NEET MDS Synopsis
Immunofluorescence
General MicrobiologyImmunofluorescence
This is precipitation or complement fixation tests. The technique can detect proteins at concentrations of around 1 µg protein per ml body fluid. Major disadvantage with this technique is frequent occurrence of nonspecific fluorescence in the tissues and other material.
The fluorescent dyes commonly used are fluorescein isothocyanate (FITC). These dyes exhibit fluorescence by absorbing UV light between 290 and 495 nm and emitting longer wavelength coloured light of 525 nm which gives shining appearance (fluorescence) to protein labelled with dye. Blue green (apple green) fluorescence is seen with FITC and orange red with rhodamine.
Enzyme Immunoassays
These are commonly called as enzyme linked immunosorbent assays or EL1SA. It is a simple and versatile technique which is as sensitive as radioimmunoassays. It is now the
technique for the detection of antigens, antibodies, hormones, toxins and viruses.
Identification of organisms by immunofluorescence
Type of agent Examples
Bacterial Neisseria gonorrhoeae, H. influenzae ,Strept pyogenes, Treponema pallidum
Viral Herpesvirus, Rabiesvirus, Epstein-Barr virus
Mycotic Candida albicans
Enzymatic activity results in a colour change which can be assessed visibly or quantified in a simple spectrophotometer.
Introduction
Dental Materials
Introduction
The science of dental materials involves a study of the composition and properties of materials and the way in which they interact with the environment in which they are placed
Selection of Dental materials
The process of materials selection should ideally follow a logical sequence involving
(1) analysis of the problem,
(2) consideration of requirements,
(3) consideration of available materials and their properties, leading to
(4) choice of material.
Evaluation of the success or failure of a material may be used to influence future decisions on materials selection.
The Effects of Enzyme Inhibitors
Biochemistry
The Effects of Enzyme Inhibitors
Enzymes can be inhibited
competitively, when the substrate and inhibitor compete for binding to the same active site or
noncompetitively, when the inhibitor binds somewhere else on the enzyme molecule reducing its efficiency.
The distinction can be determined by plotting enzyme activity with and without the inhibitor present.
Competitive Inhibition
In the presence of a competitive inhibitor, it takes a higher substrate concentration to achieve the same velocities that were reached in its absence. So while Vmax can still be reached if sufficient substrate is available, one-half Vmax requires a higher [S] than before and thus Km is larger.
Noncompetitive Inhibition
With noncompetitive inhibition, enzyme molecules that have been bound by the inhibitor are taken out
enzyme rate (velocity) is reduced for all values of [S], including
Vmax and one-half Vmax but
Km remains unchanged because the active site of those enzyme molecules that have not been inhibited is unchanged.
Immunosuppressive drugs
PharmacologyImmunosuppressive drugs are essential in managing various medical conditions,
particularly in preventing organ transplant rejection and treating autoimmune
diseases. They can be classified into five main groups:
Glucocorticoids: These are steroid hormones that reduce
inflammation and suppress the immune response. They work by inhibiting the
production of inflammatory cytokines and reducing the proliferation of
immune cells. Common glucocorticoids include prednisone and dexamethasone.
Their effects include:
Mechanism of Action: Glucocorticoids inhibit the
expression of genes coding for pro-inflammatory cytokines (e.g., IL-1,
IL-2, TNF-α).
Clinical Uses: They are used in conditions like
rheumatoid arthritis, lupus, and to prevent transplant rejection.
Side Effects: Long-term use can lead to
osteoporosis, weight gain, diabetes, and increased risk of infections.
Cytostatic Drugs: These agents inhibit cell division and
are often used in cancer treatment as well as in autoimmune diseases. They
include:
Examples: Cyclophosphamide, azathioprine, and
methotrexate.
Mechanism of Action: They interfere with DNA
synthesis and cell proliferation, particularly affecting rapidly
dividing cells.
Clinical Uses: Effective in treating cancers,
systemic lupus erythematosus, and other autoimmune disorders.
Side Effects: Can cause bone marrow suppression,
leading to increased risk of infections and anemia.
Antibodies: This group includes monoclonal and
polyclonal antibodies that target specific components of the immune system.
Types:
Monoclonal Antibodies: Such as basiliximab and
daclizumab, which target the IL-2 receptor to prevent T-cell
activation.
Polyclonal Antibodies: These are derived from
multiple B-cell clones and can broadly suppress immune responses.
Clinical Uses: Used in organ transplantation and to
treat autoimmune diseases.
Side Effects: Risk of infections and allergic
reactions due to immune suppression.
Drugs Acting on Immunophilins: These drugs modulate
immune responses by binding to immunophilins, which are proteins that assist
in the folding of other proteins.
Examples: Cyclosporine and tacrolimus.
Mechanism of Action: They inhibit calcineurin, a
phosphatase involved in T-cell activation, thereby reducing the
production of IL-2.
Clinical Uses: Primarily used in organ
transplantation to prevent rejection.
Side Effects: Nephrotoxicity, hypertension, and
increased risk of infections.
Other Drugs: This category includes various agents that
do not fit neatly into the other classifications but still have
immunosuppressive effects.
Examples: Mycophenolate mofetil and sirolimus.
Mechanism of Action: Mycophenolate inhibits
lymphocyte proliferation by blocking purine synthesis, while sirolimus
inhibits mTOR, affecting T-cell activation and proliferation.
Clinical Uses: Used in transplant patients and in
some autoimmune diseases.
Side Effects: Gastrointestinal disturbances,
increased risk of infections, and potential for malignancies.
Pulp
Dental Anatomy
Pulp
1. Four zones—listed from dentin inward
a. Odontoblastic layer
(1) Contains the cell bodies of odontoblasts.
Note: their processes remain in dentinal tubules.
(2) Capillaries, nerve fibers, and dendritic cells may also be present.
b. Cell-free or cell-poor zone (zone of Weil)
(1) Contains capillaries and unmyelinated nerve fibers.
c. Cell-rich zone
(1) Consists mainly of fibroblasts. Macrophages, lymphocytes, and dendritic cells may also be present.
d. The pulp (pulp proper, central zone)
(1) The central mass of the pulp.
(2) Consists of loose connective tissue, larger vessels, and nerves. Also contains fibroblasts and pulpal cells.
2. Pulpal innervation
a. When pulpal nerves are stimulated, they can only transmit one signal pain.
b. There are no proprioceptors in the pulp.
c. Types of nerves:
(1) A-delta fibers
(a) Myelinated sensory nerve fibers.
(b) Stimulation results in the sensation of fast, sharp pain.
(c) Found in the coronal (odontoblastic) area of the pulp.
(2) C-fibers
(a) Unmyelinated sensory nerve fibers.
(b) Transmits information of noxious stimuli centrally.
(c) Stimulation results in pain that is slower, duller, and more diffuse in nature.
(d) Found in the central region of the pulp.
(3) Sympathetic fibers
(a) Found deeper within the pulp.
(b) Sympathetic stimulation results in vasoconstriction of vessels.
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.
Antiarrhythmic Drugs-Class II Beta Blockers
Pharmacology
Class II Beta Blockers
Block SNS stimulation of beta receptors in the heart and decreasing risks of ventricular fibrillation
– Blockage of SA and ectopic pacemakers: decreases automaticity
– Blockage of AV increases the refractory period
- Increase AV nodal conduction ´
- Increase PR interval
- Reduce adrenergic activity
Treatment: Supraventricular tachycardia (AF, flutter, paroxysmal supraventricular tachycardia
– Acebutolol
– Esmolol
– Propanolol
Contraindications and Cautions
• Contraindicated in sinus bradycardia P < 45
• Cardiogenic shock, asthma or respiratory depression which could be made worse by the blocking of Beta receptors.
• Use cautiously in patients with diabetes and thyroid dysfunction, which could be altered by the blockade of Beta receptors
• Renal and hepatic dysfunction could alter the metabolism and excretion of these drugs.
Ketoprofen
Pharmacology
Ketoprofen
It acts by inhibiting the body's production of prostaglandin.