NEET MDS Synopsis
Indices used for dental caries assessment
Public Health Dentistry
Decayed-Missing-Filled Index ( DMF ) which was introduced by Klein, Palmer and Knutson in 1938 and modified by WHO:
1. DMF teeth index (DMFT) which measures the prevalence of dental caries/Teeth.
2. DMF surfaces index (DMFS) which measures the severity of dental caries.
The components are:
D component:
Used to describe (Decayed teeth) which include:
1. Carious tooth.
2. Filled tooth with recurrent decay.
3. Only the root are left.
4. Defect filling with caries.
5. Temporary filling.
6. Filled tooth surface with other surface decayed
M component:
Used to describe (Missing teeth due to caries) other cases should be excluded these are:
1. Tooth that extracted for reasons other than caries should be excluded, which include:
a- Orthodontic treatment.
b- Impaction.
c- Periodontal disease.
2. Unerupted teeth.
3. Congenitally missing.
4. Avulsion teeth due to trauma or accident.
F component:
Used to describe (Filled teeth due to caries).
Teeth were considered filled without decay when one or more permanent restorations were present and there was no secondary (recurrent) caries or other area of the tooth with primary caries.
A tooth with a crown placed because of previous decay was recorded in this category.
Teeth restored for reason other than dental caries should be excluded, which include:
1. Trauma (fracture).
2. Hypoplasia (cosmatic purposes).
3. Bridge abutment (retention).
4. Seal a root canal due to trauma.
5. Fissure sealant.
6. Preventive filling.
1. A tooth is considered to be erupted when just the cusp tip of the occlusal surface or incisor edge is exposed.
The excluded teeth in the DMF index are:
a. Supernumerary teeth.
b. The third molar according to Klein, Palmer and Knutson only.
2. Limitations - DMF index can be invalid in older adults or in children because index can overestimate caries record by cases other than dental caries.
1. DMFT: a. A tooth may have several restorations but it counted as one tooth, F. b. A tooth may have restoration on one surface and caries on the other, it should be counted as D . c. No tooth must be counted more than once, D M F or sound.
2. DMFS: Each tooth was recorded scored as 4 surfaces for anterior teeth and 5 surfaces for posterior teeth. a. Retained root was recorded as 4 D for anterior teeth, 5 D for posterior teeth. b. Missing tooth was recorded as 4 M for anterior teeth, 5 M for posterior teeth. c. Tooth with crown was recorded as 4 F for anterior teeth, 5 F for posterior teeth.
Calculation of DMFT \ DMFS:
1. For individual
DMF = D + M + F
2. For population
Minimum score = Zero
Primary teeth index:
1. dmft / dmfs Maximum scores: dmft = 20 , dmfs = 88
2. deft / defs, which was introduced by Gruebbel in 1944: d- decayed tooth. e- decayed tooth indicated for extraction . f- filled tooth.
3. dft / dfs: In which the missing teeth are ignored, because in children it is difficult to make sure whether the missing tooth was exfoliated or extracted due to caries or due to serial extraction.
Mixed dentition:
Each child is given a separate index, one for permanent teeth and another for primary teeth. Information from the dental caries indices can be derived to show the:
1. Number of persons affected by dental caries (%).
2. Number of surfaces and teeth with past and present dental caries (DMFT / dmft - DMFS / dmfs).
3. Number of teeth that need treatment, missing due to caries, and have been treated ( DT/dt, MT/mt, FT/f t).
Immunoglobulins.
General Pathology
Immunoglobulins. (Ig)
These are made up of polypeptide chains. Each molecule is constituted by two heavy and two light chains, linked by disulfide (S-S) bonds. The h~ chains are of 5 types, with corresponding, types or immunoglobulin. IgG (gamma), IgM (mu µ ), IgA(alpha α), IgD(delta ), IgE(epsilon)
Each of these can have light chains of either kappa (k) or lambda type.Each chain has a constant portion (constant for the subtype) land a variable portion (antigen specific).
Enzyme digestion can split the Ig molecule into.2 Fab (antibody binding) fragments and one Fc (crystallisable, complement binding ) fragment.
Characteristics of Immunoglobulin subclasses
I. Ig G:
(i) Predominant portion (80%) of Ig.
(ii) Molecular weight 150, 000
(iii) Sedimentation coefficient of 7S.
(iv) Crosses placental barrier and to extra cellular fluid.
(v) Mostly neutralising effect. May be complement fixing.
(vi) Half life of 23 days.
2.IgM :
(i) Pentamer of Ig.
(ii) Molecular weight 900, 000
(iii) 19S.
(iv) More effective complement fixation and cells lysis
(v) Earliest to be produced in infections.
(vi) Does not cross placental barrier.
(vii) Halflife of 5 days.
3. Ig A :
Secretory antibody. Found in intestinal, respiratory secretions tears, saliva and urine also.
Secreted usually as a dinner with secretory piece.
Mol. weight variable (160,000+)
7 S to 14 S.
Half life of 6 days.
4.Ig D :
Found in traces.
7 S.
Does not cross placenta.
5. Ig E
Normally not traceable
7-8 S (MoL weight 200,000)
Cytophilic antibody, responsible for some hypersensitivity states,
Pulmonary embolism
General Pathology
Pulmonary embolism
A pulmonary embolism (thromboembolism) occurs when a blood clot, generally a venous thrombus, becomes dislodged from its site of formation and embolizes to the arterial blood supply of one of the lungs.
Clinical presentation
Signs of PE are sudden-onset dyspnea (shortness of breath, 73%), tachypnea (rapid breathing, 70%), chest pain of "pleuritic" nature (worsened by breathing, 66%), cough (37%), hemoptysis (coughing up blood, 13%), and in severe cases, cyanosis, tachycardia (rapid heart rate), hypotension, shock, loss of consciousness, and death. Although most cases have no clinical evidence of deep venous thrombosis in the legs, findings that indicate this may aid in the diagnosis.
Diagnosis
The gold standard for diagnosing pulmonary embolism (PE) is pulmonary angiography
An electrocardiogram may show signs of right heart strain or acute cor pulmonale in cases of large PEs
In massive PE, dysfunction of the right side of the heart can be seen on echocardiography, an indication that the pulmonary artery is severely obstructed and the heart is unable to match the pressure.
Treatment
Acutely, supportive treatments, such as oxygen or analgesia
In most cases, anticoagulant therapy is the mainstay of treatment. Heparin or low molecular weight heparins are administered initially, while warfarin therapy is given
Gastric acid secretion inhibitors
Pharmacology
Gastric acid secretion inhibitors (antisecretory drugs):
HCl is secreted by parietal cells of the gastric mucosa which contain receptors for acetylcholine (muscarinic receptors: MR), histamine (H2R), prostaglandins (PGR) and gastrin (GR) that stimulate the production, except PGs which inhibit gastric acid production.
Therefore, antagonists of acetylcholine, histamine and gastrin inhibit gastric acid secretion (antisecretory). On the other hand, inhibitors of PGs biosynthesis such as NSAIDs with reduce cytoprotective mechanisms and thus promote gastric mucosal erosion. Also, the last step in gastric acid secretion from parietal cells involve a pump called H+ -K+-ATPase (proton pump). Drugs that block this pump will inhibit gastric acid secretion. Antisecretory drugs include:
1. Anticholinergic agents such as pirenzepine, dicyclomine, atropine.
2. H2-receptors blocking agents such as Cimetidine, Ranitidine, Famotidine, Nizatidine (the pharmacology of these agents has been discussed previously).
3. Gastrin-receptor blockers such as proglumide.
4. Proton pump inhibitors such as omeprazole, lansoprazole.
Major clinical indications of antisecretory drugs:
• Prevention & treatment of peptic ulcer disease.
• Zollinger Ellison syndrome.
• Reflux esophagitis.
Management of H. Pylori Infection and ZE Syndrome
Pharmacology
Management of H. Pylori Infection
- Gram – rod
- Causes erosion of protective epithelial cells -> gastritis or peptic ulcer
H2 antagonist or PPI + Abx
- Metronidazole or amoxicillin/clarithromycin
- PPI + 2 or 3 antimicrobials is standard
- Ex: Ranitidine + Peptobismol + Clarithromycin + Amoxicillin 7-14 days
-Add bismuth if resistant H. pylori
- Ex: PPI + BMT (Bismuth + Metronidazole + tetracycline) 7days
Treatment for ZE Syndrome
- Gastrinoma of the duodenum or pancreas
-Elevated gastrin levels- Peptic/gastric ulcers
- Treatment
High dose PPI until resorting to surgery or chemotherapy for tumor removal
Examples of calculations of doses of vasoconstrictors
Pharmacology
Examples of calculations of doses of vasoconstrictors
Ratio concentrations represent grams per millilitre
1:100,000 = 0.01 mg/mL or 10 µg/mL
1:200,000 = 0.005 mg/mL or 5 µg/mL
1:50,000 = 0.02 mg/mL or 20 µg/mL
1 cartridge of epinephrine 1:200,000 = 9 µg
1 cartridge of epinephrine 1:100,000 = 18 µg
1 cartridge of epinephrine 1:50,000 = 36 µg
1 cartridge of levonordefrin 1:20,000 = 90 µg
Sympathomimetics -Adrenergic Agents
Pharmacology
Sympathomimetics -Adrenergic Agents
The sympathomimetic or adrenergic or adrenomimetic drugs mimic the effects of adrenergic sympathetic nerve stimulation.
These are the important group of therapeutic agents which may be used to maintain blood pressure and in certain cases of severe bronchial asthma.
Mechanism of Action and Adrenoceptors
The catecholamines produce their action by direct combination with receptors located on the cell membrane. The adrenergic receptors are divided into two main groups – alpha and beta.
alpha receptor - stimulation produces excitatory effect and
beta receptor -stimulation usually produces inhibitory effect.
Alpha receptors: There are two major groups of alpha receptors, α1 and α2.
Activation of postsynaptic α1 receptors increases the intracellular concentration of calcium by activation of a phospholipase C in the cell membrane via G protein.
α2 receptor is responsible for inhibition of renin release from the kidney and for central aadrenergically mediated blood pressure depression.
Beta receptors:
a. Beta 1 receptors have approximately equal affinity for adrenaline and noradrenaline and are responsible for myocardial stimulation and renin release.
b. Beta 2 - receptors have a higher affinity for adrenaline than for noradrenaline and are responsible for bronchial muscle relaxation, skeletal muscle vasodilatation and uterine relaxation.
c. Dopamine receptors: The D1 receptor is typically associated with the stimulation of adenylyl cyclase. The important agonist of dopamine receptors is fenoldopam (D1) and bromocriptine (D2) and antagonist is clozapine (D4) .
Adrenergic drugs can also be classified into:
a. Direct sympathomimetics: These act directly on a or/and b adrenoceptors e.g. adrenaline, noradrenaline, isoprenaline, phenylephrine, methoxamine salbutamol etc.
b. Indirect sympathomimetics: They act on adrenergic neurones to release noradrenaline e.g. tyramine.
c. Mixed action sympathomimetics: They act directly as well as indirectly e.g. ephedrine, amphetamine, mephentermine etc.
Pharmacological Action of Sympathomimetics
Heart: Direct effects on the heart are determined largely by β1 receptors.
Adrenaline increases the heart rate, force of myocardial contraction and cardiac output
Blood vessels: Adrenaline and noradrenaline constrict the blood vessels of skin and mucous membranes.
Adrenaline also dilates the blood vessels of the skeletal muscles on account of the preponderance of β2 receptor
Blood pressure: Because of vasoconstriction (α1) and vasodilatation (β2) action of adrenaline, the net result is decrease in total peripheral resistance.
Noradrenaline causes rise in systolic, diastolic and mean blood pressure and does not cause vasodilatation (because of no action on β2 receptors) and increase in peripheral resistance due to its a action.
Isoprenaline causes rise in systolic blood pressure (because of β1 cardiac stimulant action) but marked fall in diastolic blood pressure (because of b2 vasodilatation action) but mean blood pressure generally falls.
GIT: Adrenaline causes relaxation of smooth muscles of GIT and reduce its motility.
Respiratory system: The presence of β2 receptors in bronchial smooth muscle causes relaxation and activation of these receptors by β2 agonists cause bronchodilatation.
Uterus: The response of the uterus to the atecholamines varies according to species
Eye: Mydriasis occur due to contraction of radial muscles of iris, intraocular tension is lowered due to less production of the aqueous humor secondary to vasoconstriction and conjunctival ischemia due to constriction of conjunctival blood vessels.
a. Urinary bladder: Detrusor is relaxed (b) and trigone is constricted (a) and both the actions tend to inhibit
micturition.
b. Spleen: In animals, it causes contraction (due to its a action) of the splenic capsule resulting in increase in number of RBCs in circulation.
c. It also cause contraction of retractor penis, seminal vesicles and vas deferens.
d. Adrenaline causes lacrimation and salivary glands are stimulated.
e. Adrenaline increases the blood sugar level by enhancing hepatic glycogenolysis and also by decreasing the uptake of glucose by peripheral tissues.
Adrenaline inhibits insulin release by its a-receptor stimulant action whereas it stimulates glycogenolysis by its b receptor stimulant action.
f. Adrenaline produces leucocytosis and eosinopenia and accelerates blood coagulation and also stimulates platelet aggregation.
Adverse Effects
Restlessness, anxiety, tremor, headache.
Both adrenaline and noradrenaline cause sudden increase in blood pressure, precipitating sub-arachnoid haemorrhage and occasionally hemiplegia, and ventricular arrhythmias.
May produce anginal pain in patients with ischemic heart disease.
Contraindications
a. In patients with hyperthyroidism.
b. Hypertension.
c. During anaesthesia with halothane and cyclopropane.
d. In angina pectoris.
Therapeutic Uses
Allergic reaction: Adrenaline is drug of choice in the treatment of various acute allergic disorders by acting as a physiological antagonist of histamine (a known mediator of many hypersensitivity reactions). It is used in bronchial asthma, acute angioneurotic edema, acute hypersensitivity reaction to drugs and in the treatment of anaphylactic shock.
Bronchial asthma: When given subcutaneously or by inhalation, adrenaline is a potent drug in the treatment of status asthmaticus.
Cardiac uses: Adrenaline may be used to stimulate the heart in cardiac arrest.
Adrenaline can also be used in Stokes-Adam syndrome, which is a cardiac arrest occurring at the transition of partial to complete heart block. Isoprenaline or orciprenaline may be used for the temporary treatment of partial or complete AV block.
Miscellaneous uses:
a. Phenylephrine is used in fundus examination as mydriatic agent.
b. Amphetamines are sometime used as adjuvant and to counteract sedation caused by antiepileptics.
c. Anoretic drugs can help the obese people.
d. Amphetamine may be useful in nocturnal enuresis in children.
e. Isoxsuprine (uterine relaxant) has been used in threatened abortion and dysmenorrhoea.
Progression from Gingivitis to Periodontitis
PeriodontologyProgression from Gingivitis to Periodontitis
The transition from gingivitis to periodontitis is a critical process in
periodontal disease progression. This lecture will outline the key stages
involved in this progression, highlighting the changes in microbial composition,
host response, and tissue alterations.
Pathway of Progression
Establishment and Maturation of Supragingival Plaque:
The process begins with the formation of supragingival plaque, which
is evident in gingivitis.
As this plaque matures, it becomes more complex and can lead to
changes in the surrounding tissues.
Migration of Periodontopathogenic Bacteria:
When the microbial load overwhelms the local host immune response,
pathogenic bacteria migrate subgingivally (below the gum line).
This migration establishes a subgingival niche that is conducive to
the growth of periodontopathogenic bacteria.
Initial Lesion
Timeline:
The initial lesion, characterized by subclinical gingivitis, appears
approximately 2 to 4 days after the colonization of the gingival sulcus
by bacteria.
Clinical Manifestations:
Vasculitis: Inflammation of blood vessels in the
gingival tissue.
Exudation of Serous Fluid: Increased flow of
gingival crevicular fluid (GCF) from the gingival sulcus.
Increased PMN Migration: Polymorphonuclear
neutrophils (PMNs) migrate into the sulcus in response to the
inflammatory process.
Alteration of Junctional Epithelium: Changes occur
at the base of the pocket, affecting the integrity of the junctional
epithelium.
Collagen Dissolution: Perivascular collagen begins
to dissolve, contributing to tissue breakdown.
Early Lesion
Timeline:
The early lesion forms within 4 to 7 days after the initial lesion
due to the continued accumulation of bacterial plaque.
Characteristics:
Leukocyte Accumulation: There is a significant
increase in leukocytes at the site of acute inflammation, indicating an
ongoing immune response.
Cytopathic Alterations: Resident fibroblasts
undergo cytopathic changes, affecting their function and viability.
Collagen Loss: Increased collagen loss occurs
within the marginal gingiva, contributing to tissue destruction.
Proliferation of Basal Cells: The basal cells of
the junctional epithelium proliferate in response to the inflammatory
environment.