NEET MDS Synopsis
Autoimmune Diseases
General Pathology
Autoimmune Diseases
These are a group of disease where antibodies (or CMI) are produced against self antigens, causing disease process.
Normally one's immune competent cells do not react against one's own tissues. This is due to self tolerance acquired during embryogenesis. Any antigen encountered at that stage is recognized as self and the clone of cells capable of forming the corresponding antibody is suppressed.
Mechanism of autoimmunity
(1) Alteration of antigen
-Physicochemical denaturation by UV light, drugs etc. e.g. SLE.
- Native protein may turn antigenic when a foreign hapten combines with it, e.g. Haemolytic anemia with Alpha methyl dopa.
(2) Cross reaction: Antibody produced against foreign antigen may cross react with native protein because of partial similarity e.g. Rheumatic fever.
(3) Exposure of sequestered antigens: Antigens not normally exposed to immune competent cells are not accepted as self as tolerance has not been developed to them. e.g. thyroglobulin, lens protein, sperms.
(4) Breakdown of tolerance :
Emergence of forbidden clones (due to neoplasia of immune system as in lymphomas and lymphocytic leukaemia)
Loss of suppressor T cells as in old age and CMI defects
Autoimmunity may be
Organ specific.
Non organ specific (multisystemic)
I. Organ specific
(1) Hemolytic anaemia:
Warm or cold antibodies (active at 37° C or at colder temperature)
They may lyse the RBC by complement activation or coat them and make them vulnerable to phagocytosis
(2) Hashimoto's thyroiditis:
Antibodies to thyroglobulin and microsomal antigens.
Cell mediated immunity.
Leads to chronic. destructive thyroiditis.
(3) Pernicious anemia
Antibodies to gastric parietal cells and to intrinsic factor.
2. Non organ specific.
Lesions are seen in more than one system but principally affect blood vessels and
connective tissue (collagen diseases).
1. Systemic lupus erythematosus (SLE). Antibodies to varied antigens are seen. Hence it is possible that there is abnormal reactivity of the immune system in self recognition.
Antibodies have been demonstrated against:
Nuclear material (antinuclear I antibodies) including DNA. nucleoprotein etc. Anti nuclear antibodies are demonstrated by LE cell test.
Cytoplasmic organelles- mitochondria, rib osomes, Iysosomes.
Blood constituents like RBC, WBC. platelets, coagulation factors.
Mechanism. Immune complexes of body proteins and auto antibodies deposit in various
organs and cause damage as in type III hypersensitivity
Organs involved
Skin- basal dissolution and collagen degeneration with fibrinoid vasculitis.
Heart- pancarditis.
Kidneys- glomerulonephritis of focal, diffuse or membranous type
Joints- arthritis.
Spleen- perisplenitis and vascular thickening (onion skin).
Lymph nodes- focal necrosis and follicular hyperplasia.
Vasculitis in other organs like liver, central or peripheral nervous system etc,
2. Polyarteritis nodosa. Remittant .disseminated necrotising vasculitis of small and medium sized arteries
Mechanism :- Not definitely known. Proposed immune reaction to exogenous or auto antigens
Lesion : Focal panarteritis- a segment of vessel is involved. There is fibrinoid necrosis
with initially acute and later chronic inflammatory cells. This may result in haemorrhage
and aneurysm.
Organs involved. No organ or tissue is exempt but commonly involved organs are :
- Kidneys.
- Heart.
- Spleen.
- GIT
3. Rheumatoid arthritis. A disease primarily of females in young adult life.
Antibodies
- Rheumatoid factor (An IgM antibody to self IgG)
- Antinuclear antibodies in 20% patients.
Lesions
- Arthritis which may progress on to a crippling deformity.
- Arteritis in various organs- heart, GIT, muscles.
- Pleuritis and fibrosing alveolitis.
- Amyloidosis is an important complication.
4. Sjogren's Syndrome. This is constituted by
- Kerato conjunctivitis sicca
-Xerostomia
-Rheumatoid arthritis.
Antibodies
- Rheumatoid factor
- Antinuclear factors (70%).
- Other antibodies like antithyroid, complement fixing Ab etc
- Functional defects in lymphocytes. There is a higher incidence of lymphoma
5. Scleroderma (Progressive systemic sclerosis)
Inflammation and progressive sclerosis of connective tissue of skin and viscera.
Antibodies
- Antinuclear antibodies.
- Rheumatoid factor. .
- Defect is cell mediated.
lesions
Skin- depigmentation, sclerotic atrophy followed by cakinosis-claw fingers and mask face.
Joints-synovitis with fibrosis
Muscles- myositis.
GIT- diffuse fibrous replacement of muscularis resulting in hypomotility and malabsorption
Kidneys changes as in SLE and necrotising vasculitis.
Lungs – fibrosing alveolitis.
Vasculitis in any organ or tissue.
6.Wegener’s granulomatosis. A complex of:
Necrotising lesions in upper respiratory tract.
Disseminated necrotising vasculitis.
Focal or diffuse glomerulitis.
Mechanism. Not known. It is classed with autoimmune diseases because of the vasculitis resembling other immune based disorders.
Angle's Classification of Malocclusion
OrthodonticsAngle's Classification of Malocclusion
Developed by Dr. Edward Angle in the early 20th century, this classification
is based on the relationship of the first molars and the canines. It is divided
into three main classes:
Class I Malocclusion (Normal Occlusion)
Description: The first molars are in a normal
relationship, with the mesiobuccal cusp of the maxillary first molar fitting
into the buccal groove of the mandibular first molar. The canines also have
a normal relationship.
Characteristics:
The dental arches are aligned.
There may be crowding, spacing, or other dental irregularities, but
the overall molar relationship is normal.
Class II Malocclusion (Distocclusion)
Description: The first molars are positioned such that
the mesiobuccal cusp of the maxillary first molar is positioned more than
one cusp width ahead of the buccal groove of the mandibular first molar.
Subdivisions:
Class II Division 1: Characterized by protruded
maxillary incisors and a deep overbite.
Class II Division 2: Characterized by retroclined
maxillary incisors and a deep overbite, often with a normal or reduced
overjet.
Characteristics: This class often results in an
overbite and can lead to aesthetic concerns.
Class III Malocclusion (Mesioocclusion)
Description: The first molars are positioned such that
the mesiobuccal cusp of the maxillary first molar is positioned more than
one cusp width behind the buccal groove of the mandibular first molar.
Characteristics:
This class is often associated with an underbite, where the lower
teeth are positioned more forward than the upper teeth.
It can lead to functional issues and aesthetic concerns.
2. Skeletal Classification
In addition to Angle's classification, malocclusion can also be classified
based on skeletal relationships, which consider the position of the maxilla and
mandible in relation to each other. This classification is particularly useful
in assessing the underlying skeletal discrepancies that may contribute to
malocclusion.
Class I Skeletal Relationship
Description: The maxilla and mandible are in a normal
relationship, similar to Class I malocclusion in Angle's classification.
Characteristics: The skeletal bases are well-aligned,
but there may still be dental irregularities.
Class II Skeletal Relationship
Description: The mandible is positioned further back
relative to the maxilla, similar to Class II malocclusion.
Characteristics: This can be due to a retruded mandible
or an overdeveloped maxilla.
Class III Skeletal Relationship
Description: The mandible is positioned further forward
relative to the maxilla, similar to Class III malocclusion.
Characteristics: This can be due to a protruded
mandible or a retruded maxilla.
3. Other Classifications
In addition to Angle's and skeletal classifications, malocclusion can also be
described based on specific characteristics:
Overbite: The vertical overlap of the upper incisors
over the lower incisors. It can be classified as:
Normal Overbite: Approximately 1-2 mm of overlap.
Deep Overbite: Excessive overlap, which can lead to
impaction of the lower incisors.
Open Bite: Lack of vertical overlap, where the
upper and lower incisors do not touch.
Overjet: The horizontal distance between the
labioincisal edge of the upper incisors and the linguoincisal edge of the
lower incisors. It can be classified as:
Normal Overjet: Approximately 2-4 mm.
Increased Overjet: Greater than 4 mm, often
associated with Class II malocclusion.
Decreased Overjet: Less than 2 mm, often associated
with Class III malocclusion.
Crossbite: A condition where one or more of the upper
teeth bite on the inside of the lower teeth. It can be:
Anterior Crossbite: Involves the front teeth.
Posterior Crossbite: Involves the back teeth.
COMPOSITE RESINS -Manipulation
Dental Materials
Manipulation
Selection
o Microfilled composites or hybrids for anterior class III, IV, V
o Hybrids or midifills for posterior class I, II, III, V
Conditioning of enamel and / or dentin
Do not apply fluorides before etching.-->Acid-etch --> Rinse for 20 seconds with water --> Air-dry etched area for 20 seconds but do not desiccate or dehydrate --> Apply bonding agent and polymerize
Mixing (if required)--> mix two pastes for 20 to 30 seconds
o Self-cured composite-working time is 60 to 120 seconds after mixing
o Light-cured composite-working time is unlimited (used for most anterior and some posterior composite restorations)
o Dual-cured composite-working time is > 10 minutes
o Two-stage cured composite-working time is >5 minutes
Placement
use plastic instrument or syringe --> Light curing --> Cure incrementally in <2 mm thick layers. Use matrix strip where possible to produce smooth surface and contour composite .Postcure to improve hardness
Prognosis After Traumatic Brain Injury
Oral and Maxillofacial SurgeryPrognosis After Traumatic Brain Injury (TBI)
Determining the prognosis for patients after a traumatic brain injury
(TBI) is a complex and multifaceted process. Several factors can
influence the outcome, and understanding these variables is crucial for
clinicians in managing TBI patients effectively. Below is an overview of the key
prognostic indicators, with a focus on the Glasgow Coma Scale (GCS) and other
factors that correlate with severity and outcomes.
Key Prognostic Indicators
Glasgow Coma Scale (GCS):
The GCS is a widely used tool for assessing the level of
consciousness in TBI patients. It evaluates three components: eye
opening (E), best motor response (M), and verbal response (V).
Coma Score Calculation:
The total GCS score is calculated as follows: [ \text{Coma
Score} = E + M + V ]
Prognostic Implications:
Scores of 3-4: Patients scoring in this range
have an 85% chance of dying or remaining in a vegetative
state.
Scores of 11 or above: Patients with scores in
this range have only a 5-10% chance of dying or remaining
vegetative.
Intermediate Scores: Scores between these
ranges correlate with proportional chances of recovery, indicating
that higher scores generally predict better outcomes.
Other Poor Prognosis Indicators:
Older Age: Age is a significant factor, with older
patients generally having worse outcomes following TBI.
Increased Intracranial Pressure (ICP): Elevated ICP
is associated with poorer outcomes, as it can lead to brain herniation
and further injury.
Hypoxia and Hypotension: Both conditions can
exacerbate brain injury and are associated with worse prognoses.
CT Evidence of Compression: Imaging findings such
as compression of the cisterns or midline shift indicate significant
mass effect and are associated with poor outcomes.
Delayed Evacuation of Large Intracerebral Hemorrhage:
Timely surgical intervention is critical; delays can worsen the
prognosis.
Carrier Status for Apolipoprotein E-4 Allele: The
presence of this allele has been linked to poorer outcomes in TBI
patients, suggesting a genetic predisposition to worse recovery.
Osmotic diuretics
Pharmacology
Aquaretics
An aquaretic is a class of drug that is used to promote aquaresis, the excretion of water without electrolyte loss.
Lithium, demeclocycline
Mechanism of Action
1. Block ADH action on distal tubule and collecting duct. Blocking ADH decreases H2O permeability. H2O is not recovered (distal tubule) using osmotic draw of counter-current multiplier so aquaretics reduce water reabsorption (tubule to blood stream).
2. Net effect is an increase in free water clearance
Graves disease
General Pathology
Graves disease
Graves disease is an organ-specific autoimmune disorder that results in thyrotoxicosis due to overstimulation of the thyroid gland by autoantibodies.
- It is the most common form of thyrotoxicosis, females being affected more than males by 8: 1.
- It is usually associated with a diffuse enlargement of the thyroid.
Pathogenesis
IgG-type immunoglobulins bind to TSH membrane receptors and cause prolonged stimulation of the thyroid, lasting for as long as 12 hours
(cf. 1 hour for TSH). The autoantibody binds at a site different to the hormone-binding locus and is termed the TSH-receptor autoantibody (TRAb); 95% of Graves’ disease patients are positive for TRAbs
Gross features
- The thyroid gland is diffusely and moderately enlarged
- It is usually smooth, soft, and congested
Histologically
- the gland shows diffuse hypertrophy and hyperplasia of acinar epithelium, reduction of stored colloid and local accumulations of lymphocytes with lymphoid follicle formation.
Clinical features
- Exophthalmos (protrusion of the eyeballs in their sockets)—due to the infiltration of orbital tissues by fat, mucopolysaccharides and lymphocytes. May cause compression of the optic nerve, hence blindness. However, only about 5% of Graves’ patients show signs of exophthalmos.
- Thyroid acropachy—enlargement of fingernails.
- Pretibial myxoedema—accumulation of mucoproteins in the deep dermis of the skin.
Treatment is as for thyrotoxicosis.
Ketorolac
Pharmacology
Ketorolac
Mechanism of action
primary action responsible for its anti-inflammatory/antipyretic/analgesic effects is inhibition of prostaglandin synthesis through inhibition of the enzyme cyclooxygenase (COX). Ketorolac is not a selective inhibitor of COX enzymes
Indications: short-term management of pain
Contraindications
hypersensitivity to ketorolac, and against patients with the complete or partial syndrome of nasal polyps, angioedema, bronchospastic reactivity or other allergic manifestations to aspirin or other non-steroidal anti-inflammatory drugs (due to possibility of severe anaphylaxis).
OCCLUSION AND DENTAL DEVELOPMENT-Development
Dental Anatomy
Development of occlusion.
A. Occlusion usually means the contact relationship in function. Concepts of occlusion vary with almost every specialty of dentistry.
Centric occlusion is the maximum contact and/or intercuspation of the teeth.
B. Occlusion is the sum total of many factors.
1. Genetic factors.
-Teeth can vary in size. Examples are microdontia (very small teeth) and macrodontia (very large teeth). Incidentally, Australian aborigines have the largest molar tooth size—some 35% larger than the smallest molar tooth group
-The shape of individual teeth can vary (such as third molars and the upper lateral incisors.)
-They can vary when and where they erupt, or they may not erupt at all (impaction).
-Teeth can be congenitally missing (partial or complete anodontia), or there can be extra (supernumerary) teeth.
-The skeletal support (maxilla/mandible) and how they are related to each other can vary considerably from the norm.
2. Environmental factors.
-Habits can have an affect: wear, thumbsucking, pipestem or cigarette holder usage, orthodontic appliances, orthodontic retainers have an influence on the occlusion.
3.Muscular pressure.
-Once the teeth erupt into the oral cavity, the position of teeth is affected by other teeth, both in the same dental arch and by teeth in the opposing dental arch.
-Teeth are affected by muscular pressure on the facial side (by cheeks/lips) and on the lingual side (by the tongue).
C. Occlusion constantly changes with development, maturity, and aging.
1 . There is change with the eruption and shedding of teeth as the successional changes from deciduous to permanent dentitions take place.
2. Tooth wear is significant over a lifetime. Abrasion, the wearing away of the occlusal surface reduces crown height and alters occlusal anatomy.
Attrition of the proximal surfaces reduces the mesial-distal dimensions of the teeth and significantly reduces arch length over a lifetime.
Abraision is the wear of teeth by agencies other than the friction of one tooth against another.
Attrition is the wear of teeth by one tooth rubbing against another
3. Tooth loss leaves one or more teeth without an antagonist. Also, teeth drift, tip, and rotate when other teeth in the arch are extracted.