4. INTRODUCTION
• The two adrenal glands, each of which weighs about 4
grams, lie at the superior poles of the two kidneys.
• Each gland is composed two distinct parts: the inner
medulla and the outer cortex.
5. ADRENAL CORTEX:
• Secretes corticosteroids- mineralo-corticosteroids,
gluco-corticosteroids and androgenic hormones.
• Mineralo-corticosteroids- affect electrolytes of
extracellular fluids: sodium and potassium.
• Gluco-corticosteroids- increase the blood glucose level.
• Androgenic hormones- exhibit the same effects as the
male sex hormones.
6.
7.
8. ADRENAL MEDULLA:
• Functionally related to the sympathetic nervous system.
• Secretes Epinephrine and Nor-epinephrine
• These hormones cause almost the same effects as
direct stimulation of the sympathetic nerves in all parts
of the body.
9.
10. FUNCTIONS OF MINERALO-CORTICOIDS
(ALDOSTERONE) :
• Mineralocorticoid Deficiency Causes Severe Renal
disorders like Sodium Chloride Wasting and
Hyperkalemia.
• Aldosterone Increases Renal Tubular Reabsorption
of Sodium and Secretion of Potassium.
• Aldosterone Stimulates Sodium and Potassium
Transport in Sweat Glands, Salivary Glands, and
Intestinal Epithelial Cells.
11. FUNCTIONS OF GLUCO-CORTICOIDS
(CORTISOL):
• Stimulate gluconeogenesis (formation of carbohydrate
from proteins and some other substances) by the liver.
• Cortisol also causes a moderate decrease in the rate of
glucose utilization by most cells in the body.
• It promotes mobilization of fatty acids from adipose
tissue.
12. • The cortisol has two basic anti-inflammatory effects:
(1) It can block the early stages of the inflammation
process before inflammation even begins.
(2) If inflammation has already begun, it causes rapid
resolution of the inflammation and increased rapidity of healing.
• Cortisol reduces lymphocyte production and hence, suppresses
immunity.
• Cortisol Blocks the Inflammatory Response to Allergic
Reactions.
13.
14. ACUTE ADRENAL INSUFFICIENCY: (ADRENAL CRISIS)
• A third potentially life - threatening situation that may result in
the loss of consciousness. The condition is uncommon, is
potentially life – threatening, but is readily treatable.
16. Predisposing factors:
• Lack of gluco-corticosteroid hormones
• Mechanism 1: sudden withdrawal of steroid hormones in the patient who
suffers primary adrenal insufficiency (Addison’s disease)
• Mechanism 2: After the sudden withdrawal of steroid hormones from a
patient with normal adrenal cortices but with a temporary insufficiency
resulting from cortical suppression through prolonged exogenous gluco-
corticosteroid administration (secondary insufficiency)
• Mechanism 3: Stress either physiologic or psychological.
17. If the adrenal gland cannot meet the increased demand, clinical signs and
symptoms of adrenal insufficiency develop.
• Mechanism 4: After bilateral adrenalectomy
• Mechanism 5: After sudden destruction of pituitary gland.
• Mechanism 6: Injury to the both adrenal glands (trauma, infection,
thrombosis, or tumor)
Prevention:
• History of rheumatic fever, asthma, TB, emphysema, other lung diseases,
arthritis and rheumatism
• Allergic history to drugs, food, medications, latex
Dialogue history
Rule of TWOs
• In a dose of 20 mg or more of cortisone or its equivalent
• Via oral or parenteral route for a continuous period of two weeks or longer
• Within 2 years of dental therapy
21. Management :
Conscious
Terminate dental treatment
P – Position patient comfortably if asymptomatic;
Supine with legs elevated slightly, if symptomatic
A→B→C – Assess & open airway (head tilt &chin lift); assess airway patency& breathing;
assess circulation (palpation of carotid pulse)
D – Definitive care:
Monitor vital signs
Summon medical assistance
Obtain emergency kit and O2
Administer glucocorticosteroid
23. HYPER VENTILATION
• It is defined as ventilation in excess of that required to maintain normal blood
pa O2 (arterial oxygen tension) and pa CO2 (arterial carbon dioxide tension). It is
produced by increase in frequency or depth of respiration, or both.
• Common emergency occur in dental office , almost always occur is a result of
extreme anxiety.
Prevention:
• Through prompt recognition and management of anxiety
• Physical evaluation of the patient
• The vital signs of apprehensive patients may deviate from normal. Recording
the vital signs at the patient’s initial visit
• Stress reduction protocol is the primary means of preventing hyperventilation
25. HYPERVENTILATION-DIAGNOSIS
• Patient restlessness
• Increased respiratory rate
• Increased depth of respiration
• Lightheadedness
• Tingling in hands and feet
• Carpal-pedal spasm
• Increased anxiety
• Loss of consciousness
26. Clinical manifestations:
system Signs and symptoms
cardiovascular Palpitations
Tachycardia
Precordial”pain”
Neurologic Dizziness
Lightheadedness
Disturbance of consciousness
Disturbance of vision
Numbness and tingling of
extremities
Tetany (rare)
Respiratory Shortness of breath
Chest “pain”
Dryness of mouth
Gastro intestinal Globus hystericus (subjective
feeling of a lump in the throat)
Epigastric pain
Musculoskeletal Muscle pain and cramps
Tremor
Stiffness
Carpopedal tetany
Psychological Tension
Anxiety and nightmares
27. Pathophysiology:
Anxiety
Increased rate and depth of respiration
↑ exchange of O2 & CO2 by lungs
↑ blowing off of CO2 and paCO2 decreases
Hypocapnia
↑ in blood pH
Respiratory alkalosis
29. Management:
Recognize problem (rapid , deep, uncontrolled breathing)
P – Position patient comfortably usually upright
A → B → C – Basic life support as needed
D – Definitive care:
Remove dental materials from patient’s mouth
Calm patient
Correct respiratory alkalosis – instructed to breathe 7% CO2 &93% O2 or to rebreathe the exhaled
air
Initial drug management – Benzodiazepines
Dental care may continue if both doctor and patient agree
Discharge patient
30. HYPERVENTILATION-TREATMENT1
• Stop procedure
• Clear all objects from mouth
• Verbally calm the patient
• Rebreathe CO2
•Paper bag
•Face mask
•Hands
Self-limiting problem
Diazepam 5 mg IV or midazolam 2 mg IM/IV
No O2
1.European Resuscitation Council Guidelines for Resuscitation 2010