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NEET MDS Synopsis

Str. Pneumoniae
General Pathology

Str. Pneumoniae

Probably the most important streptococci.  Primary cause of pneumonia.  Usually are diplococci.  Ste. pneumoniae are α-hemolytic and nutritionally fastidious.  Often are normal flora.

Key virulence factor is the capsule polysaccharide which prevents phagocytosis.  Other virulence factors include pneumococcal surface protein and α-hemolysin.

Major disease is pneumonia, usually following a viral respiratory infection.  Characterized by fever, cough, purulent sputum.  Bacteria infiltrates alveoli.  PMN’s fill alveoli, but don’t  cause necrosis. Also can cause meningitis, otitis, sinusitis.

There are vaccines against the capsule polysaccharide.  Resistance to penicillin, cephalosporins, erythromycins, and fluoroquinalones is increasing.

ESSENTIAL FATTY ACIDS
Biochemistry

ESSENTIAL FATTY ACIDS (EFAs) Polyunsaturated FAs,such as Linoleic acid and g(gamma)- Linolenic acid, are ESSENTIAL FATTY ACIDS — we cannot make them, and we need them, so we must get them in our diets mostly from plant sources.

Anatomy and Histology of the Periodontium
Periodontology

Anatomy and Histology of the Periodontium

Gingiva (normal clinical appearance): no muscles, no glands; keratinized


Color: coral pink but does vary with individuals and races due to cutaneous pigmentation
Papillary contour: pyramidal shape with one F and one L papilla and the col filling interproximal space to the contact area (col the starting place gingivitis)
Marginal contour: knife-edged and scalloped
Texture: stippled (orange-peel texture); blow air to dry out and see where stippling ends to see end of gingiva
Consistency: firm and resilient (push against it and won’t move); bound to underlying bone
Sulcus depth: 0-3mm
Exudate: no exudates (blood, pus, water)


  Anatomic and histological structures

Gingival unit: includes periodontium above alveolar crest of bone

a. Alveolar mucosa: histology- non-keratinized, stratified, squamous epithelium, submucosa with glands, loose connective tissue with collagen and elastin, muscles.  No epithelial ridges, no stratum granulosum (flattened cells below keratin layer)

b. Mucogingival junction: clinical demarcation between alveolar mucosa and attached gingiva

c. Attached gingiva: histology- keratinized, stratified, squamous epithelium with epithelial ridges (basal cell layer, prickle cell layer, granular cell layer (stratum granulosum), keratin layer); no submucosa


Dense connective tissue: predominantly collagen, bound to periosteum of bone by Sharpey fibers
Reticular fibers between collagen fibers and are continuous with reticulin in blood vessels


d. Free gingival groove: demarcation between attached and free gingiva; denotes base of gingival sulcus in normal gingiva; not always seen

e. Free gingival margin: area from free gingival groove to epithelial attachment (up and over ® inside)


Oral surface: stratified, squamous epithelium with epithelial ridges
Tooth side surface (sulcular epithelium): non-keratinized, stratified, squamous epithelium with no epithelial ridges (basal cell and prickle cell layers)


f. Gingival sulcus: space bounded by tooth surface, sulcular epithelium, and junctional epithelium; 0-3mm depth; space between epithelium and tooth

g. Dento-gingival junction: combination of epithelial and fibrous attachment


Junctional epithelium (epithelial attachment): attachment of epithelial cells by hemi-desmosomes and sticky substances (basal lamina- 800-1200 A, DAS-acid mucopolysaccharides, hyaluronic acid, chondroitin sulfate A, C, and B), to enamel, enamel and cementum, or cementum depending on stage of passive eruption.  Length ranges from 0.25-1.35mm.
Fibrous attachment: attachment of collagen fibers (Sharpey’s fibers) into cementum just beneath epithelial attachment; ~ 1mm thick


h. Nerve fibers: myelinated and non-myelinated (for pain) in connective tissue.  Both free and specialized endings for pain, touch pressure, and temperature -> proprioception.  If dentures, rely on TMJ.

i.Mesh of terminal argyophilic fibers (stain silver), some extending into epithelium

ii  Meissner-type corpuscles: pressure sensitive sensory nerve encased in CT

iii.Krause-type corpuscles: temperature receptors

iv. Encapsulated spindles

i. Gingival fibers:

i.  Gingivodental group:


Group I (A): from cementum to free gingival margin
Group II (B): from cementum to attached gingiva
Group III (C): from cementum over alveolar crest to periosteum on buccal and lingual plates


ii.  Circular (ligamentum circularis): encircles tooth in free gingiva

iii. Transeptal fibers: connects cementum of adjacent teeth, runs over interdental septum of alveolar bone.  Separates gingival unit from attachment apparatus.

Transeptal and Group III fibers the major defense against stuff getting into bone and ligament.

 

2.  Attachment apparatus: periodontium below alveolar crest of bone

Periodontal ligament: Sharpey’s fibers (collagen) connecting cementum to bone (bundle bone).  Few elastic and oxytalan fibers associated with blood vessels and embedded in cementum in cervical third of tooth.  Components divided as follows:

i. Alveolar crest fibers: from cementum just below CEJ apical to alveolar crest of bone

ii.Horizontal fibers: just apical to alveolar crest group, run at right angles to long axis of tooth from cementum horizontally to alveolar bone proper

iii.Oblique fibers: most numerous, from cementum run coronally to alveolar bone proper

iv. Apical fibers: radiate from cementum around apex of root apically to alveolar bone proper, form socket base

v. Interradicular fibers: found only between roots of multi-rooted teeth from cementum to alveolar bone proper

vi. Intermediate plexus: fibers which splice Sharpey’s fibers from bone and cementum

vii. Epithelial Rests of Malassez: cluster and individual epithelial cells close to cementum which are remnants of Hertwig’s epithelial root sheath; potential source of periodontal cysts.

viii. Nerve fibers: myelinated and non-myelinated; abundant supply of sensory free nerve endings capable of transmitting tactile pressure and pain sensation by trigeminal pathway and elongated spindle-like nerve fiber for proprioceptive impulses

Cementum: 45-50% inorganic; 50-55% organic (enamel is 97% inorganic; dentin 70% inorganic)

i.  Acellular cementum: no cementocytes; covers dentin (older) in coronal ½ to 2/3 of root, 16-60 mm thick

ii. Cellular cementum: cementocytes; covers dentin in apical ½ to 1/3 of root; also may cover acellular cementum areas in repair areas, 15-200 mm thick

iii. Precementum (cementoid): meshwork of irregularly arranged collagen in surface of cementum where formation starts

iv. Cemento-enamel junction (CEJ): 60-65% of time cementum overlaps enamel; 30% meet end-to-end; 5-10% space between

v. Cementum slower healing than bone or PDL.  If expose dentinotubules ® root sensitivity.

Alveolar bone: 65% inorganic, 35% organic

i. Alveolar bone proper (cribriform plate): lamina dura on x-ray; bundle bone receive Sharpey fibers from PDL

ii. Supporting bone: cancellous, trabecular (vascularized) and F and L plates of compact bone

Blood supply to periodontium

i. Alveolar blood vessels (inferior and superior)

A) Interalveolar: actually runs through bone then exits, main supply to alveolar bone and PDL

B) Supraperiosteal: just outside bone, to gingiva and alveolar bone

C) Dental (pulpal): to pulp and periapical area

D) Terminal vessels (supracrestal): anastomose of A and B above beneath the sulcular epithelium

E) PDL gets blood from: most from branches of interalveolar blood vessels from alveolar bone marrow spaces, supraperiosteal vessels when interalveolar vessels not present, pulpal (apical) vessels, supracrestal gingival vessels

ii. Lymphatic drainage: accompany blood vessels to regional lymph nodes (esp. submaxillary group)

Enzymes
General Microbiology

Enzymes:

Serum lysozyme:

Provides innate & nonspecific immunity
Lysozyme is a hydrolytic enzyme capable of digesting bacterial cell walls containing peptidoglycan 
•    In the process of cell death, lysosomal NZs fxn mainly to aulolyse necrotic cells (NOT “mediate cell degradation”)
•    Attacks bacterial cells by breaking the bond between NAG and NAM.
•    Peptidoglycan – the rigid component of cell walls in most bacteria – not found in archaebacteria or eukaryotic cells
•    Lysozyme is found in serum, tears, saliva, egg whites & phagocytic cells protecting the host nonspecifically from microorganisms

Superoxide dismutase: catalyzes the destruction of O2 free radicals protecting O2-metabolizing cells against harmful effects 

Catalase:

- catalyzes the decomposition of H2O2 into H2O & O2
- Aerobic bacteria and facultative anaerobic w/ catalase are able to resist the effects of H2O2
- Anaerobic bacteria w/o catalase are sensitive to H2O2  (Peroxide), like Strep
- Anaerobic bacteria (obligate anaerobes) lack superoxide dismutase or catalase
- Staph makes catalase, where Strep does not have enough staff to make it

Coagulase

- Converts Fibronogen to fibrin
•    Coagulase test is the prime criterion for classifying a bug as Staph aureus – from other Staph species
•    Coagulase is important to the pathogenicity of S. aureus because it helps to establish the typical abscess lesion 
•    Coagulase also coats the surface w/ fibrin upon contact w/ blood, making it harder to phagocytize

MAXILLARY SECOND MOLAR
Dental Anatomy

MAXILLARY SECOND MOLAR

The second molars are often called 12-year molars because they erupt when a child is about 12 years

Facial: The crown is shorter occluso-cervically and narrower mesiodistally whe compared to the first molar. The distobuccal cusp is visibly smaller than the mesiobuccal cusp. The two buccal roots are more nearly parallel. The roots are more parallel; the apex of the mesial root is on line with the with the buccal developmental groove. Mesial and distal roots tend to be about the same length.

Lingual: The distolingual cusp is smaller than the mesiolingual cusp. The Carabelli trait is absent.

Proximal: The crown is shorter than the first molar and the palatal root has less diverence. The roots tend to remain within the crown profile.

Occlusal: The distolingual cusp is smaller on the second than on the first molar. When it is much reduced in size, the crown outline is described as 'heart-shaped.' The Carabelli trait is usually absent. The order of cusp size, largest to smallest, is the same as the first but is more exaggerated: mesiolingual, mesiobuccal, distobuccal, and distolingual.

 

Contact Points; Height of Curvature: Both mesial and distal contacts tend to be centered buccolingually below the marginal ridges. Since themolars become shorter, moving from first to this molar, the contacts tend to appear more toward the center of the proximal surfaces.

Roots: There are three roots, two buccal and one lingual. The roots are less divergent than the first with their apices usually falling within the crown profile. The buccal roots tend to incline to the distal.

Note: The distolingual cusp is the most variable feature of this tooth. When it is large, the occlusal is somewhat rhomboidal; when reduced in size the crown is described as triangual or 'heart-shaped.' At times, the root may be fused.


Halothane

Pharmacology


Halothane (Fluothane) MAC 0.76%, Blood/gas solubility ratio 2.3
- Nonflammable.
- Any depth of anesthesia can be obtained in the absence of hypoxia.
- Halothane produces a marked hypotensive effect 
- accompanies hypotension.
- Halothane “sensitizes” the ventricular conduction system in the heart to the action of catecholamines. However, ventricular arrhythmias are rare if
- respiratory acidosis, hypoxia and other causes of sympathetic stimulation are avoided.
- Respiration is depressed by all anesthetic concentrations.
- Halothane is metabolized to a significant extent and some of its metabolic produces have been shown to be hepatotoxic.
- Can produce a malignant hyperpyrexia due to an uncontrolled hypermetabolic reaction in skeletal muscle. 

Halothane is generally used with nitrous oxide, an opiate and a neuromuscular blocking drug.

Phospholipids Functions
Biochemistry

- There are two important phospholipids, Phosphatidylcholine and Phosphatidylserine found the cell membrane without which cell cannot function normally.

- Phospholipids are also important for optimal brain health as they found the cell membrane of brain cells also which help them to communicate and influence the receptors function. That is the reason food stuff which is rich in phospholipids like soy, eggs and the brain tissue of animals are good for healthy and smart brain.

- Phospholipids are the main component of cell membrane or plasma membrane. The bilayer of phospholipid molecules determine the transition of minerals, nutrients, and drugs in and out of the cell and affect various functions of them.

- As phospholipids are main component of all cell membrane, they influence a number of organs and tissues, such as the heart, blood cells and the immune system. As we grown up the amount of phospholipids decreases and reaches to decline.

- Phospholipids present in cell membrane provide cell permeability and flexibility with various substances as well its ability to move fluently. The arrangement of phospholipid molecules in lipid bilayer prevent amino acids, carbohydrates, nucleic acids, and proteins from moving across the membrane by diffusion. The lipid bi-layer is usually help to prevent adjacent molecules from sticking to each other.

- The selectivity of cell membrane form certain substances are due to the presence of hydrophobic and hydrophilic part molecules and their arrangement in bilayer. This bilayer is also maintained the normal pH of cell to keeps it functioning properly.

- Phospholipids are also useful in the treatment of memory problem associated with chronic substances as they improve the ability of organism to adapt the chronic stress.

Epidural Hematoma
Oral and Maxillofacial Surgery

Epidural Hematoma (Extradural Hematoma)
Epidural hematoma (EDH), also known as extradural hematoma,
is a serious condition characterized by the accumulation of blood between the
inner table of the skull and the dura mater, the outermost layer of the meninges.
Understanding the etiology, clinical presentation, and management of EDH is
crucial for timely intervention and improved patient outcomes.
Incidence and Etiology


Incidence: The incidence of epidural hematomas is
relatively low, ranging from 0.4% to 4.6% of all head
injuries. In contrast, acute subdural hematomas (ASDH) occur in
approximately 50% of cases.


Source of Bleeding:

Arterial Bleeding: In about 85% of
cases, the source of bleeding is arterial, most commonly from the middle
meningeal artery. This artery is particularly vulnerable to
injury during skull fractures, especially at the pterion, where the
skull is thinner.
Venous Bleeding: In approximately 15% of
cases, the bleeding is venous, often from the bridging veins.



Locations

Common Locations:
About 70% of epidural hematomas occur laterally
over the cerebral hemispheres, with the pterion as the
epicenter of injury.
The remaining 30% can be located in the frontal,
occipital, or posterior fossa regions.



Clinical Presentation
The clinical presentation of an epidural hematoma can vary, but the
"textbook" presentation occurs in only 10% to 30% of cases and
includes the following sequence:


Brief Loss of Consciousness: Following the initial
injury, the patient may experience a transient loss of consciousness.


Lucid Interval: After regaining consciousness, the
patient may appear to be fine for a period, known as the lucid
interval. This period can last from minutes to hours, during which
the patient may seem asymptomatic.


Progressive Deterioration: As the hematoma expands, the
patient may experience:

Progressive Obtundation: Diminished alertness and
responsiveness.
Hemiparesis: Weakness on one side of the body,
indicating possible brain compression or damage.
Anisocoria: Unequal pupil size, which can indicate
increased intracranial pressure or brain herniation.
Coma: In severe cases, the patient may progress to
a state of coma.



Diagnosis

Imaging Studies:
CT Scan: A non-contrast CT scan of the head is the
primary imaging modality used to diagnose an epidural hematoma. The
hematoma typically appears as a biconvex (lens-shaped) hyperdense
area on the CT images, often associated with a skull fracture.
MRI: While not routinely used for initial
diagnosis, MRI can provide additional information about the extent of
the hematoma and associated brain injury.



Management


Surgical Intervention:

Craniotomy: The definitive treatment for an
epidural hematoma is surgical evacuation. A craniotomy is performed to
remove the hematoma and relieve pressure on the brain.
Burr Hole: In some cases, a burr hole may be used
for drainage, especially if the hematoma is small and located in a
favorable position.



Monitoring: Patients with EDH require close monitoring
for neurological status and potential complications, such as re-bleeding or
increased intracranial pressure.


Supportive Care: Management may also include supportive
care, such as maintaining airway patency, monitoring vital signs, and
managing intracranial pressure.


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