NEET MDS Synopsis
The Orbital Vessels
AnatomyThe Orbital Vessels
The orbital contents are supplied chiefly by the ophthalmic artery.
The infraorbital artery, the continuation of the maxillary, also contributes blood to this region.
Venous drainage is through the superior orbital fissure to enter the cavernous sinus.
The Ophthalmic Artery
This artery arises from the internal carotid artery as it emerges from the cavernous sinus.
It passes through the optic foramen within the dural sheath of the optic nerve and runs anteriorly, close to the superomedial wall of the orbit.
The Central Artery of the Retina
This is the one of the smallest but most important branches of the ophthalmic artery.
It arises inferior to the optic nerve until it approaches the eyeball.
It then pierces the optic nerve and runs within it to emerge through the optic disc.
The central artery of the retina spreads over the internal surface of the retina and supplies it.
The Ophthalmic Veins
The Superior Ophthalmic Vein
The superior ophthalmic vein anastomoses with the facial vein.
It has no valves and blood can flow in either direction.
It crosses superior to the optic nerve, passes through the superior orbital fissure and ends in the cavernous sinus.
The Inferior Ophthalmic Vein
This begins as a plexus on the floor of the orbit.
It communicates with the inferior orbital fissure with the pterygoid plexus, crosses inferior to the optic nerve, and ends in either the superior ophthalmic vein or the cavernous sinus.
First Generation Cephalosporins
Pharmacology
First Generation Cephalosporins
Prototype Drugs are CEFAZOLIN (for IV use) and CEPHALEXIN (oral use).
1. Staph. aureus - excellent activity against b-lactamase-producing strains
Not effective against methicillin-resistant Staph. aureus & epidermidis
2. Streptococci - excellent activity versus Streptococcus sp.
Not effective against penicillin-resistant Strep. pneumoniae
3. Other Gm + bacteria - excellent activity except for Enterococcus sp.
4. Moderate activity against gram negative bacteria.
Caution: resistance may occur in all cases.
Susceptible organisms include:
E. coli
Proteus mirabilis
Indole + Proteus sp. (many strains resistant)
Haemophilus influenzae (some strains resistant)
Neisseria sp. (some gonococci resistant)
Uses
1. Upper respiratory tract infections due to Staph. and Strep.
2. Lower respiratory tract infections due to susceptible bacteria e.g. Strep.pneumoniae in penicillin-allergic patient (previous rash)
3. Uncomplicated urinary tract infections (Cephalexin)
4. Surgical prophylaxis for orthopedic and cardiovascular operations (cefazolin preferred because of longer half-life)
5. Staphylococcal infections of skin and skin structure
Uses of NSAIDs
Pharmacology
Uses of NSAIDs
NSAIDs are usually indicated for the treatment of acute or chronic conditions where pain and inflammation are present. Research continues into their potential for prevention of colorectal cancer, and treatment of other conditions, such as cancer and cardiovascular disease.
NSAIDs are generally indicated for the symptomatic relief of the following conditions.
rheumatoid arthritis, osteoarthritis, inflammatory arthropathies (e.g. ankylosing spondylitis, psoriatic arthritis, Reiter's syndrome), acute gout, dysmenorrhoea, metastatic bone pain ,headache and migraine, postoperative pain, mild-to-moderate pain due to inflammation and tissue injury, pyrexia, renal colic
Aspirin, the only NSAID able to irreversibly inhibit COX-1, is also indicated for inhibition of platelet aggregation; an indication useful in the management of arterial thrombosis and prevention of adverse cardiovascular events.
Dental Amalgam - Applications/Use
Dental Materials
Applications/Use
Load -bearing restorations for posterior teeth (class I, II)
Pinned restorations
Buildups or cores for cast restorations
Retrograde canal filling material
(1) Alloy. An alloy is a solid mixture of two or more metals. It is possible to produce a material in which the desirable properties of each constituent are retained or even enhanced, while the less desirable properties are reduced or eliminated.
(2) Amalgam. When one of the metals in an alloy mixture is mercury, an amalgam is formed. A dental amalgam is a combination of mercury with a specially prepared silver alloy, which is used as a restorative material.
(3) Mercury. Mercury is a silver-white, poisonous, metallic element that is liquid at room temperature
BONES OF THE SKULL
Orthodontics
BONES OF THE SKULL
A) Bones of the cranial base:
A) Fontal (1)
B) Ethmoid (1)
C) Sphenoid (1)
D) Occipital (1)
B) Bones of the cranial vault:
1. Parietal (2)
2. Temporal (2)
C) Bones of the face:
Maxilla (2)
Mandible (1)
Nasal bone (2)
Lacrimal bone (2)
Zygomatic bone (2)
Palatine bone(2)
Infra nasal concha (2)
FUSION BETWEEN BONES
1. Syndesmosis: Membranous or ligamentus eg. Sutural point.
2. Synostosis: Bony union eg. symphysis menti.
3. Synchondrosis: Cartilaginous eg. sphenoccipital, spheno-ethmoidal.
GROWTH OF THE SKULL:
A) Cranium: 1. Base 2. Vault
B) Face: 1. Upper face 2.Lower face
CRANIAL BASE:
Cranial base grows at different cartilaginous suture. The cranial base may be divided into 3 areas.
1. The posterior part which extends from the occiput to the salatercica. The most important growth site spheno-occipital synchondrosis is situated here. It is active throughout the growing period and does not close until early adult life.
2. The middle portion extends from sella to foramen cecum and the sutural growth spheno-ethmoidal synchondrosis is situated here. The exact time of closing is not known but probably at the age of 7 years.
3. The anterior part is from foramen cecum and grows by surface deposition of bone in the frontal region and simultaneous development of frontal sinus.
CRANIAL VAULT:
The cranial vault grows as the brain grows. It is accelerated at infant. The growth is complete by 90% by the end of 5th year. At birth the sutures are wide sufficiently and become approximated during the 1st 2 years of life.
The development and extension of frontal sinus takes place particularly at the age of puberty and there is deposition of bone on the surfaces of cranial bone.
Antiplatelet Drugs
Pharmacology
Antiplatelet Drugs:
Whereas the anticoagulant drugs such as Warfarin and Heparin suppress the synthesis or activity of the clotting factors and are used to control venous thromboembolic disorders, the antithrombotic drugs suppress platelet function and are used primarily for arterial thrombotic disease. Platelet plugs form the bulk of arterial thrombi.
Acetylsalicylic acid (Aspirin)
• Inhibits release of ADP by platelets and their aggregation by acetylating the enzymes (cyclooxygenases or COX) of the platelet that synthesize the precursors of Thromboxane A2 that is a labile inducer of platelet aggregation and a potent vasoconstrictor.
• Low dose (160-320 mg) may be more effective in inhibiting Thromboxane A2 than PGI2 which has the opposite effect and is synthesized by the endothelium.
• The effect of aspirin is irreversible.
Haemolytic anaemia
General Pathology
Haemolytic anaemia
Anemia due to increased red cell destruction (shortened life span)
Causes:
A. Corpuscular defects:
1.Membrane defects:
- Spherocytosis.
- Elliptocytosis.
2. Haemoglobinopathies:
- Sickle cell anaemia.
- Thalassaemia
- Hb-C, HBD, HbE.
3. Enzyme defects .deficiency of:
- GIucose -6 phosphate dehydrogenase (G6-PD)
- Pyruvate kinase
4. Paroxysmal nocturnal haemoglobinuria.
B. Extracorpusular mechanisms
1. Immune based:
- Autoimmune haemolytic anaemia.
- Haemolytic disease of new born.
- Incompatible transfusion.
- Drug induced haemolysis
2. Mechanical haemolytic anaemia.
3. Miscellaneous due to :
- Drugs and chemicals.
- Infections.
- Burns.
features of haemolytic anaemia
- Evidence of increased Hb breakdown:
-> Unconjugated hyperbilirubinaemia.
-> Decreased plasma haptoglobin.
-> Increased urobilinogen and stercobilinogen.
-> Haemoglobinaemia, haemoglobinuria and haemosiderinuria if Intravascular haemolysis occurs.
- Evidence or compensatory erythroid hyperplasia:
-> Reticulocytosis and nucleated RBC in peripheral smear.
-> Polychromasia and macrocytes
-> Marrow erythroid hyperplasia
-> Skull and other bone changes.
- Evidences of damage to RBC:
-> Spherocytes and increased osmotic fragility
-> Shortened life span.
-> Fragmented RBC.
-> Heinz bodies.
The Muscles of Facial Expression
AnatomyThe Muscles of Facial Expression
These lie in the subcutaneous tissue and are attached to the skin of the face.
They enable us to move our skin and change our facial expression. They produce their effects by pulling on the skin but do not move the facial skeleton.
These muscles surround the facial orifices and act as sphincters and dilators.
All facial muscles receive their innervation from the branches of the facial nerve (CN VII)-temporal, zygomatic, buccal, marginal mandibular, cervical.