NEET MDS Synopsis
The Henderson-Hasselbalch Equation
Biochemistry
By rearranging the above equation we arrive at the Henderson-Hasselbalch equation:
pH = pKa + log[A-]/[HA]
It should be obvious now that the pH of a solution of any acid (for which the equilibrium constant is known, and there are numerous tables with this information) can be calculated knowing the concentration of the acid, HA, and its conjugate base [A-].
At the point of the dissociation where the concentration of the conjugate base [A-] = to that of the acid [HA]:
pH = pKa + log[1]
The log of 1 = 0. Thus, at the mid-point of a titration of a weak acid:
pKa = pH
In other words, the term pKa is that pH at which an equivalent distribution of acid and conjugate base (or base and conjugate acid) exists in solution.
Early Childhood Caries
Conservative DentistryEarly Childhood Caries (ECC) Classification
Early Childhood Caries (ECC) is a significant public health concern
characterized by the presence of carious lesions in young children. It is
classified into three types based on severity, affected teeth, and underlying
causes. Understanding these classifications helps in diagnosing, preventing, and
managing ECC effectively.
Type I ECC (Mild to Moderate)
A. Characteristics
Affected Teeth: Carious lesions primarily involve the
molars and incisors.
Age Group: Typically observed in children aged 2
to 5 years.
B. Causes
Dietary Factors: The primary cause is usually a
combination of cariogenic semisolid or solid foods, such as sugary snacks
and beverages.
Oral Hygiene: Lack of proper oral hygiene practices
contributes significantly to the development of caries.
Progression: As the cariogenic challenge persists, the
number of affected teeth tends to increase.
C. Clinical Implications
Management: Emphasis on improving oral hygiene
practices and dietary modifications can help control and reverse early
carious lesions.
Type II ECC (Moderate to Severe)
A. Characteristics
Affected Teeth: Labio-lingual carious lesions primarily
affect the maxillary incisors, with or without molar caries, depending on
the child's age.
Age Group: Typically seen soon after the first tooth
erupts.
B. Causes
Feeding Practices: Common causes include inappropriate
use of feeding bottles, at-will breastfeeding, or a combination of both.
Oral Hygiene: Poor oral hygiene practices exacerbate
the condition.
Progression: If not controlled, Type II ECC can
progress to more advanced stages of caries.
C. Clinical Implications
Intervention: Early intervention is crucial, including
education on proper feeding practices and oral hygiene to prevent further
carious development.
Type III ECC (Severe)
A. Characteristics
Affected Teeth: Carious lesions involve almost all
teeth, including the mandibular incisors.
Age Group: Usually observed in children aged 3
to 5 years.
B. Causes
Multifactorial: The etiology is a combination of
various factors, including poor oral hygiene, dietary habits, and possibly
socio-economic factors.
Rampant Nature: This type of ECC is rampant and can
affect immune tooth surfaces, leading to extensive decay.
C. Clinical Implications
Management: Requires comprehensive dental treatment,
including restorative procedures and possibly extractions. Education on
preventive measures and regular dental visits are essential to manage and
prevent recurrence.
The Sliding Filament mechanism of muscle contraction
PhysiologyThe Sliding Filament mechanism of muscle contraction.
When a muscle contracts the light I bands disappear and the dark A bands move closer together. This is due to the sliding of the actin and myosin myofilaments against one another. The Z-lines pull together and the sarcomere shortens
The thick myosin bands are not single myosin proteins but are made of multiple myosin molecules. Each myosin molecule is composed of two parts: the globular "head" and the elongated "tail". They are arranged to form the thick bands.
It is the myosin heads which form crossbridges that attach to binding sites on the actin molecules and then swivel to bring the Z-lines together
Likewise the thin bands are not single actin molecules. Actin is composed of globular proteins (G actin units) arranged to form a double coil (double alpha helix) which produces the thin filament. Each thin myofilament is wrapped by a tropomyosin protein, which in turn is connected to the troponin complex.
The tropomyosin-troponin combination blocks the active sites on the actin molecules preventing crossbridge formation. The troponin complex consists of three components: TnT, the part which attaches to tropomyosin, TnI, an inhibitory portion which attaches to actin, and TnC which binds calcium ions. When excess calcium ions are released they bind to the TnC causing the troponin-tropomyosin complex to move, releasing the blockage on the active sites. As soon as this happens the myosin heads bind to these active sites.
Cranial Nerves
Physiology
There Are 12 Pairs of Cranial Nerves
The 12 pairs of cranial nerves emerge mainly from the ventral surface of the brain
Most attach to the medulla, pons or midbrain
They leave the brain through various fissures and foramina of the skull
Nerve
Name
Sensory
Motor
Autonomic
Parasympathetic
I
Olfactory
Smell
II
Optic
Vision
III
Oculomotor
Proprioception
4 Extrinsic eye muscles
Pupil constriction
Accomodation
Focusing
IV
Trochlear
Proprioception
1 Extrinsic eye muscle (Sup.oblique)
V
Trigeminal
Somatic senses
(Face, tongue)
Chewing
VI
Abducens
Proprioception
1 Extrinsic eye muscle (Lat. rectus)
VII
Facial
Taste
Proprioception
Muscles of facial expression
Salivary glands
Tear glands
VIII
Auditory
(Vestibulocochlear)
Hearing, Balance
IX
Glossopharyngeal
Taste
Blood gases
Swallowing
Gagging
Salivary glands
X
Vagus
Blood pressure
Blood gases
Taste
Speech
Swallowing Gagging
Many visceral organs
(heart, gut, lungs)
XI
Spinal acessory
Proprioception
Neck muscles:
Sternocleidomastoid
Trapezius
XII
Hypoglossal
Proprioception
Tongue muscles
Speech
Many of the functions that make us distinctly human are controlled by cranial nerves: special senses, facial expression, speech.
Cranial Nerves Contain Sensory, Motor and Parasympathetic Fibers
Specific Agents
Pharmacology
Specific Agents
Hydralazine [orally effective]
MOA: Not completely understood. Seems to be partially dependent on the release of EDRF and perhaps partially due to K+-channel activation
- in clinical doses action is manifest primarily on vascular smooth muscle (non-vascular muscle is not much affected).
- Re: Metabolism & Excretion. In cases of renal failure the plasma half life may be substantially increased (4-5 fold). One mode of metabolism is
via N-Acetylation (problem of slow acetylators)
Side Effects
- those typical of vasodilation = headache, nasal congestion, tachycardia etc.
- chronic treatment with high doses > 200 mg/day may induce a rheumatoid-like state which may resemble lupus erythematosus.
Minoxidil (Loniten) [orally effective]
MOA: K+-channel agonist
- very effective antihypertensive. Used primarily to treat life-threatening hypertension or hypertension resistant to other agents.
Side effects - growth of hair
Diazoxide (Hyperstat) [used only IV]
MOA: K+-channel agonist
- Administered by rapid IV injection; action appearing after 3-5 min; action may last from 4 to 12 hours.
Nitroprusside (Nipride) [used only IV]
MOA: increase in cGMP
- unlike the other vasodilators, venous tone is substantially reduced by nitroprusside.
- rapid onset of action (.30 sec); administered as an IV-infusion.
- particularly useful for hypertension associated with left ventricular failure.
Velopharyngeal Insufficiency (VPI)
Oral and Maxillofacial SurgeryVelopharyngeal Insufficiency (VPI)
Velopharyngeal insufficiency (VPI) is
characterized by inadequate closure of the nasopharyngeal airway during speech
production, leading to speech disorders such as hypernasality and nasal
regurgitation. This condition is particularly relevant in patients who have
undergone cleft palate repair, as the surgical success does not always guarantee
proper function of the velopharyngeal mechanism.
Etiology of VPI
The etiology of VPI following cleft palate repair is multifactorial and can
include:
Inadequate Surgical Repair: Insufficient repair of the
musculature involved in velopharyngeal closure can lead to persistent VPI.
This may occur if the muscles are not properly repositioned or if there is
inadequate tension in the repaired tissue.
Anatomical Variations: Variations in the anatomy of the
soft palate, pharynx, and surrounding structures can contribute to VPI.
These variations may not be fully addressed during initial surgical repair.
Neuromuscular Factors: Impaired neuromuscular function
of the muscles involved in velopharyngeal closure can also lead to VPI,
which may not be correctable through surgical means alone.
Surgical Management of VPI
Pharyngoplasty: One of the surgical options for managing VPI
is pharyngoplasty, which aims to improve the closure of the nasopharyngeal port
during speech.
Historical Background: The procedure was first
described by Hynes in 1951 and has since been modified by various authors to
enhance its effectiveness and reduce complications.
Operative Procedure
Flap Creation: The procedure involves the creation of
two superiorly based myomucosal flaps from each posterior tonsillar pillar.
Care is taken to include as much of the palatopharyngeal muscle as possible
in the flaps.
Flap Elevation: The flaps are elevated carefully to
preserve their vascular supply and muscular integrity.
Flap Insetting: The flaps are then attached and inset
within a horizontal incision made high on the posterior pharyngeal wall.
This technique aims to create a single nasopharyngeal port rather than the
two ports typically created with a superiorly based pharyngeal flap.
Contractile Ridge Formation: The goal of the procedure
is to establish a contractile ridge posteriorly, which enhances the function
of the velopharyngeal valve, thereby improving closure during speech.
Advantages of Sphincter Pharyngoplasty
Lower Complication Rate: One of the main advantages of
sphincter pharyngoplasty over the traditional superiorly based flap
technique is the lower incidence of complications related to nasal airway
obstruction. This is particularly important for patient comfort and quality
of life post-surgery.
Improved Speech Outcomes: By creating a more effective
velopharyngeal mechanism, patients often experience improved speech
outcomes, including reduced hypernasality and better articulation.
RESPIRATORY DISORDERS - Emphysema
Physiology4. Emphysema
1. Permanent enlargement of airways with distension of alveolar walls
Thickened Bronchial Submucosa, Edema & Cellular Infiltration (loss of elasticity), Dilation of Air spaces, due to destruction of alveolar walls (Air trapped by obstruction)
2. Lower Respiratory tree destruction
Respiratory Bronchioles, Alveolar ducts, & Alveolar sacs
Types of Emphysema:
1. Centrilobular (Centriacinar) = Respiratory Bronchioles
Rarely seen in non Smokers, More in Men than Women, Found in Smokers with Bronchitis
2. Panlobular (Panacinar)
Hereditary, Single autosomal recessive gene. Deficient in 1-globulin (1-antitrypsin), Protects respiratory tract from neutrophil elastase (Enzyme that distroys lung connective tissue) , Aged persons, Results from Bronchi or Bronchiolar constriction
NOTE: Smoking = Leading cause of Bronchitis, Emphysema
Characteristics of Immunoglobulin subclasses
General Pathology
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,