NEET MDS Synopsis
Acid-Peptic disorders
Pharmacology
Acid-Peptic disorders
This group of diseases include peptic ulcer, gastroesophageal reflux and Zollinger-Ellison syndrome.
Pathophysiology of acid-peptic disorders
Peptic ulcer disease is thought to result from an imbalance between cell– destructive effects of hydrochloric acid and pepsin on the one side, and cell-protective effects of mucus and bicarbonate on the other side. Pepsin is a proteolytic enzyme activated in gastric acid (above pH of 4, pepsin is inactive); also it can digest the stomach wall. A bacterium, Helicobacter pylori, is now accepted to be involved in the pathogenesis of peptic ulcer.
In gastroesophageal reflux the acidic contents of the stomach enter into the oesophagus causing a burning sensation in the region of the heart; hence the common name heartburn or other names such as indigestion and dyspepsia.
However, Zollinger-Ellison syndrome is caused by a tumor of gastrin secreting cells of the pancreas characterized by excessive secretion of gastrin that stimulates gastric acid secretion.
These disorders can be treated by the following classes of drugs:
A. Gastric acid neutralizers (antacids)
B. Gastric acid secretion inhibitors (antisecretory drugs)
C. Mucosal protective agents
D. Drugs that exert antimicrobial action against H.pylori
Flucloxacillin
Pharmacology
Flucloxacillin, important even now for its resistance to beta-lactamases produced by bacteria such as Staphylococcus species. It is still no match for MRSA (Methicillin Resistant Staphylococcus aureus).
The last in the line of true penicillins were the antipseudomonal penicillins, such as ticarcillin, useful for their activity against Gram-negative bacteria
Apexogenesis
Pedodontics
Apexogenesis
Apexogenesis is a vital pulp therapy procedure aimed at promoting the
continued physiological development and formation of the root end of an immature
tooth. This procedure is particularly relevant in pediatric dentistry,
where the goal is to preserve the vitality of the dental pulp in young patients,
allowing for normal root development and maturation of the tooth.
Indications for Apexogenesis
Apexogenesis is typically indicated in cases where the pulp is still vital
but has been exposed due to caries, trauma, or other factors. The procedure is
designed to maintain the health of the pulp tissue, thereby facilitating the
ongoing development of the root structure. It is most commonly performed on
immature permanent teeth, where the root has not yet fully formed.
Materials Used
Mineral Trioxide Aggregate (MTA) is frequently used in apexogenesis
procedures. MTA is a biocompatible material known for its excellent
sealing properties and ability to promote healing. It serves as a
barrier to protect the pulp and encourages the formation of a calcified barrier
at the root apex, facilitating continued root development.
Signs of Success
The most important indicator of successful apexogenesis is the
continuous completion of the root apex. This means that as the pulp
remains vital and healthy, the root continues to grow and mature, ultimately
achieving the appropriate length and thickness necessary for functional dental
health.
Contraindications
While apexogenesis can be a highly effective treatment for preserving the
vitality of the pulp in young patients, it is generally contraindicated in
children with serious systemic illnesses, such as leukemia or cancer. In these
cases, the risks associated with the procedure may outweigh the potential
benefits, and alternative treatment options may be considered.
The Salivary Glands
AnatomyThe Salivary Glands
There are three large, paired salivary glands: the parotid, submandibular, and sublingual glands.
In addition to the main salivary glands, there are numerous small accessory salivary glands scattered over the palate, lips, cheeks, tonsils, and tongue.
Carbamazepine
Pharmacology
Carbamazepine (Tegretol): most common; for generalized tonic-clonic and all partial seizures; especially active in temporal lobe epilepsies
Mechanism: ↓ reactivation of Na channels (↑ refractory period, blocks high frequency cell firing, ↓ seizure spread)
Side effects: induces hepatic microsomal enzymes (can enhance metabolism of other drugs)
Pulmonary Hypertension
General Pathology
Pulmonary Hypertension
Sustained elevation of mean pulmonary arterial pressure.
Pathogenesis
Elevated pressure, through endothelial cell dysfunction, produces structural changes in the pulmonary vasculature. These changes ultimately decrease pulmonary blood flow and stress the heart to the point of failure. Based on etiology, pulmonary hypertension is divided into two categories.
Primary (idiopathic): The cause is unknown.
Secondary: The hypertension is secondary to a variety of conditions which increase pulmonary blood flow or increase resistance to blood flow. Example: Interstitial fibrosis.
Pathology
The changes involve large and small pulmonary blood vessels and range from mild to severe. The major changes include atherosclerosis, striking medial hypertrophy and intimal fibrosis of small arteries and arterioles, and plexogenic arteriopathy. Refer to Figure 15-7 in your textbook.
Pathophysiology
Dyspnea and fatigue eventually give way to irreversible respiratory insufficiency, cyanosis and cor pulmonale.
Mycobacterium leprae
General Pathology
Mycobacterium leprae
- tuberculoid type has intact cellular immunity
- forms granulomas and kill the organisms (very few present).
- evokes a positive lepromin skin test
- localized skin lesions that lack symmetry
- nerve involvement (organisms invade Schwann cells) that dominates the clinical picture and leads to skin anesthesia, muscle atrophy and autoamputation.
- lepromatous leprosy patients lack cellular immunity
- no granulomas
- organisms readily identified
- negative lepromin skin test
- Bacteremia disseminates to cooler areas like the digits.
- symmetrical, skin lesions that produce the classic leonine facies; biopsy reveals grentz zone in superficial dermis and then organisms in macrophages.
- neural involvement is a late feature of the disease.
- lepromin skin test is to determine host immunity; not a diagnostic test.
- treatment: dapsone + rifampin
Dentin
Dental Anatomy
Dentin
1. Composition
a. Inorganic (70%)—calcium hydroxyapatite crystals.
b. Organic (30%)—water and type I collagen.
2. Types of dentin
a. Primary dentin
(1) Dentin formed during tooth development, before completion of root formation.
It constitutes the majority of dentin found in a tooth.
(2) It consists of a normal organization of dentinal tubules.
(3) Circumpulpal dentin
(a) The layer of primary dentin that surrounds the pulp chamber. It is formed after the mantle dentin.
(b) Its collagen fibers are parallel to the DEJ.
b. Secondary dentin
(1) Dentin formed after root formation is complete.
(2) Is deposited unevenly around the pulp chamber, forming along the layer of dentin closest to the pulp.
It therefore contributes to the decrease in the size of the pulp chamber as one ages.
(3) It consists of a normal, or slightly less regular, organization of dentinal tubules. However,
as compared to primary dentin, it is deposited at a slower rate.
(4) Although the dentinal tubules in secondary dentin can be continuous with those in primary
dentin, there is usually a tubular angle change between the two layers.
c. Tertiary (reparative, reactive) dentin
(1) Dentin that is formed in localized areas in response to trauma or other stimuli such as caries, tooth wear, or dental work.
(2) Its consistency and organization vary. It has no defined dentinal tubule pattern
d. Mantle dentin
(1) The outermost layer of dentin
(2) Is the first layer of dentin laid down by odontoblasts adjacent to the DEJ.
(3) Is slightly less mineralized than primary dentin.
(4) Has collagen fibers that are perpendicular to the DEJ.
(5) Dentinal tubules branch abundantly in this area.
e. Sclerotic (transparent) dentin
(1) Describes dentinal tubules that have become occluded with calcified material .
(2) Occurs when the odontoblastic processes retreat, filling the dentinal tubule with calcium phosphate crystals.
(3) Occurs with aging.
f. Dead tracts
(1) When odontoblasts die, they leave behind empty dentinal tubules, or dead tracts.
(2) Occurs with aging or trauma.
(3) Empty tubules are potential paths for bacterial invasion.
3. Structural characteristics and microscopic features:
a. Dentinal tubules
(1) Tubules extend from the DEJ to the pulp chamber.
(2) The tubules taper peripherally (i.e., their diameters are wider as they get closer to the pulp). Since the tubules are distanced farther apart at the periphery, the density of tubules is greater closer to the pulp.
(3) Each tubule contains an odontoblastic process or Tomes’ fiber.
Odontoblastic processes are characterized by the presence of a network of microtubules, with
Occasional mitochondria and vesicles present.
Note: the odontoblast’s cell body remains in the pulp chamber.
(4) Coronal tubules follow an S-shaped path, which may result from the crowding of odontoblasts as they migrate toward the pulp during dentin formation.
b. Peritubular dentin (intratubular dentin)
(1) Is deposited on the walls of the dentinal tubule, which affects (i.e., narrows)the diameter of the tubule .
(2) It differs from intertubular dentin by lacking a collagenous fibrous matrix. It is also more mineralized than intertubular dentin.
c. Intertubular dentin
(1) The main part of dentin, which fills the space between dentinal tubules
(2) Is mineralized and contains a collagenous matrix.
d. Interglobular dentin
(1) Areas of hypomineralized or unmineralized dentin caused by the failure of globules or calcospherites to fuse uniformly with mature dentin.
(2) Dentinal tubules are left undisturbed as they pass through interglobular dentin; however,
No peritubular dentin is present.
(3) Interglobular dentin is found in the:
(a) Crown—just beneath the mantle dentin.
(b) Root—beneath the dentinocemental junction, giving the root the appearance of a granular
layer (of Tomes).
e. Incremental lines
(1) Dentin is deposited at a daily rate of approximately 4 microns.
(2) As dentin is laid down, small differences in collagen fiber orientation result in the formation of incremental lines.
(3) Called imbrication lines of von Ebner.
(a) Every 5 days, or about every 20 µm, the changes in collagen fiber orientation appear more
accentuated. This results in a darker staining line, known as the imbrication line of von
Ebner.
(b) These lines are similar to the lines of Retzius seen in enamel.
f. Contour lines of Owen
(1) An optical phenomenon that occurs when the secondary curvatures of adjacent dentinal tubules coincide, resulting in the appearance of lines known as contour lines of Owen.
(2) Contour lines of Owen may also refer to lines that appear similar to those just described; however, these lines result from disturbances in mineralization.
g. Granular layer of Tomes
(1) A granular or spotty-appearing band that can be observed on the root surface adjacent to the dentinocemental junction, just beneath the cementum.