NEET MDS Synopsis
CHRONIC INFLAMMATlON
General Pathology
CHRONIC INFLAMMATlON
When the inflammatory reaction instead of subsiding after the acute phase (or without entering an acute phase), persists as a smouldering lesion, it is called chronic inflammation. .
Characteristics
Predominantly mononuclear response.
Inflamation.and..repair going on simultaneously.
Usually results in more prominent-scarring.
Causes:
Chronicity may be due to :
- Defective defence mechanisms.
- Persistence of injurious agent.
(a) Certain organisms resist phagocytosis and destruction e.g tubercle bacillus, fungi
(b) insoluble particulate matter e.g., crystals. fibres suture materials.
(c) Constants supply of causative agent as in autoimmune disease where body reacts against its own tissues.
- Defective healing.
Granulomatous inflammation
It is a type of chronic inflammation characterised by localised collections of histiocytes.
These cells are usually accompanied by lymphocytes, fibroblasts and giant cells also.
Granulomas are characteristically seen in diseases like tuberculosis. syphilis, leprosy, sarcoidosis, fungal infections etc. In some of these, the lesion is morphologically distinct enough to point to the type of underlying disease. These are sometimes called' specific' granulomas. Granulomas can also be elicited by particulate, insoluble foreign material e.g. granuloma, suture granuloma, cholesterol granuloma (organising haemorrhages).
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.
Appendicular Skeleton -Upper extremity
AnatomyAppendicular Skeleton
Upper extremity
• Shoulder-clavicle and scapula
Clavicle
Articulates with the manubrium at the sternal end
Articulates with the scapula at the lateral end
Slender S-shaped bone that extends horizontally across the upper part of the thorax
Scapula
Triangular bone with the base upward and the apex downward
Lateral aspect contains the glenoid cavity that articulates with the head of the humerus
Spine extends across the upper part of the posterior surface; expands laterally and
forms the acromion (forms point of shoulder)
Coracoid process projects anteriorly from the upper part of the neck of the scapula
Arm (humerus)
Consists of a shaft (diaphysis) and two ends (epiphyses)
Proximal end has a head that articulates with the glenoid fossa of the scapula
Greater and lesser tubercles lie below the head
Intertubercular groove is located between them; long tendon of the biceps attaches here
Surgical neck is located below the tubercles
o Radial groove runs obliquely on the posterior surface; radial nerve is located here
o Deltoid muscles attaches in a V-shaped area in the middle of the shaft. called the deltoid tuberosity
Distal end has two projections. the medial and lateral epicondyles
Capitulum-articulates with the radius
Trochlea-articulates with the ulqa
Forearm
Radius
Lateral bone of the forearm
Radial tuberosity is located below the head on the medial side
Distal end is broad for articulation with the wrist: has a styloid process on its lateral side
Ulna
Medial side of the forearm
Conspicuous part of the elbow joint (olecranon)
Curved surface that articulates with the trochlea of the humerus is the trochlearnotch
Lateral ide is concave (radial notch); articulates with the head of the radius Distal end contains the styloid process
Distal end contains the styloid process
Hand
Carpal bones (8)
Aranged in two rows of four
Scaphoid. lunate. triquetral. and pisiform proximal row); trapezium. trapezoid.
capitate. and hamate (distal row)
Metacarpal bones (5)
Framework of the hand
Numbered 1 to 5 beginning on the lateral side
Phalanges (14)
Fingers
Three phalanges in each finger; two phalanges in the thumb
Approaches to the Oral Cavity in Oral Cancer Treatment
Oral and Maxillofacial SurgeryApproaches to the Oral Cavity in Oral Cancer Treatment
In the management of oral cancer, surgical approaches are tailored to the
location and extent of the lesions. The choice of surgical technique is crucial
for achieving adequate tumor resection while preserving surrounding structures
and function. Below are the primary surgical approaches used in the treatment of
oral cancer:
1. Peroral Approach
Indication: This approach is primarily used for small,
anteriorly placed lesions within the oral cavity.
Technique: The surgeon accesses the lesion directly
through the mouth without external incisions. This method is less invasive
and is suitable for superficial lesions that do not require extensive
resection.
Advantages:
Minimal morbidity and scarring.
Shorter recovery time.
Limitations: Not suitable for larger or posterior
lesions due to limited visibility and access.
2. Lip Split Approach
Indication: This approach is utilized for posteriorly
based lesions in the gingivobuccal complex and for performing marginal
mandibulectomy.
Technique: A vertical incision is made through the lip,
allowing for the elevation of a cheek flap. This provides better access to
the posterior aspects of the oral cavity and the mandible.
Advantages:
Improved access to the posterior oral cavity.
Facilitates the removal of larger lesions and allows for better
visualization of the surgical field.
Limitations: Potential for cosmetic concerns and longer
recovery time compared to peroral approaches.
3. Pull-Through Approach
Indication: This technique is particularly useful for
lesions of the tongue and floor of the mouth, especially when the posterior
margin is a concern for peroral excision.
Technique: The lesion is accessed by pulling the tongue
or floor of the mouth forward, allowing for better exposure and resection of
the tumor while ensuring adequate margins.
Advantages:
Enhanced visibility and access to the posterior margins of the
lesion.
Allows for more precise excision of tumors located in challenging
areas.
Limitations: May require additional incisions or
manipulation of surrounding tissues, which can increase recovery time.
4. Mandibulotomy (Median or Paramedian)
Indication: This approach is indicated for tongue and
floor of mouth lesions that are close to the mandible, particularly when
achieving a lateral margin of clearance is critical.
Technique: A mandibulotomy involves making an incision
through the mandible, either in the midline (median) or slightly off-center
(paramedian), to gain access to the oral cavity and the lesion.
Advantages:
Provides excellent access to deep-seated lesions and allows for
adequate resection with clear margins.
Facilitates reconstruction if needed.
Limitations: Higher morbidity associated with
mandibular manipulation, including potential complications such as nonunion
or malocclusion.
Neural Substrates of Breathing
PhysiologyNeural Substrates of Breathing
A. Medulla Respiratory Centers
Inspiratory Center (Dorsal Resp Group - rhythmic breathing) → phrenic nerve→ intercostal nerves→ diaphragm + external intercostals
Expiratory Center (Ventral Resp Group - forced expiration) → phrenic nerve → intercostal nerves → internal intercostals + abdominals (expiration)
1. eupnea - normal resting breath rate (12/minute)
2. drug overdose - causes suppression of Inspiratory Center
B. Pons Respiratory Centers
1. pneumotaxic center - slightly inhibits medulla, causes shorter, shallower, quicker breaths
2. apneustic center - stimulates the medulla, causes longer, deeper, slower breaths
C. Control of Breathing Rate & Depth
1. breathing rate - stimulation/inhibition of medulla
2. breathing depth - activation of inspiration muscles
3. Hering-Breuer Reflex - stretch of visceral pleura that lungs have expanded (vagal nerve)
D. Hypothalamic Control - emotion + pain to the medulla
E. Cortex Controls (Voluntary Breathing) - can override medulla as during singing and talking
INTRAARCH AND INTERARCH RELATIONSHIPS
Dental Anatomy
lntraarch relationship refers to the alignment of the teeth within an arch
1. In an ideal alignment teeth should contact at their proximal crests of curvature. A continuous arch form is observed in occlusal view
Curves of the occlusal plane (a line connecting the cusp tips of the canines, premolars, and molars) are observed from the proximal view
Curve of Spee: anterior to posterior curve; for mandibular teeth the curve is concave and for maxillary teeth it is convex
Curve of Wilson- medial to lateral curve for mandibular teeth the curve is also convex and for the maxillary it is convex
2. Contact does not always exist Some permanent dentitions have normal spacing
Primary dentitions often have developmental spacing in the anterior area: some primary den titions have a pattern of spacing called primate spaces between the primary maxillary lateral incisors and canine and between the mandibular canine and first mo1ar
Disturbances to the intraarch alignment are described as
a. Qpen contact where interproximal space exist because of missing teeth oral habits, dental disease, or overdeveloped frena
b. where contact or position is at an unexpected area because of developmental disturbances, crowding, dental caries or periodontal ligament for their misplaced position: facial, lingual. mesial, supra(supraerupted) infra (infraerupted) and torso (rotated) version
Aneurysm
General Pathology
Aneurysm
An aneurysm is a localized abnormal dilation of a blood vessel or the heart
Types:
1. True aneurysm - it involves all three layers of the arterial wall (intima, media, and adventitia) or the attenuated wall of the heart.
e.g. Atherosclerotic, syphilitic, and congenital aneurysms, and ventricular aneurysms that follow transmural myocardial infarctions.
2 False aneurysm
(also called pseudo-aneurysm) is a breach in the vascular wall leading to an extravascular hematoma that freely communicates with the intravascular space ("pulsating hematoma").
E.g. ventricular ruptures after MI that are contained by a pericardial adhesion
E.g. a leak at the junction of a vascular graft with a natural artery.
Aneurysms are classified by macroscopic shape and size
Saccular aneurysms
spherical outpouchings (involving only a portion of the vessel wall, and often contain thrombi.
Fusiform aneurysms
diffuse, circumferential dilation of a long vascular segment;
they vary in diameter and length and can involve extensive portions of the aortic arch, abdominal aorta, or even the iliacs.
Aortic Aneurysm
The two most important causes are:
1- atherosclerosis : the most common cause
It causes thinning and weakening of the media. The intimal plaques compress the underlying media and also compromise nutrient and waste diffusion from the vascular lumen into the arterial wall. The media consequently undergoes degeneration and necrosis, thus allowing the dilation of the vessel
2- cystic medial degeneration of the arterial media. E.g. Marfan syndrome.
3- Other causes include: trauma, congenital defects (e.g., berry aneurysms), infections (mycotic aneurysms), systemic diseases, such as vasculitis.
Mycotic Aneurysm :
Infection of a major artery that weakens its wall is called a mycotic aneurysm
possible complications: thrombosis and rupture.
It can originate from:
(1) embolization of a septic thrombus, usually as a complication of infective endocarditis
(2) extension of an adjacent suppurative process;
(3) circulating organisms directly infecting the arterial wall
Mycotic AAAs are atherosclerotic lesions infected by lodging of circulating microorganisms in the wall
- e.g. bacteremia from a primary Salmonella gastroenteritis.
Abdominal Aortic Aneurysm
Atherosclerotic aneurysms occur most frequently in the abdominal aorta ,the common iliac arteries, the arch, and descending parts of the thoracic aorta can also be involved
Pathogenesis
AAA occurs more frequently in men and rarely develops before age 50.
Atherosclerosis is a major cause of AAA
hereditary defects in structural components of the aorta (e.g., defective fibrillin production in Marfan disease affects elastic tissue synthesis)
Morphology :
Usually positioned below the renal arteries and above the bifurcation of the aorta
AAA can be saccular or fusiform
as large as 15 cm in diameter, and as long as 25 cm.
Microscopically: atherosclerosis with destruction and thinning of the underlying aortic media
the aneurysm frequently contains a laminated mural thrombus
Syphilitic Aneurysm
Caused by The spirochetes T. pallidum
Tertiary stage of syphilis can cause obliterative endarteritis of the involve small vessels in any part of the body, including the vasa vasorum of the aorta
This results in ischemic medial injury, leading to aneurysmal dilation of the aorta and aortic annulus, and eventually valvular insufficiency.
valvular insufficiency and massive volume overload lead to hypertrophy of the left ventricle. The greatly enlarged hearts are sometimes called "cor bovinum" (cow's heart).
CLINICAL CONSEQUENCES
1. Rupture → massive potentially fatal hemorrhage
2. Obstruction of downstream vessel → tissue ischemic injury
3. Embolism → from atheroma or mural thrombus
4. Impingement and compression on an adjacent structure
5. Presentation as an abdominal mass
Late mandibular growth
OrthodonticsLate mandibular growth refers to the continued development
and growth of the mandible (lower jaw) that occurs after the typical growth
spurts associated with childhood and adolescence. While most of the significant
growth of the mandible occurs during these early years, some individuals may
experience additional growth in their late teens or early adulthood.
Understanding the factors influencing late mandibular growth, its implications,
and its relevance in orthodontics and dentistry is essential.
Factors Influencing Late Mandibular Growth
Genetics:
Genetic factors play a significant role in determining the timing
and extent of mandibular growth. Family history can provide insights
into an individual's growth patterns.
Hormonal Changes:
Hormonal fluctuations, particularly during puberty, can influence
growth. Growth hormone, sex hormones (estrogen and testosterone), and
other endocrine factors can affect the growth of the mandible.
Functional Forces:
The forces exerted by the muscles of mastication, as well as
functional activities such as chewing and speaking, can influence the
growth and development of the mandible.
Environmental Factors:
Nutritional status, overall health, and lifestyle factors can impact
growth. Adequate nutrition is essential for optimal skeletal
development.
Orthodontic Treatment:
Orthodontic interventions can influence mandibular growth patterns.
For example, the use of functional appliances may encourage forward
growth of the mandible in growing patients.
Clinical Implications of Late Mandibular Growth
Changes in Occlusion:
Late mandibular growth can lead to changes in the occlusal
relationship between the upper and lower teeth. This may result in the
development of malocclusions or changes in existing malocclusions.
Facial Aesthetics:
Continued growth of the mandible can affect facial aesthetics,
including the profile and overall balance of the face. This may be
particularly relevant in individuals with a retrognathic (recessed)
mandible or those seeking cosmetic improvements.
Orthodontic Treatment Planning:
Understanding the potential for late mandibular growth is crucial
for orthodontists when planning treatment. It may influence the timing
of interventions and the choice of appliances used to guide growth.
Surgical Considerations:
In some cases, late mandibular growth may necessitate surgical
intervention, particularly in adults with significant skeletal
discrepancies. Orthognathic surgery may be considered to correct jaw
relationships and improve function and aesthetics.
Monitoring Late Mandibular Growth
Clinical Evaluation:
Regular clinical evaluations, including assessments of occlusion,
facial symmetry, and growth patterns, are essential for monitoring late
mandibular growth.
Radiographic Analysis:
Cephalometric radiographs can be used to assess changes in
mandibular growth and its relationship to the craniofacial complex. This
information can guide treatment decisions.
Patient History:
Gathering a comprehensive patient history, including growth patterns
and any previous orthodontic treatment, can provide valuable insights
into late mandibular growth.