NEET MDS Synopsis
Recent Advances
Conservative DentistryRecent Advances in Restorative DentistryRestorative dentistry has seen significant advancements in materials and
techniques that enhance the effectiveness, efficiency, and aesthetic outcomes of
dental treatments. Below are some of the notable recent innovations in
restorative dentistry:
1. Teric Evoflow
A. Description
Type: Nano-optimized flow composite.
Characteristics:
Optimum Surface Affinity: Designed to adhere well
to tooth surfaces.
Penetration: Capable of penetrating into areas that
are difficult to reach, making it ideal for various restorative
applications.
B. Applications
Class V Restorations: Particularly suitable for Class V
cavities, which are often challenging due to their location and shape.
Extended Fissure Sealing: Effective for sealing deep
fissures in teeth to prevent caries.
Adhesive Cementation Techniques: Can be used as an
initial layer under medium-viscosity composites, enhancing the overall
bonding and restoration process.
2. GO
A. Description
Type: Super quick adhesive.
Characteristics:
Time Efficiency: Designed to save valuable chair
time during dental procedures.
Ease of Use: Fast application process, allowing for
quicker restorations without compromising quality.
B. Applications
Versatile Use: Suitable for various adhesive
applications in restorative dentistry, enhancing workflow efficiency.
3. New Optidisc
A. Description
Type: Finishing and polishing discs.
Characteristics:
Three-Grit System: Utilizes a three-grit system
instead of the traditional four, aimed at achieving a higher surface
gloss on restorations.
Extra Coarse Disc: An additional extra coarse disc
is available for gross removal of material before the finishing and
polishing stages.
B. Applications
Final Polish: Allows restorations to achieve a final
polish that closely resembles the natural dentition, improving aesthetic
outcomes and patient satisfaction.
4. Interval II Plus
A. Description
Type: Temporary filling material.
Composition: Made with glass ionomer and leachable
fluoride.
Packaging: Available in a convenient 5 gm syringe.
B. Characteristics
Dependable: A one-component, ready-mixed material that
simplifies the application process.
Safety: Safe to use on resin-based materials, as it
does not contain zinc oxide eugenol (ZOE), which can interfere with bonding.
C. Applications
Temporary Restorations: Ideal for use in temporary
fillings, providing a reliable and effective solution for managing carious
lesions until permanent restorations can be placed.
The Adrenal Glands
Physiology
The Adrenal Glands
The adrenal glands are two small structures situated one at top each kidney. Both in anatomy and in function, they consist of two distinct regions:
an outer layer, the adrenal cortex, which surrounds
the adrenal medulla.
The Adrenal Cortex
cells of the adrenal cortex secrete a variety of steroid hormones.
glucocorticoids (e.g., cortisol)
mineralocorticoids (e.g., aldosterone)
androgens (e.g., testosterone)
Production of all three classes is triggered by the secretion of ACTH from the anterior lobe of the pituitary.
Glucocorticoids
They Effect by raising the level of blood sugar (glucose). One way they do this is by stimulating gluconeogenesis in the liver: the conversion of fat and protein into intermediate metabolites that are ultimately converted into glucose.
The most abundant glucocorticoid is cortisol (also called hydrocortisone).
Cortisol and the other glucocorticoids also have a potent anti-inflammatory effect on the body. They depress the immune response, especially cell-mediated immune responses.
Mineralocorticoids
The most important of them is the steroid aldosterone. Aldosterone acts on the kidney promoting the reabsorption of sodium ions (Na+) into the blood. Water follows the salt and this helps maintain normal blood pressure.
Aldosterone also
acts on sweat glands to reduce the loss of sodium in perspiration;
acts on taste cells to increase the sensitivity of the taste buds to sources of sodium.
The secretion of aldosterone is stimulated by:
a drop in the level of sodium ions in the blood;
a rise in the level of potassium ions in the blood;
angiotensin II
ACTH (as is that of cortisol)
Androgens
The adrenal cortex secretes precursors to androgens such as testosterone.
Excessive production of adrenal androgens can cause premature puberty in young boys.
In females, the adrenal cortex is a major source of androgens. Their hypersecretion may produce a masculine pattern of body hair and cessation of menstruation.
Addison's Disease: Hyposecretion of the adrenal cortices
Addison's disease has many causes, such as
destruction of the adrenal glands by infection;
their destruction by an autoimmune attack;
an inherited mutation in the ACTH receptor on adrenal cells.
Cushing's Syndrome: Excessive levels of glucocorticoids
In Cushing's syndrome, the level of adrenal hormones, especially of the glucocorticoids, is too high.It can be caused by:
excessive production of ACTH by the anterior lobe of the pituitary;
excessive production of adrenal hormones themselves (e.g., because of a tumor), or (quite commonly)
as a result of glucocorticoid therapy for some other disorder such as
rheumatoid arthritis or
preventing the rejection of an organ transplant.
The Adrenal Medulla
The adrenal medulla consists of masses of neurons that are part of the sympathetic branch of the autonomic nervous system. Instead of releasing their neurotransmitters at a synapse, these neurons release them into the blood. Thus, although part of the nervous system, the adrenal medulla functions as an endocrine gland.The adrenal medulla releases:
adrenaline (also called epinephrine) and
noradrenaline (also called norepinephrine)
Both are derived from the amino acid tyrosine.
Release of adrenaline and noradrenaline is triggered by nervous stimulation in response to physical or mental stress. The hormones bind to adrenergic receptors transmembrane proteins in the plasma membrane of many cell types.
Some of the effects are:
increase in the rate and strength of the heartbeat resulting in increased blood pressure;
blood shunted from the skin and viscera to the skeletal muscles, coronary arteries, liver, and brain;
rise in blood sugar;
increased metabolic rate;
bronchi dilate;
pupils dilate;
hair stands on end (gooseflesh in humans);
clotting time of the blood is reduced;
increased ACTH secretion from the anterior lobe of the pituitary.
All of these effects prepare the body to take immediate and vigorous action.
Psoriasis
General Pathology
Psoriasis is a chronic disorder characterized by scaly, erythematous plaques, which histologically are secondary to epidermal proliferation.
- genetic factors (HLA relationships), environmental (physical injury, infection, drugs, photosensitivity), abnormal cellular proliferation (deregulation of epidermal proliferation) and microcirculatory changes in the papillary dermis (diapedesis of neutrophils into the epidermis) are all interrelated.
- the plaques of psoriasis are characteristically well-demarcated pink or salmon colored lesions covered by a loosely-adherent silver-white scale which, when picked off, reveals pinpoint bleeding sites (Auspitz sign).
- the nail changes in psoriasis include pitting, dimpling, thickening and crumbling with a yellowish-brown discoloration of the nail plate.
- the characteristic histologic features of psoriasis include:
- hyperkeratosis
- absence of the granulosa cells (present in lichen planus).
- parakeratosis
- regular, club-shaped elongation of the rete pegs (irregular and saw toothed in lichen planus) with vessel proliferation in the papillary dermis (reason for the bleeding associated with Auspitz sign).
- characteristic subcorneal collection of neutrophils called a Munro's microabscess (diapedesis from vessels in papillary dermi).
- 7% develop HLA B27 positive psoriatic arthritis
Fatty Acid Synthesis
Biochemistry
The input to fatty acid synthesis is acetyl-CoA, which is carboxylated to malonyl-CoA.
The ATP-dependent carboxylation provides energy input. The CO2 is lost later during condensation with the growing fatty acid. The spontaneous decarboxylation drives the condensation.
fatty acid synthesis
acetyl-CoA + 7 malonyl-CoA + 14 NADPH → palmitate + 7 CO2 + 14 NADP+ + 8 CoA
ATP-dependent synthesis of malonate:
8 acetyl-CoA + 14 NADPH + 7 ATP → palmitate + 14 NADP+ + 8 CoA + 7 ADP + 7 Pi
Fatty acid synthesis occurs in the cytosol. Acetyl-CoA generated in the mitochondria is transported to the cytosol via a shuttle mechanism involving citrate
Thrombolytic Agents
Pharmacology
Thrombolytic Agents:
Tissue Plasminogen Activator (t-PA, Activase)
t-PA is a serine protease. It is a poor plasminogen activator in the absence of fibrin. t-PA binds to fibrin and activates bound plasminogen several hundred-fold more rapidly than it activates plasminogen in the circulation.
Streptokinase (Streptase)
Streptokinase is a protein produced by β-hemolytic streptococci. It has no intrinsic enzymatic activity, but forms a stable noncovalent 1:1 complex with plasminogen. This produces a conformational change that exposes the active site on plasminogen that cleaves a peptide bond on free plasminogen molecules to form free plasmin.
Urokinase (Abbokinase)
Urokinase is isolated from cultured human cells.Like streptokinase, it lacks fibrin specificity and therefore readily induces a systemic lytic state. Like t-PA, Urokinase is very expensive.
Contraindications to Thrombolytic Therapy:
• Surgery within 10 days, including organ biopsy, puncture of noncompressible vessels, serious trauma, cardiopulmonary resuscitation.
• Serious gastrointestinal bleeding within 3 months.
• History of hypertension (diastolic pressure >110 mm Hg).
• Active bleeding or hemorrhagic disorder.
• Previous cerebrovascular accident or active intracranial bleeding.
Aminocaproic acid:
Aminocaproic acid prevents the binding or plasminogen and plasmin to fibrin. It is a potent inhibitor for fibrinolysis and can reverse states that are associated with excessive fibrinolysis.
Gastric acid neutralizers (antacids)
Pharmacology
Gastric acid neutralizers (antacids)
Antacids act primarily in the stomach and are used to prevent and treat peptic ulcer. They are also used in the treatment of Reflux esophagitis and Gastritis.
Mechanism of action:
Antacids are alkaline substances (weak bases) that neutralize gastric acid (hydrochloric acid) they react with hydrochloric acid in the stomach to produce neutral or less acidic or poorly absorbed products and raise the pH of stomach secretion.
Antacids are divided into systemic and non-systemic.
• Systemic antacids (e.g. sodium bicarbonate) are highly absorbed into systemic circulation and enter body fluids. Therefore, they may alter acid–base balance. They can be used in the treatment of metabolic acidosis.
Non-systemic: they do not alter acid–base balance significantly, because they are not well-absorbed into the systemic circulation. They are used as gastric antacids; and include:
• Magnesium compounds such as magnesium hydroxide and magnesium sulphate MgS2O3. They have relatively high neutralizing capacity, rapid onset of action, however, they may cause diarrhoea and hypermagnesemia.
• Aluminium compounds such as aluminium hydroxide. Generally, these have low neutralizing capacity, slow onset of action but long duration of action. They may cause constipation.
• Calcium compounds such as. These are highly effective and have a rapid onset of action but may cause hypersecretion of acid (acid - rebound) and milk-alkali syndrome (hence rarely used in peptic ulcer disease).
Therefore, the most commonly used antacids are mixtures of aluminium hydroxide and magnesium hydroxide .
Pathogens Implicated in Periodontal Diseases
PeriodontologyPathogens Implicated in Periodontal Diseases
Periodontal diseases are associated with a variety of pathogenic
microorganisms. Below is a list of key pathogens implicated in different forms
of periodontal disease, along with their associations:
General Pathogens Associated with Periodontal Diseases
Actinobacillus actinomycetemcomitans:
Strongly associated with destructive periodontal disease.
Porphyromonas gingivalis:
A member of the "black pigmented Bacteroides group" and a
significant contributor to periodontal disease.
Bacteroides forsythus:
Associated with chronic periodontitis.
Spirochetes (Treponema denticola):
Implicated in various periodontal conditions.
Prevotella intermedia/nigrescens:
Also belongs to the "black pigmented Bacteroides group" and is
associated with several forms of periodontal disease.
Fusobacterium nucleatum:
Plays a role in the progression of periodontal disease.
Campylobacter rectus:
These organisms include members of the new genus Wolinella and are
associated with periodontal disease.
Principal Bacteria Associated with Specific Periodontal Diseases
Adult Periodontitis:
Porphyromonas gingivalis
Prevotella intermedia
Bacteroides forsythus
Campylobacter rectus
Refractory Periodontitis:
Bacteroides forsythus
Porphyromonas gingivalis
Campylobacter rectus
Prevotella intermedia
Localized Juvenile Periodontitis (LJP):
Actinobacillus actinomycetemcomitans
Capnocytophaga
Periodontitis in Juvenile Diabetes:
Capnocytophaga
Actinobacillus actinomycetemcomitans
Pregnancy Gingivitis:
Prevotella intermedia
Acute Necrotizing Ulcerative Gingivitis (ANUG):
Prevotella intermedia
Intermediate-sized spirochetes
AMYLOIDOSIS
General Pathology
AMYLOIDOSIS
Definition. Extra cellular deposition of an eosinophilic hyaline homogenous material in Various organs, occurring in a variety of clinical states.
Staining reactions
Iodine :- Brown, turning blue on addition of H2SO4 (gross and microscopic Stain).
P.A.S. – Positive (Magenta pink).
Congo Red -Orange red which on polarisation gives green birefringence.
Von Geison's –Khaki colour.
Thioflavin T -Yellow fluorescence.
Amyloid is called typical if it given the above staining reactions Other wise it is termed atypical or para-amyloid.
Classification
1. Systemic amyloidosis associated with underlying disease (secondary),
(A) Chronic infections like
- Tuberculosis.
- Bronchiectasis.
- Lung abscess.
- Osteomyelitis.
- Syphilis.
(B) Chronic inflammations of varied etiology:
- Rheumatoid arthritis.
- Ulcerative colitis.
- Regional enteritis.
- Lupus erythematosus.
(C) Neoplastic proliferations:
- Of immune system – Multiple myeloma, Hodgkin’s disease.
- Cancers like Renal cell carcinoma etc.
II Systemic primary amyloidosis with no underlying cause.
III Heredofamilial types.
- Amyloidosis with mediterranean fever.
- Amyloid polyneuropathy.
- Amyloid nephrophathy
- Familial cardiac amyloidosis
- Familial cutaneous amyloid.
- Lattice corneal dystrophy
IV. Localised amyloidosis:
- Senile - in heart, brain, seminal vesicles.
- Amyloidoma of tongue, bronchial tree, skin.
- In islets of Langerhans in Diabetes mellitus.
- In medullary thyroid carcinoma.
Deposition sites
In relation to reticulin and collagen fibres and to basement, membranes especially
subendothelial.
Organs involved commonly are :
Secondary amyloidosis
- Liver.
- Spleen.
- Kidney
- Lymph nodes.
- Adrenals.
Primary amyloidosis
- Heart
- Tongue and gingiva.
- Gastro intestinal tract.
- Lung.
- Wall of small vessels.
Nature and pathogenesis of amyloid
It is primarily made up of protein arranged in two patterns
- There are filaments twisted together to from the fibrils. These chemically resemble light chains of immunoglobulins
- Rods composed of stacked rings. These are made up of alpha globulin components of plasma proteins (P-components)
- In addition to these, extracts of crude amyloid contain mucopolysacharides complement and gamma globulins.
- Origin of amyloid :- current concept is that it is a direct product of cells of the immune sustem with some abnormality in their immune response
The abnormality may be due to :
- A genetic enzyme defect.
- Prolonged antigenic challenge.
- Neoplastic transformation
- Supression of normal. Response as in induced tolerance.