NEET MDS Synopsis
Blastomycosis (North American Blastomycosis; Gilchrist's Disease)
General Pathology
Blastomycosis (North American Blastomycosis; Gilchrist's Disease)
A disease caused by inhalation of mold conidia (spores) of Blastomyces dermatitidis, which convert to yeasts and invade the lungs, occasionally spreading hematogenously to the skin or focal sites in other tissues.
Pulmonary blastomycosis tends to occur as individual cases of progressive infection
Symptoms are nonspecific and may include a productive or dry hacking cough, chest pain, dyspnea, fever, chills, and drenching sweats. Pleural effusion occurs occasionally. Some patients have rapidly progressive infections, and adult respiratory distress syndrome may develop.
Antifungal
Pharmacology
Antifungal
There are several classes of antifungal drugs.
The polyenes bind with sterols in the fungal cell wall, principally ergosterol. This causes the cell's contents to leak out and the cell dies. Human (and other animal) cells contain cholesterol rather than ergosterol so are much less suceptible.
Nystatin
Amphotericin B
Natamycin
The imidazole and triazole groups of antifungal drugs inhibit the enzyme cytochrome P450 14α-demethylase. This enzyme converts lanosterol to ergosterol, and is required in fungal cell wall synthesis. These drugs also block steroid synthesis in humans.
Imidazoles:
Miconazole
Ketoconazole
Clotrimazole
The triazoles are newer, and are less toxic and more effective:
Fluconazole
Itraconazole
Allylamines inhibit the enzyme squalene epoxidase, another enzyme required for ergosterol synthesis:
Terbinafine
Echinocandins inhibit the synthesis of glucan in the cell wall, probably via the enzyme 1,3-β glucan synthase:
Caspofungin
Micafungin
Others:
Flucytosine is an antimetabolite.
Griseofulvin binds to polymerized microtubules and inhibits fungal mitosis.
Gow-Gates Technique for Mandibular Anesthesia
Oral and Maxillofacial SurgeryGow-Gates Technique for Mandibular Anesthesia
The Gow-Gates technique is a well-established method for
achieving effective anesthesia of the mandibular teeth and associated soft
tissues. Developed by George Albert Edwards Gow-Gates, this technique is known
for its high success rate in providing sensory anesthesia to the entire
distribution of the mandibular nerve (V3).
Overview
Challenges in Mandibular Anesthesia: Achieving
successful anesthesia in the mandible is often more difficult than in the
maxilla due to:
Greater anatomical variation in the mandible.
The need for deeper penetration of soft tissues.
Success Rate: Gow-Gates reported an astonishing success
rate of approximately 99% in his experienced hands, making
it a reliable choice for dental practitioners.
Anesthesia Coverage
The Gow-Gates technique provides sensory anesthesia to the following nerves:
Inferior Alveolar Nerve
Lingual Nerve
Mylohyoid Nerve
Mental Nerve
Incisive Nerve
Auriculotemporal Nerve
Buccal Nerve
This comprehensive coverage makes it particularly useful for procedures
involving multiple mandibular teeth.
Technique
Equipment
Needle: A 25- or 27-gauge long needle is
recommended for this technique.
Injection Site and Target Area
Area of Insertion:
The injection is performed on the mucous membrane on
the mesial aspect of the mandibular ramus.
The insertion point is located on a line drawn from the intertragic
notch to the corner of the mouth, just distal
to the maxillary second molar.
Target Area:
The target for the injection is the lateral side of the
condylar neck, just below the insertion of the lateral
pterygoid muscle.
Landmarks
Extraoral Landmarks:
Lower Border of the Tragus: This serves as a reference
point. The center of the external auditory meatus is the ideal landmark, but
since it is concealed by the tragus, the lower border is used as a visual
aid.
Corner of the Mouth: This helps in aligning the
injection site.
Intraoral Landmarks:
Height of Injection: The needle tip should be placed
just below the mesiopalatal cusp of the maxillary second
molar to establish the correct height for the injection.
Penetration Point: The needle should penetrate the soft
tissues just distal to the maxillary second molar at the height established
in the previous step.
Graded Contractions and Muscle Metabolism
PhysiologyGraded Contractions and Muscle Metabolism
The muscle twitch is a single response to a single stimulus. Muscle twitches vary in length according to the type of muscle cells involved. .
Fast twitch muscles such as those which move the eyeball have twitches which reach maximum contraction in 3 to 5 ms (milliseconds). [superior eye] and [lateral eye] These muscles were mentioned earlier as also having small numbers of cells in their motor units for precise control.
The cells in slow twitch muscles like the postural muscles (e.g. back muscles, soleus) have twitches which reach maximum tension in 40 ms or so.
The muscles which exhibit most of our body movements have intermediate twitch lengths of 10 to 20 ms.
The latent period, the period of a few ms encompassing the chemical and physical events preceding actual contraction.
This is not the same as the absolute refractory period, the even briefer period when the sarcolemma is depolarized and cannot be stimulated. The relative refractory period occurs after this when the sarcolemma is briefly hyperpolarized and requires a greater than normal stimulus
Following the latent period is the contraction phase in which the shortening of the sarcomeres and cells occurs. Then comes the relaxation phase, a longer period because it is passive, the result of recoil due to the series elastic elements of the muscle.
We do not use the muscle twitch as part of our normal muscle responses. Instead we use graded contractions, contractions of whole muscles which can vary in terms of their strength and degree of contraction. In fact, even relaxed muscles are constantly being stimulated to produce muscle tone, the minimal graded contraction possible.
Muscles exhibit graded contractions in two ways:
1) Quantal Summation or Recruitment - this refers to increasing the number of cells contracting. This is done experimentally by increasing the voltage used to stimulate a muscle, thus reaching the thresholds of more and more cells. In the human body quantal summation is accomplished by the nervous system, stimulating increasing numbers of cells or motor units to increase the force of contraction.
2) Wave Summation ( frequency summation) and Tetanization- this results from stimulating a muscle cell before it has relaxed from a previous stimulus. This is possible because the contraction and relaxation phases are much longer than the refractory period. This causes the contractions to build on one another producing a wave pattern or, if the stimuli are high frequency, a sustained contraction called tetany or tetanus. (The term tetanus is also used for an illness caused by a bacterial toxin which causes contracture of the skeletal muscles.) This form of tetanus is perfectly normal and in fact is the way you maintain a sustained contraction.
Treppe is not a way muscles exhibit graded contractions. It is a warmup phenomenon in which when muscle cells are initially stimulated when cold, they will exhibit gradually increasing responses until they have warmed up. The phenomenon is due to the increasing efficiency of the ion gates as they are repeatedly stimulated. Treppe can be differentiated from quantal summation because the strength of stimulus remains the same in treppe, but increases in quantal summation
Length-Tension Relationship: Another way in which the tension of a muscle can vary is due to the length-tension relationship. This relationship expresses the characteristic that within about 10% the resting length of the muscle, the tension the muscle exerts is maximum. At lengths above or below this optimum length the tension decreases.
Trigeminal Neuralgia
Oral and Maxillofacial SurgeryTrigeminal Neuralgia
Trigeminal neuralgia (TN) is a type of orofacial neuralgia
characterized by severe, paroxysmal pain that follows the anatomical
distribution of the trigeminal nerve (cranial nerve V). It is often described as
one of the most painful conditions known, and understanding its features,
triggers, and patterns is essential for effective management.
Features of Trigeminal Neuralgia
Anatomical Distribution:
Trigeminal neuralgia follows the distribution of the trigeminal
nerve, which has three main branches:
V1 (Ophthalmic): Supplies sensation to the
forehead, upper eyelid, and parts of the nose.
V2 (Maxillary): Supplies sensation to the
cheeks, upper lip, and upper teeth.
V3 (Mandibular): Supplies sensation to the
lower lip, chin, and lower teeth.
Pain can occur in one or more of these dermatomes, but it is
typically unilateral.
Trigger Zones:
Patients with trigeminal neuralgia often have specific trigger
zones on the face. These are areas where light touch, brushing,
or even wind can provoke an episode of pain.
Stimulation of these trigger zones can initiate a paroxysm of pain,
leading to sudden and intense discomfort.
Pain Characteristics:
The pain associated with trigeminal neuralgia is described as:
Paroxysmal: Occurs in sudden bursts or attacks.
Excruciating: The pain is often severe and
debilitating.
Sharp, shooting, or lancinating: Patients may
describe the pain as electric shock-like.
Unilateral: Pain typically affects one side of
the face.
Intermittent: Attacks can vary in frequency and
duration.
Latency and Refractory Period:
Latency: This refers to the short time interval
between the stimulation of the trigger area and the onset of pain. It
can vary among patients.
Refractory Period: After an attack, there may be a
refractory period during which further stimulation does not elicit pain.
This period can vary in length and is an important aspect of the pain
cycle.
Pain Cycles:
Paroxysms of pain often occur in cycles, with each cycle lasting for
weeks or months. Over time, these cycles may become more frequent, and
the intensity of pain can increase with each attack.
Patients may experience a progressive worsening of symptoms, leading
to more frequent and severe episodes.
Psychosocial Impact:
The unpredictable nature of trigeminal neuralgia can significantly
impact a patient's quality of life, leading to anxiety, depression, and
social withdrawal due to fear of triggering an attack.
Management of Trigeminal Neuralgia
Medications:
Anticonvulsants: Medications such as carbamazepine
and oxcarbazepine are commonly used as first-line treatments to help
control pain.
Other Medications: Gabapentin, pregabalin,
and baclofen may also be effective in managing symptoms.
Surgical Options:
For patients who do not respond to medication or experience
intolerable side effects, surgical options may be considered. These can
include:
Microvascular Decompression: A surgical
procedure that relieves pressure on the trigeminal nerve.
Rhizotomy: A procedure that selectively
destroys nerve fibers to reduce pain.
Alternative Therapies:
Some patients may benefit from complementary therapies such as
acupuncture, physical therapy, or biofeedback.
ERUPTION - The mixed dentition
Dental Anatomy
The mixed dentition
I. Transition dentition between 6 and 12 years of age with primary tooth exfoliation and permanent tooth eruption
2. Its characteristic features have led this to be called the ugly duckling stage because of
a. Edentulated areas
b. Disproportionately sized teeth
c. Various clinical crown heights
d. Crowding
e. Enlarged and edematous gingiva
f. Different tooth colors
BONES OF THE SKULL
Orthodontics
BONES OF THE SKULL
A) Bones of the cranial base:
A) Fontal (1)
B) Ethmoid (1)
C) Sphenoid (1)
D) Occipital (1)
B) Bones of the cranial vault:
1. Parietal (2)
2. Temporal (2)
C) Bones of the face:
Maxilla (2)
Mandible (1)
Nasal bone (2)
Lacrimal bone (2)
Zygomatic bone (2)
Palatine bone(2)
Infra nasal concha (2)
FUSION BETWEEN BONES
1. Syndesmosis: Membranous or ligamentus eg. Sutural point.
2. Synostosis: Bony union eg. symphysis menti.
3. Synchondrosis: Cartilaginous eg. sphenoccipital, spheno-ethmoidal.
GROWTH OF THE SKULL:
A) Cranium: 1. Base 2. Vault
B) Face: 1. Upper face 2.Lower face
CRANIAL BASE:
Cranial base grows at different cartilaginous suture. The cranial base may be divided into 3 areas.
1. The posterior part which extends from the occiput to the salatercica. The most important growth site spheno-occipital synchondrosis is situated here. It is active throughout the growing period and does not close until early adult life.
2. The middle portion extends from sella to foramen cecum and the sutural growth spheno-ethmoidal synchondrosis is situated here. The exact time of closing is not known but probably at the age of 7 years.
3. The anterior part is from foramen cecum and grows by surface deposition of bone in the frontal region and simultaneous development of frontal sinus.
CRANIAL VAULT:
The cranial vault grows as the brain grows. It is accelerated at infant. The growth is complete by 90% by the end of 5th year. At birth the sutures are wide sufficiently and become approximated during the 1st 2 years of life.
The development and extension of frontal sinus takes place particularly at the age of puberty and there is deposition of bone on the surfaces of cranial bone.
Hepatitis A virus.
General Pathology
Hepatitis A virus.
- Hepatitis A (HAV) is a self-limited hepatitis caused by an RNA virus
- Symptoms last 2 to 4 weeks.
- There is no risk of developing chronic hepatitis in the future.
- Incubation period is short, lasting 2 to 6 weeks.
- Infection is identified by HAV-specific antibodies (IgM if acute, IgG if past disease).
- The usual route of infection is fecal-oral transmission by contaminated food. There is no carrier state and no chronic disease
- Laboratory diagnosis: ELISA test for IgM antibody.
- Vaccine: killed virus.
- Prevention: serum immunoglobulins are available.