NEET MDS Synopsis
Walsham’s Forceps
General SurgeryWalsham’s Forceps
Walsham’s forceps are specialized surgical instruments used
primarily in the manipulation and reduction of fractured nasal fragments. They
are particularly useful in the management of nasal fractures, allowing for
precise adjustment and stabilization of the bone fragments during the reduction
process.
Design:
Curved Blades: Walsham’s forceps feature two curved
blades—one padded and one unpadded. The curvature of the blades allows
for better access and manipulation of the nasal structures.
Padded Blade: The padded blade is designed to
provide a gentle grip on the external surface of the nasal bone and
surrounding tissues, minimizing trauma during manipulation.
Unpadded Blade: The unpadded blade is inserted into
the nostril and is used to secure the internal aspect of the nasal bone
and associated fragments.
Usage:
Insertion: The unpadded blade is carefully passed
up the nostril to reach the fractured nasal bone and the associated
fragment of the frontal process of the maxilla.
Securing Fragments: Once in position, the nasal
bone and the associated fragment are secured between the padded blade
externally and the unpadded blade internally.
Manipulation: The surgeon can then manipulate the
fragments into their correct anatomical position, ensuring proper
alignment and stabilization.
Indications:
Walsham’s forceps are indicated for use in cases of nasal fractures,
particularly when there is displacement of the nasal bones or associated
structures. They are commonly used in both emergency and elective
settings for nasal fracture management.
Advantages:
Precision: The design of the forceps allows for
precise manipulation of the nasal fragments, which is crucial for
achieving optimal alignment and aesthetic outcomes.
Minimized Trauma: The padded blade helps to reduce
trauma to the surrounding soft tissues, which can be a concern during
the reduction of nasal fractures.
Postoperative Considerations:
After manipulation and reduction of the nasal fragments, appropriate
postoperative care is essential to monitor for complications such as
swelling, infection, or malunion. Follow-up appointments may be
necessary to assess healing and ensure that the nasal structure remains
stable.
Periodontal Medicaments
Periodontology
Periodontal Medicaments
Periodontal diseases often require adjunctive therapies to traditional
mechanical treatments such as scaling and root planing. Various medicaments have
been developed to enhance the healing process and control infection in
periodontal tissues. This lecture will discuss several periodontal medicaments,
their compositions, and their clinical applications.
1. Elyzol
Composition:
Elyzol is an oil-based gel containing 25% metronidazole.
It is formulated with glyceryl mono-oleate and sesame oil.
Clinical Use:
Elyzol has been found to be equivalent to scaling and root
planing in terms of effectiveness for treating periodontal
disease.
However, no adjunctive effects beyond those achieved with mechanical
debridement have been demonstrated.
2. Actisite
Composition:
Actisite consists of tetracycline-containing fibers.
Each fiber has a diameter of 0.5 mm and contains 12.7
mg of tetracycline per 9 inches of fiber.
Clinical Use:
The fibers are placed directly into periodontal pockets, where they
release tetracycline over time, helping to reduce bacterial load and
promote healing.
3. Arestin
Composition:
Arestin contains minocycline, which is delivered as
a biodegradable powder in a syringe.
Clinical Use:
Arestin is indicated for the treatment of periodontal disease and is
applied directly into periodontal pockets, where it provides localized
antibiotic therapy.
4. Atridox
Composition:
Atridox contains 10% doxycycline in a syringeable
gel system that is biodegradable.
Clinical Use:
The gel is injected into periodontal pockets, where it solidifies
and releases doxycycline over time, aiding in the management of
periodontal disease.
5. Dentamycin and Periocline
Composition:
Both Dentamycin and Periocline contain 2% minocycline
hydrochloride.
Clinical Use:
These products are used similarly to other local delivery systems,
providing localized antibiotic therapy to reduce bacterial infection in
periodontal pockets.
6. Periochip
Composition:
Periochip is a biodegradable chip that contains chlorhexidine.
Clinical Use:
The chip is placed in the gingival crevice, where it releases
chlorhexidine over time, providing antimicrobial action and helping to
control periodontal disease.
ANTIDEPRESSANTS
Pharmacology
ANTIDEPRESSANTS
Monoamine uptake inhibitors
1. Tricyclic antidepressants (TCAs)
2. Selective serotonin reuptake inhibitors (SSRIs)
3. Serotonin-norepinephrine reuptake inhibitors(SNRIs)
4. Norepinephrine reuptake inhibitor
Monoamine oxidase inhibitors (MAOIs)
Monoamine receptor antagonists
AMYLOIDOSIS
General Pathology
AMYLOIDOSIS
Definition. Extra cellular deposition of an eosinophilic hyaline homogenous material in Various organs, occurring in a variety of clinical states.
Staining reactions
Iodine :- Brown, turning blue on addition of H2SO4 (gross and microscopic Stain).
P.A.S. – Positive (Magenta pink).
Congo Red -Orange red which on polarisation gives green birefringence.
Von Geison's –Khaki colour.
Thioflavin T -Yellow fluorescence.
Amyloid is called typical if it given the above staining reactions Other wise it is termed atypical or para-amyloid.
Classification
1. Systemic amyloidosis associated with underlying disease (secondary),
(A) Chronic infections like
- Tuberculosis.
- Bronchiectasis.
- Lung abscess.
- Osteomyelitis.
- Syphilis.
(B) Chronic inflammations of varied etiology:
- Rheumatoid arthritis.
- Ulcerative colitis.
- Regional enteritis.
- Lupus erythematosus.
(C) Neoplastic proliferations:
- Of immune system – Multiple myeloma, Hodgkin’s disease.
- Cancers like Renal cell carcinoma etc.
II Systemic primary amyloidosis with no underlying cause.
III Heredofamilial types.
- Amyloidosis with mediterranean fever.
- Amyloid polyneuropathy.
- Amyloid nephrophathy
- Familial cardiac amyloidosis
- Familial cutaneous amyloid.
- Lattice corneal dystrophy
IV. Localised amyloidosis:
- Senile - in heart, brain, seminal vesicles.
- Amyloidoma of tongue, bronchial tree, skin.
- In islets of Langerhans in Diabetes mellitus.
- In medullary thyroid carcinoma.
Deposition sites
In relation to reticulin and collagen fibres and to basement, membranes especially
subendothelial.
Organs involved commonly are :
Secondary amyloidosis
- Liver.
- Spleen.
- Kidney
- Lymph nodes.
- Adrenals.
Primary amyloidosis
- Heart
- Tongue and gingiva.
- Gastro intestinal tract.
- Lung.
- Wall of small vessels.
Nature and pathogenesis of amyloid
It is primarily made up of protein arranged in two patterns
- There are filaments twisted together to from the fibrils. These chemically resemble light chains of immunoglobulins
- Rods composed of stacked rings. These are made up of alpha globulin components of plasma proteins (P-components)
- In addition to these, extracts of crude amyloid contain mucopolysacharides complement and gamma globulins.
- Origin of amyloid :- current concept is that it is a direct product of cells of the immune sustem with some abnormality in their immune response
The abnormality may be due to :
- A genetic enzyme defect.
- Prolonged antigenic challenge.
- Neoplastic transformation
- Supression of normal. Response as in induced tolerance.
Time for tooth development
Dental Anatomy
Time for tooth development
Entire primary dentition initiated between 6 and 8 weeks of embryonic development.
Successional permanent teeth initiated between 20th week in utero and 10th month after birth Permanent molars between 20th week in utero (first molar) and 5th year of life (third molar)
Miscellaneous Bone Tumors
General Pathology
Miscellaneous Bone Tumors
1. Ewing Sarcoma & Primitive Neuroectodermal Tumor (PNET) are primary malignant small round-cell tumors of bone and soft tissue. They are viewed as the same tumor because they share an identical chromosome translocation; they differ only in degree of differentiation. PNETs demonstrate neural differentiation whereas Ewing sarcomas are undifferentiated. After osteosarcomas, they are the second most common pediatric bone sarcomas. Most patients are 10 to 15 years old. The common chromosomal abnormality is a translocation that causes fusion of the EWS gene with a member of the ETS family of transcription factors. The resulting hybrid protein functions as an active transcription factor to stimulate cell proliferation. These translocations are of diagnostic importance since almost all patients with Ewing tumor have t(11;22).
Pathological features
• Ewing sarcoma and PNETs arise in the medullary cavity but eventually invade the cortex and periosteum to produce a soft tissue mass.
• The tumor is tan-white, frequently with foci of hemorrhage and necrosis.
Microscopic features
• There are sheets of uniform small, round cells that are slightly larger than lymphocytes with few mitoses and little intervening stroma.
• The cells have scant glycogen-rich cytoplasm.
• The presence of Homer-Wright rosettes (tumor cells circled about a central fibrillary space) indicates neural differentiation, and hence indicates by definition PNET.
Ewing sarcoma and PNETs typically present as painful enlarging masses in the diaphyses of long tubular bones (especially the femur) and the pelvic flat bones. The tumor may be confused with osteomyelitis because of its association with systemic signs & symptoms of infection. X-rays show a destructive lytic tumor with infiltrative margins and extension into surrounding soft tissues. There is a characteristic periosteal reaction depositing bone in an onionskin fashion.
2. Giant-Cell Tumor of Bone (GCT) is dominated by multinucleated osteoclast-type giant cells, hence the synonym osteoclastoma. GCT is benign but locally aggressive, usually arising in individuals in their 20s to 40s. Current opinion suggests that the giant cell component is likely a reactive macrophage population and the mononuclear cells are neoplastic. Tumors are large and red-brown with frequent cystic degeneration. They are composed of uniform oval mononuclear cells with frequent mitoses, with scattered osteoclast-type giant cells that may contain 30 or more nuclei.
The majority of GCTs arise in the epiphysis of long bones around the knee (distal femur and proximal tibia).
Radiographically, GCTs are large, purely lytic, and eccentric; the overlying cortex is frequently destroyed, producing a bulging soft tissue mass with a thin shell of reactive bone. Although GCTs are benign, roughly 50% recur after simple curettage; some malignant examples (5%) metastasize to the lungs
Neurophysiology
PhysiologyNeurophysiology
Transmission of an action potential. This occurs in two ways:
1) across the synapse - synaptic transmission. This is a chemical process, the result of a chemical neurotransmitter.
2) along the axon - membrane transmission. This is the propagation of the action potential itself along the membrane of the axon.
Synaptic transmission - What you learned about the neuromuscular junction is mostly applicable here as well. The major differences in our current discussion are:
1) Transmission across the synapse does not necessarily result in an action potential. Instead, small local potentials are produced which must add together in summation to produce an action potential.
2) Although ACh is a common neurotransmitter, there are many others and the exact effect at the synapse depends on the neurotransmitter involved.
3) Neurotransmitters can be excitatory or inhibitory. The result might be to turn off the next neuron rather than to produce an action potential
The basic steps of synaptic transmission are the same as described at the neuromuscular junction
1) Impulse arrives at the axon terminus causing opening of Ca2+ channels and allows Ca2+ to enter the axon. The calcium ions are in the extracellular fluid, pumped there much like sodium is pumped. Calcium is just an intermediate in both neuromuscular and synaptic transmission.
2) Ca2+ causes vesicles containing neurotransmitter to release the chemical into the synapse by exocytosis across the pre-synaptic membrane.
3) The neurotransmitter binds to the post-synaptic receptors. These receptors are linked to chemically gated ion channels and these channels may open or close as a result of binding to the receptors to cause a graded potential which can be either depolarization, or hyperpolarization depending on the transmitter. Depolarization results from opening of Na+ gates and is called an EPSP. Hyperpolarization could result from opening of K+ gates and is called IPSP.
4) Graded potentials spread and overlap and can summate to produce a threshold depolarization and an action potential when they stimulate voltage gated ion channels in the neuron's trigger region.
5) The neurotransmitter is broken down or removed from the synapse in order for the receptors to receive the next stimulus. As we learned there are enzymes for some neurotransmitters such as the Ach-E which breaks down acetylcholine. Monoamine oxidase (MAO) is an enzyme which breaks down the catecholamines (epinephrine, nor-epinephrine, dopamine) and nor-epinephrine (which is an important autonomic neurotransmitter) is removed by the axon as well in a process known as reuptake. Other transmitters may just diffuse away.
Graded Potentials - these are small, local depolarizations or hyperpolarizations which can spread and summate to produce a threshold depolarization. Small because they are less than that needed for threshold in the case of the depolarizing variety. Local means they only spread a few mm on the membrane and decline in intensity with increased distance from the point of the stimulus. The depolarizations are called EPSPs, excitatory post-synaptic potentials, because they tend to lead to an action potential which excites or turns the post-synaptic neuron on. Hyperpolarizations are called IPSPs, inhibitory post-synaptic potentials, because they tend to inhibit an action potential and thus turn the neuron off.
Summation - the EPSPs and IPSPs will add together to produce a net depolarization (or hyperpolarization).
Temporal summation- this is analogous to the frequency (wave, tetany) summation discussed for muscle. Many EPSPs occurring in a short period of time (e.g. with high frequency) can summate to produce threshold depolarization. This occurs when high intensity stimulus results in a high frequency of EPSPs.
Spatial summation - this is analogous to quantal summation in a muscle. It means that there are many stimuli occurring simultaneously. Their depolarizations spread and overlap and can build on one another to sum and produce threshold depolarization.
Inhibition - When the brain causes an IPSP in advance of a reflex pathway being stimulated, it reduces the likelihood of the reflex occurring by increasing the depolarization required. The pathway can still work, but only with more than the usual number or degree of stimulation. We inhibit reflexes when allowing ourselves to be given an injection or blood test for instance.
Facilitation - When the brain causes an EPSP in advance of a reflex pathway being stimulated, it makes the reflex more likely to occur, requiring less additional stimulation. When we anticipate a stimulus we often facilitate the reflex.
Learned Reflexes - Many athletic and other routine activities involve learned reflexes. These are reflex pathways facilitated by the brain. We learn the pathways by performing them over and over again and they become facilitated. This is how we can perfect our athletic performance, but only if we learn and practice them correctly. It is difficult to "unlearn" improper techniques once they are established reflexes. Like "riding a bike" they may stay with you for your entire life!
Post-tetanic potentiation - This occurs when we perform a rote task or other repetitive action. At first we may be clumsy at it, but after continuous use (post-tetanic) we become more efficient at it (potentiation). These actions may eventually become learned reflexes
The Action Potential
The trigger region of a neuron is the region where the voltage gated channels begin. When summation results in threshold depolarization in the trigger region of a neuron, an action potential is produced. There are both sodium and potassium channels. Each sodium channel has an activation gate and an inactivation gate, while potassium channels have only one gate.
A) At the resting state the sodium activation gates are closed, sodium inactivation gates are open, and potassium gates are closed. Resting membrane potential is at around -70 mv inside the cell.
B) Depolarizing phase: The action potential begins with the activation gates of the sodium channels opening, allowing Na+ ions to enter the cell and causing a sudden depolarization which leads to the spike of the action potential. Excess Na+ ions enter the cell causing reversal of potential becoming briefly more positive on the inside of the cell membrane.
C) Repolarizing phase: The sodium inactivation gates close and potassium gates open. This causes Na+ ions to stop entering the cell and K+ ions to leave the cell, causing repolarization. Until the membrane is repolarized it cannot be stimulated, called the absolute refractory period.
D) Excess potassium leaves the cell causing a brief hyperpolarization. Sodium activation gates close and potassium gates begin closing. The sodium-potassium pump begins to re-establish the resting membrane potential. During hyperpolarization the membrane can be stimulated but only with a greater than normal depolarization, the relative refractory period.
Action potentials are self-propagated, and once started the action potential progresses along the axon membrane. It is all-or-none, that is there are not different degrees of action potentials. You either have one or you don't.
Hormones of the Pituitary -The Posterior Lobe
Physiology
The Posterior Lobe
The posterior lobe of the pituitary releases two hormones, both synthesized in the hypothalamus, into the circulation.
Antidiuretic Hormone (ADH).
ADH is a peptide of 9 amino acids. It is also known as arginine vasopressin. ADH acts on the collecting ducts of the kidney to facilitate the reabsorption of water into the blood.
A deficiency of ADH
leads to excessive loss of urine, a condition known as diabetes nsipidus.
Oxytocin
Oxytocin is a peptide of 9 amino acids. Its principal actions are:
stimulating contractions of the uterus at the time of birth
stimulating release of milk when the baby begins to suckle