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Walls of the Tympanic Cavity or Middle Ear

  • This cavity is shaped like a narrow six-sided box that has convex medial and lateral walls.
  • It has the shape of the biconcave lens in cross-section (like a red blood cell).

 

The Roof or Tegmental Wall

  • This is formed by a thin plate of bone, called the tegmen tympani (L. tegmen, roof).
  • It separates the tympanic cavity from the dura on the floor of middle cranial fossa.
  • The tegmen tympani also covers the aditus ad antrum.

 

The Floor or Jugular Wall

  • This wall is thicker than the roof.
  • It separates the tympanic cavity from the superior bulb of the internal jugular vein. The internal jugular vein and the internal carotid artery diverge at the floor of the tympanic cavity.
  • The tympanic nerve, a branch of the glossopharyngeal nerve (CN IX), passes through an aperture in the floor of the tympanic cavity and its branches form the tympanic plexus.

The Lateral or Membranous Wall

  • This is formed almost entirely by the tympanic membrane.
  • Superiorly it is formed by the lateral bony wall of the epitympanic recess.
  • The handle of the malleus is incorporated in the tympanic membrane, and its head extends into the epitympanic recess.

The Medial or Labyrinthine Wall

  • This separates the middle ear from the membranous labyrinth (semicircular ducts and cochlear duct) encased in the bony labyrinth.
  • The medial wall of the tympanic cavity exhibits several important features.
  • Centrally, opposite the tympanic membrane, there is a rounded promontory (L. eminence) formed by the first turn of the cochlea.
  • The tympanic plexus of nerves, lying on the promontory, is formed by fibres of the facial and glossopharyngeal nerves.
  • The medial wall of the tympanic cavity also has two small apertures or windows.
  • The fenestra vestibuli (oval window) is closed by the base of the stapes, which is bound to its margins by an annular ligament.
  • Through this window, vibrations of the stapes are transmitted to the perilymph window within the bony labyrinth of the inner ear.
  • The fenestra cochleae (round window) is inferior to the fenestra vestibuli.
  • This is closed by a second tympanic membrane.

 

The Posterior or Mastoid Wall

  • This wall has several openings in it.
  • In its superior part is the aditus ad antrum (mastoid antrum), which leads posteriorly from the epitympanic recess to the mastoid cells.
  • Inferiorly is a pinpoint aperture on the apex of a tiny, hollow projection of bone, called the pyramidal eminence (pyramid).
  • This eminence contains the stapedius muscle.
  • Its aperture transmits the tendon of the stapedius, which enters the tympanic cavity and inserts into the stapes.
  • Lateral to the pyramid, there is an aperture through which the chorda tympani nerve, a branch of the facial nerve (CN VII), enters the tympanic cavity.

The Anterior Wall or Carotid Wall

  • This wall is a narrow as the medial and lateral walls converge anteriorly.
  • There are two openings in the anterior wall.
  • The superior opening communicates with a canal occupied by the tensor tympani muscle.
  • Its tendon inserts into the handle of the malleus and keeps the tympanic membrane tense.
  • Inferiorly, the tympanic cavity communicates with the nasopharynx through the auditory tube.

Anti-Histamines:
 
The effect of histamine can be opposed in three ways:
1. Physiological antagonism: by using a drug to oppose the effect (e.g adrenaline). Histamine constricts bronchi,
causes vasodilatation which increases capillary permeability. Adrenaline opposes this effect by a mechanism unrelated to histamine.
2. By preventing histamine from reaching its site of action (receptors), By competition with H1-H2 receptors (Drug antagonisms).
3. By preventing the release of histamine. (adrenal steroids and sodium-cromoglycate can suppress the effect on the tissues)

Types of Anti-histamine drugs

Selected H1 antagonist drugs

First-generation H1 receptor antagonists:

Chlorpheniramine (Histadin) & Dexchlorpheniramine 
Diphenhydramine (Allermine)
Promethazine (Phenergan) -  strong CNS depressants
Cyproheptadine (Periactin)

ACTION
These drugs bind to both central and peripheral H1 receptors and can cause CNS depression or stimulation.

- They usually cause CNS depression (drowsiness,sedation) with usual therapeutic doses
- Cause CNS stimulation (anxiety, agitation) 
with excessive doses, especially in children. 
They also have Anticholinergic effects (e.g. dry mouth, urinary retention, constipation, blurred vision).


Second-generation H1 receptor antagonists (non-sedating) agents

Terfenadine
Fexofenadine
Loratadine
Acravistine and Cetirizine
Astemizol

Action

They cause less CNS epression because they are selective for peripheral H1 receptors and do not cross the blood brain barrier.

Indications for use

The drugs can relieve symptoms but don’t relieve hypersensitivity.

1) Allergic rhinitis. Some relief of sneezing, rhinorrhea, nasal airway obstruction and conjunctivitis are with the use of antihistamine.
2) Anaphylaxis. Antihistamine is helpful in treating urticaria and pruritus.
3) Allergic conjunctivitis. This condition, which is characterized by redness, itching and tearing of the eyes.
4) Drug allergies. Antihistamines may be given to prevent or treat reactions to drugs (e.g, before a dignostic test that
uses an iodine preparation).
5) Transfusions of blood and blood products.
6) Dermatologic conditions. Antihistamines are the drug of choice for treatment of allergic contact dermatitis and
acute Urticaria. Urticaria often occurs because the skin has many mast cells to release histamine.
7) Miscellaneous. Some antihistamines are commonly used for non-allergic disorder such as motion sickness, nausea, vomiting, sleep, cough or add to cough mixtures.

Contraindication

hypersensitivity to the drugs, narrow-angle glaucoma, prostatic hypertroph, stenosing peptic ulcer, bladder neck obstruction, during pregnancy and lactating women

Adverse effects:

Drowsiness and sedation
Anticholinergic
Some antihistamines may cause dizziness, fatigue, hypotention, headache, epigastric distress and photosensitivity
Serious adverse reaction including cardiac arrest & death, have been reported in patients receiving high dose astemizole

H2-receptor antagonists

 Cimetidine (Tagamate), Ranitidine (Zantac), Fomatidine, Nizatidine. 

Mechanism of action

Numerous factors influence acid secretion by the stomach, including food, physiological condition and drugs. H2 receptor blockers reduce basal acid-secretion by about 95% and food stimulated acid-secretion by about 70%. Both conc. and vol. of H ions will decrease.

Pharmacokinetics:
1) They are all well absorbed after oral dose.
2) Antacids decrease their absorption in about 10-20%

Uses
Cimetidine -  reduction of gastric secretion is beneficial, these are in main duodenal ulcer, benign gastric ulcer, stomach ulcer and reflux eosophagitis.

Rantidine -used as alternative for duodenal ulcer

Adverse effects:
headache, dizziness, constipation, diarrhoea, tiredness and muscular pain. 

Periodontics: Dental specialty deals with the supporting and surrounding tissues of the teeth. 

1. Periodontium: tissues that invest and support teeth Includes Gingiva, Alveolar mucosa  Cementum, Periodontal ligament, Alveolar bone, Support bone

2. Periodontal disease: changes to periodontium beyond normal range of variation

a. Specific plaque hypothesis: specific microorganisms cause periodontal disease; mostly anaerobes. Three implicated: Actinobacillus actinomycetemcomitans, Porphyromonas gingivalis, and Bacteriodes forsythus

b. Contributing factors: often a combination of factors

i. Local: calculus (tarter, home for bacteria, ­ with age), traumatic occlusal forces, caries (root caries), overhangs and over-contoured restorations, open contacts with food impaction, missing/malaligned teeth

Invasion of biological width: from free gingival margin -> attached gingiva need ~ 3 mm.  If enter this area -> problems (e.g., resorption)

ii. Host factors: exacerbate periodontal problems; e.g., smoking/tobacco use, pregnancy and puberty (hormonal changes, ­ blood vessel permeability), stress, poor diet

iii.Medications: often -> tissue overgrowth; e.g., oral contraceptives, antidepressants, heart medicines, transplant anti-rejection drugs

iv.Systemic diseases: e.g., diabetes, immunosuppression

B. Gingivitis: inflammation of gingiva; ­ with age; generally reversible

C. Periodontitis: inflammation of supporting tissues of teeth, characterized by loss of attachment (PDL) and bone; generally irreversible

D.       Periodontal disease as risk factor for systemic diseases:

1.        Causes difficulty for diabetics to control blood sugar

2.        Pregnant women with periodontal disease ~ 7 times more likely to have premature and/or underweight baby

3.        Periodontal diseased patients may be at risk for heart disease

Bronchitis

Bronchitis is an obstructive pulmonary disease characterized by inflammation of the bronchi of the lungs

Signs and symptoms

persistent cough that produces sputum

shortness of breath (dyspnea) on exertion

hypercapnia

insufficient oxygenation of the blood hypoxemia leading to cynosis

Severe chronic bronchitis will commonly lead to cor pulmonale and heart failure.

Pathology

an increase in the number of goblet cells with mucus blocking the airway clusters of pigmented alveolar macrophages

the presence of inflammatory cells (e.g. neutrophils) scarring (fibrosis) of the walls of the bronchioles

Diagnosis

  • decreased intensity of breath sounds (rhonchi) and extended expiration.
  • a sputum culture has pathogenic microorganisms
  • a chest x-ray that reveals hyperinflation and increased bronchovascular markings
  • a pulmonary function test that shows an increase in the lung's residual volume and a decreased vital capacity

Pathophysiology

  • The initiating event in developing bronchitis appears to be chronic irritation due to inhalation of certain chemicals
  • earliest clinical feature of bronchitis is increased secretion of mucus by submucousal glands of the trachea and bronchi
  • Damage caused by irritation of the airways leads to inflammation and infiltration of the lung tissue by neutrophils
  • The neutrophils release substances that promote mucousal hypersecretion
  • As bronchitis persists to become chronic bronchitis, a substantial increase in the number of goblet cells in the small airways is seen
  • The role of infection in the pathogenesis of chronic bronchitis appears to be secondary.

Treatment

Quit smoking, Oxygen therapy, bronchodilator drugs

Prognosis

Pulmonary hypertension, cor pulmonale, and chronic respiratory failure are possible complications of chronic bronchitis

In severe chronic bronchitis is poor