NEET MDS Synopsis
ADRENAL INSUFFICIENCY
General Pathology
ADRENAL INSUFFICIENCY
Adrenocortical hypofunction is either primary (adrenocrtical) or secondary (ACTH deficiency). Primary insufficiency is divided into acute & chronic.
Acute Adrenocortical Insufficiency occurs most commonly in the following clinical settings
- massive adrenal hemorrhage including Waterhouse-Friderichsen syndrome
- Sudden withdrawal of long-term corticosteroid therapy
- Stress in those with chronic adrenal insufficiency
Massive adrenal hemorrhage may destroy the adrenal cortex sufficiently to cause acute adrenocortical
insufficiency. This condition may occur
1. in patients maintained on anticoagulant therapy
2. in postoperative patients who develop DIC
3. during pregnancy
4. in patients suffering from overwhelming sepsis (Waterhouse-Friderichsen syndrome)
Waterhouse-Friderichsen syndrome is a catastrophic syndrome classically associated with Neisseria meningitidis septicemia but can also be caused by other organisms, including Pseudomonas species, pneumococci & Haemophilus influenzae. The pathogenesis of the syndrome remains unclear, but probably involves endotoxin-induced vascular injury with associated DIC.
Chronic adrenocortical insufficiency (Addison disease) results from progressive destruction of the adrenal cortex. More than 90% of all cases are attributable to one of four disorders:
1. autoimmune adrenalitis (the most common cause; 70% of cases)
2. tuberculosis &fungal infections
3. AIDS
4. Metastatic cancers
In such primary diseases, there is hyperpigmentation of the skin oral mucosa due to high levels of MSH (associated with high levels of ACTH).
Autoimmune adrenalitis is due to autoimmune destruction of steroid-producing cells. It is either isolated associated other autoimmune diseases, such as Hashimoto disease, pernicious anemia, etc.
Infections, particularly tuberculous and fungal
Tuberculous adrenalitis, which once was responsible for as many as 90% of cases of Addison disease, has become less common with the advent of antituberculous therapy. When present, tuberculous adrenalitis is usually associated with active infection elsewhere, particularly the lungs and genitourinary tract. Among fungi, disseminated infections caused by Histoplasma capsulatum is the main cause.
AIDS patients are at risk for developing adrenal insufficiency from several infectious (cytomegalovirus, Mycobacterium avium-intracellulare) and noninfectious (Kaposi sarcoma) complications.
Metastatic neoplasms: the adrenals are a fairly common site for metastases in persons with disseminated carcinomas. Although adrenal function is preserved in most such patients, the metastatic growths sometimes destroy sufficient adrenal cortex to produce a degree of adrenal insufficiency. Carcinomas of the lung and breast are the major primary sources.
Secondary Adrenocortical Insufficiency
Any disorder of the hypothalamus and pituitary, such as metastatic cancer, infection, infarction, or irradiation, that reduces the output of ACTH leads to a syndrome of hypoadrenalism having many similarities to Addison disease. In such secondary disease, the hyperpigmentation of primary Addison disease is lacking because melanotropic hormone levels are low.
Secondary adrenocortical insufficiency is characterized by low serum ACTH and a prompt rise in plasma cortisol levels in response to ACTH administration.
Pathological features of adrenocortical deficiency
- The appearance of the adrenal glands varies with the cause of the insufficiency.
- In secondary hypoadrenalism the adrenals are reduced to small, uniform, thin rim of atrophic yellow cortex that surrounds a central, intact medulla. Histologically, there is atrophy of cortical cells with loss of cytoplasmic lipid, particularly in the zonae fasciculata and reticularis.
- In primary autoimmune adrenalitis there is also atrophy of the cortex associated with a variable lymphoid infiltrate that may extend into the subjacent medulla. The medulla is otherwise normal.
- In tuberculosis or fungal diseases there is granulomatous inflammatory reaction. Demonstration of the responsible organism may require the use of special stains.
- With metastatic carcinoma, the adrenals are enlarged and their normal architecture is obscured by the infiltrating neoplasm.
Amalgam Bonding Agents
Conservative DentistryAmalgam Bonding Agents
Amalgam bonding agents can be classified into several categories based on
their composition and mechanism of action:
A. Adhesive Systems
Total-Etch Systems: These systems involve etching both
enamel and dentin with phosphoric acid to create a rough surface that
enhances mechanical retention. After etching, a bonding agent is applied to
the prepared surface before the amalgam is placed.
Self-Etch Systems: These systems combine etching and
bonding in one step, using acidic monomers that partially demineralize the
tooth surface while simultaneously promoting bonding. They are less
technique-sensitive than total-etch systems.
B. Glass Ionomer Cements
Glass ionomer cements can be used as a base or liner under amalgam
restorations. They bond chemically to both enamel and dentin, providing a
good seal and some degree of fluoride release, which can help in caries
prevention.
C. Resin-Modified Glass Ionomers
These materials combine the properties of glass ionomer cements with
added resins to improve their mechanical properties and bonding
capabilities. They can be used as a liner or base under amalgam
restorations.
Mechanism of Action
A. Mechanical Retention
Amalgam bonding agents create a roughened surface on the tooth
structure, which increases the surface area for mechanical interlocking
between the amalgam and the tooth.
B. Chemical Bonding
Some bonding agents form chemical bonds with the tooth structure,
particularly with dentin. This chemical interaction can enhance the overall
retention of the amalgam restoration.
C. Sealing the Interface
By sealing the interface between the amalgam and the tooth, bonding
agents help prevent microleakage, which can lead to secondary caries and
postoperative sensitivity.
Applications of Amalgam Bonding Agents
A. Sealing Tooth Preparations
Bonding agents are used to seal the cavity preparation before the
placement of amalgam, reducing the risk of microleakage and enhancing the
longevity of the restoration.
B. Bonding New to Old Amalgam
When repairing or replacing an existing amalgam restoration, bonding
agents can be used to bond new amalgam to the old amalgam, improving the
overall integrity of the restoration.
C. Repairing Marginal Defects
Bonding agents can be applied to repair marginal defects in amalgam
restorations, helping to restore the seal and prevent further deterioration.
Clinical Considerations
A. Technique Sensitivity
The effectiveness of amalgam bonding agents can be influenced by the
technique used during application. Proper surface preparation, including
cleaning and drying the tooth structure, is essential for optimal bonding.
B. Moisture Control
Maintaining a dry field during the application of bonding agents is
critical. Moisture contamination can compromise the bond strength and lead
to restoration failure.
C. Material Compatibility
It is important to ensure compatibility between the bonding agent and
the amalgam used. Some bonding agents may not be suitable for all types of
amalgam, so clinicians should follow manufacturer recommendations.
D. Longevity and Performance
While amalgam bonding agents can enhance the performance of amalgam
restorations, their long-term effectiveness can vary. Regular monitoring of
restorations is essential to identify any signs of failure or degradation.
Dental Porcelain and PFM Porcelains
Dental Materials
Dental Porcelain and PFM Porcelains
Applications/Use
a. Porcelain inlays and jacket crowns
b. PFM crowns and bridges
c. Denture teeth
Terms
PFM-porcelain fused to metal
Fusing-adherence of porcelain particles into a single porcelain mass
Classification
Dental porcelain is manufactured as a powder. When it is heated to a very high temperature in a special oven, it fuses into a homogeneous mass. The heating process is called baking. Upon cooling, the mass is hard and dense. The material is made in a variety of shades to closely match most tooth colors. Baked porcelain has a translucency similar to that of dental enamel, so that porcelain crowns, pontics, and inlays of highly pleasing appearance can be made. Ingredients of porcelain include feldspar, kaolin, silica in the form of quartz, materials which act as fluxes to lower the fusion point, metallic oxide, and binders. Porcelains are classified into high-, medium-, and low-fusing groups, depending upon the temperature at which fusion takes place.
High-Fusing Porcelains. High-fusing porcelains fuse at 2,400o Fahrenheit or over. They are used for the fabrication of full porcelain crowns (jacket crowns).
Medium-Fusing Porcelains. Medium-fusing porcelains fuse between 2,000o and 2,400o Fahrenheit. They are used in the fabrication of inlays, crowns, facings, and pontics. A pontic is the portion of a fixed partial denture, which replaces a missing tooth.
Low-Fusing Porcelains. Low-fusing porcelains fuse between 1,600o and 2,000o Fahrenheit. They are used primarily to correct or modify the contours of previously baked high- or medium-fusing porcelain restorations. Eg for PFM restorations
Structure
Components
a. Large number of oxides but principally silicon oxide, aluminum oxide. and potassium oxide
b. Oxides are supplied by mixing clay, feldspar, and quartz.
Manipulation
Porcelain powders mixed with water and compacted into position for firing
Shrinkage is 30% on firing because of fusing and so must be made oversized and built up by several firing steps
Properties
1. Physical
a. Excellent electrical and thermal insulation
b. Low coefficient of thermal expansion and contraction
c. Good color and translucency; excellent aesthetics
2. Chemical
a. Not resistant to acids (and can be dissolved by contact with APF topical fluoride treatments)
b. Can be acid-etched with phosphoric acid or hydrofluoric acid for providing microll1echanical retention for cements
3. Mechanical
a. Harder than tooth structure and ,will cause opponent wear
b. Can be polished with aluminum oxide pastes
Modified Widman Flap
PeriodontologyModified Widman Flap Procedure
The modified Widman flap procedure is a surgical technique used in
periodontal therapy to treat periodontal pockets while preserving the
surrounding tissues and promoting healing. This lecture will discuss the
advantages and disadvantages of the modified Widman flap, its indications, and
the procedural steps involved.
Advantages of the Modified Widman Flap Procedure
Intimate Postoperative Adaptation:
The main advantage of the modified Widman flap procedure is the
ability to establish a close adaptation of healthy collagenous
connective tissues and normal epithelium to all tooth surfaces. This
promotes better healing and integration of tissues post-surgery
Feasibility for Bone Implantation:
The modified Widman flap procedure is advantageous over curettage,
particularly when the implantation of bone and other substances is
planned. This allows for better access and preparation of the surgical
site for grafting .
Conservation of Bone and Optimal Coverage:
Compared to conventional reverse bevel flap surgery, the modified
Widman flap conserves bone and provides optimal coverage of root
surfaces by soft tissues. This results in:
A more aesthetically pleasing outcome.
A favorable environment for oral hygiene.
Potentially less root sensitivity and reduced risk of root
caries.
More effective pocket closure compared to pocket elimination
procedures .
Minimized Gingival Recession:
When reattachment or minimal gingival recession is desired, the
modified Widman flap is preferred over subgingival curettage, making it
a suitable choice for treating deeper pockets (greater than 5 mm) and
other complex periodontal conditions.
Disadvantages of the Modified Widman Flap Procedure
Interproximal Architecture:
One apparent disadvantage is the potential for flat or concave
interproximal architecture immediately following the removal of the
surgical dressing, particularly in areas with interproximal bony
craters. This can affect the aesthetic outcome and may require further
management .
Indications for the Modified Widman Flap Procedure
Deep Pockets: Pockets greater than 5 mm, especially in
the anterior and buccal maxillary posterior regions.
Intrabony Pockets and Craters: Effective for treating
pockets with vertical bone loss.
Furcation Involvement: Suitable for managing
periodontal disease in multi-rooted teeth.
Bone Grafts: Facilitates the placement of bone grafts
during surgery.
Severe Root Sensitivity: Indicated when root
sensitivity is a significant concern.
Procedure Overview
Incisions and Flap Reflection:
Vertical Incisions: Made to access the periodontal
pocket.
Crevicular Incision: A horizontal incision along
the gingival margin.
Horizontal Incision: Undermines and removes the
collar of tissue around the teeth.
Conservative Debridement:
Flap is reflected just beyond the alveolar crest.
Careful removal of all plaque and calculus while preserving the root
surface.
Frequent sterile saline irrigation is used to maintain a clean
surgical field.
Preservation of Proximal Bone Surface:
The proximal bone surface is preserved and not curetted, allowing
for better healing and adaptation of the flap.
Exact flap adaptation is achieved with full coverage of the bone.
Suturing:
Suturing is aimed at achieving primary union of the proximal flap
projections, ensuring proper healing and tissue integration.
Postoperative Care
Antibiotic Ointment and Periodontal Dressing:
Traditionally, antibiotic ointment was applied over sutures, and a
periodontal dressing was placed. However, these practices are often omitted
today.
Current Recommendations: Patients are advised not to
disturb the surgical area and to use a chlorhexidine mouth rinse every 12
hours for effective plaque control and to promote healing.
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Neutrophil Disorders Associated with Periodontal Diseases
Neutrophils play a crucial role in the immune response, particularly in
combating infections, including those associated with periodontal diseases.
Various neutrophil disorders can significantly impact periodontal health,
leading to increased susceptibility to periodontal diseases. This lecture will
explore the relationship between neutrophil disorders and specific periodontal
diseases.
Neutrophil Disorders
Diabetes Mellitus
Description: A metabolic disorder characterized by
high blood sugar levels due to insulin resistance or deficiency.
Impact on Neutrophils: Diabetes can impair
neutrophil function, including chemotaxis, phagocytosis, and the
oxidative burst, leading to an increased risk of periodontal infections.
Papillon-Lefevre Syndrome
Description: A rare genetic disorder characterized
by palmoplantar keratoderma and severe periodontitis.
Impact on Neutrophils: Patients exhibit neutrophil
dysfunction, leading to early onset and rapid progression of periodontal
disease.
Down’s Syndrome
Description: A genetic disorder caused by the
presence of an extra chromosome 21, leading to various developmental and
health issues.
Impact on Neutrophils: Individuals with Down’s
syndrome often have impaired neutrophil function, which contributes to
an increased prevalence of periodontal disease.
Chediak-Higashi Syndrome
Description: A rare genetic disorder characterized
by immunodeficiency, partial oculocutaneous albinism, and neurological
problems.
Impact on Neutrophils: This syndrome results in
defective neutrophil chemotaxis and phagocytosis, leading to increased
susceptibility to infections, including periodontal diseases.
Drug-Induced Agranulocytosis
Description: A condition characterized by a
dangerously low level of neutrophils due to certain medications.
Impact on Neutrophils: The reduction in neutrophil
count compromises the immune response, increasing the risk of
periodontal infections.
Cyclic Neutropenia
Description: A rare genetic disorder characterized
by recurrent episodes of neutropenia (low neutrophil count) occurring
every 21 days.
Impact on Neutrophils: During neutropenic episodes,
patients are at a heightened risk for infections, including periodontal
disease.
Problems in Film Processing
Radiology
Common Problems in Film Processing
1. Light Radiographs
Causes:
Under Development:
Temperature too low
Time too short
Depleted developer solution
Under Exposure:
Insufficient milliamperage
Insufficient kVp
Insufficient exposure time
Film-source distance too great
Film packet reversed in the mouth
2. Dark Radiographs
Causes:
Over Development:
Temperature too high
Time too long
Accidental exposure to light
Improper safe lighting
Developer concentration too high
Over Exposure:
Excessive milliamperage
Excessive kVp
Excessive exposure time
Film-source distance too short
3. Insufficient Contrast
Causes:
Improper processing conditions (under or over development)
Depleted developer solution
Contaminated solutions
4. Film Fog
Causes:
Excessive kVp
Improper safe lighting
Light leaks in the darkroom
Contaminated developer solution
5. Dark Spots or Tines
Causes:
Contaminated solutions
Film contaminated with developer before processing
Film in contact with tank or another film during fixation
6. Light Spots
Causes:
Insufficient washing
Film contaminated with fixer before processing
Film in contact with tank or another film during development
7. Yellow or Brown Stains
Causes:
Insufficient washing after fixation
Depleted fixer solution
Contaminated solutions
8. Blurring
Causes:
Movement of the patient during exposure
Movement of the X-ray tube head
Double exposure
Misalignment of the X-ray tube head (cone cut)
9. Partial Images
Causes:
Top of film not immersed in developing solution
Film in contact with tank or another film during processing
10. Emulsion Peel
Causes:
Excessive bending of the film
Improper handling of the film
11. Static Discharge
Causes:
Static discharge to film before processing (results in dark lines
with a tree-like image)
12. Fingerprint Contamination
Causes:
Fingerprint contamination during handling of the film
13. Excessive Roller Pressure
Causes:
Excessive roller pressure during processing can lead to artifacts on
the film.
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
Articulations and Movement
Anatomy
Articulations
Classified according to their structure, composition,and movability
• Fibrous joints-surfaces of bones almost in direct contact with limited movement
o Syndesmosis-two bones united by interosseous ligaments
o Sutures-serrated margins of bones united by a thin layer of fibrous tissue
o Gomphosis-insertion of a cone-shaped process into a socket
• Cartilaginous joints-no joint cavity and contiguous bones united by cartilage
o Synchondrosis-ends of two bones approximated by hyaline cartilage
o Symphyses-approximating bone surfaces connected by fibrocartilage
• Synovial joints-approximating bone surfaces covered with cartilage; may be separated by a disk; attached by ligaments
o Hinge-permits motion in one plane only
o Pivot-permits rotary movement in which a ring rotates around a central axis
o Saddle-opposing surfaces are convexconcave. allowing great freedom of motion
o Ball and socket - capable of movement in an infinite number of axes; rounded head of one bone moves in a cuplike cavity of the approximating bone
Bursae
• Sacs filled with synovial fluid that are present where tendons rub against bone or where skjn rubs across bone
• Some bursae communicate with a joint cavity
• Prominent bursae found at the elbow. hip, and knee'
Movements
• Gliding
o Simplest kind of motion in a joint
o Movement on a joint that does not involve any angular or rotary motions
• Flexion-decreases the angle formed by the union of two bones
• Extension-increases the angle formed by the union of two bones
• Abduction-occurs by moving part of the appendicular skeleton away from the median plane of the body
• Adduction-occurs by moving part of the appendicular skeleton toward the median plane of the body
• Circumduction
o Occurs in ball-and-socket joints
o Circumscribes the conic space of one bone by the other bone
• Rotation-turning on an axis without being displaced from that axis
Ketamine
Pharmacology
Ketamine
- Causes a dissociative anesthesia.
- Is similar to but less potent than phencyclidine.
- Induces amnesia, analgesia, catalepsy and anesthesia, but does not induce convulsions.
- The principal disadvantage of ketamine is its adverse psychic effects during emergence from anesthesia. These include: hallucinations, changes in mood and body image.
- During anesthesia, many of the protective reflexes are maintained, such as laryngeal, pharyngeal, eyelid and corneal reflexes.
- Muscle relaxation is poor.
- It is not indicated for intracranial operations because it increases cerebrospinal fluid pressure.
- Respiration is well maintained.
- Arterial blood pressure, cardiac output, and heart rate are all elevated.