NEET MDS Synopsis
Nucleic Acids
PhysiologyNucleic Acids:
Two major types: DNA
RNA (including mRNA, tRNA, & rRNA)
Both types have code which specifies the sequence of amino acids in proteins
DNA = archival copy of genetic code, kept in nucleus, protected
RNA = working copy of code, used to translate a specific gene into a protein, goes into cytoplasm & to ribosomes, rapidly broken down
Nucleic acids are made of 5 nucleotide bases, sugars and phosphate groups
The bases make up the genetic code ; the phosphate and sugar make up the backbone
RNA is a molecule with a single strand
DNA is a double strand (a double helix) held together by hydrogen bonds between the bases
A = T; C= G because:
A must always hydrogen bond to T
C must always hydrogen bond to G
Public health Dentistry
Public Health Dentistry
Terms
Health—state of complete physical, mental, and social well-being where basic human needs are met. not merely the absence of disease or infirmity; free from disease or pain
Public health — science and art of preventing disease. prolonging life, and promoting physical and mental health and efficiency through organized community efforts
1. Public health is concerned with the aggregate health of a group, a community, a state, a nation. or a group of nations
2. Public health is people’s health
3. Concerned with four broad areas
a. Lifestyle and behavior
b. The environment
c. Human biology
d. The organization of health programs and systems
Dental public health—science and art of preventing and controlling dental diseases and promoting dental health through organized community efforts; that form of dental practice that serves the community as a patient rather than the individual; concerned with the dental education of the public, with applied dental research, and with the administration of group dental care programs. as well as the prevention and control of dental diseases on a community basis
Community health—same as public health full range of health services, environmental and personal, including major activities such as health education of the public and the social context of life as it affects the community; efforts that are organized to promote and restore the health and quality of life of the people
Community dental health services are directed to ward developing, reinforcing, and enhancing the oral health status of people either as individuals or collectively as groups and communities
Orofacial Pain - Local Anesthetics
Anaesthesia
Pain: sensory and emotional experience associated with actual or potential tissue damage
1. Components: sensory (objective characteristics of pain e.g., location, duration, intensity; thermal, mechanical, or chemical) and motivational/affective (associated with past experience, fear, suffering, anxiety, culture)
2. Anatomy and physiology: nociceptors specialized to convey noxious stimuli (mechanical, chemical, thermal)
a. Hyperalgesia: exaggerated pain response to stimulus that was previously painful.
i. Primary: nociceptors in area of tissue damage fire or due to algesic chemicals (bradykinin, SP, etc.)
ii. Secondary: absence of local causes so due to changes in CNS that result in nociceptor firing (e.g., referred pain due to convergence)
b. Allodynia: pain caused by stimulus that is normally innocuous (non-painful); e.g., abcess- just touch, hurts
c. Fiber types: local anesthetics target Ad and C fibers
i. A-b: myelinated cutaneous mechanoreceptor (25-50 m/s); innervates Ruffini endings
ii. A-d: myelinated nociceptor that mediates sharp, well-localized pain (10-30 m/s)
iii. C: have Schwan cells but no myelin; nociceptor that mediates dull, poorly-localized pain (<2.5 m/s)
d. Neurotransmitters:
i. Excitatory: glutamate (most common, works on NMDA receptors), substance P (SP, p for pain; act at neurokinin, NK, receptors), calcitonin G-receptor peptide (CGRP; co-released with SP), prostaglandins (products of cyclooxygenase), and kinins
ii. Inhibitory: GABA (amino acid; hyperpolarizes neurons so ¯ pain sensation), monoamines (e.g., seratonin, NE), and opioids (e.g., endorphins- give runner’s high; 3 made by body: 1) b-endorphin, 2) dynorphin, 3) enkephalins; 3 receptors: 1) mu- most important for pain, 2) delta, and 3) kappa)
Treatment:
a. Opioids: indicated for moderate to severe acute (post-op) pain, chronic cancer pain, or as sedative/pain reliever during general anesthesia. A narcotic = sleep-inducing.
i. Mechanism of action: bind opioid receptor in spinal cord and brainstem (mu, d, and kappa; found in periaqueductal grey- area in brain with tons of opioid receptors, when activated ® ¯ pain), inhibit peripheral nociceptors, activate descending pain control system, improve affective components of pain
ii. Side-effects: euphoria, sedation, respiratory depression, nausea/vomiting, constipation (especially with elderly), addiction, tolerance (does not remain once drug removed)
b. NSAIDS (non-steroidal anti-inflammatory drugs): indicated for mild to moderate pain that has inflammatory component, fever. Aspirin first made in 1853 from parts of willow bark.
i. Mechanism of action: inhibits cyclooxygenase (COX) which makes prostaglandins and other inflammatory agents. Anti-pyretic (fever-reducing) actions mediated by effects on hypothalamus- center of brain that regulates body T.
ii. Side effects: since acidic- nausea, vomiting (rare), GI bleeding, prolonged bleeding time since inhibit platelets. Warnings if ulcer history, combining NSAIDS (® ringing in ears), and flu/chicken pox in children ® risk of Rie syndrome (fatal brain inflammation)
c. Tylenol (acetaminophen): analgesic and anti-pyretic but no significant effect on inflammation. OD kills liver.
d. Muscle relaxants: don’t act directly on muscles; indicated for myofascial pain (muscle/CT pain) but not analgesic (not good for pain control)
i. Mechanism of action: depends on drug but most GABA-mediated signals in spinal cord
ii. Side-effects: sedation, weakness
e. Anti-depressants: low-doses indicated for chronic pain that is unresponsive to conventional analgesics, 1st choice for some types of neuropathic pain. Side effects: sedation, xerostomia, CV effects.
i. Mechanism of action: activate descending pain control systems ® pre-synaptic a-2 receptor to monoamine (NE, seratonin) in brain ® inhibit SP, glutamate, etc. release from peripheral nociceptors.
4. Descending pain modulatory pathways: neuronal cell bodies in brainstem send projections to dorsal horn where release NT that inhibit incoming pain info or decrease sensitivity of neurons in dorsal horn to that info. Opioids and antidepressants act in part by these pathways.
ATROPHY
General Pathology
ATROPHY
It is the acquired decrease in the size of an organ due to decrease in the size and/or number of its constituent cells.
Causes:
(1) Physiological
- Foetal involution.
o Branchial clefts.
o Ductus arterious.
- Involution of thymus and other lymphoid organs in childhood and adolescence.
- In adults:
o Post-partum uterus.
o Post-menopausal ovaries and uterus
o Post-lactational breast
o Thymus.
(2) Pathological:
- Generalised as in
o Ageing.
o Severe starvation and cachexia
- Localised :
o Disuse atropy of bone and muscle.
o Ischaemic atrophy as in arteriosclerotic kidney. .
o Pressure atrophy due to tumours and of kidney in hydronephrosis.
o Lack of trophic stimulus to endocrines and gonads.
Clinical importance of cementum
Dental Anatomy
Clinical importance of cementum
1) Deposition of cementum continues throughout life.
The effects of the continuous deposition of cementum are the maintenance of total length of the tooth (good) and constriction of the apical foramen (bad).
2) With age, the smooth surface of cementum becomes more irregular due to calcification of some ligament fiber bundles. This is referred to as spikes.
Behavior of cementum in pathologic conditions
Dentin
Dental Anatomy
Dentin
Composition: 70% inorganic, 20% organic, 10% water by weight and 45%, 33%, and 22% in volume respectively
Hydroxyapatite crystals and collagen type I
Physical characteristics: Harder than bone and softer than enamel
Yellow in color in normal teeth
Radiographic appearance: More radiolucent than enamel
Primary (circumpulpal) dentin: forms most of the tooth
Mantle dentin: first dentin to form; forms the outline of dentin in the adult tooth
Predentin: lines the innermost portion of dentin (faces the pulp)
Secondary dentin: after root formation dentin continues to form, continuous to primary dentin but with structural irregularities
Tertiary dentin: reactive or reparative dentin; may or may not have characteristics of primary dentin; produced in the area of an external stimulus; osteodentin
Dentin is formed by cells called odontoblasts.
These cells derive from the ectomesenchyme and produce the organic matrix that will calcify and become the dentin.
Formation of dentin initiates formation of enamel.
The formation of dentin starts during late bell-stage in the area of the future cusp.
First coronal dentin and then root dentin.
Completion of dentin does not occur until about 18 months after eruption of primary and 2-3 years after eruption of permanent teeth.
The rate of dentin development varies.
The role of the internal (inner) dental (enamel) epithelium
Cuboidal - Columnar (reverse polarization)
Ectomesenchymal cells of the dental papilla become preodontoblasts - odontoblasts
Acellular zone disappears
Histologic features of dentin
Odontoblasts
Dentinal tubules
Extend through the entire thickness of dentin
S-shaped (primary curvatures) path in the crown, less S-shaped in the root, almost straight in the cervical aspect
Secondary curvatures
Tubular microbranches
Presence of fluid
Intratubular dentin
Dentin in the tubule that is hypermineralized
The term peritubular dentin should not be used
Sclerotic dentin
Dentinal tubules that are occluded with calcified material
Most likely a physiologic response
Reduction of permeability of dentin
Intertubular dentin
Dentin between the tubules
Interglobular dentin
Areas of unmineralized or hypomineralized dentin
The defect affects mineralization and not the architecture of dentin
Incremental lines
Lines of von Ebner: lines associated with 5-day rythmic pattern of dentin deposition
Contour lines of Owen: Originally described by Owen they result from a coincidence of the secondary curvatures between neighboring dentinal tubules.
Granular Layer of Tomes
Seen only in ground sections in the root area covered by cementum
Originally, they were thought to be areas of hypomineralization
They are true spaces obtained by sections going through the looped terminal portions dentinal tubules
DE junction :Scalloped area
Enamel tissue with incremental lines of Retzius and dentin tissue with parallel, curved dentinal tubules are in contact at the irregular dentino-enamel junction. The junction often has a scalloped-shaped morphology
DC junction Dentin Cemental Junction
Water Acid Bases & Buffers -pKa
Biochemistry
Acids and bases can be classified as proton donors and proton acceptors, respectively. This means that the conjugate base of a given acid will carry a net charge that is more negative than the corresponding acid. In biologically relavent compounds various weak acids and bases are encountered, e.g. the acidic and basic amino acids, nucleotides, phospholipids etc.
Weak acids and bases in solution do not fully dissociate and, therefore, there is an equilibrium between the acid and its conjugate base. This equilibrium can be calculated and is termed the equilibrium constant = Ka. This is also referred to as the dissociation constant as it pertains to the dissociation of protons from acids and bases.
In the reaction of a weak acid:
HA <-----> A- + H+
the equlibrium constant can be calculated from the following equation:
Ka = [H+][A-]/[HA]
As in the case of the ion product:
pKa = -logKa
Therefore, in obtaining the -log of both sides of the equation describing the dissociation of a weak acid we arrive at the following equation:
-logKa = -log[H+][A-]/[HA]
Since as indicated above -logKa = pKa and taking into account the laws of logrithms:
pKa = -log[H+] -log[A-]/[HA]
pKa = pH -log[A-]/[HA]
From this equation it can be seen that the smaller the pKa value the stronger is the acid. This is due to the fact that the stronger an acid the more readily it will give up H+ and, therefore, the value of [HA] in the above equation will be relatively small.
Phases of cardiac cycle
Physiology
Phases of cardiac cycle :
1. Early diastole ( also called the atrial diastole , or complete heart diastole) : During this phase :
- Atria are relaxed
- Ventricles are relaxed
- Semilunar valves are closed
- Atrioventricular valves are open
During this phase the blood moves passively from the venous system into the ventricles ( about 80 % of blood fills the ventricles during this phase.
2. Atrial systole : During this phase :
- Atria are contracting
- Ventricles are relaxed
- AV valves are open
- Semilunar valves are closed
- Atrial pressure increases.the a wave of atrial pressure appears here.
- P wave of ECG starts here
- intraventricular pressure increases due to the rush of blood then decrease due to continuous relaxation of ventricles.
The remaining 20% of blood is moved to fill the ventricles during this phase , due to atrial contraction.
3. Isovolumetric contraction : During this phase :
- Atria are relaxed
- Ventricles are contracting
- AV valves are closed
- Semilunar valves are closed
- First heart sound
- QRS complex.
The ventricular fibers start to contract during this phase , and the intraventricular pressure increases. This result in closing the AV valves , but the pressure is not yet enough to open the semilunar valves , so the blood volume remain unchanged , and the muscle fibers length also remain unchanged , so we call this phase as isovolumetric contraction ( iso : the same , volu= volume , metric= length).
4. Ejection phase : Blood is ejected from the ventricles into the aorta and pulmonary artery .
During this phase :
- Ventricles are contracting
- Atria are relaxed
- AV valves are closed
- Semilunar valves are open
- First heart sound
- Intraventricular pressure is increased , due to continuous contraction
- increased aortic pressure .
- T wave starts.
5. Isovolumetric relaxation: This phase due to backflow of blood in aorta and pulmonary system after the ventricular contraction is up and the ventricles relax . This backflow closes the semilunar valves .
During this phase :
- Ventricles are relaxed
- Atrial are relaxed
- Semilunar valves are closed .
- AV valves are closed.
- Ventricular pressure fails rapidly
- Atrial pressure increases due to to continuous venous return. the v wave appears here.
- Aortic pressure : initial sharp decrease due to sudden closure of the semilunar valve ( diacrotic notch) , followed by secondary rise in pressure , due to elastic recoil of the aorta ( diacrotic wave) .
- T wave ends in this phase