NEET MDS Synopsis
SHOCK
General Surgery
SHOCK
Shock is defined as a pathological state causing inadequate oxygen delivery to the peripheral tissues and resulting in lactic acidosis, cellular hypoxia and disruption of normal metabolic condition.
CLASSIFICATION
Shock is generally classified into three major categories:
1. Hypovolemic shock
2. Cardiogenic shock
3. Distributive shock
Distributive shock is further subdivided into three subgroups:
a. Septic shock
b. Neurogenic shock
c. Anaphylactic shock
Hypovolemic shock is present when marked reduction in oxygen delivery results from diminished cardiac output secondary to inadequate vascular volume. In general, it results from loss of fluid from circulation, either directly or indirectly.
e.g. ? Hemorrhage
• Loss of plasma due to burns
• Loss of water and electrolytes in diarrhea
• Third space loss (Internal fluid shift into inflammatory exudates in
the peritoneum, such as in pancreatitis.)
Cardiogenic shock is present when there is severe reduction in oxygen delivery secondary to impaired cardiac function. Usually it is due to myocardial infarction or pericardial tamponade.
Septic Shock (vasogenic shock) develops as a result of the systemic effect of infection. It is the result of a septicemia with endotoxin and exotoxin release by gram-negative and gram-positive bacteria. Despite normal or increased cardiac output and oxygen delivery, cellular oxygen consumption is less than normal due to impaired extraction as a result of impaired metabolism.
Neurogenic shock results primarily from the disruption of the sympathetic nervous system which may be due to pain or loss of sympathetic tone, as in spinal cord injuries.
PATHO PHYSIOLOGY OF SHOCK
Shock stimulates a physiologic response. This circulatory response to hypotension is to conserve perfusion to the vital organs (heart and brain) at the expense of other tissues. Progressive vasoconstriction of skin, splanchnic and renal vessels leads to renal cortical necrosis and acute renal failure. If not corrected in time, shock leads to organ failure and sets up a vicious circle with hypoxia and acidosis.
CLINICAL FEATURES
The clinical presentation varies according to the cause. But in general patients with hypotension and reduced tissue perfusion presents with:
• Tachycardia
• Feeble pulse
• Narrow pulse pressure
• Cold extremities (except septic shock)
• Sweating, anxiety
• Breathlessness / Hyperventilation
• Confusion leading to unconscious state
PATHO PHYSIOLOGY OF SHOCK
Shock stimulates a physiologic response. This circulatory response to hypotension is to conserve perfusion to the vital organs (heart and brain) at the expense of other tissues. Progressive vasoconstriction of skin, splanchnic and renal vessels leads to renal cortical necrosis and acute renal failure. If not corrected in time, shock leads to organ failure and sets up a vicious circle with hypoxia and acidosis.
CLINICAL FEATURES
The clinical presentation varies according to the cause. But in general patients with hypotension and reduced tissue perfusion presents with:
• Tachycardia
• Feeble pulse
• Narrow pulse pressure
• Cold extremities (except septic shock)
• Sweating, anxiety
• Breathlessness / Hyperventilation
• Confusion leading to unconscious state
Dental Practice Considerations
Conservative DentistryImplications for Dental Practice
A. Health and Safety Considerations
Mercury Exposure: Understanding the amounts of mercury
released during these procedures is crucial for assessing potential health
risks to dental professionals and patients.
Regulatory Guidelines: Dental practices should adhere
to guidelines and regulations regarding mercury handling and exposure limits
to ensure a safe working environment.
B. Best Practices
Use of Wet Polishing: Whenever possible, wet polishing
should be preferred over dry polishing to minimize mercury release.
Proper Ventilation: Ensuring adequate ventilation in
the dental operatory can help reduce the concentration of mercury vapor in
the air.
Personal Protective Equipment (PPE): Dental
professionals should use appropriate PPE, such as masks and gloves, to
minimize exposure during amalgam handling.
C. Patient Safety
Informed Consent: Patients should be informed about the
materials used in their restorations, including the presence of mercury in
amalgam, and the associated risks.
Monitoring: Regular monitoring of dental practices for
mercury exposure levels can help maintain a safe environment for both staff
and patients.
1. Noise Levels of Turbine Handpieces
Turbine Handpieces
Ball Bearings: Turbine handpieces equipped with ball
bearings can operate efficiently at air pressures of around 30 pounds.
Noise Levels: At high frequencies, these handpieces may
produce noise levels ranging from 70 to 94 dB.
Hearing Damage Risk: Exposure to noise levels exceeding
75 dB, particularly in the frequency range of 1000 to 8000 cycles per second
(cps), can pose a risk of hearing damage for dental professionals.
Implications for Practice
Hearing Protection: Dental professionals should
consider using hearing protection, especially during prolonged use of
high-speed handpieces, to mitigate the risk of noise-induced hearing loss.
Workplace Safety: Implementing noise-reduction
strategies in the dental operatory can enhance the comfort and safety of
both staff and patients.
2. Post-Carve Burnishing
Technique
Post-Carve Burnishing: This technique involves lightly
rubbing the carved surface of an amalgam restoration with a burnisher of
suitable size and shape.
Purpose: The goal is to improve the smoothness of the
restoration and produce a satin finish rather than a shiny appearance.
Benefits
Enhanced Aesthetics: A satin finish can improve the
aesthetic integration of the restoration with the surrounding tooth
structure.
Surface Integrity: Burnishing can help to compact the
surface of the amalgam, potentially enhancing its resistance to wear and
marginal integrity.
3. Preparing Mandibular First Premolars for MOD Amalgam Restorations
Considerations for Tooth Preparation
Conservation of Tooth Structure: When preparing a
mesio-occluso-distal (MOD) amalgam restoration for a mandibular first
premolar, it is important to conserve the support of the small lingual cusp.
Occlusal Step Preparation: The occlusal step should
be prepared more facially than lingually, which helps to maintain the
integrity of the lingual cusp.
Bur Positioning: The bur should be tilted slightly
lingually to establish the correct direction for the pulpal wall.
Cusp Reduction
Lingual Cusp Consideration: If the lingual margin of
the occlusal step extends more than two-thirds the distance from the central
fissure to the cuspal eminence, the lingual cusp may need to be reduced to
ensure proper occlusal function and stability of the restoration.
4. Universal Matrix System
Overview
Tofflemire Matrix System: Designed by B.R. Tofflemire,
the Universal matrix system is a commonly used tool in restorative
dentistry.
Indications: This system is ideally indicated when
three surfaces (mesial, occlusal, distal) of a posterior tooth have been
prepared for restoration.
Benefits
Retention and Contour: The matrix system helps in
achieving proper contour and retention of the restorative material, ensuring
a well-adapted restoration.
Ease of Use: The design allows for easy placement and
adjustment, facilitating efficient restorative procedures.
5. Angle Former Excavator
Functionality
Angle Former: A special type of excavator used
primarily for sharpening line angles and creating retentive features in
dentin, particularly in preparations for gold restorations.
Beveling Enamel Margins: The angle former can also be
used to place a bevel on enamel margins, enhancing the retention of
restorative materials.
Clinical Applications
Preparation for Gold Restorations: The angle former is
particularly useful in preparations where precise line angles and retention
are critical for the success of gold restorations.
Versatility: Its ability to create retentive features
makes it a valuable tool in various restorative procedures.
Estimation of the risk of anesthesia
Pharmacology
Estimation of the risk of anesthesia (American Society of Anesthesiologists scale)
• ASA 1: healthy patient.
• ASA 2: patient with stable, treated illness like arterial hypertension, diabetes melitus, asthma bronchiale, obesity
• ASA 3: patient with systemic illness decreasing sufficiency like heart illness, late infarct
• ASA 4: patient with serious illness influencing his state like renal insuficiency, unstable hypertension, circulatory insuficiency
• ASA 5: patient in life treatening illness
• ASA 6: brain death- potential organ donor
Pharyngeal Arch
Anatomy
Pharyngeal Arch
Arch Artery
Cranial Nerve
Skeletal elements
Muscles
1
Terminal Branch of maxillary artery
Maxillary and mandibular division of trigemenial (V)
Derived from arch cartilages (originating from neural crest):
From maxillary cartilages:
Alispenoid, incus
From mandibular:
Mackel’s cartilage, malleus
Upper portion of external ear (auricle) is derived from dorsal aspect of 1st pharyngeal arch.
Derived by direct ossification from arch dermal mesenchyme:
Maxilla, zygomatic, squamous portion of temporal bone, mandible
Muscles of mastication (temporalis, masseter, and pterygoids), mylohyoid, anterior belly of digastric, tensor tympani, tensor veli palatini (originate from cranial somitomere 4)
2
Stapedius artery (embryologic) and cortiotympanic artery (adult)
Facial nerve (VII)
Stapes, styloid process, stylohyoid ligament, lesser horns and upper rim of hyoid (derived from the second arch cartilage; originate from neural crest).
Lower portion of external ear (auricle) is derived from 2nd pharyngeal arch.
Muscles of facial expression (orbicularis oculi, orbicularis oris, auricularis, platysma, fronto-ooccipitalis, buccinator), posterior belly of digastric, stylohyoid, stapedius (originate from cranial somitomere 6)
3
Common carotid artery, most of internal carotid
Glossopharyngeal (IX)
Lower rim and greater horn of hyoid (derived from the third arch cartilage; originate from neural crest cells)
Sytlopharyngeus (originate from cranial somitomere 7)
4
Left: Arch of aorta;
Right: Right subclavian artery;
Original sprouts of pulmonary arteries
Superior laryngeal branch of vagus (X)
Laryngeal cartilages (Derived from the 4th arch cartilage, originate from lateral plate mesoderm)
Constrictors of pharynx, cricothyroid, levator veli palatine (originate from occipital somites 2-4)
6
Ductus arteriosus; roots of definitive pulmonary arteries
Recurrent laryngeal branch of vagus (X)
Laryngeal cartilages (derived from the 6th-arch cartilage; originate from lateral plate mesoderm)
Intrinsic muscles of larynx (originate from occipital somites 1 and 2)
Changes in Plaque pH After Sucrose Rinse
PeriodontologyChanges in Plaque pH After Sucrose Rinse
The pH of dental plaque is a critical factor in the development of dental
caries and periodontal disease. Key findings from
various studies that investigated the changes in plaque pH following
carbohydrate rinses, particularly focusing on sucrose and glucose.
Key Findings from Studies
Monitoring Plaque pH Changes:
A study reported that changes in plaque pH after a sucrose rinse
were monitored using plaque sampling, antimony and glass electrodes, and
telemetry.
Results:
The minimum pH at approximal sites (areas between teeth) was
approximately 0.7 pH units lower than that on buccal surfaces (outer
surfaces of the teeth).
The pH at the approximal site remained below resting levels for
over 120 minutes.
The area under the pH response curves from approximal sites was
five times greater than that from buccal surfaces, indicating a more
significant and prolonged acidogenic response in interproximal
areas.
Stephan's Early Studies (1935):
Method: Colorimetric measurement of plaque pH
suspended in water.
Findings:
The pH of 211 plaque samples ranged from 4.6 to 7.0.
The mean pH value was found to be 5.9, indicating a generally
acidic environment in dental plaque.
Stephan's Follow-Up Studies (1940):
Method: Use of an antimony electrode to measure in
situ plaque pH after rinsing with sugar solutions.
Findings:
A 10% solution of glucose or sucrose caused a rapid drop in
plaque pH by about 2 units within 2 to 5 minutes, reaching values
between 4.5 and 5.0.
A 1% lactose solution lowered the pH by 0.3 units, while a 1%
glucose solution caused a drop of 1.5 units.
A 1% boiled starch solution resulted in a reduction of 1.5 pH
units over 51 minutes.
In all cases, the pH tended to return to initial values within
approximately 2 hours.
Investigation of Proximal Cavities:
Studies of actual proximal cavities opened mechanically showed that
the lowest pH values ranged from 4.6 to 4.1.
After rinsing with a 10% glucose or sucrose solution, the pH in the
plaque dropped to between 4.5 and 5.0 within 2 to 5 minutes and
gradually returned to baseline levels within 1 to 2 hours.
Implications
The studies highlight the significant impact of carbohydrate exposure,
particularly sucrose and glucose, on the pH of dental plaque.
The rapid drop in pH following carbohydrate rinses indicates an
acidogenic response from plaque microorganisms, which can contribute to
enamel demineralization and caries development.
The prolonged acidic environment in approximal sites suggests that these
areas may be more susceptible to caries due to the slower recovery of pH
levels.
Amelogenesis Imperfecta
PedodonticsClassification of Amelogenesis Imperfecta
Amelogenesis imperfecta (AI) is a group of genetic conditions that affect the
development of enamel, leading to various enamel defects. The classification of
amelogenesis imperfecta is based on the phenotype of the enamel and the mode of
inheritance. Below is a detailed classification of amelogenesis imperfecta.
Type I: Hypoplastic
Hypoplastic amelogenesis imperfecta is characterized by a deficiency in the
amount of enamel produced. The enamel may appear thin, pitted, or smooth,
depending on the specific subtype.
1A: Hypoplastic Pitted
Inheritance: Autosomal dominant
Description: Enamel is pitted and has a rough
surface texture.
1B: Hypoplastic, Local
Inheritance: Autosomal dominant
Description: Localized areas of hypoplasia
affecting specific teeth.
1C: Hypoplastic, Local
Inheritance: Autosomal recessive
Description: Similar to 1B but inherited in an
autosomal recessive manner.
1D: Hypoplastic, Smooth
Inheritance: Autosomal dominant
Description: Enamel appears smooth with a lack of
pits.
1E: Hypoplastic, Smooth
Inheritance: Linked dominant
Description: Similar to 1D but linked to a dominant
gene.
1F: Hypoplastic, Rough
Inheritance: Autosomal dominant
Description: Enamel has a rough texture with
hypoplastic features.
1G: Enamel Agenesis
Inheritance: Autosomal recessive
Description: Complete absence of enamel on affected
teeth.
Type II: Hypomaturation
Hypomaturation amelogenesis imperfecta is characterized by enamel that is
softer and more prone to wear than normal enamel, often with a mottled
appearance.
2A: Hypomaturation, Pigmented
Inheritance: Autosomal recessive
Description: Enamel has a pigmented appearance,
often with brown or yellow discoloration.
2B: Hypomaturation
Inheritance: X-linked recessive
Description: Similar to 2A but inherited through
the X chromosome.
2D: Snow-Capped Teeth
Inheritance: Autosomal dominant
Description: Characterized by a white, snow-capped
appearance on the incisal edges of teeth.
Type III: Hypocalcified
Hypocalcified amelogenesis imperfecta is characterized by enamel that is
poorly mineralized, leading to soft, chalky teeth that are prone to rapid wear
and caries.
3A:
Inheritance: Autosomal dominant
Description: Enamel is poorly calcified, leading to
significant structural weakness.
3B:
Inheritance: Autosomal recessive
Description: Similar to 3A but inherited in an
autosomal recessive manner.
Type IV: Hypomaturation, Hypoplastic with Taurodontism
This type combines features of both hypomaturation and hypoplasia, along with
taurodontism, which is characterized by elongated pulp chambers and short roots.
4A: Hypomaturation-Hypoplastic with Taurodontism
Inheritance: Autosomal dominant
Description: Enamel is both hypoplastic and
hypomature, with associated taurodontism.
4B: Hypoplastic-Hypomaturation with Taurodontism
Inheritance: Autosomal dominant
Description: Similar to 4A but with a focus on
hypoplastic features.
Fixation of Condylar Fractures
Oral and Maxillofacial SurgeryFixation of Condylar Fractures
Condylar fractures of the mandible can be challenging to manage due to their
location and the functional demands placed on the condylar region. Various
fixation techniques have been developed to achieve stable fixation and promote
healing. Below is an overview of the different methods of fixation for condylar
fractures, including their advantages, disadvantages, and indications.
1. Miniplate Osteosynthesis
Overview:
Miniplate osteosynthesis involves the use of condylar plates and
screw systems designed to withstand biochemical forces, minimizing
micromotion at the fracture site.
Primary Bone Healing:
Under optimal conditions of stability and fracture reduction,
primary bone healing can occur, allowing new bone to form along the
fracture surface without the formation of fibrous tissue.
Plate Placement:
High condylar fractures may accommodate only one plate with two
screws above and below the fracture line, parallel to the posterior
border, providing adequate stability in most cases.
For low condylar fractures, two plates may be required. The
posterior plate should parallel the posterior ascending ramus, while the
anterior plate can be angulated across the fracture line.
Mechanical Advantage:
The use of two miniplates at the anterior and posterior borders of
the condylar neck restores tension and compression trajectories,
neutralizing functional stresses in the condylar neck.
Research Findings:
Studies have shown that the double mini plate method is the only
system able to withstand normal loading forces in cadaver mandibles.
2. Dynamic Compression Plating
Overview:
Dynamic compression plating is generally not recommended for
condylar fractures due to the oblique nature of the fractures, which can
lead to overlap of fragment ends and loss of ramus height.
Current Practice:
The consensus is that treatment is adequate with miniplates placed
in a neutral mode, avoiding the complications associated with dynamic
compression plating.
3. Lag Screw Osteosynthesis
Overview:
First described for condylar fractures by Wackerbauer in 1962, lag
screws provide a biomechanically advantageous method of fixation.
Mechanism:
A true lag screw has threads only on the distal end, allowing for
compression when tightened against the near cortex. This central
placement of the screw enhances stability.
Advantages:
Rapid application of rigid fixation and close approximation of
fractured parts due to significant compression generated.
Less traumatic than miniplates, as there is no need to open the
joint capsule.
Disadvantages:
Risk of lateralization and rotation of the condylar head if the
screw is not placed centrally.
Requires a steep learning curve for proper application.
Contraindications:
Not suitable for cases with loss of bone in the fracture gap or
comminution that could lead to displacement when compression is applied.
Popular Options:
The Eckelt screw is one of the most widely used lag screws in
current practice.
4. Pin Fixation
Overview:
Pin fixation involves the use of 1.3 mm Kirschner wires (K-wires)
placed into the condyle under direct vision.
Technique:
This method requires an open approach to the condylar head and
traction applied to the lower border of the mandible. A minimum of three
convergent K-wires is typically needed to ensure stability.
5. Resorbable Pins and Plates
Overview:
Resorbable fixation devices may take more than two years to fully
resorb. Materials used include self-reinforced poly-L-lactide screws
(SR-PLLA), polyglycolide pins, and absorbable alpha-hydroxy polyesters.
Indications:
These materials are particularly useful in pediatric patients or in
situations where permanent hardware may not be desirable.
Niacin: Vitamin B3, Nicotinamide, Nicotinic Acid Niacin, or vitamin B3
Biochemistry
Niacin: Vitamin B3, Nicotinamide, Nicotinic Acid Niacin, or vitamin B3,
is involved in energy production, normal enzyme function, digestion, promoting normal appetite, healthy skin, and nerves.
RDA Males: 16 mg/day; Females: 14 mg/day
Niacin Deficiency : Pellagra is the disease state that occurs as a result of severe niacin deficiency. Symptoms include cramps, nausea, mental confusion, and skin problems.