NEET MDS Synopsis
Cardiac arrhythmia
General Pathology
Cardiac arrhythmia
Cardiac arrhythmia is a group of conditions in which muscle contraction of the heart is irregular for any reason.
Tachycardia :A rhythm of the heart at a rate of more than 100 beats/minute , palpitation present
Causes : stress, caffeine, alcohol, hyperthyroidism or drugs
Bradycardia : slow rhythm of the heart at a rate less than 60 beats/min
Atrial Arrhythmias
- Atrial fibrillation
Atrial Dysrhythmias
- Premature atrial contraction
- Atrial flutter
- Supraventricular tachycardia
- Sick sinus syndrome
Ventricular Arrhythmias
- Ventricular fibrillation
Ventricular Dysrhythmias
- Premature ventricular contraction
- Pulseless electrical activity
- Ventricular tachycardia
- Asystole
Heart Blocks
- First degree heart block
- Second degree heart block
o Type 1 Second degree heart block a.k.a. Mobitz I or Wenckebach
o Type 2 Second degree heart block a.k.a. Mobitz II
- Third degree heart block a.k.a. complete heart block
Atrial fibrillation
Atrial fibrillation is a cardiac arrhythmia (an abnormality of heart rate or rhythm) originating in the atria.
AF is the most common cardiac arrhythmia
Signs and symptoms
Rapid and irregular heart rates
palpitations, exercise intolerance, and occasionally produce angina and congestive symptoms of shortness of breath or edema
Paroxysmal atrial fibrillation is the episodic occurence of the arrhythmia Episodes may occur with sleep or with exercise
Diagnosis:
Electrocardiogram
- absence of P waves
- unorganized electrical activity in their place
- irregularity of R-R interval due to irregular conduction of impulses to the ventricles
Causes:
- Arterial hypertension
- Mitral valve disease (e.g. due to rheumatic heart disease or mitral valve prolapse)
- Heart surgery
- Coronary heart disease
- Excessive alcohol consumption ("binge drinking" or "holiday heart")
- Hyperthyroidism
- Hyperstimulation of the vagus nerve, usually by having large meals
Treatment
Rate control by
Beta blockers (e.g. metoprolol)
Digoxin
Calcium channel blockers (e.g. verapamil)
Rhythm control
Electrical cardioverion by application of a DC electrical shock
Chemical cardioversion is performed with drugs eg amiodarone
Radiofrequency ablation : uses radiofrequency energy to destroy abnormal electrical pathways in heart tissue It is used in recurrent AF
In confirmed AF, anticoagulant treatment is a crucial way to prevent stroke
Atrial flutter
Atrial flutter is a regular, rhythmic tachycardia originating in the atria. The rate in the atria is over 220 beats/minute, and typically about 300 beats/minute
he morphology on the surface EKG is typically a sawtooth pattern.
The ventricles do not beat as fast as the atria in atrial flutter
Supraventricular tachycardia
apid rhythm of the heart in which the origin of the electrical signal is either the atria or the AV node
it is important to determine whether a wide-complex tachycardia is an SVT or a ventricular tachycardia, since they are treated differently
Sick sinus syndrome : a group of abnormal heartbeats (arrhythmias) presumably caused by a malfunction of the sinus node, the heart's "natural" pacemaker.
Ventricular fibrillation
is a cardiac condition which consists of a lack of coordination of the contraction of the muscle tissue of the large chambers of the heart. The ventricular muscle twitches randomly, rather than contracting in unison, and so the ventricles fail to pump blood into the arteries and into systemic circulation.
Ventricular fibrillation is a medical emergency: if the arrhythmia continues for more than a few seconds, blood circulation will cease, as evidenced by lack of pulse, blood pressure and respiration, and death will occur. Ventricular fibrillation is a cause of cardiac arrest and sudden cardiac death
Lymphocytosis
General Pathology
Lymphocytosis:
Causes
-Infections in children and the neutropenic infections in adults.
-Lymphocytic leukaemia.
-Infectious mononucleosis.
-Toxdplasmosis.
-Myast'henia gravis.
Asthma
General Pathology
Asthma
Asthma is
(1) An obstructive lung disease characterized by narrowing of the airways.
Inflammation of the airways is a major component of asthma.
(2) Common symptoms are dyspnea, wheezing on expiration, and coughing.
(3) Two types:
(a) Extrinsic (allergic, atopic) asthma
(i) An atopic allergy caused by a type I immediate hypersensitivity immune reaction to an allergen.
(ii) Seen in children, adults.
(b) Intrinsic (nonallergic) asthma
(i) Not caused by an allergic reaction.
(ii) Mostly seen in adults.
The disorder is a chronic inflammatory condition in which the airways develop increased responsiveness to various stimuli, characterized by bronchial hyper-responsiveness, inflammation, increased mucus production, and intermittent airway obstruction.
Signs and symptoms
The clinical hallmarks of an attack are shortness of breath (dyspnea) and wheezing
A cough—sometimes producing clear sputum—may also be present
The onset is often sudden; there is a "sense of constriction" in the chest, breathing becomes difficult, and wheezing occurs
Signs of an asthmatic episode are wheezing, rapid breathing (tachypnea), prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), and over-inflation of the chest.
During very severe attacks asthma sufferer can turn blue due to lack of oxygen , can experience chest pain or even loss of consciousness, may lead to respiratory arrest and death
Pathophysiology
Bronchoconstriction : asthma is the result of an abnormal immune response in the bronchial airways. The airways of asthmatics are "hypersensitive" to certain triggers, also known as stimuli, these stimuli include allergens, medications , air pollution, early child hood infection, exercise, emotional stress
Bronchial inflammation asthma resulting from an immune response to inhaled allergens—are the best understood of the causal factors. In both asthmatics and non-asthmatics, inhaled allergens that find their way to the inner airways are ingested by a type of cell known as antigen presenting cells These activate an humoral immune response. The humoral immune system produces antibodies against the inhaled allergen. Later, when an asthmatic inhales the same allergen, these antibodies "recognize" it and activate a humoral response. Inflammation results: chemicals are produced that cause the airways to constrict and release more mucus, and the cell-mediated arm of the immune system is activated. The inflammatory response is responsible for the clinical manifestations of an asthma attack
Symptomatic Treatment
Episodes of wheeze and shortness of breath generally respond to inhaled bronchodilators which work by relaxing the smooth muscle in the walls of the bronchi., More severe episodes may need short courses of inhaled, oral, or intravenous steroids which suppress inflammation and reduce the swelling of the lining of the airway.
Bronchodilators (usually inhaled)
Short-acting selective beta2-adrenoceptor agonists(salbutamol, terbutaline)
less selective adrenergic agonists, such as inhaled epinephrine and ephedrine tablets
Antimuscarinics
Systemic steroids
Oxygen to alleviate the hypoxia that is the result of extreme asthma attacks.
If chronic acid indigestion ( GERD) is part of the attack, it is necessary to treat it as well or it will restart the inflammatory process
Preventive Treatment
most effective preventive medication are
Inhaled corticosteroids
Long-acting beta2-adrenoceptor agonists
Leukotriene modifiers
Mast cell stabilizers
Methylxanthines (theophylline and aminophylline),
Antihistamines, often used to treat allergic symptoms
Anatomy of MANDIBULAR Ridge
Prosthodontics
LIMITING STRUCTURES
A) Labial, lingual & buccal frenum
- It is fibrous band extending from the labial aspect of the residual alveolar ridge to the lip containing a band of the fibrous connective tissue the that helps in attachment of the orbicularis oris muscle.
- It is quite sensitive hence the denture should have an appropriate labial notch.
- The fibers of buccinator are attached to the buccal frenum.
- Should be relieved to prevent displacement of the denture during function.
- The lingual frenum relief should be provided in the anterior portion of the lingual flange.
- This anterior portion of the lingual flange called sub-lingual crescent area.
- The lingual notch of the denture should be well adapted otherwise it will affect the denture stability.
B) Labial & buccal vestibule
- The labial sulcus runs from the labial frenum to the buccal frenum on each side.
- Mentalis muscle is quite active in this region.
- The buccal sulcus extends posteriorly from the buccal frenum to outside back corner of the retromolar region.
- Area maximization can be safely done here as because the fibers of the buccinator runs parallel to the border and hence displacing action due to buccinator during its contraction is slight.
- The impression is the widest in this region.
C) Alveololingual sulcus
- Between lingual frenum to retromylohyoid curtain.
- Overextension causes soreness and instability.
It can be divided into three parts:
i) Anterior part :
- From lingual frenum to mylohyoid ridge
- The shallowest portion(least height) of the lingual flange
ii) Middle region :
- From the premylohyoid fossa to the the distal end of the mylohyoid region
iii) Posterior portion :
- From the end of the mylohyoid ridge end to the retromylohyoid curtain
- Provides for a valuable undercut area so important retention
- Overextension causes soreness and instability
- Proper recording gives typical S –form of the lingual flange
D) Retromolar pad
- Pear-shaped triangular soft pad of tissue at the distal end of the lower ridge is referred to as the retromolar pad.
- It is an important structure, which forms the posterior seal of the mandibular denture.
- The denture base should extend up to 2/3rd of the retromolar pad triangle.
E) Pterygomandibular raphe
SUPPORTING STRUCTURES
A) Primary stress bearing area / Supporting area
1. Buccal shelf area
- Extends from buccal frenum to retromolar pad.
- Between external oblique ridge and crest of alveolar ridge.
Its boundaries are:
1. Medially the crest of the ridge
2. Laterally the external oblique ridge
3. Distally the retromolar pad
4. Mesially the buccal frenum
The width of this area increases as the alveolar resorption continues.
B) Secondary stress bearing area / Supporting area
1. Residual alveolar ridge
- Buccal and lingual slopes are secondary stress bearing areas.
RELIEF AREAS
A) Mylohyoid ridge
- Attachment for the mylohyoid muscle.
- Running along the lingual surface of the mandible.
- Anteriorly: the ridge lies close to the inferior border of the mandible.
- Posteriorly it lies close to the residual ridge.
- Covered by the thin mucosa which may be traumatized by denture base hence it should be relieved.
- The extension of the lingual flange is to be beyond the palpable position of the mylohyoid ridge but not in the undercut.
B) Mental foramen
- Lies on the external surface of the mandible in between the 1st and the 2nd premolar region.
- It should be relieved specially in case it lies close to the residual alveolar ridge due to ridge resorption to prevent parasthesia.
C) Genial tubercle
- Area of muscle attachment (Genioglossus and Geniohyoid).
- Lies away from the crest of the ridge.
- Prominent in resorbed ridges therefore adequate relief to be provided.
D) Torus mandibularis
- Abnormal bony prominence.
- Bilaterally on the lingual side near the premolar area.
- Covered by thin mucosa so it should be relieved
Osteomyelitis
Oral Maxillofacial Surgery
Osteomyelitis
Staphylococcus aureus causes osteomyelitis.
TYPES OF OSTEOMYELITIS
1.Suppurative Osteomyelitis - onset 4 weeks - Deep bacterial invasion into medullary & cortical bone - polymicrobial infection anaerobes such as Bacteriods, Porphyromonas or Provetella.
Staphylococci may be a cause when an open fracture is involved. Mandible is more prone than maxilla as vascular supply is readily compromised.
2.Focal Sclerosing Osteomylitis(Condensing osteitis) - Localized areas of bone sclerosis. Bony reaction to low-grade peri-apical infection or unusually strong host defensive response. Association with an area of inflammation is critical.
3. Diffuse Sclerosing Osteomylitis - Chronic intraosseous bacterial infection creates a smoldering mass of chronically inflammed granulation tissue.
4. Proliferative Periostitis(Periostitis ossificans & Garee’s osteomyelitis) - periosteal reaction to the presence of inflammation. Affected periosteum forms several rows of reactive vital bone that parallel each other & expand surface of altered bone.
- Radiopaque laminations of bone roughly parallel each other & underlying cortical surface. Laminations may vary from 1-12 in number. Radiolucent separations often are present between new bone & original cortex.
Conditions that weaken the immune system increase a person's risk for osteomyelitis, including:
Diabetes (most cases of osteomyelitis stem from diabetes)
Sickle cell disease
HIV or AIDS
Rheumatoid arthritis
Intravenous drug use
Alcoholism
Long-term use of steroids
Hemodialysis
Poor blood supply
Recent injury
Bone surgery, including hip and knee replacements, also increase the chance of bone infection.
Osteomyelitis in Children and Adults
In children, osteomyelitis is usually acute. Acute osteomyelitis comes on quickly, is easier to treat, and overall turns out better than chronic osteomyelitis. In children, osteomyelitis usually shows up in arm or leg bones.
In adults, osteomyelitis can be either acute or chronic.
Acute osteomyelitis develops rapidly over a period of seven to 10 days. The symptoms for acute and chronic osteomyelitis are very similar
Clinical features of chronic osteomyelitis are usually limited to :
- Pain and tenderness: the pain is minimal,
- Non healing bony and overlying soft tissue wounds with induration of soft tissues,
- Intraoral or extraoral draining fistulae,
- Thickened or “wooden” character of bone,
- Enlargement of mandible, because of deposition of subperiosteal new bone.
- Pathological fractures may occur,
- Sterile abscess (Brodie’s abscess), common to long bones is rare in jaws.
- Teeth in the area tend to become loose and sensitive to palpation and percussion.
Beveling in Restorative Dentistry
Conservative Dentistry
Beveling in Restorative Dentistry
Beveling: Beveling refers to the process of angling the
edges of a cavity preparation to create a smooth transition between the
tooth structure and the restorative material. This technique can enhance the
aesthetics and retention of certain materials.
Characteristics of Ceramic Materials
Brittleness: Ceramic materials, such as porcelain, are
inherently brittle and can be prone to fracture under stress.
Bonding Mechanism: Ceramics rely on adhesive bonding to
tooth structure, which can be compromised by beveling.
Contraindications
Cavosurface Margins: Beveling the cavosurface margins
of ceramic restorations is contraindicated because:
It can weaken the bond between the ceramic and the tooth structure.
It may create unsupported enamel, increasing the risk of chipping or
fracture of the ceramic material.
Beveling with Amalgam Restorations
Amalgam Characteristics
Strength and Durability: Amalgam is a strong and
durable material that can withstand significant occlusal forces.
Retention Mechanism: Amalgam relies on mechanical
retention rather than adhesive bonding.
Beveling Guidelines
General Contraindications: Beveling is generally
contraindicated when using amalgam, as it can reduce the mechanical
retention of the restoration.
Exception for Class II Preparations:
Gingival Floor Beveling: In Class II preparations
where enamel is still present, a slight bevel (approximately 15 to 20
degrees) may be placed on the gingival floor. This is done to:
Remove unsupported enamel rods, which can lead to enamel
fracture.
Enhance the seal between the amalgam and the tooth structure,
improving the longevity of the restoration.
Technique for Beveling
Preparation: When beveling the gingival floor:
Use a fine diamond bur or a round bur to create a smooth, angled
surface.
Ensure that the bevel is limited to the enamel portion of the wall
to maintain the integrity of the underlying dentin.
Clinical Implications
A. Material Selection
Understanding the properties of the restorative material is essential
for determining the appropriate preparation technique.
Clinicians should be aware of the contraindications for beveling based
on the material being used to avoid compromising the restoration's success.
B. Restoration Longevity
Proper preparation techniques, including appropriate beveling when
indicated, can significantly impact the longevity and performance of
restorations.
Regular monitoring of restorations is essential to identify any signs of
failure or degradation, particularly in areas where beveling has been
performed.
DNA (Deoxyribonucleic acid)
PhysiologyDNA (Deoxyribonucleic acid) - controls cell function via transcription and translation (in other words, by controlling protein synthesis in a cell)
Transcription - DNA is used to produce mRNA
Translation - mRNA then moves from the nucleus into the cytoplasm & is used to produce a protein . requires mRNA, tRNA (transfer RNA), amino acids, & a ribosome
tRNA molecule
sequence of amino acids in a protein is determined by sequence of codons (mRNA). Codons are 'read' by anticodons of tRNAs & tRNAs then 'deliver' their amino acid.
Amino acids are linked together by peptide bonds (see diagram to the right)
As mRNA slides through ribosome, codons are exposed in sequence & appropriate amino acids are delivered by tRNAs. The protein (or polypeptide) thus grows in length as more amino acids are delivered.
The polypeptide chain then 'folds' in various ways to form a complex three-dimensional protein molecule that will serve either as a structural protein or an enzyme.
NON-SPECIFIC KILLER CELLS
General Microbiology
NON-SPECIFIC KILLER CELLS
Several different cells including NK and LAK cells, K cells, activated macrophages and eosinophils are capable of killing foreign and altered self target cells in a non-specific manner. These cells play an important role in the innate immune system.
A. NK and LAK cells
Natural killer (NK) cells are also known as large granular lymphocytes (LGL) because they resemble lymphocytes in their morphology, except that they are slightly larger and have numerous granules.
NK cells can be identified by the presence of CD56 and CD16 and a lack of CD3 cell surface markers.
NK cells are capable of killing virus-infected and malignant target cells but they are relatively inefficient in doing so.
However, upon exposure to IL-2 and IFN-gamma, NK cells become lymphokine-activated killer (LAK) cells, which are capable of killing malignant cells.
Continued exposure to IL-2 and IFN-gamma enables the LAK cells to kill transformed as well as malignant cells. LAK cell therapy is one approach for the treatment of malignancies.
NK and LAK cells have two kinds of receptors on their surface – a killer activating receptor (KAR) and a killer inhibiting receptor (KIR).
When the KAR encounters its ligand, a killer activating ligand (KAL) on the target cell the NK or LAK cells are capable of killing the target. However, if the KIR also binds to its ligand then killing is inhibited even if KAR binds to KAL.
The ligands for KIR are MHC-class I molecules. Thus, if a target cell expresses class I MHC molecules it will not be killed by NK or LAK cells even if the target also has a KAL which could bind to KAR.
Normal cells constitutively express MHC class I molecules on their surface, however, virus infected and malignant cells down regulate expression of class I MHC. Thus, NK and LAK cells selectively kill virus-infected and malignant cells while sparing normal cells.
B. K cells
Killer (K) cells are not a morphologically distinct type of cell. Rather a K cell is any cell that mediates antibody-dependent cellular cytotoxicity (ADCC).
In ADCC antibody acts as a link to bring the K cell and the target cell together to allow killing to occur. K cells have on their surface an Fc receptor for antibody and thus they can recognize, bind and kill target cells coated with antibody.
Killer cells which have Fc receptors include NK, LAK, and macrophages which have an Fc receptor for IgG antibodies and eosinophils which have an Fc receptor for IgE antibodies.