NEET MDS Synopsis
The Soft Palate
Anatomy
This is the posterior curtain-like part, and has no bony support. It does, however, contain a membranous aponeurosis.
The soft palate, or velum palatinum (L. velum, veil), is a movable, fibromuscular fold that is attached to the posterior edge of the hard palate.
It extends posteroinferiorly to a curved free margin from which hangs a conical process, the uvula (L. uva, grape).
The soft palate separates the nasopharynx superiorly and the oropharynx inferiorly.
During swallowing the soft palate moves posteriorly against the wall of the pharynx, preventing the regurgitation of food into the nasal cavity.
Laterally, the soft palate is continuous with the wall of the pharynx and is joined to the tongue and pharynx by the palatoglossal and palatopharyngeal folds.
The soft palate is strengthened by the palatine aponeurosis, formed by the expanded tendon of the tensor veli palatini muscle.
This aponeurosis attaches to the posterior margin of the hard palate.
ACRYLIC RESINS
Dental Materials
ACRYLIC RESINS
Use. Acrylic (unfilled) resins are used as temporary crown material. Temporary crowns are placed to protect the crown preparation and provide patient comfort during the time the permanent crown is being constructed
Cerebral palsy and Treatment
PedodonticsCerebral palsy (CP) is a neurological disorder resulting from damage to the
brain during its development before, during, or shortly after birth. This
condition is non-progressive, meaning that it does not worsen over time, but it
manifests as a range of neurological problems that can significantly impact a
child's mobility, muscle control, and posture.
Causes:
The primary cause of CP is any factor that leads to decreased oxygen supply
(hypoxia) to the developing brain. This can occur due to various reasons,
including complications during pregnancy, childbirth, or immediately after
birth.
Classification of Cerebral Palsy:
Based on Anatomical Involvement:
Monoplegia: One limb is affected.
Hemiplegia: One side of the body is affected.
Paraplegia: Both legs are affected.
Quadriplegia: All four limbs are affected.
Based on Neuromuscular Involvement:
Spasticity: Characterized by stiff and tight muscles; this
is the most common type, seen in 70% of cases. Affected individuals may
have limited head movement and a limp gait.
Athetosis: Involves involuntary, writhing movements, seen in
15% of cases. Symptoms include excessive head movement and drooling.
Ataxia: Affects balance and coordination, seen in 5% of
cases. Individuals may exhibit a staggering gait and slow tremor-like
movements.
Mixed: A combination of more than one type of cerebral
palsy, seen in about 10% of cases.
1. Spastic Cerebral Palsy (70% of cases)
Characteristics:
Limited Head Movement: Individuals have restrictions in moving their
head due to increased muscle tone.
Involvement of Cerebral Cortex: Indicates that the motor control areas
of the brain (especially those concerning voluntary movement) are affected.
Limping Gait with Circumduction of the Affected Leg: When walking, the
patient often swings the affected leg around instead of lifting it normally,
due to spasticity.
Hypertonicity of Facial Muscles: Increased muscle tension in the facial
region, contributing to a fixed or tense facial expression.
Unilateral or Bilateral Manifestations: Symptoms can occur on one side
of the body (hemiplegia) or affect both sides (diplegia or quadriplegia).
Slow Jaw Movement: Reduced speed in moving the jaw, potentially leading
to functional difficulties.
Hypertonic Orbicularis Oris Muscles: Increased muscle tone around the
mouth, affecting lip closure and movement.
Mouth Breathing (75%): The individual may breathe through their mouth
due to poor control of oral musculature.
Spastic Tongue Thrust: The tongue pushes forward excessively, which can
disrupt swallowing and speech.
Class II Division II Malocclusion (75%): Dental alignment issue often
characterized by a deep overbite and anterior teeth that are retroclined,
sometimes accompanied by a unilateral crossbite.
Speech Involvement: Difficulties with speech articulation due to muscle
coordination problems.
Constricted Mandibular Arch: The lower jaw may have a narrower
configuration, complicating dental alignment and oral function.
2. Athetoid Cerebral Palsy (15% of cases)
Characteristics:
Excessive Head Movement: Involuntary, uncontrolled movements lead to
difficulties maintaining a stable head position.
Involvement of Basal Ganglia: Damage to this area affects muscle tone
and coordination, leading to issues like chorea (involuntary movements).
Bull Neck Appearance: The neck may appear thicker and less defined,
owing to abnormal muscle development or tone.
Lack of Head Balance, Drawn Back: The head may be held in a retracted
position, affecting posture and balance.
Quick Jaw Movement: Involuntary rapid movements can lead to difficulty
with oral control.
Hypotonic Orbicularis Oris Muscles: Reduced muscle tone around the mouth
can lead to drooling and lack of control of oral secretions.
Grimacing and Drooling: Facial expressions may be exaggerated or
inappropriate due to muscle tone issues, and there may be problems with
managing saliva.
Continuous Mouth Breathing: Patients may consistently breathe through
their mouths rather than their noses.
Tissue Biting: Increased risk of self-biting due to lack of muscle
control.
Tongue Protruding: The tongue may frequently stick out, complicating
speech and intake of food.
High and Narrow Palatal Vault: Changes in the oral cavity structures can
lead to functional difficulties.
Class II Division I Malocclusion (90%): Characterized by a deep bite and
anterior open bite.
Speech Involvement: Affected due to uncontrolled muscle movements.
Muscle of Deglutition Involvement: Difficulties with swallowing due to
affected muscles.
Bruxism: Involuntary grinding or clenching of teeth.
Auditory Organs May be Involved: Hearing impairments can coexist.
3. Ataxic Cerebral Palsy (5% of cases)
Characteristics:
Slow Tremor-like Head Movement: Unsteady, gradual movements of the head,
indicative of coordination issues.
Involvement of Cerebellum: The cerebellum, which regulates balance and
motor control, is impacted.
Lack of Balance Leading to Staggering Gait: Individuals may have
difficulty maintaining equilibrium, leading to a wide-based and unsteady
gait.
Hypotonic Orbicularis Oris Muscles: Reduced muscle tone leading to
difficulties with oral closure and control.
Slow Jaw Movement: The jaw may move slower, affecting chewing and
speech.
Speech Involvement: Communication may be affected due to poor
coordination of the speech muscles.
Visual Organ May be Involved (Nystagmus): Involuntary eye movements may
occur, affecting visual stability.
Varied Type of Malocclusion: Dental alignment issues can vary widely in
this population.
4. Mixed:
Mixed cerebral palsy involves a combination of the above types, where the
individual may exhibit spasticity, athetosis, and ataxia to varying degrees.
Dental Considerations for Mixed CP:
- Dental care for patients with mixed CP is highly individualized and depends on
the specific combination and severity of symptoms.
- The dentist must consider the unique challenges that arise from the
combination of muscle tone issues, coordination problems, and potential for
involvement of facial muscles.
- A multidisciplinary approach, including occupational therapy and speech
therapy, may be necessary to address oral function and hygiene.
- The use of sedation or general anesthesia might be considered for extensive
dental treatments due to the difficulty in managing the patient's movements and
ensuring safety during procedures.
Associated Symptoms:
Children with CP may exhibit persistent reflexes such as the asymmetric tonic
neck reflex, which can influence their dental treatment. Other symptoms may
include mental retardation, seizure disorders, speech difficulties, and joint
contractures.
Dental Problems:
Children with cerebral palsy often experience specific dental challenges:
They may have a higher incidence of dental caries (tooth decay) due to
difficulty in maintaining oral hygiene and dietary preferences.
There is a greater likelihood of periodontal disease, often exacerbated
by medications like phenytoin, which can lead to gum overgrowth and dental
issues.
Dental Treatment Considerations:
When managing dental care for children with cerebral palsy, dentists need to
consider:
Patient Stability: The child’s head should be stabilized, and their back
should be elevated to minimize swallowing difficulties.
Physical Restraints: These can help manage uncontrolled movements during
treatment.
Use of Mouth Props and Finger Splints: These tools can assist in
controlling involuntary jaw movements.
Gentle Handling: Avoid abrupt movements to prevent triggering the
startle reflex.
Local Anesthesia (LA): Administered with caution, ensuring stabilization
to prevent sudden movements.
Premedication: Medications may be given to alleviate muscle
hypertonicity, manage anxiety, and reduce involuntary movements.
General Anesthesia (GA): Reserved for cases that are too challenging to
manage with other methods.
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
HYPERTENSIVE VASCULAR DISEASE
General Pathology
HYPERTENSIVE VASCULAR DISEASE
Malignant hypertension
A small percentage of HTN patients (5%) present with a rapidly rising blood pressure that, if untreated, leads to death within 1 to 2 years.
systolic pressures -> 200 mm Hg or diastolic pressures -> 120 mm Hg
Associated with renal failure and retinal hemorrhages
Most commonly is superimposed on preexisting benign hypertension
Hypertension (HTN) has the following complications
- stroke (CVD)
- multi-infarct dementia
- atherosclerotic coronary heart disease
- cardiac hypertrophy and heart failure (hypertensive heart disease)
- aortic dissection
- renal failure
Essential HTN Accounts for 90% to 95% of all cases
SecondaryHTN
Renal - > Acute glomerulonephritis Chronic renal disease
Endocrine - > Cushing syndrome, Hypothyroidism (myxedema) Hyperthyroidism (thyrotoxicosis) Pregnancy-induced (pre-eclampsia)
Cardiovascular - > Coarctation of aorta
Neurologic
Psychogenic, Increased intracranial pressure
PATHOGENESIS
most cases (95%) are idiopathic (essential hypertension)
Most of the remaining cases (secondary hypertension) are due to primary renal disease, renal artery narrowing
Gene defects in enzymes involved in aldosterone metabolism
Mutations in proteins that affect sodium resorption as in Liddle syndrome
Genetic factors - > familial clustering of hypertension
Environmental factors such as stress, obesity, smoking, physical inactivity, and high levels of salt consumption, modify the impact of genetic determinants
Morphology
HTN is associated with arteriolosclerosis (small arterial disease)
Two forms of small blood vessel disease are hypertension-related:
1- hyaline arteriolosclerosis
2- hyperplastic arteriolosclerosis
Hyaline arteriolosclerosis
Associated with benign hypertension.
-marked by homogeneous, pink hyaline thickening of the arteriolar walls, and luminal narrowing.
Hyperplastic arteriolosclerosis
It is more typical of severe hypertension.
- "onionskin," concentric, laminated thickening of arteriolar walls and luminal narrowing.
- The laminations consist of smooth muscle cells and thickened, reduplicated basement membrane.
DISORDERS OF BLOOD VESSEL HYPERREACTIVITY
Several disorders are characterized by inappropriate or exaggerated vasoconstriction of blood vessels:
1- Raynaud Phenomenon
2- Myocardial Vessel Vasospasm
Raynaud Phenomenon
- results from exaggerated vasoconstriction of arteries and arterioles in the extremities (the fingers and toes, but also sometimes the nose, earlobes, or lips).
-restricted blood flow induces paroxysmal pallor or cyanosis
- involved digits characteristically show "red-white-andblue" color changes from most proximal to most distal
Myocardial Vessel Vasospasm
Causes: 1- vasoactive mediators - > prolonged vascular contraction;
- endogenous (e.g., epinephrine released by pheochromocytomas) or exogenous (cocaine or phenylephrine).
2- Elevated thyroid hormone -> increase sensitivity of vessels to catecholamines
3- autoantibodies and T cells in scleroderma vascular instability and vasospasm.
4- extreme psychological stress (release of catecholamines)
Cardiac raynaud
When vasospasm of cardiac arterial or arteriolar bed is of sufficient duration (20 to 30 min ) myocardial infarction occurs
acute microscopic area of necrosis characterized by mycotic hypercontraction (contraction band necrosis)
subacute and chronic cases - > microscopic foci of granulation tissue or scar
Hepatitis C virus
General Pathology
Hepatitis C virus.
It is most often mild and anicteric but occasionally severe with fulminant hepatic failure. It is caused an RNA virus, which may be transmitted parenterally (a cause of post-transfusion hepatitis); the route of transmission undetermined in 40%-50% of cases
a. 90% of blood transfusion-related hepatitis is caused by hepatitis C.
b. 50% progress to chronic disease.
c. Increased risk for hepatocellular carcinoma.
d. Incubation period: ranges from 2 to 26 weeks, but averages 8 weeks.
- Antibody is detected by enzyme-linked immunosorbent,assay (ELISA). The incubation period is between 2 and weeks with peak onset of illness 6-8 weeks after infection
- Most patients progress to chronic liver disease, specifically chronic persistent hepatitis or chronic active hepatitis
- Cirrhosis is common in patients with chronic active hepatitis and occurs in 20%-25% of infected patients. HCV is also associated with hepatocellular carcinoma.
e. Treatment and prevention: α-interferon is used to treat chronic hepatitis C. There is currently no vaccine available.
IMMUNO PATHOLOGY
General Pathology
IMMUNO PATHOLOGY
Abnormalities of immune reactions are of 3 main groups
Hypersensitivity,
Immuno deficiency,
Auto immunity.
Hypersensitivity (ALLERGY)
This is an exaggerated or altered immune response resulting in adverse effects
They are classified into 4 main types.
I. Type I-(reaginic, anaphylactic). This is mediated by cytophylic Ig E antibodies, which get bound to mast cells. On re-exposure, the Ag-Ab reaction occurs on the mast cell surface releasing histamine.
Clinical situations
I. Systemic anaphylaxis, presenting with bronchospasm oedema hypertension, and even death.
2. Local (atopic) allergy.
Allergic rhinitis (hay fever)
Asthma
Urticaria.
Food allergies.
2. Type II. (cytotoxic). Antibody combines with antigen present on-cell surface. The antigen may be naturally present on the surface or an extrinsic substance (e.g.drug) attached to cell surface.
The cell is then destroyed by complement mediated lysis (C89) or phagocytosis of the antibody coated cell.
Clinical situations
Haemolytic anemia.
Transfusion reaction
Auto immune haemolytic anemia.
Haemolysis due to some drugs like Alpha methyl dopa
Drug induced thrombocytopenia (especially sedormid).
Agranulocytosis due to sensitivity to some drugs.
Goodpasture’s syndrome-glomermerulonephritis due to anti basement membrane antibodies.
3. Type III. (Immune complex disease). Circulating immune complexes especially
small soluble complexes tend to deposit in tissues especially kidney, joints, heart and
arteries.
These then cause clumping of platelets with subsequent release of histamine. and
serotonin resulting in increased permeability. Also, complement activation occurs which
being chemotactic results in aggregation of polymorphs and necrotising vasculitis due to
release of lysosmal enzymes
Clinical situations
Serum sickness.
Immune complex glomerulonephritis.
Systemic lupus erythematosus.
Allergic alveolitis.
Immune based vasculitis like
Drug induced vasculitis.
Henoch – Schonlein purpura
4. Type IV. (Cell mediated). The sensitized lymphocytes may cause damage by
cytotoxicity or by lymphokines and secondarily involving macrophages in the reaction.
Clinical situations
I. Caseation necrosis in tuberculosis.
2. Contact dermatitis to
Metals.
Rubber.
Drugs (topical).
Dinitrochlorbenzene (DNCB).
5. Type V. (stimulatory) This is classed by some workers separately and by other with
cytotoxic type (Type II) with a stimulatory instead of toxic effect
Clinical Situations :
LATS (long acting thyroid stimulator) results in thyrotoxicosis (Grave’s disease)
Chronic hepatitis
General Pathology
Chronic hepatitis
Chronic hepatitis occurs in 5%-10% of HBV infections and in well over 50% of HCV; it does not occur in HAV. Most chronic disease is due to chronic persistent hepatitis. The chronic form is more likely to occur in the very old or very young, in males, in immunocompromised hosts, in Down's syndrome, and in dialysis patients.
a. Chronic persistent hepatitis is a benign, self-limited disease with a prolonged recovery. Patients are asymptomatic except for elevated transaminases.
b. Chronic active hepatitis features chronic inflammation with hepatocyte destruction, resulting in cirrhosis and liver failure.
(1) Etiology. HBV, HCV, HDV, drug toxicity, Wilson's disease, alcohol, a,-antitrypsin deficiency, and autoimmune hepatitis are common etiologies.
(2) Clinical features may include fatigue, fever, malaise, anorexia, and elevated liver function tests.
(3) Diagnosis is made by liver biopsy.
8. Carrier state for HBV and HCV may be either asymptomatic or with liver disease; in the latter case, the patient has elevate transaminases.
a. Incidence is most common in immunodeficient, drug addicted, Down's syndrome, and dialysis patients.
b. Pathology of asymptomatic carriers shows "ground-glass"" hepatocytes with finely granular eosinophilic cytoplasm.