NEET MDS Synopsis
Respiratory system
PhysiologyRespiratory system plays important role in maintaining homeostasis . Other than its major function , which is supplying the cells with needed oxygen to produce energy and getting rid of carbon dioxide , it has other functions :
1 Vocalization , or sound production.
2 Participation in acid base balance .
3 Participation in fluid balance by insensible water elimination (vapors ).
4 Facilitating venous return .
5 Participation in blood pressure regulation : Lungs produce Angiotensin converting enzyme ( ACE ) .
6 Immune function : Lungs produce mucous that trap foreign particles , and have ciliae that move foreign particles away from the lung. They also produce alpha 1 antitrepsin that protect the lungs themselves from the effect of elastase and other proteolytic enzymes
Salivary gland pathology
General Pathology
Salivary gland pathology
Inflammation
a. Sialolithiasis produces a secondary inflammatory reaction to obstruction and the resultant enlargement of ducts by stones. It may be complicated by actual infection with mouth flora.
b. Sialadenitis is a primary inflammatory reaction, but it is not always infectious. It may be part of an autoimmune disease (e.g., Sjogren's syndrome), or the result of bacterial or virals (e.g., mumps) infection.
Sjögren’s syndrome
a. An autoimmune disease of the salivary and lacrimal glands.
b. Autonuclear antibodies (ANAs) against salivary ducts may be seen.
c. Triad of symptoms include:
(1) Xerostomia—from decreased saliva production.
(2) Keratoconjunctivitis sicca (dry eyes)—from decreased tear production.
(3) Rheumatoid arthritis.
(4) Enlargement of the salivary or lacrimal glands, known as Mikulicz syndrome, may also be observed.
d. Histologically, a dense infiltration of the gland by lymphocytes is observed.
Tumors
The parotid gland accounts for more than three-quarters of these tumors, most of which are benign. Of the remainder, more occur in the submandibular gland than in the sublingual, and most of these are malignant. Many are surgically, cured, but local recurrence is common.
a. Pleomorphic adenoma is generally benign and accounts for approximately three-quarters of all salivary gland tumors. If is composed of multiple epithelial and mesenchymal cell types. Complications may arise due to involvement of cranial nerve VII.
(a) The most common salivary gland tumor.
(b) Is benign.
(c) Prognosis is good after proper surgical excision.
b. Warthin's tumor (adenolymphoma) is also benign, occuring almost exclusively in the parotid gland. It is grossly cystic.
Microscopic examination reveals cell types suggestive of branchial cleft origin embedded in a lymphoid matrix.
c. Mucoepidermoid tumors also occur primarily in the parotid and have a high rate of malignant transformation.The malignant component is usually squamous cell. Prognosis of tumor depends on grade and stage of disease.
d. Cylindroma (adenoid cysticc. Mucoepidermoid tumors carcinoma) is more common in the minor salivary glands found in the oral mucosa, and metastases are more common than in other tumors of the salivary glands. Facial nerve complications are frequent.
(1) Grossly, the tumor forms multiple lobules surrounded by a capsule.
(2) Microscopically, small cells form glands containin mucoid material
AUTOCOIDS
Pharmacology
AUTOCOIDS
An organic substance, such as a hormone, produced in one part of organism and transported by the blood or lymph to another part of the organism where it exerts a physiologic effect on that part.
TYPES OF AUTACOIDS:
Amines : Histamine,5-Hydroxytryptamine.
Lipids : Prostaglandins, Leukotriens, Platelet activating factor.
Peptide : Bradykinin , angiotensin.
Piroxicam
Pharmacology
Piroxicam:
Half‐life of 45 hrs. Once‐daily dosing. Delay onset of action.
High doses inhibits PMN migration, decrease oxygen radical production, inhibits lymphocyte function.
used to relieve the symptoms of arthritis, primary dysmenorrhoea, pyrexia; and as an analgesic,non-selective cyclooxygenase (COX) inhibitor
The risk of adverse side efects is nearly ten times higher than with other NSAIDs. Peptic ulcer (9.5 higher)
Events in Muscle Contraction
PhysiologyEvents in Muscle Contraction - the sequence of events in crossbridge formation:
1) In response to Ca2+ release into the sarcoplasm, the troponin-tropomyosin complex removes its block from actin, and the myosin heads immediately bind to active sites.
2) The myosin heads then swivel, the Working Stroke, pulling the Z-lines closer together and shortening the sarcomeres. As this occurs the products of ATP hydrolysis, ADP and Pi, are released.
3) ATP is taken up by the myosin heads as the crossbridges detach. If ATP is unavailable at this point the crossbridges cannot detach and release. Such a condition occurs in rigor mortis, the tensing seen in muscles after death, and in extreme forms of contracture in which muscle metabolism can no longer provide ATP.
4) ATP is hydrolyzed and the energy transferred to the myosin heads as they cock and reset for the next stimulus.
Excitation-Contraction Coupling: the Neuromuscular Junction
Each muscle cell is stimulated by a motor neuron axon. The point where the axon terminus contacts the sarcolemma is at a synapse called the neuromuscular junction. The terminus of the axon at the sarcolemma is called the motor end plate. The sarcolemma is polarized, in part due to the unequal distribution of ions due to the Sodium/Potassium Pump.
1) Impulse arrives at the motor end plate (axon terminus) causing Ca2+ to enter the axon.
2) Ca2+ binds to ACh vesicles causing them to release the ACh (acetylcholine) into the synapse by exocytosis.
3) ACH diffuses across the synapse to bind to receptors on the sarcolemma. Binding of ACH to the receptors opens chemically-gated ion channels causing Na+ to enter the cell producing depolarization.
4) When threshold depolarization occurs, a new impulse (action potential) is produced that will move along the sarcolemma. (This occurs because voltage-gated ion channels open as a result of the depolarization -
5) The sarcolemma repolarizes:
a) K+ leaves cell (potassium channels open as sodium channels close) returning positive ions to the outside of the sarcolemma. (More K+ actually leaves than necessary and the membrane is hyperpolarized briefly. This causes the relative refractory period) (b) Na+/K+ pump eventually restores resting ion distribution. The Na+/K+ pump is very slow compared to the movement of ions through the ion gates. But a muscle can be stimulated thousands of times before the ion distribution is substantially affected.
6) ACH broken down by ACH-E (a.k.a. ACHase, cholinesterase). This permits the receptors to respond to another stimulus.
Excitation-Contraction Coupling:
1) The impulse (action potential) travels along the sarcolemma. At each point the voltaged-gated Na+ channels open to cause depolarization, and then the K+ channels open to produce repolarization.
2) The impulse enters the cell through the T-tublules, located at each Z-disk, and reach the sarcoplasmic reticulum (SR), stimulating it.
3) The SR releases Ca2+ into the sarcoplasm, triggering the muscle contraction as previously discussed.
4) Ca2+ is pumped out of the sarcoplasm by the SR and another stimulus will be required to continue the muscle contraction.
Chemical Mediators In Inflammation
General Pathology
Chemical Mediators In Inflammation
Can be classified as :
A. Neurogenic
Also called the Triple Response of Lewis. It involves neurogenic vasodilatation of arterioles due to antidromic axon reflex arc. The constituents of the response are:
1. arteriolar vasoconstriction followed by
2. arteriolar vasodilatation
3. swelling
B. Chemical
1. Amines: Histamine and 5 hydroxytryptamine. Released from platelets and mast cells.
Actions: Immediate and short lived.
Dilatation of arterioles.
Increased capillary premeability.
Kinins: Bradykinin and kallidin These are present in inactive from and are activated by kinin forming proteases
Actions:
Arteriolar dilatation.
Increased vascular permeability
Pain
Kinin forming proteases Plasmin and Kallikrein. Present as inactive precursors.
Cleavage products of complement C3a und C5a are called anaphylatoxins
Actions:
Histamine release from mast cells
Chemotaxis (also C567 )
Enhance phagocytosis.
Polymorph components
Cationic: proteins which cause
Increased permeability
Histamine release.
Chemotaxis of monocytes
Neutral proteases which:
Cleave C3 and C5 to active form
Convert Kininogen to Kinin
Increase permeability.
Acid proteases which liberate leucokinins
Slow reacting. substance of anaphylaxis: (SRS-A) is a lipid released from mast cell.
Action --Increases vascular permeability
Prostaglandins: E1 + E2 .
Platelets are rich source
Action:
Platelets are a rich source.
Vasodilatation.
Increased permeability.
Pain.
VIII. Miscellaneous: like
Tissue lactic acid.
Bacterial toxins.
Basic Principles of Treatment of a Fracture
Oral and Maxillofacial SurgeryBasic Principles of Treatment of a Fracture
The treatment of fractures involves a systematic approach to restore the
normal anatomy and function of the affected bone. The basic principles of
fracture treatment can be summarized in three key steps: reduction, fixation,
and immobilization.
1. Reduction
Definition: Reduction is the process of restoring the
fractured bone fragments to their original anatomical position.
Methods of Reduction:
Closed Reduction: This technique involves
realigning the bone fragments without direct visualization of the
fracture line. It can be achieved through:
Reduction by Manipulation: The physician uses
manual techniques to manipulate the bone fragments into alignment.
Reduction by Traction: Gentle pulling forces
are applied to align the fragments, often used in conjunction with
other methods.
Open Reduction: In some cases, if closed reduction is
not successful or if the fracture is complex, an open reduction may be
necessary. This involves surgical exposure of the fracture site to directly
visualize and align the fragments.
2. Fixation
Definition: After reduction, fixation is the process of
stabilizing the fractured fragments in their normal anatomical relationship to
prevent displacement and ensure proper healing.
Types of Fixation:
Internal Fixation: This involves the use of devices
such as plates, screws, or intramedullary nails that are placed inside
the body to stabilize the fracture.
External Fixation: This method uses external
devices, such as pins or frames, that are attached to the bone through
the skin. External fixation is often used in cases of open fractures or
when internal fixation is not feasible.
Goals of Fixation: The primary goals are to maintain the
alignment of the bone fragments, prevent movement at the fracture site, and
facilitate healing.
3. Immobilization
Definition: Immobilization is the phase during which the
fixation device is retained to stabilize the reduced fragments until clinical
bony union occurs.
Duration of Immobilization: The length of the
immobilization period varies depending on the type of fracture and the bone
involved:
Maxillary Fractures: Typically require 3 to
4 weeks of immobilization.
Mandibular Fractures: Generally require 4
to 6 weeks of immobilization.
Condylar Fractures: Recommended immobilization
period is 2 to 3 weeks to prevent temporomandibular
joint (TMJ) ankylosis.
Classification
Pharmacology
Classification Based on
a. Chemical structure
I. Sulphonamidcs.and others - c.g.. sulphadiazine. etc.
2. Beta-lactum ring - e.g.. penicillin
3. Tetracycline - e.g.. Oxytetracycline,.doxycycline.etc.
b. Mechanism of action
1. Inhibits cell-wall synthesis - penicillin. cephalosporin..cycloserine. etc.
2. Cause leakage from cell-membrane – polypeptides (polymyxin, Bacitracin), polyenes (Nystatin)
3. Inhibit protein synthesis - tetracyclines. chloramphenicols. erythromycin.
4. Cause mis-reading of mRNA code - aminoglycosides
5. Interfere with DNA function - refampicin.. metronidazole
6. Interfere with intermediary metabolism - sulphonamides. ethambutole
c. Type of organism against which it is primarily activate
I. Antibacterial - penicillin.
2. Antifungal - nystatin.
d. Spectrum of activity
1. Broad spectrum - tetracylines .
2. Narrow spectrum - penicillin G (penG). streptomycin.erythromycin
e. Type of action
I. Bacteriostatic - sulphonamides, erythromycin.tertracyclines
2. Bacteriocidal - penicillin. aminoglycoside
f. Source
I. Fungi - penicillin. cephalosporins
2. Bacteria - Polymyxin B