar features.
Accommodation:
Accommodation occurs when a child changes their existing concepts or
strategies in response to new information that does not fit into their
current schemas. This leads to the development of new schemas. For
instance, after learning that a cat is different from a dog, the child
creates a new category for cats.
Equilibration:
Equilibration refers to the process of balancing assimilation and
accommodation to create stable understanding. When children encounter
new information that challenges their existing knowledge, they adjust
their understanding to achieve a better fit with the facts.
Stages of Cognitive Development
Piaget categorized cognitive development into four major stages:
Sensorimotor Stage (0 to 2 years):
In this stage, infants learn about the world through their senses
and actions. They develop object permanence and begin to understand that
objects continue to exist even when they cannot be seen.
Pre-operational Stage (2 to 6 years):
During this stage, children begin to use language and engage in
symbolic play. However, their thinking is still intuitive and
egocentric, meaning they have difficulty understanding perspectives
other than their own.
Concrete Operational Stage (6 to 12 years):
Children in this stage develop logical thinking but are still
concrete in their reasoning. They can perform operations on tangible
objects and understand concepts such as conservation (the idea that
quantity does not change even when its shape does).
Formal Operational Stage (11 to 15 years):
In this final stage, adolescents develop the ability to think
abstractly and hypothetically. They can formulate and test hypotheses
and engage in systematic planning.
Merits of Piaget’s Theory
Comprehensive Framework: Piaget's theory is one of the
most comprehensive theories of cognitive development, providing a structured
understanding of how children think and learn.
Insight into Learning: The theory suggests that
examining children's incorrect answers can provide valuable insights into
their cognitive processes, just as much as correct answers can.
Demerits of Piaget’s Theory
Underestimation of Abilities: Critics argue that Piaget
underestimated the cognitive abilities of children, particularly in the
pre-operational stage.
Overestimation of Age Differences: The theory may
overestimate the differences in thinking abilities between age groups,
suggesting a more rigid progression than may actually exist.
Vagueness in Change Processes: There is some vagueness
regarding how changes in thinking occur, particularly in the transition
between stages.
Underestimation of Social Environment: Piaget's theory
has been criticized for underestimating the role of social interactions and
cultural influences on cognitive development.
Pulmonary edema
General Pathology
Pulmonary edema
Pulmonary edema is swelling and/or fluid accumulation in the lungs. It leads to impaired gas exchange and may cause respiratory failure.
Signs and symptoms
Symptoms of pulmonary edema include difficulty breathing, coughing up blood, excessive sweating, anxiety and pale skin. If left untreated, it can lead to death, generally due to its main complication of acute respiratory distress syndrome.
Diagnosis
physical examination: end-inspiratory crackles during auscultation (listening to the breathing through a stethoscope) can be due to pulmonary edema. The diagnosis is confirmed on X-ray of the lungs, which shows increased vascular filling and fluid in the alveolar walls.
Low oxygen saturation and disturbed arterial blood gas readings may strengthen the diagnosis
Causes
Cardiogenic causes:
Heart failure
Tachy- or bradyarrhythmias
Severe heart attack
Hypertensive crisis
Excess body fluids, e.g. from kidney failure
Pericardial effusion with tamponade
Non-cardiogenic causes, or ARDS (acute respiratory distress syndrome):
Inhalation of toxic gases
Multiple blood transfusions
Severe infection
Pulmonary contusion, i.e. high-energy trauma
Multitrauma, i.e. severe car accident
Neurogenic, i.e. cerebrovascular accident (CVA)
Aspiration, i.e. gastric fluid or in case of drowning
Certain types of medication
Upper airway obstruction
Reexpansion, i.e. postpneumonectomy or large volume thoracentesis
Reperfusion injury, i.e. postpulmonary thromboendartectomy or lung transplantation
Lack of proper altitude acclimatization.
Treatment
When circulatory causes have led to pulmonary edema, treatment with loop diuretics, such as furosemide or bumetanide, is the mainstay of therapy. Secondly, one can start with noninvasive ventilation. Other useful treatments include glyceryl trinitrate, CPAP and oxygen.