NEET MDS Synopsis
Antiarrhythmic Drugs - Class III Potassium Channel Blockers
Pharmacology
Class III Potassium Channel Blockers
Prolong effective refractory period by prolonging Action Potential
Treatment: ventricular tachycardia and fibrillation, conversion of atrial fibrillation or flutter to sinus rhythm, maintenance of sinus rhythm
– Amiodarone (Cordarone) – maintenance of sinus rhythm
– Bretylium (Bretylol)
– Ibutilide (Corvert)
– Dofetilide (Tykosyn)
– Sotalol (Betapace)
Amiodarone
- Has characteristics of sodium channel blockers, beta blockers, and calcium channel blockers
- Has vasodilating effects and decreases systemic vascular resistance
- Prolongs conduction in all cardiac tissue
- Decreases heart rate
- Decreases contractility of the left ventricles
Class III - Adverse Effects
- GI- Nausea vomiting and GI distress
- CNS- Weakness and dizziness
- CV-Hypotension, CHF, and arrhythmias are common.
- Amiodarone associated with potentially fatal Hepatic toxicity, ocular abnormalities and serious cardiac arrhythmias.
Drug – Drug Interactions
These drugs can cause serious toxic effects if combined with digoxin or quinidine.
Post viral cirrhosis
General Pathology
Post viral (post hepatitic) cirrhosis (15-20%)
Cause:- Viral hepatitis (mostly HBV or HCV)
Acute hepatitis → chronic hepatitis → cirrhosis.
Pathology
Liver is shrunken. Fatty change is absent (except with HCV). Cirrhosis is mixed.
M/E :-
Hepatocytes-show degeneration, necrosis as other types of cirrhosis.
Fibrous septa -They are thick and immature (more cellular and vascular).
- Irregular margins (piece meal necrosis).
- Heavy lymphocytic infiltrate.
Prognosis:- - More rapid course than alcoholic cirrhosis.Hepatocellular carcinoma is more liable to occur
Morphine
Pharmacology
Morphine
Morphine is effective orally, but is much less effective than when given parenterally due to first-pass metabolism in the liver. Metabolism involves glucuronide formation, the product of which is excreted in the urine.
1. Central Nervous System Effects
• Morphine has mixed depressant and stimulatory actions on the CNS.
• Analgesia:
• Dysphoria – Euphoria
- morphine directly stimulates the chemoreceptor trigger zone, but later depresses the vomiting center in the brain stem. This center is outside the blood/brain barrier.
- opiates appear to relieve anxiety
• Morphine causes the release of histamine and abolishes hunger.
- causes the body to feel warm and the face and nose to itch.
• Pupils are constricted.- due to stimulation of the nuclei of the third cranial nerves.
- tolerance does not develop to this effect.
• Cough reflex is inhibited. - this is not a stereospecific effect.
- dextromethorphan will suppress cough but will not produce analgesia.
• Respiration is depressed
- due to a direct effect on the brain stem respiratory center.
- death from narcotic overdose is nearly always due to respiratory arrest.
- the mechanism of respiratory depression involves:
• a reduction in the responsiveness of the brain stem respiratory centers to an increase in pCO2.
• depression of brain stem centers that regulate respiratory rhythm.
- hypoxic stimulation of respiration is less affected and O2 administration can produce apnea.
2. Cardiovascular Effects
• Postural orthostatic hypotension.- due primarily to peripheral vasodilation, which may be due in part to histamine release.
• Cerebral circulation is also indirectly influenced by increased pCO2, which leads to cerebral vasodilation and increased cerebrospinal fluid pressure.
• In congestive heart failure, morphine decreases the left ventricular workload and myocardial oxygen demand.
3. Endocrine Effects
• Increases prolactin secretion
• Increases vasopressin (ADH) secretion
• Decreases pituitary gonadotropin (LH & FSH) secretion.
• Decreases stress induced ACTH secretion.
4. Gastrointestinal Tract Effects
• Constipation (tolerance does not develop to this effect).
• Several of these agents can be used in the treatment of diarrhea.
There is an increase in smooth muscle tone and a decrease in propulsive contractions.
Adverse Reactions
Generally direct extensions of their pharmacological actions.
1. respiratory depression, apnea
2. nausea and vomiting
3. dizziness, orthostatic hypotension, edema
4. mental clouding, drowsiness
5. constipation, ileus
6. biliary spasm (colic)
7. dry mouth
8. urine retention, urinary hesitancy
9. hypersensitivity reactions (contact dermatitis, urticaria)
Precautions
1. respiratory depression, particularly in the newborn
3. orthostatic hypotension
4. histamine release (asthma, shock)
5. drug interactions (other CNS depressants)
6. tolerance:
- analgesia, euphoria, nausea and vomiting, respiratory depression
7. physical dependence (psychological & physiological)
Clinical Physiology CVS
Physiology
Clinical Physiology
Heart Failure : Heart failure is inability of the heart to pump the enough amount of blood needed to sustain the needs of organism .
It is usually called congestive heart failure ( CHF) .
To understand the pathophysiology of the heart failure , lets compare it with the physiology of the cardiac output :
Cardiac output =Heart rate X stroke volume
Stroke volume is determined by three determinants : Preload ( venous return ) , contractility , and afterload (peripheral resistance ) . Any disorder of these factors will reduce the ability of the heart to pump blood .
Preload : Any factor that decrease the venous return , either by decreasing the intravenous pressure or increasing the intraatrial pressure will lead to heart failure .
Contractility : Reducing the power of contraction such as in myocarditis , cardiomyopathy , preicardial tamponade ..etc , will lead to heart failure .
Afterload : Any factor that may increase the peripheral resistance such as hypertension , valvular diseases of the heart may cause heart failure.
Pathophysiology : When the heart needs to contract more to meet the increased demand , compensatory mechanisms start to develope to enhance the power of contractility . One of these mechanism is increasing heart rate , which will worsen the situation because this will increase the demands of the myocardial cells themselves . The other one is hypertrophy of the cardiac muscle which may compensate the failure temporarily but then the hypertrophy will be an additional load as the fibers became stiff .
The stroke volume will be reduced , the intraventricular pressure will increase and consequently the intraatrial pressure and then the venous pressure . This will lead to decrease reabsorption of water from the interstitium ( see microcirculation) and then leads to developing of edema ( Pulmonary edema if the failure is left , and systemic edema if the failure is right) .
SELECTION OF SPRUE
Dental Materials
SELECTION OF SPRUE
1 . DIAMETER :
It should be approximately the same size of the thickest portion of the wax pattern .
Too small sprue diameter suck back porosity results .
2 . SPRUE FORMER ATTACHMENT :
Sprue should be attached to the thickest portion of the wax pattern .
It should be Flared for high density alloys & Restricted for low density alloys .
3 . SPRUE FORMER POSITION
Based on the
1. Individual judgement .
2. Shape & form of the wax pattern .
Patterns may be sprued directly or indirectly .
Indirect method is commonly used
Periodontal Bone Grafts
PeriodontologyPeriodontal Bone Grafts
Bone grafting is a critical procedure in periodontal surgery, aimed at
restoring lost bone and supporting the regeneration of periodontal tissues.
1. Bone Blend
Bone blend is a mixture of cortical or cancellous bone that is procured using a trephine or rongeurs, placed in an
amalgam capsule, and triturated to achieve a slushy osseous mass. This technique
allows for the creation of smaller particle sizes, which enhances resorption and
replacement with host bone.
Particle Size: The ideal particle size for bone blend is
approximately 210 x 105 micrometers.
Rationale: Smaller particle sizes improve the chances of
resorption and integration with the host bone, making the graft more effective.
2. Types of Periodontal Bone Grafts
A. Autogenous Grafts
Autogenous grafts are harvested from the patient’s own body, providing the
best compatibility and healing potential.
Cortical Bone Chips
History: First used by Nabers and O'Leary in 1965.
Characteristics: Composed of shavings of cortical
bone removed during osteoplasty and ostectomy from intraoral sites.
Challenges: Larger particle sizes can complicate
placement and handling, and there is a potential for sequestration. This
method has largely been replaced by autogenous osseous coagulum and bone
blend.
Osseous Coagulum and Bone Blend
Technique: Intraoral bone is obtained using high-
or low-speed round burs and mixed with blood to form an osseous coagulum
(Robinson, 1969).
Advantages: Overcomes disadvantages of cortical
bone chips, such as inability to aspirate during collection and
variability in quality and quantity of collected bone.
Applications: Used in various periodontal
procedures to enhance healing and regeneration.
Intraoral Cancellous Bone and Marrow
Sources: Healing bony wounds, extraction sockets,
edentulous ridges, mandibular retromolar areas, and maxillary
tuberosity.
Applications: Provides a rich source of osteogenic
cells and growth factors for bone regeneration.
Extraoral Cancellous Bone and Marrow
Sources: Obtained from the anterior or posterior
iliac crest.
Advantages: Generally offers the greatest potential
for new bone growth due to the abundance of cancellous bone and marrow.
B. Bone Allografts
Bone allografts are harvested from donors and can be classified into three
main types:
Undermineralized Freeze-Dried Bone Allograft (FDBA)
Introduction: Introduced in 1976 by Mellonig et al.
Process: Freeze drying removes approximately 95% of
the water from bone, preserving morphology, solubility, and chemical
integrity while reducing antigenicity.
Efficacy: FDBA combined with autogenous bone is
more effective than FDBA alone, particularly in treating furcation
involvements.
Demineralized (Decalcified) FDBA
Mechanism: Demineralization enhances osteogenic
potential by exposing bone morphogenetic proteins (BMPs) in the bone
matrix.
Osteoinduction vs. Osteoconduction: Demineralized
grafts induce new bone formation (osteoinduction), while
undermineralized allografts facilitate bone growth by providing a
scaffold (osteoconduction).
Frozen Iliac Cancellous Bone and Marrow
Usage: Used sparingly due to variability in
outcomes and potential complications.
Comparison of Allografts and Alloplasts
Clinical Outcomes: Both FDBA and DFDBA have been
compared to porous particulate hydroxyapatite, showing little difference in
post-treatment clinical parameters.
Histological Healing: Grafts of DFDBA typically heal
with regeneration of the periodontium, while synthetic bone grafts (alloplasts)
heal by repair, which may not restore the original periodontal architecture.
Aspects of Pathology
General Pathology
Pathology gives explanations of a disease by studying the following four aspects of the disease.
1. Etiology,
2. Pathogenesis,
3. Morphologic changes and
4. Functional derangements and clinical significance.
1. Etiology Etiology of a disease means the cause of the disease. If the cause of a disease is known it is called primary etiology. If the cause of the disease is unknown it is called idiopathic. Knowledge or discovery of the primary cause remains the backbone on which a diagnosis can be made, a disease understood, & a treatment developed. There are two major classes of etiologic factors: genetic and acquired (infectious, nutritional, chemical, physical, etc).
2. Pathogenesis Pathogenesis means the mechanism through which the cause operates to produce the pathological and clinical manifestations. The pathogenetic mechanisms could take place in the latent or incubation period. Pathogenesis leads to morphologic changes.
3. Morphologic changes The morphologic changes refer to the structural alterations in cells or tissues that occur following the pathogenetic mechanisms. The structural changes in the organ can be seen with the naked eye or they may only be seen under the microscope. Those changes that can be seen with the naked eye are called gross morphologic changes & those that are seen under the microscope are called microscopic changes. the morphologic changes will lead to functional alteration & to the clinical signs & symptoms of the disease.
4. Functional derangements and clinical significance The morphologic changes in the organ influence the normal function of the organ. By doing so, they determine the clinical features (symptoms and signs), course, and prognosis of the disease.
ANTICHOLINERGIC DRUGS
Pharmacology
ANTICHOLINERGIC DRUGS
Blocks the action of Ach on autonomic effectors.
Classification
Natural Alkaloids - Atropine. Hyoscine
Semi-synthetic deriuvatives:- Homatropine, Homatropine methylbromide, Atropine methonitrate.
Synthetic compounds
(a) Mydriatics - Cyclopentolate. Tropicamide.
(b) Antisecretory - Antispasmodics - Propantha1ine. Oxy-phenonium, Pirenzipine.
c) Antiparkinsonism- Benzotopine, Ethopropazine, Trihexyphenidyl, Procyclidine, Biperiden
Other drugs with anticholinergic properties • Tricyclic Antidepressants • Phenothiazines • Antihistaminics • Disopyramide
MUSCARINIC RECEPTORS SUBTYPES & ANTAGONISTS
• M 1 Antagonists – Pirenzepine, Telenzepine, dicyclomine, trihexyphenidyl
• M 2 Antagonists – Gallamine, methoctramine
• M 3 Antagonists – Darifenacin, solifenacin, oxybutynin, tolterodine
Pharmacological Actions
CNS - stimulation of medullary centres like vagal. respiratory. vasomotor and inhibition of vestibular excitation and has anti-motion sickness properties.
CVS - tachycardia.
Eye - mydriasis
Smooth muscles - relaxation of the muscles receiving parnsympathetic motor innervation.
Glands - decreased secretion of sweat and salivary glands
Body Temperature - is increased as there is stimulation of temperature regulating centre.
Respiratory System- Bronchodilatation & decrease in secretions. For COPD or Asthma - antimuscarinic drugs are effective
GIT - Pirenzepine & Telenzepine - decrease gastric secretion with lesser side effects.