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NEET MDS Synopsis


Ketoconazole

Pharmacology


Ketoconazole

synthetic antifungal drug

used for infections such as  athlete's foot, ringworm, candidiasis (yeast infection or thrush), jock itch.

Ketoconazole is used to treat eumycetoma, the fungal form of mycetoma.

MOA: Ketoconazole is imidazole structured, and interferes with the fungal synthesis of  ergosterol, the main constituent of cell membranes, as well as certain enzymes. It is specific for fungi, as mammalian cell membranes contain no ergosterol.

Sensitive fungi Ketoconazole inhibits growth of  dermatophytes and  yeast species (such as Candida albicans).

Oral Medicine Questions 1
Oral Medicine

1. Where does a follicular cyst form?

1) Gingiva
2) Root
3) Crown
4) Basel cell

Answer: 3

Follicular cysts form around the crown of an unerupted, developing tooth. It is the second most common cyst. The cyst usually develops on the third molar, maxillary canine, or maxillary third molar.


2. Stevens-Johnson syndrome and TENs are variants of which disease?

1. Aphthous ulcers
2. Penphigus vulgaris
3. Erythema multiforme
4. Lichen Planus

Answer: 3

 - Stevens-Johnson syndrome and TENs are variants of erythema multiforme.
 
The origins of the lesions are from sulfa drugs, vaccinations, and viral infections. These lesions primarily present on the face and extremities. Oral lesions present as vesicles and ulcerations and spread widely throughout the oral cavity. Stevens-Johnson syndrome is considered erythema multiforme miner. If it is severe, lesions display on skin, conjunctiva, genitalia, and oral mucosa, and triggered by drugs. Treatment includes systemic corticosteroids, acyclovir, and the discontinuation of causative drugs. TENs, the most severe form of erythema multiforme, must be treated in a burn unit.

3. White sponge nevus is caused by a mutation of what gene:

1. Keratin 4 and 13
2. Keratin 5 and 12
3. Keratin 1 and 49
4. Keratin 21 and 23

Answer:1

- White sponge nevus is caused by a mutation of genes keratin 4 and keratin13. It is an autosomal dominate genetic disorder. The condition is also known as familial epithelial hyperplasia, or Cannon's disease. The mass is bilateral and rough due to epithelial thickening in the buccal mucosa. There is not treatment required.


4. Erythroplakia is:

1. Greenish plaque
2. Brown plaque
3. Red plaque
4. Yellowish plaque

Answer: 3

 - Erythroplakia is red plaque that has no clinical diagnoses and fails to resolve with several weeks with or without treatment. Biopsy is the only way to diagnose. There are three Erythroplakia conditions: median rhomboid glossitis, hereditary hemorrhagic telangiectasias, and hemangioma. Treatment is not often required beyond corticosteroid therapy to larger lesions.

5. Inflammatory papillary hyperplasia is also known as:

1. Papilloma
2. Verruca vulgaris
3. Denture papillomatosis
4. Inflammatory papillary hyperplasia

Answer: 3

 - Inflammatory papillary hyperplasia is also known as denture papillomatosis. The condition is caused by poor oral hygiene by denture wearers, poor fitting dentures, or reactive tissue growth from the wearing of dentures. Treatment options are the readjustment of dentures, removal of dentures to allow lesion-healing time, and removal of lesion by cryosurgery or curettage.

 

Classification for antiasthmatic drugs.
Pharmacology

ANTIASTHMATIC AGENTS

 Classification for antiasthmatic drugs.
 
I. Bronchodilators

i. Sympathomimetics (adrenergic receptor agonists)

Adrenaline, ephedrine, isoprenaline, orciprenaline, salbutamol, terbutaline, salmeterol, bambuterol

ii. Methylxanthines (theophylline and its derivatives)

Theophylline 
Hydroxyethyl theophylline 
Theophylline ethanolate of piperazine

iii. Anticholinergics

Atropine methonitrate 
Ipratropium bromide

II. Mast cell stabilizer

Sodium cromoglycate
Ketotifen 


III. Corticosteroids

Beclomethasone dipropionate 
Beclomethasone (200 µg) with salbutamol

IV. Leukotriene pathway inhibitors 

Montelukast 
Zafirlukast

Acute pericarditis
General Pathology

Acute pericarditis

1. Characterized by inflammation of the pericardium.
2. Causes include:
a. Viral infection.
b. Bacterial infection, including Staphylococcus, Pneumococcus.
c. Tuberculosis.
d. MI.
e. Systemic lupus erythematosus.
f. Rheumatic fever.

3. Signs and symptoms include:
a. Pericardial friction rub on cardiac auscultation.
b. Angina.
c. Fever.

4. Consequences include constrictive pericarditis,which results from fusion and scarring of the pericardium. This may lead to the restriction of ventricular expansion, preventing the heart chambers from filling normally.

Nasogastric Tube (Ryles Tube)
Oral and Maxillofacial Surgery

Nasogastric Tube (Ryles Tube)
A nasogastric tube (NG tube), commonly referred to as a Ryles
tube, is a medical device used for various purposes, primarily
involving the stomach. It is a long, hollow tube made of polyvinyl chloride
(PVC) with one blunt end and multiple openings along its length. The tube is
designed to be inserted through the nostril, down the esophagus, and into the
stomach.
Description and Insertion


Structure: The NG tube has a blunt end that is inserted
into the nostril, and it features multiple openings to allow for the passage
of fluids and air. The open end of the tube is used for feeding or drainage.


Insertion Technique:

The tube is gently passed through one of the nostrils and advanced
through the nasopharynx and into the esophagus.
Care is taken to ensure that the tube follows the natural curvature
of the nasal passages and esophagus.
Once the tube is in place, its position must be confirmed before any
feeds or medications are administered.



Position Confirmation:

To check the position of the tube, air is pushed into the tube using
a syringe.
The presence of air in the stomach is confirmed by auscultation with
a stethoscope, listening for the characteristic "whoosh" sound of air
entering the stomach.
Only after confirming that the tube is correctly positioned in the
stomach should feeding or medication administration begin.



Securing the Tube: The tube is fixed to the nose using
sticking plaster or adhesive tape to prevent displacement.


Uses of Nasogastric Tube


Nutritional Support:

Enteral Feeding: The primary use of a nasogastric
tube is to provide nutritional support to patients who are unable to
take oral feeds due to various reasons, such as:
Neurological conditions (e.g., stroke, coma)
Surgical procedures affecting the gastrointestinal tract
Severe dysphagia (difficulty swallowing)





Gastric Lavage:

Postoperative Care: NG tubes can be used for
gastric lavage to flush out blood, fluids, or other contents from the
stomach after surgery. This is particularly important in cases where
there is a risk of aspiration or when the stomach needs to be emptied.
Poisoning: In cases of poisoning or overdose,
gastric lavage may be performed using an NG tube to remove toxic
substances from the stomach. This procedure should be done promptly and
under medical supervision.



Decompression:

Relieving Distension: The NG tube can also be used
to decompress the stomach in cases of bowel obstruction or ileus,
allowing for the removal of excess gas and fluid.



Medication Administration:

The tube can be used to administer medications directly into the
stomach for patients who cannot take oral medications.



Considerations and Complications


Patient Comfort: Insertion of the NG tube can be
uncomfortable for patients, and proper technique should be used to minimize
discomfort.


Complications: Potential complications include:

Nasal and esophageal irritation or injury
Misplacement of the tube into the lungs, leading to aspiration
Sinusitis or nasal ulceration with prolonged use
Gastrointestinal complications, such as gastric erosion or
ulceration



Hyperparathyroidism 
General Pathology

Hyperparathyroidism 

Abnormally high levels of parathyroid hormone (PTH) cause hypercalcemia. This can result from either primary or secondary causes. Primary hyperparathyroidism is caused usually by a parathyroid adenoma, which is associated with autonomous PTH secretion. Secondary  hyperparathyroidism, on the other hand, can occur in the setting of chronic renal failure. In either situation, the presence of excessive amounts of this hormone leads to significant skeletal changes related to a persistently exuberant osteoclast activity that is associated with increased bone resorption and calcium mobilization. The entire skeleton is affected. PTH is directly responsible for the bone changes seen in primary hyperparathyroidism, but in secondary hyperparathyroidism additional influences also contribute. In chronic renal failure there is inadequate 1,25- (OH)2-D synthesis that ultimately affects gastrointestinal calcium absorption. The hyperphosphatemia of renal
failure also suppresses renal α1-hydroxylase, which further impair vitamin D synthesis; all these eventuate in hypocalcemia, which stimulates excessive secretion of PTH by the parathyroid glands, & hence elevation in PTH serum levels. 

Gross features
• There is increased osteoclastic activity, with bone resorption. Cortical and trabecular bone are lost and replaced by loose connective tissue. 
• Bone resorption is especially pronounced in the subperiosteal regions and produces characteristic radiographic changes, best seen along the radial aspect of the middle phalanges of the second and third fingers.

Microscopical features

• There is increased numbers of osteoclasts and accompanying erosion of bone surfaces.
• The marrow space contains increased amounts of loose fibrovascular tissue.
• Hemosiderin deposits are present, reflecting episodes of hemorrhage resulting from microfractures of the weakened bone.
• In some instances, collections of osteoclasts, reactive giant cells, and hemorrhagic debris form a distinct mass, termed "brown tumor of hyperparathyroidism". Cystic change is common in such lesions (hence the name osteitis fibrosa cystica). Patients with hyperparathyroidism have reduced bone mass, and hence are increasingly susceptible to fractures and bone deformities.

Str. Pneumoniae
General Pathology

Str. Pneumoniae

Probably the most important streptococci.  Primary cause of pneumonia.  Usually are diplococci.  Ste. pneumoniae are α-hemolytic and nutritionally fastidious.  Often are normal flora.

Key virulence factor is the capsule polysaccharide which prevents phagocytosis.  Other virulence factors include pneumococcal surface protein and α-hemolysin.

Major disease is pneumonia, usually following a viral respiratory infection.  Characterized by fever, cough, purulent sputum.  Bacteria infiltrates alveoli.  PMN’s fill alveoli, but don’t  cause necrosis. Also can cause meningitis, otitis, sinusitis.

There are vaccines against the capsule polysaccharide.  Resistance to penicillin, cephalosporins, erythromycins, and fluoroquinalones is increasing.

The Lips
Anatomy

The Lips


These are mobile muscular folds that surround the mouth, the entrance of the oral cavity.



The lips (L. labia) are covered externally by skin and internally by mucous membrane.
In between these are layers of muscles, especially the orbicularis oris muscle.



The upper and lower lips are attached to the gingivae in the median plane by raised folds of mucous membrane, called the labial frenula.


Sensory Nerves of the Lips


The sensory nerves of the upper and lower lips are from the infraorbital and mental nerves, which are branches of the maxillary (CN V2) and mandibular (CN V3) nerves.

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