NEET MDS Synopsis
Ludwig's Angina
Oral and Maxillofacial SurgeryLudwig's Angina
Ludwig's angina is a serious, potentially life-threatening
cellulitis or connective tissue infection of the submandibular space. It is
characterized by bilateral swelling of the submandibular and sublingual areas,
which can lead to airway obstruction. The condition is named after the German
physician Wilhelm Friedrich Ludwig, who provided a classic
description of the disease in the early 19th century.
Historical Background
Coining of the Term: The term "Ludwig's angina" was
first coined by Camerer in 1837, who
presented cases that included a classic description of the condition. The
name honors W.F. Ludwig, who had described the features of
the disease in the previous year.
Etymology:
The word "angina" is derived from the Latin word "angere," which
means "to suffocate" or "to choke." This reflects the potential for
airway compromise associated with the condition.
The name "Ludwig" recognizes the contributions of
Wilhelm Friedrich Ludwig to the understanding of this medical entity.
Ludwig's Personal Connection: Interestingly, Ludwig
himself died of throat inflammation in 1865, which
underscores the severity of infections in the head and neck region.
Clinical Features
Ludwig's angina typically presents with the following features:
Bilateral Swelling: The most characteristic sign is
bilateral swelling of the submandibular area, which can extend to the
sublingual space. This swelling may cause the floor of the mouth to elevate.
Pain and Tenderness: Patients often experience pain and
tenderness in the affected area, which may worsen with movement or
swallowing.
Dysphagia and Dysarthria: Difficulty swallowing
(dysphagia) and changes in speech (dysarthria) may occur due to swelling and
discomfort.
Airway Compromise: As the swelling progresses, there is
a risk of airway obstruction, which can be life-threatening. Patients may
exhibit signs of respiratory distress.
Systemic Symptoms: Fever, malaise, and other systemic
signs of infection may be present.
Etiology
Ludwig's angina is most commonly caused by infections that originate from the
teeth, particularly the second or third molars. The infection can spread from
dental abscesses or periodontal disease into the submandibular space. The most
common pathogens include:
Streptococcus species
Staphylococcus aureus
Anaerobic bacteria
Diagnosis and Management
Diagnosis: Diagnosis is primarily clinical, based on the
characteristic signs and symptoms. Imaging studies, such as CT scans, may be
used to assess the extent of the infection and to rule out other conditions.
Management:
Airway Management: Ensuring a patent airway is the
top priority, especially if there are signs of respiratory distress.
Antibiotic Therapy: Broad-spectrum intravenous
antibiotics are initiated to target the likely pathogens.
Surgical Intervention: In cases of significant
swelling or abscess formation, surgical drainage may be necessary to
relieve pressure and remove infected material.
Structure of a nerve
PhysiologyStructure of a nerve:
A peripheral nerve is arranged much like a muscle in terms of its connective tissue. It has an outer covering which forms a sheath around the nerve, called the epineurium. Often a nerve will run together with an artery and vein and their connective coverings will merge. Nerve fibers, which are axons, organize into bundles known as fascicles with each fascicle surrounded by the perineurium. Between individual nerve fibers is an inner layer of endoneurium.
The myelin sheath in peripheral nerves consists of Schwann cells wrapped in many layers around the axon fibers. Not all fibers in a nerve will be myelinated, but most of the voluntary fibers are. The Schwann cells are portrayed as arranged along the axon like sausages on a string. Gaps between the Schwann cells are called nodes of Ranvier. These nodes permit an impulse to travel faster because it doesn't need to depolarize each area of a membrane, just the nodes. This type of conduction is called saltatory conduction and means that impulses will travel faster in myelinated fibers than in unmyelinated ones.
The myelin sheath does several things:
1) It provides insulation to help prevent short circuiting between fibers.
2) The myelin sheath provides for faster conduction.
3) The myelin sheath provides for the possibility of repair of peripheral nerve fibers. Schwann cells help to maintain the micro-environments of the axons and their tunnel (the neurilemma tunnel) permits re-connection with an effector or receptor CNS fibers, not having the same type of myelination accumulate scar tissue after damage, which prevents regeneration.
Antiarrhythmic Drugs
Pharmacology
Antiarrhythmic Drugs
Cardiac Arrhythmias
Can originate in any part of the conduction system or from atrial or ventricular muscle.
Result from
– Disturbances in electrical impulse formation (automaticity)
– Conduction (conductivity)
– Both
MECHANISMS OF ARRHYTHMIA
ARRHYTHMIA – absence of rhythm
DYSRRHYTHMIA – abnormal rhythm
ARRHYTHMIAS result from:
1. Disturbance in Impulse Formation
2. Disturbance in Impulse Conduction
- Block results from severely depressed conduction
- Re-entry or circus movement / daughter impulse
Types of Arrhythmias
• Sinus arrhythmias
– Usually significant only
– if they are severe or prolonged
• Atrial arrhythmias
– Most significant in the presence of underlying heart disease
– Serious: atrial fibrillation can lead to the formation of clots in the heart
• Nodal arrhythmias
– May involve tachycardia and increased workload of the heart or bradycardia from heart block
• Ventricular arrhythmias
– Include premature ventricular contractions (PVCs), ventricular tachycardia, and ventricular fibrillation
Class
Action
Drugs
I
Sodium Channel Blockade
IA
Prolong repolarization
lengthen AP duration
Intermediate interaction with Na+ channels
Quinidine, procainamide, disopyramide
IB
Shorten repolarization
shorten AP duration
rapid interaction with Na+ channels
Lidocaine, mexiletine, tocainide, phenytoin
IC
Little effect on repolarization
no effect or minimal ↑ AP duration
slow interaction with Na+ channels
Encainide, flecainide, propafenone
II
Beta-Adrenergic Blockade
Propanolol, esmolol, acebutolol, l-sotalol
III
Prolong Repolarization (Potassium Channel Blockade; Other)
Ibutilide, dofetilide, sotalol (d,l), amiodarone, bretylium
IV
Calcium Channel Blockade
Verapamil, diltiazem, bepridil
Miscellaneous
Miscellaneous Actions
Adenosine, digitalis, magnesium
Indications
• To convert atrial fibrillation (AF) or flutter to normal sinus rhythm (NSR)
• To maintain NSR after conversion from AF or flutter
• When the ventricular rate is so fast or irregular that cardiac output is impaired
– Decreased cardiac output leads to symptoms of decreased systemic, cerebral, and coronary circulation
• When dangerous arrhythmias occur and may be fatal if not quickly terminated
– For example: ventricular tachycardia may cause cardiac arrest
Mechanism of Action
• Reduce automaticity (spontaneous depolarization of myocardial cells, including ectopic pacemakers)
• Slow conduction of electrical impulses through the heart
• Prolong the refractory period of myocardial cells (so they are less likely to be prematurely activated by adjacent cells
Plate Fixation Techniques
Oral and Maxillofacial SurgeryManagement of Mandibular Fractures: Plate Fixation Techniques
The management of mandibular fractures involves various techniques for
fixation, depending on the type and location of the fracture. .
1. Plate Placement in the Body of the Mandible
Single Plate Fixation:
A single plate is recommended to be placed just below the apices of
the teeth but above the inferior alveolar nerve canal. This positioning
helps to avoid damage to the nerve while providing adequate support to
the fracture site.
Miniplate Fixation: Effective for non-displaced or
minimally displaced fractures, provided the fracture is not severely
comminuted. The miniplate should be placed at the superior border of the
mandible, acting as a tension band that prevents distraction at the
superior border while maintaining compression at the inferior border
during function.
Additional Plates:
While a solitary plate can provide adequate rigidity, the placement
of an additional plate or the use of multi-armed plates (Y or H plates)
can enhance stability, especially in more complex fractures.
2. Plate Placement in the Parasymphyseal and Symphyseal Regions
Two Plates for Stability:
In the parasymphyseal and symphyseal regions, two plates are
recommended due to the torsional forces generated during function.
First Plate: Placed at the inferior aspect of
the mandible.
Second Plate: Placed parallel and at least 5 mm
superior to the first plate (subapical).
Plate Placement Behind the Mental Foramen:
A plate can be fixed in the subapical area and another near the
lower border. Additionally, plates can be placed on the external oblique
ridge or parallel to the lower border of the mandible.
3. Management of Comminuted or Grossly Displaced Fractures
Reconstruction Plates:
Comminuted or grossly displaced fractures of the mandibular body
require fixation with a locking reconstruction plate or a standard
reconstruction plate. These plates provide the necessary stability for
complex fractures.
4. Management of Mandibular Angle Fractures
Miniplate Fixation:
When treating mandibular angle fractures, the plate should be placed
at the superolateral aspect of the mandible, extending onto the broad
surface of the external oblique ridge. This placement helps to
counteract the forces acting on the angle of the mandible.
5. Stress Patterns and Plate Design
Stress Patterns:
The zone of compression is located at the superior border of the
mandible, while the neutral axis is approximately at the level of the
inferior alveolar canal. Understanding these stress patterns is crucial
for optimal plate placement.
Miniplate Characteristics:
Developed by Michelet et al. and popularized by Champy et al.,
miniplates utilize monocortical screws and require a minimum of two
screws in each osseous segment. They are smaller than standard plates,
allowing for smaller incisions and less soft tissue dissection, which
reduces the risk of complications.
6. Other Fixation Techniques
Compression Osteosynthesis:
Indicated for non-oblique fractures that demonstrate good body
opposition after reduction. Compression plates, such as dynamic
compression plates (DCP), are used to achieve this. The inclined plate
within the hole allows for translation of the bone toward the fracture
site as the screw is tightened.
Fixation Osteosynthesis:
For severely oblique fractures, comminuted fractures, and fractures
with bone loss, compression plates are contraindicated. In these cases,
non-compression osteosynthesis using locking plates or reconstruction
plates is preferred. This method is also suitable for patients with
questionable postoperative compliance or a non-stable mandible.
Hormones of the Pituitary -The Posterior Lobe
Physiology
The Posterior Lobe
The posterior lobe of the pituitary releases two hormones, both synthesized in the hypothalamus, into the circulation.
Antidiuretic Hormone (ADH).
ADH is a peptide of 9 amino acids. It is also known as arginine vasopressin. ADH acts on the collecting ducts of the kidney to facilitate the reabsorption of water into the blood.
A deficiency of ADH
leads to excessive loss of urine, a condition known as diabetes nsipidus.
Oxytocin
Oxytocin is a peptide of 9 amino acids. Its principal actions are:
stimulating contractions of the uterus at the time of birth
stimulating release of milk when the baby begins to suckle
Carbenicillin
Pharmacology
Carbenicillin
Antibiotic that is chemically similar to ampicillin. Active against gram-negative germs. It is well soluble in water and acid-labile.
Caries Risk Assessment Tool
PedodonticsThe American Academy of Pediatric Dentistry (AAPD) Caries Risk Assessment
Tool is designed to evaluate a child's risk of developing dental caries
(cavities). The tool considers various factors to categorize a child's risk
level as low, moderate, or high.
Low Risk:
- No carious (cavitated) teeth in the past 24 months
- No enamel white spot lesions (initial stages of tooth decay)
- No visible dental plaque
- Low incidence of gingivitis (mild gum inflammation)
- Optimal exposure to fluoride (both systemic and topical)
- Limited consumption of simple sugars (at meal times only)
Moderate Risk:
- Carious teeth in the past 12 to 24 months
- One area of white spot lesion
- Gingivitis present
- Suboptimal systemic fluoride exposure (e.g., not receiving fluoride
supplements or living in a non-fluoridated water area)
- One or two between-meal exposures to simple sugars
High Risk:
- Carious teeth in the past 12 months
- More than one area of white spot lesion
- Visible dental plaque
- Suboptimal topical fluoride exposure (not using fluoridated toothpaste or
receiving professional fluoride applications)
- Presence of enamel hypoplasia (developmental defect of enamel)
- Wearing orthodontic or dental appliances that may increase caries risk
- Active caries in the mother, which can increase the child's risk due to oral
bacteria transmission
- Three or more between-meal exposures to simple sugars
Membrane Potential
PhysiologyMembrane Potential
Membrane potentials will occur across cell membranes if
1) there is a concentration gradient of an ion
2) there is an open channel in the membrane so the ion can move from one side to the other
The Sodium Pump Sets Up Gradients of Na and K Across Cell Membranes
All cells have the Na pump in their membranes
Pumps 3 Nas out and 2 Ks in for each cycle
Requires energy from ATP
Uses about 30% of body's metabolic energy
This is a form of active transport- can pump ions "uphill", from a low to a high concentration
This produces concentration gradients of Na & K across the membrane
Typical concentration gradients:
In mM/L
Out mM/L
Gradient orientation
Na
10
150
High outside
K
140
5
High inside
The ion gradients represent stored electrical energy (batteries) that can be tapped to do useful work
The Na pump is of ancient origin, probably originally designed to protect cell from osmotic swelling
Inhibited by the arrow poisons ouabain and digitalis