NEET MDS Synopsis
Dental trauma types in endodontics
EndodonticsIn endodontics, dental trauma often results in the luxation of teeth, which
is the displacement of a tooth from its normal position in the alveolus (the
bone socket that holds the tooth). There are several types of luxation injuries,
each with different endodontic implications. Here are the main types of dental
luxation:
1. Concussion: A tooth is injured but not displaced from its socket. The
periodontal ligament (PDL) is compressed and may experience hemorrhage. The
tooth is usually not loose and does not require repositioning. However, it can
be tender to percussion and may exhibit some mobility. The pulp may remain
vital, but it can become inflamed or necrotic due to the trauma.
2. Subluxation: The tooth is partially displaced but remains in the socket. It
shows increased mobility in all directions but can be repositioned with minimal
resistance. The PDL is stretched and may be damaged, leading to pulpal and
periodontal issues. Endodontic treatment is often not necessary unless symptoms
of pulp damage arise.
3. Lateral luxation: The tooth is displaced in a horizontal direction and may be
pushed towards the adjacent teeth. The PDL is stretched and possibly torn. The
tooth may be pushed out of alignment or into an incorrect position in the arch.
Prompt repositioning and splinting are crucial. The pulp can be injured, and the
likelihood of endodontic treatment may increase.
4. Intrusion: The tooth is pushed into the alveolar bone, either partially or
completely. This can cause significant damage to the PDL and the surrounding
bone tissue. The tooth may appear shorter than its neighbors. The pulp is often
traumatized and can die if not treated quickly. Endodontic treatment is usually
required after repositioning and stabilization.
5. Extrusion: The tooth is partially displaced out of its socket. The PDL is
stretched and sometimes torn. The tooth appears longer than its neighbors. The
pulp is frequently exposed, which increases the risk of infection and necrosis.
Repositioning and endodontic treatment are typically necessary.
6. Avulsion: The tooth is completely knocked out of its socket. The PDL is
completely severed, and the tooth may have associated soft tissue injuries. Time
is of the essence in these cases. If the tooth can be replanted within 30
minutes and properly managed, the chances of saving the pulp are higher.
Endodontic treatment is usually needed, with the possibility of a root canal or
revascularization.
7. Inverse luxation: This is a rare type of luxation where the tooth is
displaced upwards into the alveolar bone. The tooth is pushed into the bone,
which can cause severe damage to the PDL and surrounding tissues. Endodontic
treatment is often necessary.
8. Dystopia: Although not a true luxation, it's worth mentioning that a tooth
can be displaced during eruption. This can cause the tooth to emerge in an
abnormal position. Endodontic treatment may be necessary if the tooth does not
respond to orthodontic treatment or if the displacement causes pain or
infection.
The endodontic management of luxated teeth varies depending on the severity of
the injury and the condition of the pulp. Treatments can range from simple
monitoring to root canal therapy, apicoectomy, or even tooth extraction in
severe cases. The goal is always to preserve the tooth and prevent further
complications.
Adult Respiratory Distress Syndrome
General Pathology
Adult Respiratory Distress Syndrome
A constellation of pathologic and clinical findings initiated by diffuse injury to alveolar capillaries. This syndrome is associated with a multitude of clinical conditions which primarily damage the lung or secondarily as part of a systemic disorder.
Pathogenesis
There are many types of injuries which lead to the ultimate, common pathway, i.e., damage to the alveolar capillary unit. The initial injury most frequently affects the endothelium, less frequently the alveolar epithelium. Injury produces increased vascular permeability, edema, fibrin-exudation (hyaline membranes). Leukocytes (primarily neutrophils) plays a key role in endothelial damage.
Pathology
Heavy, red lungs showing congestion and edema. The alveoli contain fluid and are lined by hyaline membranes.
Pathophysiology
Severe respiratory insufficiency with dyspnea, cyanosis and hypoxemia refractory to oxygen therapy.
Desquamative Gingivitis
PeriodontologyDesquamative Gingivitis
Characteristics: Desquamative gingivitis is
characterized by intense erythema, desquamation, and ulceration of both free
and attached gingiva.
Associated Diseases:
Lichen Planus
Pemphigus
Pemphigoid
Linear IgA Disease
Chronic Ulcerative Stomatitis
Epidermolysis Bullosa
Systemic Lupus Erythematosus (SLE)
Dermatitis Herpetiformis
Nephrolithiasis, urolithiasis
General Pathology
Nephrolithiasis, urolithiasis
Formation of calculi (calcium stones) in the kidney (nephrolithiasis) or urinary tract (urolithiasis).
Commonly associated with hyperparathyroidism.
Signs and symptoms
urinary tract obstruction, severe pain, and pyelonephritis.
Note: an enlarged prostate can also cause urinary tract obstruction in males.
THE PLASMIDS
General Microbiology
THE PLASMIDS
The extrachromosomal genetic elements, called as plasmids are autonomously replicating , cyclic ,double stranded DNA molecules which are distinct from the cellular chromosome
Classification
Plasmids can be broadly classified as conjugative and nonconjugative.
Conjugative plasmids are large and self-transmissible i.e. they have an apparatus through which they can mediate their own transfer to another cell after coming in contact with the same. Example: RF and certain bacteriocinogen plasmids.
Nonconjugative plasmids are small in size and can be mobilised for transfer into another cell only through the help of a conjugative plasmid. To this group belong some ‘r’ determinants and few bacteriocinogenic plasmids. Plasmids can also be transferred without cell contact by the process of transfection.
Properties of plasmids
Double stranded DNA , Autonomously replicate in host cell, Plasmd specific, Free DNA is transferred b transfection
Significance of Plasmids :The spread of resistance to antibiotics is one such well known example. These also play an important role in the geochemical cycle by spreading genes for the degradation of complex organic compounds.
SMALL INTESTINE pathology
General Pathology
SMALL INTESTINE
Congenital anomalies
1. Meckel's diverticulum (a true diverticulum) is due to persistence of the omphalomesenteric vitelline duct.
2. Atresia is a congenital absence of a region of bowel, leaving a blind pouch or solid fibrous cord.
3. Stenosis refers to a narrowing of any region of the gastrointestinal tract, which may cause obstruction.
4. Duodenal diverticula are areas of congenital weakness permitting saccular enlargement. The duodenum is the most common region of the small bowel to contain diverticula.
5. Diverticula of jejunum and ileum are herniations of mucosa and submucosa at points where the mesenteric vessels and nerves enter.
Infections
1. Bacterial enterocolitis may be caused by the ingestion of preformed bacterial toxins, producing symptoms ranging from severe but transient nausea, vomiting, and diarrhea (Staphylococcus aureus toxin) to lethal paralysis (Clostridium botulinum toxin). Ingestion of toxigenic bacteria with colonization of the gut (e.g., Vibrio cholera, toxigenic E. coli, various species of Campylobacter jejuni, Shigella, salmonel
Yersinia, and many others) is another potential cause.
2. Nonbacterial gastroenterocolitis
a. Viral
(1) Rotavirus (children)
(2) Parvovirus (adults)
b. Fungal-Candida
c. Parasitic
(1 ) Entamoeba histolytica
(2) Giardia lamblia
3. In HIV patients. Causes of infectious diarrhea in HIV patients include Cryptosporidium, Microsporidia, isospora belli, CMV, and M. avium-intracellulare.
C. Malabsorption is defined as impaired intestinal absorption of dietary constituents.
Clinical features include diarrhea,steatorrhea, weakness, lassitude, and weight loss. Steatorrhea results in deficiency of fat-soluble vitamins (A, D, E, K) and calcium.
1. Celiac sprue
a. Etiology. Celiac sprue (nontropical sprue or gluten enteropathy) is caused by an allergic, immunologic, or toxic reaction to the gliadin component of gluten. There is a genetic predisposition.
Symptoms:
– Steatorrhea, abdominal distention, flatulence, fatigue, and weight loss
Complications:
– Iron and vitamin deficiency
– Risk of lymphoma (T-cell type)
Extraintestinal manifestation:
– Dermatitis herpetiformis (a pruritic papulovesicular rash with IgA deposits at the dermoepidermal junction)
2. Tropical sprue
Etiology. Tropical sprue is of unknown etiology, but may be caused by enterotoxigenic E. coli.
3. Disaccharidase deficiency is due to a deficiency of brush border enzymes. Lactase deficiency is most common.
4. Diverticulosis Coli
- Acquired colonic diverticula are present in nearly half of the population over the age of 50
- Diverticula are associated with low-fiber, low-residue diets
- Etiology is most likely high intraluminal pressure required for propulsion of hard, small stools
- Complications include hemorrhage, acute diverticulitis, perforation, fistula formation
Obstructive lesions
Hernias cause 15% of small intestinal obstruction. They are due to a protrusion of a serosa-lined sac through a weakness in the wall of the peritoneal cavity. They occur most commonly at the inguinal and femoral canals, at the umbilicus, and with scars. They may lead to entrapment, incarceration, and strangulation of the bowel.
Tumors of the small bowel account for only 5% of gastrointestinal tumors.
Benign tumors in descending order of frequency include:
leiomyomas, lipomas, adenomas (polyps), angiomas, and fibromas. Adenomatous polyps are most common in the stomach and duodenum and may be single or multiple, sessile or pedunculated. The larger the polyp, the greater the incidence of malignant transformation.
Malignant tumors, in descending order of frequency, include: endocrine cell tumors, lymphomas, adenocarcinomas, and leiomyosarcomas.
Idiopathic Inflammatory Bowel Disease (IBD)
- Chronic, relapsing, idiopathic inflamamtory disease of the GI tract
Crohn’s Disease
– Transmural granulomatous disease affecting any portion of the GI tract
Ulcerative Colitis
– Superficial, non-granulomatous inflammatory disease restricted to the colon
Ulcerative Colitis
- Bloody mucoid diarrhea, rarely toxic megacolon
- Can begin at any age, peaks at 20-25 years
- Annual incidence of ~10 per 100,000 in US
- Negligible risk of cancer in the first 10 years, but 1% per year risk of cancer thereafter
- Good response to total colectomy if medical therapy fails
Macroscopic
- Normal serosa
- Bowel normal thickness
- Continuous disease
- Confluent mucosal ulceration
- Pseudopolyp formation
Microscopic
- Crypt distortion + shortening
- Paneth cell metaplasia
- Diffuse mucosal inflammation
- Crypt abscesses
- Mucin depletion
- Mucosal ulceration
Crohn’s Disease
- Variable and elusive clinical presentation with diarrhea, pain, weight loss, anorexia, fever
- Can begin at any age, peaks at 15-25 years
- Annual incidence of ~3 per 100,000 in US
- Many GI complications and extracolonic manifestations
- Risk of cancer less than in UC
- Poor response to surgery
Macroscopic
Fat wrapping
Thickened bowel wall
Skip Lesions
Stricture formation
Cobblestoned mucosa
Ulceration
Microscopic
- Cryptitis and crypt abscesses
- Transmural inflammation
- Lymphoid aggregates +/- granulomas
- “Crohn’s rosary”
- Fissuring
- Neuromuscular hyperplasia
SALIVARY GLANDS Embryonic development
Dental Anatomy
Embryonic development
The parotid derives from ectoderm
The sublingual-submandibular glands thought to derive from endoderm
Differentiation of the ectomesenchyme
Development of fibrous capsule
Formation of septa that divide the gland into lobes and lobules
The parotid develops around 4-6 weeks of embryonic lofe
The submandibular gland develops around the 6th week
The sublingual and the minor glands develop around the 8-12 week
Pneumoconioses
General Pathology
Pneumoconioses—are environmentally related lung diseases that result from chronic inhalation of various substances.
1. Silicosis (stone mason’s disease)
a. Inhalant: silica dust.
b. Associated with extensive fibrosis of the lungs.
c. Patients have a higher susceptibility to tuberculosis infections.
2. Asbestosis
a. Inhalant: asbestos fibers.
b. Associated with the presence of pleural plaques.
c. Consequences include:
(1) Mesothelioma (malignant mesothelial tumor).
(2) Bronchogenic carcinoma.
3. Anthracosis
a. Inhalant: carbon dust.
b. Usually not as harmful as silicosis or asbestosis.
c. Associated with the presence of macrophages containing carbon.