NEET MDS Synopsis
Chemical Controls of Respiration
PhysiologyChemical Controls of Respiration
A. Chemoreceptors (CO2, O2, H+)
1. central chemoreceptors - located in the medulla
2. peripheral chemoreceptors - large vessels of neck
B. Carbon Dioxide Effects
1. a powerful chemical regulator of breathing by increasing H+ (lowering pH)
a. hypercapnia Carbon Dioxide increases ->
Carbonic Acid increases ->
pH of CSF decreases (higher H+)- >
DEPTH & RATE increase (hyperventilation)
b. hypocapnia - abnormally low Carbon Dioxide levels which can be produced by excessive hyperventilation; breathing into paper bag increases blood Carbon Dioxide levels
C. Oxygen Effects
1. aortic and carotid bodies - oxygen chemoreceptors
2. slight Ox decrease - modulate Carb Diox receptors
3. large Ox decrease - stimulate increase ventilation
4. hypoxic drive - chronic elevation of Carb Diox (due to disease) causes Oxygen levels to have greater effect on regulation of breathing
D. pH Effects (H+ ion)
1. acidosis - acid buildup (H+) in blood, leads to increased RATE and DEPTH (lactic acid)
E. Overview of Chemical Effects
Chemical Breathing Effect
increased Carbon Dioxide (more H+) increase
decreased Carbon Dioxide (less H+) decrease
slight decrease in Oxygen effect CO2 system
large decrease in Oxygen increase ventilation
decreased pH (more H+) increase
increased pH (less H+) decrease
NECROSIS
General Pathology
NECROSIS
Definition: Necrosis is defined as the morphologic changes caused by the progressive degradative
action of enzymes on the lethally injured cell.
These changes are due to
I. Autolysis and
2. Heterolysis.
The cellular changes of necrosis i.e. death of circumscribed group of cells in continuity with living tissues are similar to changes in tissues following somatic death, except that in the former, there is leucocytic infiltration in reaction to the dead cells and the lytic
enzymes partly come from the inflammatory cell also. (Heterolysis). Cell death occurs in the normal situation of cell turnover also and this is called apoptosis-single cellular dropout.
Nuclear changes in necrosis
As cytoplasmic changes are a feature of degeneration ,similarly nuclear changes are the hallmark of necrosis. These changes are:
(i) Pyknosis –condensation of chromatin
(ii) Karyorrhexis - fragmentation
(iii) Karyolysis - dissolution
Types of necrosis
(1) Coagulative necrosis: Seen in infarcts. The architectural outlines are maintained though structural details are lost. E.g, myocardial infarct.
(2) Caseous necrosis: A variant of coagulative necrosis seen in tuberculosis. The architecture is destroyed, resulting in an eosinophilic amorphous debris.
(3) Colliquative (liquifactive). Necrosis seen in Cerebral infarcts and suppurative necrosis.
Gangrenous necrosis: It is the necrosis with superadded putrefaction
May be:
a. dry - coagulative product.
b. Wet - when there is bacterial liquifaction.
Fat necrosis
May be:
a. Traumatic (as in breast and subcutaneous tissue).
b Enzymatic (as in pancreatitis). It shows inflammation of fat with formation of lipophages and giant cells.
This is often followed by deposition of calcium as calcium soaps.
Hyaline necrosis: Seen in skeletal muscles in typhoid and in liver ceIs in some forms of hepatitis.
Fibrinoid necrosis: In hypertension and in immune based diseases.
Chronic Osteomyelitis
Oral Pathology
Chronic Osteomyelitis
As soon as pus drains intra or extraorally, condition ceases to spread and chronic phase commences.
Infection is localized but persistent as bacteria are able to grow in dead bone inaccessible to body’s defenses.
Clinical features
Primary – insidious in onset , slight pain , gradual increase in jaw size.
Secondary - Pain is deep pain and intermittent, temperature fluctuations , pyrexia , cellulitis eventually leading to abscess
New bone formation leads to thickening causing facial asymmetry.
Thickened or “wooden” character of bone in cr sec osteomyelitis.
Eventually cures itself as the last sequestra is discharged.
Radiographic Features
Trabeculae in the involved area become thin or appear fuzzy & then lose their continuity.
After some time “moth eaten” appearance is seen
Sequestra appear denser on radiographs.
Where the subperiosteal new bone formation , the new bone is superimposed upon that of jaw, “fingerprint” or “orange peel” appearance is seen
Cloacae seen as dark shadows passing through opacity.
Histologic features
Areas of acute and subacute inflammation in the cancellous spaces of the necrotic bone.
Foci of acute inflammation
Active osteoclastic resorption of bone noted in peripheral portions
Chronic Subperiosteal Osteomyelitis
Cortical plate deprived of its blood supply undergoes necrosis, underlying medullary bone is slightly affected.
Multiple small sequestra form, eventually discharged through sinuses with pus.
Following extrusion of sequestra, healing occurs.
Spontaneous drainage poor in submassetric area.
Much of body of mandible is lost due to poor central blood supply of the region.
D/D
Paget’s disease – particularly wen periosteal bone is involved
Fibrous dysplasia
Osteosarcoma
Chronic sclerosing osteomyelitis
– focal
- diffuse
Focal Sclerosing Osteomyelitis
Clinical features
Most commonly in children and young adults, rarely in older individuals.
Tooth most commonly involved is the mandibular third molar presenting with a large carious lesion.
No signs or symptoms other than mild pain associated with infected pulp.
Radiographic features
Entire root outline always visible with intact lamina dura.
Periodontal ligament space widened.
Border smooth & distinct appearing to blend into surrounding bone
D/D for focal sclerosing osteomyelitis
Local bone sclerosis
Sclerosing cementoma
Gigantiform cementoma
Treatment & prognosis
Affected tooth may be treated endodontically or extracted.
Sclerotic bone not attached to tooth and remains behind after tooth is removed.
This dense area may not get remodeled.
Recognizable on bone years later and is referred as bone scar.
Diffuse Sclerosing Osteomyelitis
May occur at any age, most common in older persons, esp in edentulous mandibles
vague pain, unpleasant taste.
Many times spontaneous formation of fistula seen opening onto mucosal surface to establish drainage
Slowly progressive, not particularly dangerous since it is non destructive & seldom produces complications
Radiographic features
Diffuse patchy, sclerosis of bone – “cotton wool” appearance
Radiopacity may be extensive and bilateral.
Due to diffuse nature, border between sclerosis & normal bone is often indistinct
D/D for DIFFUSE sclerosing osteomyelitis
FLORID OSSEOUS DYSPLASIA
SCLEROTIC CEMENTAL MASSES
TRUE CHR DIFFUSE SCLEROSING OSTEOMYELITIS
FIBROUS DYSPLASIA
Treatment & Prognosis
Resolution of adjacent foci of chronic infection often leads to improvement.
Usually too extensive to be removed surgically,
Acute episodes treated with antibiotics.
PROPERTIES OF TRIACYLGTYCEROLS
Biochemistry
PROPERTIES OF TRIACYLGTYCEROLS
1. Hydrolysis : Triacylglycerols undergo stepwise enzymatic hydrolysis to finally liberate free fatty acids and glycerol.
The process of hydrolysis, catalysed by lipases is important for digestion of fat in the gastrointestinal tract and fat mobilization from the adipose tissues.
2. Saponification : The hydrolysis of triacylglycerols by alkali to produce glycerol and soaps is known as saponification.
3.Rancidity: Rancidity is the term used to represent the deterioration of fats and oils resulting in an unpleasant taste. Fats containing unsaturated fatty acids are more susceptible to rancidity.
Hydrolytic rancidity occurs due to partial hydrolysis of triacylglycerols by bacterial enzymes.
Oxidative rancidity is due to oxidation of unsaturated fatty acids.
This results in the formation of unpleasant products such as dicarboxylic acids, aldehydes, ketones etc.
Antioxidants : The substances which can prevent the occurrence of oxidative rancidity are known as antioxidants.
Trace amounts of antioxidants such as tocopherols (vitamin E), hydroquinone, gallic acid and c,-naphthol are added to the commercial preparations of fats and oils to prevent rancidity. Propylgallate, butylatedhydroxyanisole (BHA) and butylated hydroxytoluene (BHT) are the antioxidants used in food preservation.
Lipid peroxidation in vivo: In the living cells, lipids undergo oxidation to produce peroxides and free radicals which can damage the tissue. .
The free radicals are believed to cause inflammatory diseases, ageing, cancer , atherosclerosis etc
Iodine number : lt is defined as the grams (number) of iodine absorbed by 100 g of fat or oil. lodine number is useful to know the relative
unsaturation of fats, and is directly proportional to the content of unsaturated fatty acids
Determination of iodine number will help to know the degree of adulteration of a given oil
Saponification number : lt is defined as the mg (number) of KOH required to hydrolyse (saponify) one gram of fat or oiL
Reichert-Meissl (RM) number: lt is defined as the number of ml 0.1 N KOH required to completely neutralize the soluble volatile fatty acids distilled from 5 g fat. RM number is useful in testing the purity of butter since it contains a good concentration of volatile fatty acids (butyric acid, caproic acid and caprylic acid).
Acid number : lt is defined as the number of mg of KOH required to completely neutralize free fatty acids present in one gram fat or oil. In normal circumstances, refined oils should be free from any free fatty acids.
FACTORS AFFECTING ENZYME ACTIVITY
Biochemistry
FACTORS AFFECTING ENZYME ACTIVITY
Velocity or rate of enzymatic reaction is assessed by the rate of change in concentration of substrate or product at a given time duration. Various factors which affect the activity of enzymes include:
1. Substrate concentration
2. Enzyme concentration
3. Product concentration
4. Temperature 5. Hydrogen ion concentration (pH)
6. Presence of activators
7. Presence of inhibitor
Effect of substrate Concentration : Reaction velocity of an enzymatic process increases with constant enzyme concentration and increase in substrate concentration.
Effect of enzyme Concentration: As there is optimal substrate concentration, rate of an enzymatic reaction or velocity (V) is directly proportional to the enzyme concentration.
Effect of product concentration In case of a reversible reaction catalyzed by a enzyme, as per the law of mass action the rate of reaction is slowed down with equilibrium. So, rate of reaction is slowed, stopped or even reversed with increase in product concentration
Effect of temperature: Velocity of enzymatic reaction increases with temperature of the medium which they are most efficient and the same is termed as optimum temperature.
Effect of pH: Many enzymes are most efficient in the region of pH 6-7, which is the pH of the cell. Outside this range, enzyme activity drops off very rapidly. Reduction in efficiency caused by changes in the pH is due to changes in the degree of ionization of the substrate and enzyme.
Highly acidic or alkaline conditions bring about a denaturation and subsequent loss of enzymatic activity
Exceptions such as pepsin (with optimum pH 1-2), alkaline phosphatase (with optimum pH 9-10) and acid phosphatase (with optimum pH 4-5)
Presence of activators Presence of certain inorganic ions increases the activity of enzymes. The best examples are chloride ions activated salivary amylase and calcium activated lipases.
Effect of Inhibitors The catalytic enzymatic reaction may be inhibited by substances which prevent the formation of a normal enzyme-substrate complex. The level of inhibition then depends entirely upon the relative concentrations of the true substrate and the inhibitor
Anti-Parkinson Drugs
Pharmacology
Anti-Parkinson Drugs
The disease involves degeneration of dopaminergic neurons in the nigral-striatal pathway in the basal ganglia. The cause is usually unknown. Sometimes it is associated with hypoxia, toxic chemicals, or cerebral infections.
Strategy
1. Increase dopamine in basal ganglia.
2. Block muscarinic receptors in the basal ganglia, since cholinergic function opposes the action of dopamine in the basal ganglia.
3. Newer therapies, such as the use of β-adrenergic receptor blockers.
Drugs
a. L-dopa plus carbidopa (Sinemet).
b. Bromocriptine, pergolide, pramipexole, ropinirole.
c. Benztropine, trihexyphenidyl, biperiden, procyclidine.
d. Diphenhydramine.
e. Amantadine.
f. Tolcapone and entacapone.
g. Selegiline.
Mechanisms of action of three drugs affecting DOPA
1. L-dopa plus carbidopa:
L-dopa is able to penetrate the blood–brain barrier and is then converted into dopamine. Carbidopa inhibits dopa decarboxylase, which catalyzes the formation of dopamine.
Carbidopa does not penetrate the blood–brain barrier; it therefore prevents the conversion of L-dopa to dopamine outside the CNS but allows
the conversion of L-dopa to dopamine inside the CNS.
2. Bromocriptine, pergolide, pramipexole, and ropinirole are direct dopamine receptor agonists.
3. Benztropine, trihexyphenidyl, biperiden, and procyclidine are antimuscarinic drugs.
4. Diphenhydramine is an antihistamine that has antimuscarinic action.
5. Amantadine releases dopamine and inhibits neuronal uptake of dopamine.
6. Selegiline is an irreversible inhibitor of monoamine oxidase B (MAO-B), which metabolizes dopamine. Selegiline therefore increases the level of dopamine.
7. Tolcapone is an inhibitor of catechol-O-methyl transferase (COMT), another enzyme that metabolizes dopamine.
8. Entacapone is another COMT inhibitor.
Dopamine and acetylcholine.
Loss of dopaminergic neurons in Parkinsonism leads to unopposed action by cholinergic neurons. Inhibiting muscarinic receptors can help alleviate symptoms of Parkinsonism
Adverse effects
1. L-dopa
- The therapeutic effects of the drug decrease with time.
- Oscillating levels of clinical efficacy of the drug (“on-off” effect).
- Mental changes—psychosis.
- Tachycardia and orthostatic hypotension.
- Nausea.
- Abnormal muscle movements (dyskinesias).
2. Tolcapone, entacapone (similar to L-dopa).
3. Direct dopamine receptor agonists (similar to L-dopa).
4. Antimuscarinic drugs
- Typical antimuscarinic adverse effects such as dry mouth.
b. Sedation.
5. Diphenhydramine (see antimuscarinic drugs).
6. Amantadine
- Nausea.
- Dizziness.
- Edema.
- Sweating.
7. Selegiline
- Nausea.
- Dry mouth.
- Dizziness.
- Insomnia.
- Although selegiline is selective for MAO-B, it still can cause excessive toxicity in the presence of tricyclic antidepressants, SSRIs, and meperidine.
Indications
Parkinson’s disease is the obvious major use of the above drugs. Parkinson-like symptoms can occur with many antipsychotic drugs. These symptoms are often treated with antimuscarinic drugs or diphenhydramine.
Dental implications of anti-Parkinson drugs
1. Dyskinesia caused by drugs can present a challenge for dental treatment.
2. Orthostatic hypotension poses a risk when changing from a reclining to a standing position.
3. The dentist should schedule appointments at a time of day at which the best control of the disease occurs.
4. Dry mouth occurs with several of the drugs.
The Oropharynx
AnatomyThe Oropharynx
The oral part of the pharynx has a digestive function.
It is continuous with the oral cavity through the oropharyngeal isthmus.
The oropharynx is bounded by the soft palate superiorly, the base of the tongue inferiorly, and the palatoglossal and palatopharyngeal arches laterally.
It extends from the soft palate to the superior border of the epiglottis.
The Palatine Tonsils
These are usually referred to as "the tonsils".
They are collections of lymphoid tissue the lie on each side of the oropharynx in the triangular interval between the palatine arches.
The palatine tonsils vary in size from person to person.
In children, the palatine tonsils tend to be large, whereas in older persons they are usual small and inconspicuous.
The visible part of the tonsil is no guide to its actual size because much of it may be hidden by the tongue and buried in the soft palate.
MAXILLARY CENTRAL INCISORS
Dental Anatomy
MAXILLARY CENTRAL INCISORS
Viewed mesially or distally, a maxillary central incisor looks like a wedge, with the point of the wedge at the incisal (cutting) edge of the tooth.
Facial Surface- The mesial margin is nearly straight and meets the incisal edge at almost a 90° angle, but the distal margin meets the incisal edge in a curve. The incisal edge is straight, but the cervical margin is curved like a half moon. Two developmental grooves are on the facial surface.
Lingual Surface:- The lingual aspect presents a distinctive lingual fossa that is bordered by mesial and distal marginal ridges, the incisal edge, and the prominent cingulum at the gingival. Sometimes a deep pit, the lingual pit, is found in conjunction with a cingulum.
Incisal: The crown is roughly triangular in outline; the incisal edge is nearly a straight line, though slightly crescent shaped
Contact Points: The mesial contact point is just about at the incisal, owing to the very sharp mesial incisal angle. The distal contact point is located at the junction of the incisal third and the middle third.
Root Surface:-As with all anterior teeth, the root of the maxillary central incisor is single. This root is from one and one-fourth to one and one-half times the length of the crown. Usually, the apex of the root is inclined slightly distally.