NEET MDS Synopsis
Recurrent Aphthous Ulcers
Pedodontics
Recurrent Aphthous Ulcers (Canker Sores)
Overview of Recurrent Aphthous Ulcers (RAU)
Definition:
Recurrent aphthous ulcers, commonly known as canker sores, are painful
ulcerations that occur on the unattached mucous membranes of the mouth.
They are characterized by their recurrent nature and can significantly
impact the quality of life for affected individuals.
Demographics:
RAU is most prevalent in school-aged children and young adults, with a
peak incidence between the ages of 10 and 19 years.
It is reported to be the most common mucosal disorder across various
ages and races globally.
Clinical Features
Characteristics:
RAU is defined by recurrent ulcerations on the moist mucous membranes of
the mouth.
Lesions can be discrete or confluent, forming rapidly in certain areas.
They typically feature:
A round to oval crateriform base.
Raised, reddened margins.
Significant pain.
Types of Lesions:
Minor Aphthous Ulcers:
Usually single, smaller lesions that heal without scarring.
Major Aphthous Ulcers (RAS):
Larger, more painful lesions that may take longer to heal and can
leave scars.
Also referred to as periadenitis mucosa necrotica recurrens or
Sutton disease.
Herpetiform Ulcers:
Multiple small lesions that can appear in clusters.
Duration and Healing:
Lesions typically persist for 4 to 12 days and heal uneventfully, with
scarring occurring only rarely and usually in cases of unusually large
lesions.
Epidemiology
Prevalence:
The condition occurs approximately three times more frequently in white
children compared to black children.
Prevalence estimates of RAU range from 2% to 50%, with most estimates
falling between 5% and 25%. Among medical and dental students, the
estimated prevalence is between 50% and 60%.
Associated Conditions
Systemic Associations:
RAS has been linked to several systemic diseases, including:
PFAPA Syndrome: Periodic fever, aphthous stomatitis,
pharyngitis, and adenitis.
Behçet Disease: A systemic condition characterized by
recurrent oral and genital ulcers.
Crohn's Disease: An inflammatory bowel disease that can
present with oral manifestations.
Ulcerative Colitis: Another form of inflammatory bowel
disease.
Celiac Disease: An autoimmune disorder triggered by gluten.
Neutropenia: A condition characterized by low levels of
neutrophils, leading to increased susceptibility to infections.
Immunodeficiency Syndromes: Conditions that impair the
immune system.
Reiter Syndrome: A type of reactive arthritis that can
present with oral ulcers.
Systemic Lupus Erythematosus: An autoimmune disease that
can cause various oral lesions.
MAGIC Syndrome: Mouth and genital ulcers with inflamed
cartilage.
Oral Habits
PedodonticsClassification of Oral Habits
Oral habits can be classified based on various criteria, including their
nature, impact, and the underlying motivations for the behavior. Below is a
detailed classification of oral habits:
1. Based on Nature of the Habit
Obsessive Habits (Deep Rooted):
International or Meaningful:
Examples: Nail biting, digit sucking, lip biting.
Masochistic (Self-Inflicting):
Examples: Gingival stripping (damaging the gums).
Unintentional (Empty):
Examples: Abnormal pillowing, chin propping.
Non-Obsessive Habits (Easily Learned and Dropped):
Functional Habits:
Examples: Mouth breathing, tongue thrusting, bruxism (teeth
grinding).
2. Based on Impact
Useful Habits:
Habits that may have a positive or neutral effect on oral health.
Harmful Habits:
Habits that can lead to dental issues, such as malocclusion,
gingival damage, or tooth wear.
3. Based on Author Classifications
James (1923):
a) Useful Habits
b) Harmful Habits
Kingsley (1958):
a) Functional Oral Habits
b) Muscular Habits
c) Combined Habits
Morris and Bohanna (1969):
a) Pressure Habits
b) Non-Pressure Habits
c) Biting Habits
Klein (1971):
a) Empty Habits
b) Meaningful Habits
Finn (1987):
I. a) Compulsive Habits
b) Non-Compulsive Habits
II. a) Primary Habits
4. Based on Functionality
Functional Habits:
Habits that serve a purpose, such as aiding in speech or feeding.
Dysfunctional Habits:
Habits that disrupt normal oral function or lead to negative
consequences.
Skeletal System Formation
Anatomy
Bones begin to form during the eighth week of embryomic life in the fibrous membranes (intramembranous ossification) and hyaline cartilage (endochondral ossification)
Viscera/organ development
AnatomyEye
At week 4, two depressions are evident on each of the forebrain hemispheres. As the anterior neural fold closes, the optic pits elongate to form the optic vesicles. The optic vesicles remain connected to the forebrain by optic stalks.
The invagination of the optic vesicles forms a bilayered optic cup. The bilayered cup becomes the dual layered retina (neural and pigmented layer)
Surface ectoderm forms the lens placode, which invaginates with the optic cup.
The optic stalk is deficient ventrally to contain choroids fissure to allow blood vessels into the eye (hyaloid artery). The artery feeds the growing lens, but will its distal portion will eventually degenerate such that the adult lens receives no hyaloid vasculature.
At the 7th week, the choroids fissure closes and walls fuse as the retinal nerve get bigger.
The anterior rim of the optic vesicles forms the retina and iris. The iris is an outgrowth of the distal edge of the retina.
Optic vesicles induces/maintains the development of the lens vesicle, which forms the definitive lens. Following separation of the lens vesicle from the surface ectoderm, the cornea develops in the anterior 1/5th of the eye.
The lens and retina are surrounded by mesenchyme which forms a tough connective tissue, the sclera, that is continuous with the dura mater around the optic nerve.
Iridopupillary membrane forms to separate the anterior and posterior chambers of the eye. The membrane breaks down to allow for the pupil
Mesenchyme surrounding the forming eye forms musculature (ciliary muscles and pupillary muscles – from somitomeres 1 and 2; innervated by CN III), supportive connective tissue elements and vasculature.
Eyelids
Formed by an outgrowth of ectoderm that is fused at its midline in the 2nd trimester, but later reopen.
Lipids
PhysiologyLipids:
about 40% of the dry mass of a typical cell
composed largely of carbon & hydrogen
generally insoluble in water
involved mainly with long-term energy storage; other functions are as structural components (as in the case of phospholipids that are the major building block in cell membranes) and as "messengers" (hormones) that play roles in communications within and between cells
Subclasses include:
Triglycerides - consist of one glycerol molecule + 3 fatty acids (e.g., stearic acid in the diagram below). Fatty acids typically consist of chains of 16 or 18 carbons (plus lots of hydrogens).
phospholipids - Composed of 2 fatty acids, glycerol, phosphate and polar groups , phosphate group (-PO4) substitutes for one fatty acid & these lipids are an important component of cell membranes
steroids - have 4 rings- cholesterol, some hormones, found in membranes include testosterone, estrogen, & cholesterol
Smallpox (variola)
General Pathology
Smallpox (variola)
- vesicles are well synchronized (same stage of development) and cover the skin and mucous membranes.
- vesicles rupture and leave pock marks with permanent scarring.
STOMACH pathology
General Pathology
STOMACH
Congenital malformations
1. Pyloric stenosis
Clinical features. Projectile vomiting 3-4 weeks after birth associated with a palpable "olive" mass in the epigastric region is observed.
Pathology shows hypertrophy of the muscularis of the pylorus and failure to relax.
2. Diaphragmatic hernias are due to weakness in or absence of parts of the diaphragm, allowing herniation of the abdominal contents into the thorax.
Inflammation
1. Acute gastritis (erosive)
Etiology. Alcohol, aspirin and other NSAIDs, smoking, shock, steroids, and uremia may all cause disruption of the mucosal barrier, leading to inflammation.
Clinical features. Patients experience heartburn, epigastric pain, nausea, vomiting, hematemesis, and even melena.
2. Chronic gastritis (nonerosive) may lead to atrophic mucosa with lymphocytic infiltration.
Types
(1) Fundal (Type A) gastritis is often autoimmune in origin. It is the type associated with pernicious anemia and, therefore, achlorhydria and intrinsic factor deficiency.
(2) Antral (Type B) gastritis is most commonly caused by Helicobacter pylori and is the most common form of chronic gastritis in the U.S. H. pylori is also responsible for proximal duodenitis in regions of gastric metaplasia.
Clinical features. The patient may be asymptomatic or suffer epigastric pain, nausea, vomiting, and bleeding. Gastritis may predispose to peptic ulcer disease, probably related to H. pylori infection.
3. Peptic ulcers
Peptic ulcers are usually chronic, isolated ulcers observed in areas bathed by pepsin and HCI; they are the result of mucosal breakdown
Common locations are the proximal duodenum, the stomach, and the esophagus, often in areas of Barrett's esophagus.
Etiology. There are several important etiologic factors.
Duodenal ulcers occur predominantly in patients with excess acid secretion, while gastric ulcers usually occur in patients with lower than average acid secretion.
Other predisposing conditions include smoking, cirrhosis, pancreatitis, hyperparathyroidism, and H. pylori infection. Aspirin, steroids, and NSAlDs are known to be assoicated with peptic ulcer disease. Next to H. pylori colonization, aspirin or NSAID ingestion is the most common cause of peptic ulcer.
Clinical features. Patients experience episodic epigastric pain. Duodenal and most gastric ulcers are relieved by food or antacids. Approximately one-fifth of gastric ulcer patients get no relief from eating or experience pain again within 30 minutes.
Pathology. Benign peptic ulcers are well-circumscribed lesions with a loss of the mucosa, underlying scarring, and sharp walls.
Complications include hemorrhage, perforation, obstruction, and pain. Duodenal ulcers do not become malignant .Gastric ulcers do so only rarely; those found to be ma1ignant likely originated as a cancer that ulcerated.
Diagnosis is made by upper gastrointestinal Series , endoscopy, and biopsy to rule out malignancy or to demonstrate the presence of H. pylori.
4. Stress ulcers
are superficial mucosal ulcers of the stomach or duodenum or both. Stress may be induced by burns, sepsis shock, trauma, or increased intracranial pressure.
Tumors
1. Benign
a. Leiomyoma, often multiple, is the most common benign neoplasm of the stomach. Clinical features include bleeding, pain, and iron deficiency anemia.
b. Gastric polyps are due to proliferation of the mucosal epithelium.
2. Malignant tumors
a. Carcinoma
Etiology. Primary factors include genetic predisposition and diet; other factors include hypochlorhydria, pernicious anemia, atrophic gastritis, adenomatous polyps, and exposure to nitrosamines. H. pylori are also implicated.
Clinical features. Stomach cancer is usually asymptomatic until late, then presents with anorexia, weight loss, anemia, epigastric pain, and melena. Virchow's node is a common site of metastasis.
Pathology. Symptomatic late gastric carcinoma may be expanding or infiltrative. In both cases the prognosis is poor (approximately 10% 5-year survival), and metastases are frequently present at the time of diagnosis.
Adenocarcinomas are most common.
b. Gastrointestinal lymphomas may be primary In the gastrointestinal tract as solitary masses.
c. Sarcoma is a rare, large, ulcerating mass that extends into the lumen.
d. Metastatic carcinoma. Krukenberg's tumor is an ovaria metastasis from a gastric carcinoma.
e. Kaposi's sarcoma. The stomach is the most commonly involved GI organ in Kaposi's sarcoma. It primarily occurs in homosexual men, appearing as hemorrhagic polypoid, umbilicated nodular lesions, typically in a submucosal location. It rarely causes symptoms
Serum Lipids
PhysiologySerum Lipids
LIPID
Typical values (mg/dl)
Desirable (mg/dl)
Cholesterol (total)
170–210
<200
LDL cholesterol
60–140
<100
HDL cholesterol
35–85
>40
Triglycerides
40–160
<160
Total cholesterol is the sum of
HDL cholesterol
LDL cholesterol and
20% of the triglyceride value
Note that
high LDL values are bad, but
high HDL values are good.
Using the various values, one can calculate a
cardiac risk ratio = total cholesterol divided by HDL cholesterol
A cardiac risk ratio greater than 7 is considered a warning.