NEET MDS Synopsis
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)
The Palate
AnatomyThe Palate
The palate forms the arched roof of the mouth and the floor of the nasal cavities.
The palate consists of two regions: the anterior 2/3 or bony part, called the hard palate, and the mobile posterior 1/3 or fibromuscular part, known as the soft palate.
The Hard Palate
The anterior bony part of the palate is formed by the palatine process of the maxillae and the horizontal plates of the palatine bones.
Anteriorly and laterally, the hard palate is bounded by the alveolar processes and the gingivae.
Posteriorly, the hard palate is continuous with the soft palate.
The incisive foramen is the mouth of the incisive canal.
This foramen is located posterior to the maxillary central incisor teeth.
This foramen is the common opening for the right and left incisive canals.
The incisive canal and foramen transmit the nasopalatine nerve and the terminal branches of the sphenopalatine artery.
Medial to the third molar tooth, the greater palatine foramen pierces the lateral border of the bony palate.
The greater palatine vessels and nerve emerge from this foramen and run anteriorly into two grooves on the palate.
The lesser palatine foramen transmits the lesser palatine nerve and vessels.
This runs to the soft palate and adjacent structures.
Functions of the blood
PhysiologyFunction of Blood
transport through the body of
oxygen and carbon dioxide
food molecules (glucose, lipids, amino acids)
ions (e.g., Na+, Ca2+, HCO3−)
wastes (e.g., urea)
hormones
heat
defense of the body against infections and other foreign materials. All the WBCs participate in these defenses
The Soft Palate
Anatomy
This is the posterior curtain-like part, and has no bony support. It does, however, contain a membranous aponeurosis.
The soft palate, or velum palatinum (L. velum, veil), is a movable, fibromuscular fold that is attached to the posterior edge of the hard palate.
It extends posteroinferiorly to a curved free margin from which hangs a conical process, the uvula (L. uva, grape).
The soft palate separates the nasopharynx superiorly and the oropharynx inferiorly.
During swallowing the soft palate moves posteriorly against the wall of the pharynx, preventing the regurgitation of food into the nasal cavity.
Laterally, the soft palate is continuous with the wall of the pharynx and is joined to the tongue and pharynx by the palatoglossal and palatopharyngeal folds.
The soft palate is strengthened by the palatine aponeurosis, formed by the expanded tendon of the tensor veli palatini muscle.
This aponeurosis attaches to the posterior margin of the hard palate.
Pneumocystis Pneumonia
Pathology
- Caused by fungal organism called Pneumocystis jiroveci. Previously known as Pneumocystis carinii (PCP).
- Causes a pneumonia in the immunosuppressed, typically HIV with CD4 <200 therefore may require prophylaxis. Also seen in lymphoproliferative disorders, organ transplants and chemotherapy patients.
- Insidious onset, increasing dyspnoea, dry cough and fever. Patient may have bilateral fine crepitations and signs of hypoxia.
- CXR - can be normal, or classically showing bilateral perihilar interstitial shadowing. The CXR above also shows cavitating lesions.
- CT - ground glass appearance. This CT shows multiple cavitations.
- Diagnosis - direct visualisation on microscopy specimen from bronchoalveolar lavage or biopsy.
- Management - ASAP give high dose IV co-trimoxazole or IV penamidine. Steroids useful in severe hypoxia. Supportive therapy with oxygen. May require CPAP or mechanical ventilation.
Ketoprofen
Pharmacology
Ketoprofen
It acts by inhibiting the body's production of prostaglandin.
Degrees of Mental Disability
PedodonticsDegrees of Mental Disability
Mental disabilities are often classified based on the severity of cognitive
impairment, which can be assessed using various intelligence scales, such as the
Wechsler Intelligence Scale and the Stanford-Binet Scale. Below is a detailed
overview of the degrees of mental disability, including IQ ranges and
communication abilities.
1. Mild Mental Disability
IQ Range: 55-69 (Wechsler Scale) or 52-67 (Stanford-Binet
Scale)
Description:
Individuals in this category may have some difficulty with academic
skills but can often learn basic academic and practical skills.
They typically can communicate well enough for most communication
needs and may function independently with some support.
They may have social skills that allow them to interact with peers
and participate in community activities.
2. Moderate Mental Disability
IQ Range: 40-54 (Wechsler Scale) or 36-51
(Stanford-Binet Scale)
Description:
Individuals with moderate mental disability may have significant
challenges in academic learning and require more support in daily
living.
Communication skills may be limited; they can communicate at a basic
level with others but may struggle with more complex language.
They often need assistance with personal care and may benefit from
structured environments and support.
3. Severe or Profound Mental Disability
IQ Range: 39 and below (Severe) or 35 and below
(Profound)
Description:
Individuals in this category have profound limitations in cognitive
functioning and adaptive behavior.
Communication may be very limited; some may be mute or communicate
only in grunts or very basic sounds.
They typically require extensive support for all aspects of daily
living, including personal care and communication.
Herpetic Gingivostomatitis
PedodonticsHerpetic Gingivostomatitis
Herpetic gingivostomatitis is an infection of the oral cavity caused by the
herpes simplex virus (HSV), primarily HSV type 1. It is characterized by
inflammation of the gingiva and oral mucosa, and it is most commonly seen in
children.
Etiology and Transmission
Causative Agent: Herpes simplex virus (HSV).
Transmission: The virus is communicated through
personal contact, particularly via saliva. Common routes include:
Direct contact with an infected individual.
Transmission from mother to child, especially during the neonatal
period.
Epidemiology
Prevalence: Studies indicate that antibodies to HSV are
present in 40-90% of individuals across different populations, suggesting
widespread exposure to the virus.
Age of Onset:
The incidence of primary herpes simplex infection increases after 6
months of age, peaking between 2 to 5 years.
Infants under 6 months are typically protected by maternal
antibodies.
Clinical Presentation
Incubation Period: 3 to 5 days following exposure to
the virus.
Symptoms:
General Symptoms: Fever, headache, malaise, and
oral pain.
Oral Symptoms:
Initial presentation includes acute herpetic gingivostomatitis,
with the gingiva appearing red, edematous, and inflamed.
After 1-2 days, small vesicles develop on the oral mucosa, which
subsequently rupture, leading to painful ulcers with diameters of
1-3 mm.
Course of the Disease
Self-Limiting Nature: The primary herpes simplex
infection is usually self-limiting, with recovery typically occurring within
10 days.
Complications: In severe cases, complications may
arise, necessitating hospitalization or antiviral treatment.
Treatment
Supportive Care:
Pain management with analgesics for fever and discomfort.
Ensuring adequate hydration through fluid intake.
Topical anesthetic ointments may be used to facilitate eating and
reduce pain.
Severe Cases:
Hospitalization may be required for severe symptoms or
complications.
Antiviral agents (e.g., acyclovir) may be administered in severe
cases or for immunocompromised patients.
Recurrence of Herpetic Infections
Reactivation: Recurrent herpes simplex infections are
due to the reactivation of HSV, which remains dormant in nerve tissue after
the primary infection.
Triggers for Reactivation:
Mucosal injuries (e.g., from dental treatment).
Environmental factors (e.g., sunlight exposure, citrus fruits).
Location of Recurrence: Recurrent infections typically
occur at the same site as the initial infection, commonly manifesting as
herpes labialis (cold sores).