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NEET MDS Synopsis

Seizure classification
Pharmacology

Seizure classification:

based on degree of CNS involvement, involves simple ( Jacksonian; sensory or motor cortex) or complex symptoms (involves temporal lobe)

1.    Generalized (whole brain involved): 

a.    Tonic-clonic:

Grand Mal; ~30% incidence; unconsiousness, tonic contractions (sustained contraction of muscle groups) followed by clonic contractions (alternating contraction/relaxation); happens for ~ 2-3 minutes and people don’t breathe during this time

Drugs: phenytoin, carbamazepine, Phenobarbital, lamotrigine, valproic acid

Status epilepticus: continuous seizures; use diazepam (short duration) or diazepam + phenytoin

b.    Absence:

Petit Mal; common in children; frequent, brief lapses of consciousness with or without clonic motor activity; see spike and wave EEg at 3 Hz (probably relates to thalamocorticoreverburating circuit)

Drugs: ethosuximide, lamotrigine, valproic acid

c.    Myoclonic: uncommon; isolated clinic jerks associated with bursts of EEG spikes; 

Drugs: lamotrigine, valproic acid

d.    Atonic/akinetic: drop seizures; uncommon; sudden, brief loss of postural muscle tone
Drugs: valproic acid and lamotrigine


2.    Partial:  focal


a.    Simple:  Jacksonian; remain conscious; involves motor or sensory seizures (hot, cold, tingling common)

Drugs: carbamazepine, phenytoin, Phenobarbital, lamotrigine, valproic acid, gabapentin

b.    Complex: temporal lobe or psychomotor; produced by abnormal electrical activity in temporal lobe (involves emotional functions)

Symptoms: abnormal psychic, cognitive, and behavioral function; seizures consist of confused/altered behavior with impaired consciousness (may be confused with psychoses like schizophrenia or dementia)

Drugs: carbamazepine, phenytoin, laotrigine, valproic acid, gabapentin


Generalizations: most seizures can’t be cured but can be controlled by regular administration of anticonvulsants (many types require treatment for years to decades); drug treatment can effectively control seizures in ~ 80% of patients

HEART DISORDERS
Physiology

HEART DISORDERS


Pump failure => Alters pressure (flow) =>alters oxygen carrying capacity.

Renin release (Juxtaglomerular cells) Kidney
Converts Angiotensinogen => Angiotensin I
In lungs Angiotensin I Converted => Angiotensin II
Angiotensin II = powerful vasoconstrictor (raises pressure, increases afterload)

stimulates thirst
stimulates adrenal cortex to release Aldosterone
(Sodium retention, potassium loss)
stimulates kidney directly to reabsorb Sodium
releases ADH from Posterior Pituitary




Myocardial Infarction
 


Myocardial Cells die from lack of Oxygen
Adjacent vessels (collateral) dilate to compensate
Intracellular Enzymes leak from dying cells (Necrosis)

Creatine Kinase CK (Creatine Phosphokinase) 3 forms

One isoenzyme = exclusively Heart (MB)
CK-MB blood levels found 2-5 hrs, peak in 24 hrs
Lactic Dehydrogenase found 6-10 hours after. points less clearly to infarction


Serum glutamic oxaloacetic transaminase (SGOT)

Found 6 hrs after infarction, peaks 24-48 hrs at 2 to 15 times normal,
SGOT returns to normal after 3-4 days




Myocardium weakens = Decreased CO & SV (severe - death)
Infarct heal by fibrous repair
Hypertrophy of undamaged myocardial cells

Increased contractility to restore normal CO
Improved by exercise program


Prognosis

10% uncomplicated recovery
20% Suddenly fatal
Rest MI not fatal immediately, 15% will die from related causes




Congenital heart disease (Affect oxygenation of blood)

Septal defects
Ductus arteriosus
Valvular heart disease

Stenosis = cusps, fibrotic & thickened, Sometimes fused, can not open
Regurgitation = cusps, retracted, Do not close, blood moves backwards





Liver cirrhosis
General Pathology

Liver cirrhosis

It is a chronic, progressive diffuse process characterized by 
a. Hepatocellular necrosis           
b. Replacement by fibrosis and inflammation 
c. Hyperplasia of surviving liver cells forming regenerating nodules 
d. Vascular derangement. 

All these changes lead to loss of the normal liver architecture. 

Pathology of cirrhosis
At first the liver is enlarged or of normal size. Late in the disease, it is reduced in size and weight. 
Consistency- Firm. 
Colour -May be yellow (fatty change), red (congestion), green (cholestaisis), or pale gray (recent nodules due to absence of pigment). 

Morphologically  According to the size of these nodules, cirrhosis can be classified
    
    Micronodular (regular) cirrhosis. Small nodules 2-3 mm.in diameter.
    Macronodular (irregular) cirrhosis, nodules up to one cm in diameter.
    Mixed cirrhosis is the end stage of all types of cirrhosis
    
Microscopic picture 

1 Regenerating nodulesn- Proliferated hepatocytes arranged in thick plates and separated by blood sinusoids.  Central vein in abnormal sites (eccentric) - Hepatocytes may be small , large , or binucleated 

2- Fibrosis- It replaces damaged hepatocytes. It develops at certain sites:-
a-perivenular    b -perisinusoidal    c -pericellular  and d -in relation to portal tracts.

- It may be young, cellular and highly vascular or mature with diminished vasculsarity. It encloses groups of hepatocytes, lobules or regenerating nodules.

-As a result of hepatocyte injury and fibrosis, there’s loss of normal liver architecture including the lobular and acinar pattern as well as the liver cell plates 

3- Bile ductular proliferation:- Occurs in the fibrous septa.Focal choestaisis with feathery degeneration of hepatocytes occur at the margins of regenerating nodules. It becomes diffuse terminally.  

4- Inflammatory cells:-   Lymphocytes, macrophages and plasma cells infiltrate the fibrous septa and regenerating nodules 

Etiological classification of cirrhosis

Congenital Occurs at childhood
- congenital syphilis   
  
Hereditary diseases:- 
a. Primary idiopathic haemochromatosis      b. Thalassemia      c. Wilson’s disease      d.α 1-antitrypsin deficien e. glycogen storage disease

Acquired

-Cryptogenic (10-50%).             
-Alcoholic (30-70%)
-Post viral  (15-20%)                
- Biliary cirrhosis (16%) primary or secondary. 

Behavioral Classification
Pedodontics

Behavioral Classification Systems in Pediatric Dentistry
Understanding children's behavior in the dental environment is crucial for
effective treatment and management. Various classification systems have been
developed to categorize these behaviors, which can assist dentists in guiding
their approach, systematically recording behaviors, and evaluating research
validity.
Importance of Behavioral Classification

Behavior Guidance: Knowledge of behavioral
classification systems helps dentists tailor their behavior guidance
strategies to individual children.
Systematic Recording: These systems provide a
structured way to document children's behaviors during dental visits,
facilitating better communication and understanding among dental
professionals.
Research Evaluation: Behavioral classifications can aid
in assessing the validity of current research and practices in pediatric
dentistry.

Wright’s Clinical Classification
Wright’s clinical classification categorizes children into three main groups
based on their cooperative abilities:


Cooperative:

Children in this category exhibit positive behavior and are
generally relaxed during dental visits. They may show enthusiasm and can
be treated using straightforward behavior-shaping approaches. These
children typically follow established guidelines and perform well within
the framework provided.



Lacking in Cooperative Ability:

This group includes children who demonstrate significant
difficulties in cooperating during dental procedures. They may require
additional support and alternative strategies to facilitate treatment.



Potentially Cooperative:

Children in this category may show some willingness to cooperate but
may also exhibit signs of apprehension or reluctance. They may need
encouragement and reassurance to engage positively in the dental
environment.



Frankl Behavioral Rating Scale
The Frankl behavioral rating scale is a widely used tool that divides
observed behavior into four categories, ranging from definitely positive to
definitely negative. The scale is as follows:


Rating 1: Definitely Negative:

Characteristics: Refusal of treatment, forceful crying, fearfulness,
or any other overt evidence of extreme negativity.



Rating 2: Negative:

Characteristics: Reluctance to accept treatment, uncooperativeness,
and some evidence of a negative attitude (e.g., sullen or withdrawn
behavior).



Rating 3: Positive:

Characteristics: Acceptance of treatment with cautious behavior at
times; willingness to comply with the dentist, albeit with some
reservations. The patient generally follows the dentist’s directions
cooperatively.



Rating 4: Definitely Positive:

Characteristics: Good rapport with the dentist, interest in dental
procedures, and expressions of enjoyment (e.g., laughter).



Application of the Frankl Scale

Research Tool: The Frankl method is popular in research
settings for assessing children's behavior in dental contexts.
Shorthand Recording: Dentists can use shorthand
notations (e.g., “+” for positive behavior, “-” for negative behavior) to
quickly document children's responses during visits.
Limitations: While the scale is useful, it may not
provide sufficient clinical information regarding uncooperative children.
For example, simply recording “-” does not convey the nuances of a child's
behavior. A more descriptive notation, such as “- tearful,” offers better
insight into the clinical problem.

Cement Applications
Dental Materials

Root canal sealers

Applications

Cementation of silver cone gutta-percha point
Paste filling material

Types

Zinc oxide-eugenol cement types
Noneugenol cement types
Therapeutic cement types

properties

Physical-radiopacity
Chemical-insolubility
Mechanical-flow; tensile strength
Biologic-inertness

Gingival tissue packs

Application-provide temporary displacement of gingival tissues
Composition-slow setting zinc oxide-eugenol cement mixed with cotton twills for texture and strength


Surgical dressings
1.Application-gingival covering after periodontal surgery
2. Composition-modified zinc oxide-eugenol cement (containing tannic, acid. rosin, and various oils)

Orthodontic cements

Application-cementation of orthodontic bands
Composition-zinc phosphate cement 

Manipulation

Zinc phosphate types are routinely mixed with cold or frozen mixing slab to extend the working time
Enamel bonding agent types use acid etching for improved bonding
Band, bracket, or cement removal requires special care
 

Direct Pulp Capping
Endodontics

Direct pulp capping is a minimally invasive endodontic procedure used to
preserve the vitality of the tooth's pulp when it is exposed due to caries or
trauma. The goal is to induce a biological response that leads to the formation
of dentin-bridge to seal the pulp and prevent further infection.

Indications:
- Cariously exposed pulp that is asymptomatic and has no evidence of
irreversible pulpitis.
- Recent traumatic exposure of the pulp with no signs of necrosis or infection.
- Presence of a thin layer of residual dentin over the pulp.

Contraindications:
- Signs of irreversible pulpitis or pulpal necrosis.
- Presence of a deep carious lesion that may lead to pulpal exposure during
restoration.
- Large pulp exposures or when the pulp is exposed for an extended period.
- Immunocompromised patients or those with poor oral hygiene.

Procedure:
1. Local anesthesia: Numb the tooth and surrounding tissue to ensure patient
comfort.
2. Caries removal: Carefully remove caries and any infected dentin using a
high-speed handpiece with water spray to prevent pulp exposure.
3. Hemostasis: Apply a mild hemostatic agent if necessary to control bleeding.
4. Pulp conditioning: Apply a calcium hydroxide paste or a bioactive material to
the exposed pulp for a brief period.
5. Application of the capping material: Place a bioactive material, such as
mineral trioxide aggregate (MTA), calcium silicate, or a glass ionomer cement,
directly over the pulp.
6. Restoration: Seal the tooth with a temporary restoration material and place a
final restoration (usually a composite resin) to protect the pulp from further
trauma.
7. Follow-up: Monitor the tooth for signs of pain, swelling, or discoloration.
If these symptoms occur, a root canal treatment may be necessary.

Advantages:
- Preservation of pulp vitality.
- Reduced need for root canal treatment.
- Faster healing and less post-operative sensitivity.
- Conservative approach, maintaining more natural tooth structure.

Disadvantages:
- Limited success in deep or prolonged exposures.
- Higher risk of failure in certain cases, such as extensive caries or pulp
exposure.
- Requires careful technique to avoid further pulp damage.

The Tongue
Anatomy

The Tongue


The tongue (L. lingua; G. glossa) is a highly mobile muscular organ that can vary greatly in shape.
It consists of three parts, a root, body, and tip.



The tongue is concerned with mastication, taste, deglutition (swallowing), articulation (speech), and oral cleansing.
Its main functions are squeezing food into the pharynx when swallowing, and forming words during speech.


 

Gross Features of the Tongue


The dorsum of the tongue is divided by a V-shaped sulcus terminalis into anterior oral (presulcal) and posterior pharyngeal (postsulcal) parts.
The apex of the V is posterior and the two limbs diverge anteriorly.
The oral part forms about 2/3 of the tongue and the pharyngeal part forms about 1/3.


 

Oral Part of the Tongue


This part is freely movable, but it is loosely attached to the floor of the mouth by the lingual frenulum.



On each side of the frenulum is a deep lingual vein, visible as a blue line.
It begins at the tip of the tongue and runs posteriorly.
All the veins on one side of the tongue unite at the posterior border of the hyoglossus muscle to form the lingual vein, which joins the facial vein or the internal jugular vein.



On the dorsum of the oral part of the tongue is a median groove.
This groove represents the site of fusion of the distal tongue buds during embryonic development.


 

The Lingual Papillae and Taste Buds


The filiform papillae (L. filum, thread) are numerous, rough, and thread-like.
They are arranged in rows parallel to the sulcus terminalis.



The fungiform papillae are small and mushroom-shaped.
They usually appear are pink or red spots.



The vallate (circumvallate) papillae are surrounded by a deep, circular trench (trough), the walls of which are studded with taste buds.



The foliate papillae are small lateral folds of lingual mucosa that are poorly formed in humans.



The vallate, foliate and most of the fungiform papillae contain taste receptors, which are located in the taste buds.


 

The Pharyngeal Part of the Tongue


This part lies posterior to the sulcus terminalis and palatoglossal arches.
Its mucous membrane has no papillae.



The underlying nodules of lymphoid tissue give this part of the tongue a cobblestone appearance.
The lymphoid nodules (lingual follicles) are collectively known as the lingual tonsil.

Spruing Technique
Dental Materials

Spruing Technique:

Direct Spruing:

The flow of the molten metal is straight(direct) from the casting crucible to pattern area in the ring. Even with the ball reservoir, the Spruing method is still direct. A basic weakness of direct Spruing is the potential for suck-back porosity at the junction of restoration and the Sprue.

Indirect Spruing:

Molten alloy does not flow directly from the casting crucible into the pattern area, instead the alloy takes a circuitous (indirect) route. The connector (or runner) bar is often used to which the wax pattern Sprue formers area attached. Indirect Spruing offers advantages such as greater reliability & predictability in casting plus enhanced control of solidification shrinkage .The Connector bar is often referred to as a “reservoir .

Armamentarium :
1 . Sprue
2 . Sticky wax
3 . Rubber crucible former
4 . Casting ring 
5 . Pattern cleaner 
6 . Scalpel blade & Forceps 
7 . Bunsen burner

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