NEET MDS Synopsis
Antimania Drugs
Pharmacology
Antimania Drugs
MANIC SYMPTOMSMANIC SYMPTOMS
Elevated or irritable mood
Increased activity or psychomotor agitation
Reduced need for sleep
Inflated self esteem or grandiosity
Increased or pressure of speech
Flight of ideas
These drugs are used to treat manic-depressive illness.
1. Lithium
2. Carbamazepine
3. Valproic acid
Mechanisms of action
1. Lithium works inside the cell to block conversion of inositol phosphate to inositol.
2. Carbamazepine blocks sodium channels
3. Valproic acid blocks sodium and calcium channels
PHARMACOKINETICS
Absorbed readily and almost completely from the GI tract; peak concentrations in 1-2 hrs
Lithium toxicity
1. Nausea, diarrhea, convulsions, coma, hyperreflexia, cardiac arrhythmias, hypotension.
2. Thyroid enlargement; increases thyroid stimulating hormone (TSH) secretion; may cause hypothyroidism.
3. Polydipsia, polyuria (lithium inhibits the effect of antidiuretic hormone on the kidney).
Clinical applications concerning lithium
- Patients must be warned against sodium-restricted diets because sodium restriction leads to greater retention of lithium by the kidney.
- Patients must have regular (e.g., monthly) blood checks because the margin of safety is narrow.
Endocrine Effects – Goitre and hypothyroidism commonly
Cardiac Effects:– ECG changes(common) - T-wave flattening/inversion and appearance of U wavesflattening/inversion and appearance of U waves
Li and Pregnancy -1st Trimester:Cardiovascular anomalies of the newborn, especially Ebstein's malformation
- 3rd Trimester: Neonatal goiter, CNS depression, hypotonia ("floppy baby" syndrome)
Drug–drug interactions of lithium
Diuretics and newer nonsteroidal anti-inflammatory drugs (NSAIDs) reduce lithium excretion and may cause lithium toxicity.
CLASSIFICATION OF LIPIDS
Biochemistry
CLASSIFICATION OF LIPIDS
Lipids are classified as follows:
1. Simple lipids: Esters of fatty acids with various alcohols.
(a) Fats: Esters of fatty acids with glycerol. Oils are fats in the liquid state. A long-chain carboxylic acid; those in animal fats and vegetable oils often have 12–22 carbon atoms.
(b) Waxes: Esters of fatty acids with higher molecular weight monohydric alcohols. Waxes are carboxylic acid esters, RCOOR’ ,with long, straight hydrocarbon chains in both R groups
2. Complex lipids: Esters of fatty acids containing groups in addition to an alcohol and a fatty acid.
(a) Phospholipids: Lipids containing, in addition to fatty acids and an alcohol, a phosphoric acid residue. They frequently have nitrogen containing bases and other substituents,
Eg glycerophospholipids the alcohol is glycerol
sphingophospholipids the alcohol is sphingosine.
(b) Glycolipids (glycosphingolipids): Lipids containing a fatty acid, sphingosine, and carbohydrate. These lipids contain a fatty acid, carbohydrate and nitrogenous base. The alcohol is sphingosine, hence they are also called as glycosphingolipids. Clycerol and phosphate are absent
e.g., cerebrosides, gangliosides.
(c) Other complex lipids: Lipids such as sulfolipids and aminolipids. Lipoproteins may also be placed in this category.
3. Precursor and derived lipids: These include fatty acids, glycerol, steroids, other alcohols, fatty aldehydes, and ketone bodies, hydrocarbons, lipid soluble vitamins, and hormones. Because they are uncharged, acylglycerols (glycerides), cholesterol, and cholesteryl esters are termed neutral lipids
4. Miscellaneous lipids: These include a large number of compounds possessing the characteristics of lipids e.g., carotenoids, squalene, hydrocarbons such as pentacosane (in bees wax), terpenes etc.
NEUTRAL LIPIDS: The lipids which are uncharged are referred to as neutral lipids. These are mono-, di-, and triacylglycerols, cholesterol and cholesteryl esters.
Connective tissue diseases
General Pathology
Connective tissue diseases
Marfan’s syndrome
a. Genetic transmission: autosomal dominant.
b. Characterized by a defective microfibril glycoprotein, fibrillin.
c. Clinical findings include tall stature, joints that can be hyperextended, and cardiovascular defects, including mitral valve prolapse and dilation of the ascending aorta.
Ehlers-Danlos syndrome
a. Genetic transmission: autosomal dominant or recessive.
b. This group of diseases is characterized by defects in collagen.
c. Clinical findings include hypermobile joints and highly stretchable skin. The skin also bruises easily. Oral findings include Gorlin’s sign and possible temporomandibular joint (TMJ) subluxation.
The oral mucosa may also appear more fragile and vulnerable to trauma.
Factors Considered for Prescribing Fluoride Tablets
Public Health Dentistry
Factors Considered for Prescribing Fluoride Tablets
Child's Age:
Different age groups require different dosages.
Children older than 4 years may receive lozenges or chewable tablets,
while those younger than 4 are typically prescribed liquid fluoride drops.
Fluoride Concentration in Drinking Water:
The fluoride level in the child's drinking water is crucial.
If the fluoride concentration is less than 1 part per million (ppm),
systemic fluoride supplementation is recommended.
Risk of Dental Caries:
Children at higher risk for dental decay may need additional fluoride
supplementation.
Regular dental assessments help determine the need for fluoride.
Overall Health and Dietary Needs:
Consideration of the child's overall health and any dietary restrictions
that may affect fluoride intake.
Recommended Doses of Fluoride Tablets
For Children Aged 6 Months to 4 Years:
Liquid drops are typically prescribed in doses of 0.125, 0.25, and 0.5
mg of fluoride ion.
For Children Aged 4 Years and Older:
Chewable tablets or lozenges are recommended, usually at doses of 0.5 mg
to 1 mg of fluoride ion.
Adjustments Based on Water Fluoride Levels:
Doses may be adjusted based on the fluoride content in the child's
drinking water to ensure adequate protection against dental caries.
Duration of Supplementation:
Fluoride supplementation is generally continued until the child reaches
16 years of age, depending on their fluoride exposure and dental health
status.
Endodontics - Pulp Pain & Diagnostics
Endodontics
Tooth avulsion
PedodonticsTooth Replantation and Avulsion Injuries
Tooth avulsion is a dental emergency that occurs when a tooth is completely
displaced from its socket. The success of replantation, which involves placing
the avulsed tooth back into its socket, is influenced by several factors,
including the time elapsed since the avulsion and the condition of the
periodontal ligament (PDL) tissue.
Key Factors Influencing Replantation Success
Time Elapsed Since Avulsion:
The length of time between the loss of the tooth and its
replantation is critical. The sooner a tooth can be replanted, the
better the prognosis for retention and vitality.
Prognosis Statistics:
Replantation within 30 minutes: Approximately
90% of replanted teeth show no evidence of root resorption after 2
or more years.
Replantation after 2 hours: About 95% of these
teeth exhibit root resorption.
Condition of the Tooth:
The condition of the tooth at the time of replantation, particularly
the health of the periodontal ligament tissue remaining on the root
surface, significantly affects the outcome.
Immediate replacement of a permanent tooth can sometimes lead to
vitality and indefinite retention, but this is not guaranteed.
Temporary Measure:
While replantation can be successful, it should generally be viewed
as a temporary solution. Many replanted teeth may be retained for 5 to
10 years, with a few lasting a lifetime, but others may fail shortly
after replantation.
Common Avulsion Injuries
Most Commonly Avulsed Tooth: The maxillary central
incisor is the tooth most frequently avulsed in both primary and permanent
dentition.
Demographics:
Avulsion injuries typically involve a single tooth and are three
times more common in boys than in girls.
The highest incidence occurs in children aged 7 to 9 years,
coinciding with the eruption of permanent incisors.
Structural Factors: The loosely structured periodontal
ligament surrounding erupting teeth may predispose them to complete
avulsion.
Recommendations for Management of Avulsed Teeth
Immediate Action: If a tooth is avulsed, it should be
replanted as soon as possible. If immediate replantation is not feasible,
the tooth should be kept moist.
Storage Options: The tooth can be stored in:
Cold milk (preferably whole milk)
Saline solution
Patient's own saliva (by placing it in the buccal vestibule)
A sterile saline solution
Avoid: Storing the tooth in water, as this can
damage the periodontal ligament cells.
Professional Care: Seek dental care immediately after an
avulsion injury to ensure proper replantation and follow-up care.
Pheochromocytoma
General Pathology
Pheochromocytoma
Pheochromocytomas are neoplasms composed of chromaffin cells, which as their normal counterparts synthesize and release catecholamines.
1. Arise in association with one of several familial syndromes such as MEN syndromes, type 1 neurofibromatosis, von Hippel-Lindau disease, and Sturge-Weber syndrome.
2. Are extra-adrenal, occurring in sites such as the organ of Zuckerkandl and the carotid body, where they are usually called paragangliomas rather than pheochromocytomas.
3. Are bilateral; but in association with familial syndromes, this figure may rise to 50%.
4. Are malignant; frank malignancy, however, is more common in extra-adrenal tumors.
Gross features
- The size of these tumors is quite variable ranging from small to huge masses.
- Sectioning shows yellow-tan, well-defined tumor that compress the adjacent adrenal. Large lesions display areas of hemorrhage, necrosis, and cystic degeneration.
- Incubation of the fresh tissue with potassium dichromate solutions converts the tumor a dark brown color.
Microscopic features
- These tumors are composed of polygonal to spindle-shaped chromaffin cells and their supporting sustentacular cells, arranged in well-defined small nests (Zellballen)," rimmed by a rich vascular network.
- The cytoplasm is often finely granular (catecholamine-containing granules)
- The nuclei are often quite pleomorphic.
- Both capsular and vascular invasion may be encountered in benign lesions, and the presence of mitotic figures per se does not imply malignancy. Therefore, the definitive diagnosis of malignancy in pheochromocytomas is based exclusively on the presence of metastases. These may involve regional lymph nodes as well as more distant sites, including liver, lung, and bone.
The laboratory diagnosis of pheochromocytoma is based on demonstration of increased urinary excretion of free catecholamines and their metabolites, such as vanillylmandelic acid (VMA)& metanephrines.
Muscles of the Tongue
AnatomyMuscles of the Tongue
The tongue is divided into halves by a medial fibrous lingual septum that lies deep to the medial groove.
In each half of the tongue there are four extrinsic and four intrinsic muscles.
The lingual muscles are all supplied by the hypoglossal nerve (CN XII).
The only exception is palatoglossus, which is supplied by the pharyngeal branch of the vagus nerve, via the pharyngeal plexus.
Extrinsic Muscles of the Tongue
The Genioglossus Muscle
This is a bulky, fan-shaped muscle that contributes to most of the bulk of the tongue.
It arises from a short tendon from the genial tubercle (mental spine) of the mandible.
It fans out as it enters the tongue inferiorly and its fibres attach to the entire dorsum of the tongue.
Its most inferior fibres insert into the body of the hyoid bone.
The genioglossus muscle depresses the tongue and its posterior part protrudes it.
The Hyoglossus Muscle
This is a thin, quadrilateral muscle.
It arises from the body and greater horn of the hyoid bone and passes superoanteriorly to insert into the side and inferior aspect of the tongue.
It depresses the tongue, pulling its sides inferiorly; it also aids in retrusion of the tongue.
The Styloglossus Muscle
This small, short muscle arises from the anterior border of the styloid process near its tip and from the stylohyoid ligament.
It passes inferoanteriorly to insert into the side and inferior aspect of the tongue.
The styloglossus retrudes the tongue and curls its sides to create a trough during swallowing.
The Palatopharyngeus Muscle
Superior attachment: hard palate and palatine aponeurosis.
Inferior attachment: lateral wall of pharynx.
Innervation: cranial part of accessory nerve (CN XI) through the pharyngeal branch of vagus (CN X) via the pharyngeal plexus.
This thin, flat muscle is covered with mucous membrane to form the palatopharyngeal arch.
It passes posteroinferiorly in this arch.
This muscle tenses the soft palate and pulls the walls of the pharynx superiorly, anteriorly and medially during swallowing.
Intrinsic Muscles of the Tongue
The Superior Longitudinal Muscle of the Tongue
The muscle forms a thin layer deep to the mucous membrane on the dorsum of the tongue, running from its tip to its root.
It arises from the submucosal fibrous layer and the lingual septum and inserts mainly into the mucous membrane.
This muscle curls the tip and sides of the tongue superiorly, making the dorsum of the tongue concave.
The Inferior Longitudinal Muscle of the Tongue
This muscle consists of a narrow band close to the inferior surface of the tongue.
It extends from the tip to the root of the tongue.
Some of its fibres attach to the hyoid bone.
This muscle curls the tip of the tongue inferiorly, making the dorsum of the tongue convex.
The Transverse Muscle of the Tongue
This muscle lies deep to the superior longitudinal muscle.
It arises from the fibrous lingual septum and runs lateral to its right and left margins.
Its fibres are inserted into the submucosal fibrous tissue.
The transverse muscle narrows and increases the height of the tongue.
The Vertical Muscle of the Tongue
This muscle runs inferolaterally from the dorsum of the tongue.
It flattens and broadens the tongue.
Acting with the transverse muscle, it increases the length of the tongue.