NEET MDS Synopsis
Cor pulmonale
General Pathology
Cor pulmonale
a failure of the right side of the heart. It is caused by prolonged high blood pressure in the right ventricle of the heart, which in turn is most often caused by pulmonary hypertension - prolonged high blood pressure in the arteries or veins of the lungs. People with heart disease, or lung diseases such as cystic fibrosis, are at greater risk.
Pathophysiology
There are several mechanisms leading to pulmonary hypertension and cor pulmonale:
Pulmonary vasoconstriction
Anatomic changes in vascularisation
Increased blood viscosity
Primary pulmonary hypertension
Causes
Acute:
• Massive pulmonary embolization
• Exacerbation of chronic cor pulmonale
Chronic:
• COPD
• Loss of lung tissue following trauma or surgery
Nerves of the Palate
AnatomyNerves of the Palate
The sensory nerves of the palate, which are branches of the pterygopalatine ganglion, are the greater and lesser palatine nerves.
They accompany the arteries through the greater and lesser palatine foramina, respectively.
The greater palatine nerve supplies the gingivae, mucous membrane, and glands of the hard palate.
The lesser palatine nerve supplies the soft palate.
Another branch of the pterygopalatine ganglion, the nasopalatine nerve, emerges from the incisive foramen and supplies the mucous membrane of the anterior part of the hard palate.
The Parathyroid Glands
Physiology
The Parathyroid Glands
The parathyroid glands are 4 tiny structures embedded in the rear surface of the thyroid gland. They secrete parathyroid hormone (PTH) a polypeptide of 84 amino acids. PTH increases the concentration of Ca2+ in the blood in three ways. PTH promotes
release of Ca2+ from the huge reservoir in the bones. (99% of the calcium in the body is incorporated in our bones.)
reabsorption of Ca2+ from the fluid in the tubules in the kidneys
absorption of Ca2+ from the contents of the intestine (this action is mediated by calcitriol, the active form of vitamin D.)
PTH also regulates the level of phosphate in the blood. Secretion of PTH reduces the efficiency with which phosphate is reclaimed in the proximal tubules of the kidney causing a drop in the phosphate concentration of the blood.
Hyperparathyroidism
Elevate the level of PTH causing a rise in the level of blood Ca2+ .Calcium may be withdrawn from the bones that they become brittle and break.
Patients with this disorder have high levels of Ca2+ in their blood and excrete small amounts of Ca2+ in their urine. This causes hyperparathyroidism.
Hypoparathyroidism
This disorder have low levels of Ca2+ in their blood and excrete large amounts of Ca2+ in their urine.
Rhythmicity
Physiology
1.Rhythmicity ( Chronotropism ) : means the ability of heart to beat regularly ( due to repetitive and stable depolarization and repolarization ) . Rhythmicity of heart is a myogenic in origin , because cardiac muscles are automatically excited muscles and does not depend on the nervous stimulus to initiate excitation and then contraction . The role of nerves is limited to the regulation of the heart rate and not to initiate the beat.
There are many evidences that approve the myogenic and not neurogenic origin of the rhythmicity of cardiac muscle . For example :
- transplanted heart continues to beat regularly without any nerve supply.
- Embryologically the heart starts to beat before reaching any nerves to them.
- Some drugs that paralyze the nerves ( such as cocaine ) do not stop the heart in given doses.
Spontaneous rhythmicity of the cardiac muscle due to the existence of excitatory - conductive system , which is composed of self- exciting non-contractile cardiac muscle cells . The SA node of the mentioned system excites in a rate , that is the most rapid among the other components of the system ( 110 beats /minute ) , which makes it the controller or ( the pacemaker ) of the cardiac rhythm of the entire heart.
Mechanism , responsible for self- excitation in the SA node and the excitatory conductive system is due to the following properties of the cell membrane of theses cells :
1- Non-gated sodium channels
2- Decreased permeability to potassium
3- existence of slow and fast calcium channels.
These properties enable the cations ( sodium through the none-gated sodium voltage channels , calcium through calcium slow channels) to enter the cell and depolarize the cell membrane without need for external stimulus.
The resting membrane potential of non-contractile cardiac cell is -55 - -60 millivolts ( less than that of excitable nerve cells (-70) ) .
The threshold is also less negative than that of nerve cells ( -40 millivolts ).
The decreased permeability to potassium from its side decrease the eflux of potassium during the repolarization phase of the pacemaker potential . All of these factors give the pacemaker potential its characteristic shape
Repeating of the pacemaker potential between the action potentials of contractile muscle cells is the cause of spontaneous rhythmicity of cardiac muscle cells.
Factors , affecting the rhythmicity of the cardiac muscle :
I. Factors that increase the rate ( positive chronotropic factors) :
1. sympathetic stimulation : as its neurotransmitter norepinephrine increases the membrane permeability to sodium and calcium.
2. moderate warming : moderate warming increases temperature by 10 beats for each 1 Fahrenheit degree increase in body temperature, this due to decrease in permeability to potassium ions in pacemaker membrane by moderate increase in temperature.
3. Catecholaminic drugs have positive chronotropic effect.
4. Thyroid hormones : have positive chronotropic effect , due to the fact that these drugs increase the sensitivity of adrenergic receptors to adrenaline and noreadrenaline .
5. mild hypoxia.
6. mild alkalemia : mild alkalemia decreases the negativity of the resting potential.
7. hypocalcemia.
8. mild hypokalemia
II. Factors that decrease rhythmicity ( negative chronotropic):
1.Vagal stimulation : the basal level of vagal stimulation inhibits the sinus rhythm and decrease it from 110-75 beats/ minute. This effect due to increasing the permeability of the cardiac muscle cell to potassium , which causes rapid potassium eflux , which increases the negativity inside the cardiac cells (hyperpolarization ).
2. moderate cooling
3. severe warming : due to cardiac damage , as a result of intercellular protein denaturation. Excessive cooling on the other hand decrease metabolism and stops rhythmicity.
4. Cholenergic drugs ( such as methacholine , pilocarpine..etc) have negative chronotropic effect.
5. Digitalis : these drugs causes hyperpolarization . This effect is similar to that of vagal stimulation.
6. Hypercapnia ( excessive CO2 production )
7. Acidemia.
8. hyper- and hyponatremia .
9. hyperkalemia
10. hypercalcemia
11. Typhoid or diphteria toxins.
Emergency conditions in Dental Clinics p2
Oral Medicine
Emergency conditions in Dental Clinics
Hypoadrenalism - Usually the patient is known to have Addison's disease or to be taking steroids long term and has forgotten to take the tablets.
Signs and symptoms
• Pallor
• Confusion
• Rapid weak pulse.
Treatment:
Give oxygen
Give 200 mg hydrocortisone sodium succinate by slow i.v. injection.
Give steroid replacement
Determining and managing underlying cause once the crisis over.
If required:
• Transfer to Emergeny hostpital
• Fluids and further hydrocortisone, both i.v.
Acute asthma - Exposure to antigen but precipitated by many factors including anxiety.
Signs and symptoms
• Persistent shortness of breath poorly relieved by bronchodilators
• Restlessness and exhaustion
• Tachycardia greater than 110 beats/min and low peak expiratory flow
• Respirations may be so shallow in severe cases that wheezing is absent.
Treatment
Excluded respiratory obstruction
Sit the patient up
Give oxygen
Salbutamol (Ventolin) via a nebuliser (2.5-5 mg of 1 mg/ml nebuliser solution) or via a large-volume spacer (two puffs of a metered dose inhaler 10-20 times: one puff every 30 seconds up to 10 puffs for a child)
Reassure and allow home if recovered.
• Bronchodilatation.
If Major Problem recommend to hospital Emergeny
• Hydrocortisone sodium succinate i.v.: adults 200 mg; child 100 mg
• Add ipratropium 0.5 mg to nebulised salbutamol
• Aminophylline slow i.v. injection of 250 mg in 10 ml over at least 20 minutes: monitor or keep finger on pulse during injection.
Caution in epilepsy: rapid injection of aminophylline may cause arrhythmias and convulsions.
Caution in patients already receiving theophylline: arrhythmias or convulsions may occur.
Anaphylactic shock
Signs and symptoms
• Paraesthesia, flushing and swelling of face, especially eyelids and lips (Fig. 13)
• generalised urticaria, especially hands and feet
• wheezing and difficulty in breathing
• rapid weak pulse.
These may develop over 15 to 30 minutes following the oral administration of a drug or rapidly over a few minutes following i.v. drug administration.
Treatment
Lay patient flat and raise feet
Give oxygen
Give 0.5 ml epinephrine (adrenaline) 1 mg/ml (1 in
1000) intramuscular
— 0.25 ml for 6-12 years
— 0.12 ml for 6 months to 6 years
repeated every 10 min until improvement.
Requires prompt energetic treatment of
• laryngeal oedema
• bronchospasm
• hypotension.
• Chlorphenamine (chlorpheniramine) 10 mg in 1 ml intramuscular or slow i.v. injection
• Hydrocortisone sodium succinate 200 mg by slow i.v. injection: valuable as action persists after that of adrenaline has worn off
• Fluids i.v. (colloids) infused rapidly if shock not responding quickly to adrenaline.
Stroke - Stroke results from either cerebral haemorrhage or cerebral ischaemia.
Signs and symptoms
• Confusion followed by signs and symptoms of focal brain damage
• Hemiplegia or quadriplegia
• Sensory loss
• Dysphasia
• Locked-in syndrome (aware, but unable to respond).
Treatment
Maintain and transfer for further investigation.
Benzodiazepine overdose - Overdose can result from a large or a fast dose of benzodiazepine or can occur in a sensitive patient.
Signs and symptoms
• Deeply sedated
• Severe respiratory depression.
Treatment
Flumazenil (Annexate) 200 mg over 15 seconds as 100 mg/ml i.v. followed by 100 mg every 1 minute up to maximum of 1 mg Maintain airway with head tilt/chin lift
Give oxygen.
Treatment
The action of the benzodiazepine is reversed with the specific antagonist.
Angina and myocardial infarction
Signs and symptoms
• Sudden onset of severe crushing pain across front of chest, which may radiate towards the shoulder and down the left arm or into the neck and jaw; pain from angina usually radiates down left arm
Skin pale and clammy
Shallow respirations
Nausea
Weak pulse and hypotension
If the pain not relieved by glyceryl trinitrate (GTN) then cause is myocardial infarction rather than angina.
First-line treatment of angina and myocardial infarction
Allow patient to rest in position that feels most comfortable:
• in presence of breathlessness this is likely to be the sitting position, whereas syncopal patients will want to lie flat
• often an intermediate position will be most appropriate.
Angina -
Angina results from reduced coronary artery lumen diameter because of atheromatous plaques
Myocardial infarction is usually the result of thrombosis in a coronary artery.
Angina is relieved by rest and nitrates:
• Glyceryl trinitrate spray 400 mg metered dose (sprayed on oral mucosa or under tongue and mouth then closed)
• Give oxygen
• Allow home if attack is mild and the patient recovers rapidly.
Myocardial infarction
If a myocardial infarction is suspected:
• give oxygen
• aspirin tablet 300 mg chewed.
• Pain control
• Vasodilatation of blood vessels to reduce load on heart.
Further management for severe angina or myocardial infarction
• Transfer to Emergency
• Diamorphine 5 mg (2.5 mg in older people) by slow i.v. injection (1 mg/min)
• Early thrombolytic therapy reduces mortality.
Cardiac arrest
• Most cardiac arrests result from arrhythmias associated with acute myocardial infarction or chronic ischaemic heart disease
• The heart arrests in one of three rhythms
— VF (ventricular fibrillation) or pulseless VT (ventricular tachycardia)
— asystole
— PEA (pulseless electrical activity) or EMD (electromechanical dissociation).
Signs and symptoms
• Unconscious
• No breathing
• Absent carotid pulse.
Treatment
• Circulation failure for 4 minutes, or less if the patient is already hypoxaemic, will lead to irreversible brain damage
• Institute early basic life support as holding procedure until early advanced life support is available.
• Transfer to Emergency
• Advanced life support.
Advanced life support for cardiac arrest
Advanced airway management techniques and specific treatment of the underlying cause of cardiac arrest constitute advanced life support (ALS).
Mercury Exposure and Safety
Conservative DentistryMercury Exposure and Safety
Concentrations of Mercury in Air
Typical Levels: Mercury concentrations in air can vary
significantly:
Pure air: 0.002 µg/m³
Urban air: 0.05 µg/m³
Air near industrial parks: 3 µg/m³
Air in mercury mines: 300 µg/m³
Threshold Limit Value (TLV): The generally accepted TLV
for exposure to mercury vapor for a 40-hour work week is 50 µg/m³.
Understanding these levels is crucial for ensuring safety in dental
practices where amalgam is used.
Cardiac Conduction
Physiology
A small fraction of cardiac muscle fibers have myogenicity and autorhythmicity.
Myogenicity is the property of spontaneous impulse generation. The slow sodium channels are leaky and cause the polarity to spontaneously rise to threshold for action potential generation. The fastest of these cells, those in the SA node, set the pace for the heartbeat.
Autorhythmicity - the natural rhythm of spontaneous depolarization. Those with the fastest autorhythmicity act as the 1. heart's pacemaker.
Contractility - like skeletal muscle, most cardiac muscle cells respond to stimuli by contracting. The autorhythmic cells have very little contractility however. Contractility in the other cells can be varied by the effect of neurotransmitters.
Inotropic effects - factors which affect the force or energy of muscular contractions. Digoxin, epinephrine, norepinephrine, and dopamine have positive inotropic effects. Betal blockers and calcium channel blockers have negative inotropic effects
Sequence of events in cardiac conduction: The electrical events in the cardiac cycle.
1) SA node depolarizes and the impulse spreads across the atrial myocardium and through the internodal fibers to the AV node. The atrial myocardium depolarizes resulting in atrial contraction, a physical event.
2) AV node picks up the impulse and transfers it to the AV Bundle (Bundle of His). This produces the major portion of the delay seen in the cardiac cycle. It takes approximately .03 sec from SA node depolarization to the impulse reaching the AV node, and .13 seconds for the impulse to get through the AV node and reach the Bundle of His. Also during this period the atria repolarize.
3) From the AV node the impulse travels through the bundle branches and through the Purkinje fibers to the ventricular myocardium, causing ventricular depolarization and ventricular contraction, a physical event.
4) Ventricular repolarization occurs.
The Thyroid
Physiology
The thyroid gland is a double-lobed structure located in the neck. Embedded in its rear surface are the four parathyroid glands.
The Thyroid Gland
The thyroid gland synthesizes and secretes:
thyroxine (T4) and
calcitonin
T4 and T3
Thyroxine (T4 ) is a derivative of the amino acid tyrosine with four atoms of iodine. In the liver, one atom of iodine is removed from T4 converting it into triiodothyronine (T3). T3 is the active hormone. It has many effects on the body. Among the most prominent of these are:
an increase in metabolic rate
an increase in the rate and strength of the heart beat.
The thyroid cells responsible for the synthesis of T4 take up circulating iodine from the blood. This action, as well as the synthesis of the hormones, is stimulated by the binding of TSH to transmembrane receptors at the cell surface.
Diseases of the thyroid
1. hypothyroid diseases; caused by inadequate production of T3
cretinism: hypothyroidism in infancy and childhood leads to stunted growth and intelligence. Can be corrected by giving thyroxine if started early enough.
myxedema: hypothyroidism in adults leads to lowered metabolic rate and vigor. Corrected by giving thyroxine.
goiter: enlargement of the thyroid gland. Can be caused by:
inadequate iodine in the diet with resulting low levels of T4 and T3;
an autoimmune attack against components of the thyroid gland (called Hashimoto's thyroiditis).
2. hyperthyroid diseases; caused by excessive secretion of thyroid hormones
Graves´ disease. Autoantibodies against the TSH receptor bind to the receptor mimicking the effect of TSH binding. Result: excessive production of thyroid hormones. Graves´ disease is an example of an autoimmune disease.
Osteoporosis. High levels of thyroid hormones suppress the production of TSH through the negative-feedback mechanism mentioned above. The resulting low level of TSH causes an increase in the numbers of bone-reabsorbing osteoclasts resulting in osteoporosis.
Calcitonin
Calcitonin is a polypeptide of 32 amino acids. The thyroid cells in which it is synthesized have receptors that bind calcium ions (Ca2+) circulating in the blood. These cells monitor the level of circulating Ca2+. A rise in its level stimulates the cells to release calcitonin.
bone cells respond by removing Ca2+ from the blood and storing it in the bone
kidney cells respond by increasing the excretion of Ca2+
Both types of cells have surface receptors for calcitonin.
Because it promotes the transfer of Ca2+ to bones, calcitonin has been examined as a possible treatment for osteoporosis