NEET MDS Synopsis
ULCER
General Surgery
An ulcer is a break in the continuity of the skin or the mucous membrane.
Mode of onset: Traumatic ulcers heal when the traumatic agent is removed., If it persists it becomes chronic as in the case of dental ulcer of the tongue. Ulcers may develop spontaneously as in the case of gumma (syphilitic ulcer). It may develop with varicose veins called varicose ulcer, which develops in the lower third of the leg.
Sometimes a malignant ulcer develops in a scar called Marjolin’s ulcer. Special features are:
No pain - as there are no nerves. It does not spread - as there is scar tissue. No metastases - as there are no lymphatics Treatment:- Wide excision.
Classification of Ulcer
A) Pathologically
I. Non-specific ulcers:
a. Due to infected wound after trauma, that is physical or chemical agents.
b. Due to local infection example dental ulcer, pressure sore
Specific ulcers: Caused by specific infection
a. Syphilitic ulcers (Hunterian chancre)
b. Tubercular ulcers, actinomycosis
Trophic ulcer:- Caused by two factors:
Diminished nutrition due to inadequate blood supply to the tissues
Eg. Ulcers in Buerger’s Disease, Artherosclerosis
b. Diminished or absence of sensation of the skin leading to perforating ulcer of the foot
iv. Malignant ulcer: Due to squamous cell carcinoma, rodent ulcers and melanoma.
B) Clinical classification of ulcers
1. Acute Ulcer: The edge is inflamed oedematous and painful with slough in the floor and n o granulation tissue. Profuse purulent Discgarge seen
2. Healing ulcers: edge sloping with bluish margin The floor is covered with a red, healthy granulation tissue.
3. Chronic or callous ulcer (non- healing) There is no tendency to heal by itself, the base is jndurated unhealthy granulation tissue is present in the floor The edge is rounded and thickened.
Chronic ulcer occur due to:
Chronic infection , Defective circulation , Foreign body, Persistent local oedema , Malignancy , Diabetes , Malnutrition (loss of proteins), Gout
Specific Ulcers
Tubeculous Ulcer
Edge Undermined, floor contains granulation tissue a watery discharge is present. Caseous material is found in the floor of the ulcer. It usually occurs in tubercular lymphadenitis in the neck, axilla or groin.
Syphilitic Ulcer
a) Huntarian Chancre or primary sore or hard chancre: usuaIly occurs over the genitalia especially on penis. Occurs in the primary stage of syphilis Ulcer is round or oval, it is hard,indurated, elevated and painless It feels like a button, discharges serum containing spirochetes (cork screw) which is highly infective.
b) In the Secondary stage mucous patches and condylomata occurs The ulcers are shallow white patches, of sodden thickness which occur in the mouth and tongue. Condyloma are hypertrophied epithelium with serous discharge occurring in mucocutaneous junction around the anus. The regional lymphnod (inguinal transverse chain) are enlarged.
c) In tertiary stage of syphilis gummatous ulcers occur They have a punched out edge and wash Ieather floor. They occur on the subcutaneous bones like sternum and tibia. They are painless and refuse to heal.
Soft Sore (chanchroid)
They are painful muitiple ulcers, with copious discharge. They are caused by Bacillus Ducrey lncubation time is 3 to 4 days. located on glans penis and prepuce is due to venereal infection. They are associated with enlarged called bilateral inguinal lymphnodes
Tropical ulcer:
a) Oriental Sore - due to L. Tropica (lieshmaniasis)
b) Ulcers and sinuses are due to guinea worm abscess
c) Histoplasmosis with multiple ulcers on the tibia.
d) Chronic ulcers due to yaws
e) Amoebic ulcers occur in colon_and rectum , flask shaped ulcers , undermined edge , caused by Entamoeba Histolytica
Varicose Ulcer:
Associated with varicose veins. Occurs on the inner aspect of the lower third of leg , chronic ulcer The surrounding area is pigmented and eczema is present. The sore is longitudinally oval It does not penetrate the deep fascia and is painless The base is adherent to the periosteum of the tibia
Rodent ulcer
Usually Occurs on the face above a line joining the lobule of the ear to the angle of the mouth. Usually occurs at the inner canthous of the eye . Edge is raised and rolled, Erodes the deeper structures and the bone, the lyrnph nodes are not involved.
Treatment: If small wide excision is done with skin grafting, If large, radiotherapy is given.
Malignant Ulcer
Occurs due to chronic irritation as in the case of malignant ulcer of the tongue. The edge is everted. The floor is covered with slough and tumor tissue The regional lymph nodes are hard.
Initially mobile later becomes hard
Treatment: Wide excision is done.
Marjolin ulcer: Malignant Ulcer occurring on scar of Burns
Blood Supply to the Head and Neck
AnatomyBlood Supply to the Head and Neck
Most arteries in the anterior cervical triangle arise from the common carotid artery or one of the branches of the external carotid artery.
Most veins in the anterior cervical triangle are tributaries of the large internal jugular vein.
The Common Carotid Arteries
The right common carotid artery begins at the bifurcation of the brachiocephalic trunk, posterior to the right sternoclavicular joint.
The left common carotid artery begins arises from the arch of the aorta and ascends into the neck, posterior to the left sternoclavicular joint.
Each common carotid artery ascends into the neck within the carotid sheath to the level of the superior border of the thyroid cartilage.
Here it terminates by dividing into the internal and external carotid arteries.
The Internal Carotid Artery
This is the direct continuation of the common carotid artery and it has no branches in the neck.
It supplies structures inside the skull.
The internal carotid arteries are two of the four main arteries that supply blood to the brain.
Each artery arises from the common carotid at the level of the superior border of the thyroid cartilage.
It then passes superiorly, almost in a vertical plane, to enter the carotid canal in the petrous part of the temporal bone.
A plexus of sympathetic fibres accompany it.
During its course through the neck, the internal carotid artery lies on the longus capitis muscle and the sympathetic trunk.
The vagus nerve (CN X) lies posterolateral to it.
The internal carotid artery enters the middle cranial fossa beside the dorsum sellae of the sphenoid bone.
Within the cranial cavity, the internal carotid artery and its branches supply the hypophysis cerebri (pituitary gland), the orbit, and most of the supratentorial part of the brain.
The External Carotid Arteries
This vessel begins at the bifurcation of the common carotid, at the level of the superior border of the thyroid cartilage.
It supplies structures external to the skull.
The external carotid artery runs posterosuperiorly to the region between the neck of the mandible and the lobule of the auricle.
It terminates by dividing into two branches, the maxillary and superficial temporal arteries.
The stems of most of the six branches of the external carotid artery are in the carotid triangle.
The Superior Thyroid Artery
This is the most inferior of the 3 anterior branches of the external carotid.
It arises close to the origin of the vessel, just inferior to the greater horn of the hyoid.
The superior thyroid artery runs anteroinferiorly, deep to the infrahyoid muscles and gives off the superior laryngeal artery. This artery pierces the thyrohyoid membrane in company with the internal laryngeal nerve and supplies the larynx.
The Lingual Artery
This arises from the external carotid artery as it lies on the middle constrictor muscle of the pharynx.
It arches superoanteriorly, about 5 mm superior to the tip of the greater horn of the hyoid bone, and then passes deep to the hypoglossal nerve, the stylohyoid muscle, and the posterior belly of digastric muscle.
It disappears deep to the hyoglossus muscle.
At the anterior border of this muscle, it turns superiorly and ends by becoming the deep lingual artery.
The Facial Artery
This arises from the carotid artery either, in common with the lingual artery, or immediately superior to it.
In the neck the facial artery gives off its important tonsillar branch and branches to the palate and submandibular gland.
The facial artery then passes superiorly under the cover of the digastric and stylohyoid muscles and the angle of the mandible.
It loops anteriorly and enters a deep groove in the submandibular gland.
The facial artery hooks around the inferior border of the mandible and enters the face. Here the pulsation of this artery can be felt (anterior to the masseter muscle).
The Ascending Pharyngeal Artery
This is the 1st or 2nd branch of the external carotid artery.
This small vessel ascends on the pharynx, deep to the internal carotid artery.
It sends branches to the pharynx, prevertebral muscles, middle ear and meninges.
The Occipital Artery
This arises from the posterior surface of the external carotid near the level of the facial artery.
It passes posteriorly along the inferior border of the posterior belly of digastric.
It ends in the posterior part of the scalp.
During its course, it is superficial to the internal carotid artery and three cranial nerves (CN IX, CN X and CN XI).
The Posterior Auricular Artery
This is a small posterior branch of the external carotid artery.
It arises from it at the superior border of the posterior belly of the digastric muscle.
It ascends posteriorly to the external acoustic meatus and supplies adjacent muscles, the parotid gland, the facial nerve, structures in the temporal bone, the auricle, and the scalp.
The Internal Jugular Vein
This is usually the largest vein in the neck.
The internal jugular vein drains blood from the brain and superficial parts of the face and neck.
Its course corresponds to a line drawn from a point immediately inferior to the external acoustic meatus to the medial end of the clavicle.
This large vein commences at the jugular foramen in the posterior cranial fossa, as the direct continuation of the sigmoid sinus.
The dilation at its origin is called the superior bulb of the internal jugular vein.
From here it runs inferiorly through the neck in the carotid sheath.
The internal jugular vein leaves the anterior triangle of the neck by passing deep to the SCM muscle.
Posterior to the sternal end of the clavicle, it unites with the subclavian vein to form the brachiocephalic vein.
Near its termination is the inferior bulb of the jugular vein contains a bicuspid valve similar to that of the subclavian vein.
The deep cervical lymph nodes lie along the course of the internal jugular vein, mostly lateral and posterior.
Tributaries of the Internal Jugular Vein
This large vein is joined at its origin by the: inferior petrosal sinus, the facial, lingual, pharyngeal, superior and middle thyroid veins, and often the occipital vein.
Periodontium
Dental Anatomy
The periodontium, which is the supporting structure of a tooth, consists of the cementum, periodontal ligaments, gingiva, and alveolar bone. Cementum is the only one of these that is a part of a tooth. Alveolar bone surrounds the roots of teeth to provide support and creates what is commonly called a "socket". Periodontal ligaments connect the alveolar bone to the cementum, and the gingiva is the surrounding tissue visible in the mouth.
Periodontal ligaments
Histology of the Periodontal Ligament (PDL)
Embryogenesis of the periodontal ligament
The PDL forms from the dental follicle shortly after root development begins
The periodontal ligament is characterized by connective tissue. The thinnest portion is at the middle third of the root. Its width decreases with age. It is a tissue with a high turnover rate.
OCCLUSION AND DENTAL DEVELOPMENT-Stages-Deciduous dentition period
Dental Anatomy
Deciduous dentition period.
-The deciduous teeth start to erupt at the age of six months and the deciduous dentition is complete by the age of approximately two and one half years of age.
-The jaws continue to increase in size at all points until about age one year.
-After this, growth of the arches is lengthening of the arches at their posterior (distal) ends. Also, there is slightly more forward growth of the mandible than the maxilla.
1. Many early developmental events take place.
-The tooth buds anticipate the ultimate occlusal pattern.
-Mandibular teeth tend to erupt first. The pattern for the deciduous incisors is usually in this distinctive order:
(1) mandibular central
(2) maxillary central incisors
(3) then all four lateral incisors.
-By one year, the deciduous molars begin to erupt.
-The eruption pattern for the deciduous dentition as a whole is:
(1) central incisor
(2) lateral incisor
(3) deciduous first molar
(4) then the canine
(5) then finally the second molar.
-Eruption times can be variable.
2. Occlusal changes in the deciduous dentition.
-The overjet tends to diminish with age. Wear and mandibular growth are a factor in this process.
-The overbite often diminishes with the teeth being worn to a flat plane occlusion.
-Spacing of the incisors in anticipation of the soon-to-erupt permanent incisors appears late. Permanent anterior teeth (incisors and canines) are wider mesiodistally than deciduous anterior teeth. In contrast, the deciduous molar are wider mesiodistally that the premolars that later replace them.
-Primate spaces occur in about 50% of children. They appear in the deciduous dentition. The spaces appear between the upper lateral incisor and the upper canine. They also appear between the lower canine and the deciduous first molar.
Actinic keratosis
General Pathology
Actinic keratosis
1. Dry, scaly plaques with an erythematous base.
2. Similar to actinic cheilosis, which occurs along the vermilion border of the lower lip.
3. Caused by sun damage to the skin.
4. Dysplastic lesion, may be premalignant.
IMMUNITY AND RESISTANCE TO INFECTION
General Pathology
IMMUNITY AND RESISTANCE TO INFECTION
Body's resistance to infection depends upon:
I. Defence mechanisms at surfaces and portals of entry.
II. Nonspecific or innate immunity
Ill. Specific immune response.
I. Surface Defence Mechanisms
1. Skin:
(i) Mechanical barrier of keratin and desquamation.
(ii) Resident commensal organisms
(iii)Acidity of sweat.
(iv) Unsaturated fatty acids of sebum
2. Oropharyngeal
(i)Resident flora
(ii) Saliva, rich in lysozyme, mucin and Immunoglobulins (lgA).
3. Gastrointestinal tract.-
(i) Gastric HCI
(ii) Commensal organisms in Intestine
(iii) Bile salts
(iv) IgA.
(v) Diarrhoeal expulsion of irritants.
4. Respiratory tract:
(i) Trapping in turbinates
(ii) Mucus trapping
(iii) Expulsion by coughing and sneezing.
(iv) Ciliary propulsion.
(V) Lysozymes and antibodies in secretion.
(vi) Phagocytosis by alveolar macrophages.
5. Urinary tract:
(i) Flushing action.
(ii) Acidity
(iii) Phagocytosis by urothelial cells.
6. Vagina.-
(i) Desquamation.
(ii) Acid barrier.
(iii) Doderlein's bacilli (Lactobacilli)
7. Conjunctiva:
Lysozymes and IgA in tears
II. Nonspecific or Innate Immunity
1. Genetic factors
Species: Guinea pig is very susceptible to tuberculosis.
Race: Negroes are more susceptible to tuberculosis than whites
Sickle cells (HbS-a genetic determined Haemoglobinopathy resistant to Malarial parasite.
2. Age Extremes of age are more susceptible.
3. Hormonal status. Low resistance in:
Diabetes Mellitus.
Increased corticosteroid levels.
Hypothyroidism
4. Phagocytosis. Infections can Occur in :
Qualitative or quantitative defects in neutrophils and monocytes.
Diseases of mononuclear phagocytic system (Reticuloendothelial cells-RES).
Overload blockade of RES.
5. Humoral factors
Lysozyme.
Opsonins.
Complement
Interferon (antiviral agent secreted by cells infected by virus)
III. The Specific Immune Response
Definition
The immune response comprises all the phenomenon resulting from specific interaction
of cells of the immune-system with antigen. As a consequence of this interaction cells
, appear that mediate cellular immune response as well cells that synthesis and secrete
immunoglobulins
Hence the immune response has 2 components.
1. Cell mediated immunity (CMI).
2:. Humoral immunity (antibodies)
(I) Macrophages. Constituent of the M. P. S. These engulf the antigenic material.
(i) Most of the engulfed antigen is destroyed to' prevent a high dose paralysis of the Immune competent cells.
(ii) Some of it persists in the macrophage, retaining immunogenecity for continued stimulus to the immune system.
(iii)The antigenic information is passed on to effectors cells. There are two proposed mechanisms for this:
(a) As messenger RNA with code for the specific antibody.
(b) As antigen-RNA complexes.
(2) Lymphocytes. There are 2 main classes recognized by surface characteristics.
(A) T-Lymyhocytes (thymus dependant) :- These are responsible for cellular immunity . On exposure to antigen
They transform to immunoblasts which divide to form the effectors cells.
They secrete lymphokines These are
Monocyte migration inhibition factor
Macrophage activation factor
Chemotactic factor
Mitogenic factor
Transfer factor
Lymphotoxin which kills target cell
Interferon.
Inflammatory factor which increases permeability. .
Some remain as 1onglived memory cell for a quicker recognition on re-exposure
They also modify immune response by other lymphocytes in the form of “T – helper cells “ and “T-suppressor” cells
They are responsible for graft rejection
(B) B-Lymphocytes (Bursa dependent). In birds the Bursa of Fabricious controls these cells. In man, its role is taken up by," gut associated lymphoid tissue)
(i) They are responsible for antibody synthesis. On stimulation they undergo blastic transformation and then differentiation to plasma cells, the site of immunoglobulin synthesis.
(ii) They also form memory cells. But these are probably short lived.
(C) In addition to T & B lymphocytes, there are some lymphocytes without the surface markers of either of them. These are 'null' cells-the-natural Killer (N,K.) cells and cells responsible for antibody dependent cellular-cytotoxicity.
(3) Plasma cells. These are the effectors cells of humoral immunity. They produce the immunoglobins, which are the effector molecules.
Blood Pressure
Physiology
Blood Pressure
Blood moves through the arteries, arterioles, and capillaries because of the force created by the contraction of the ventricles.
Blood pressure in the arteries.
The surge of blood that occurs at each contraction is transmitted through the elastic walls of the entire arterial system where it can be detected as the pulse. Even during the brief interval when the heart is relaxed — called diastole — there is still pressure in the arteries. When the heart contracts — called systole — the pressure increases.
Blood pressure is expressed as two numbers, e.g., 120/80.
Blood pressure in the capillaries
The pressure of arterial blood is largely dissipated when the blood enters the capillaries. Capillaries are tiny vessels with a diameter just about that of a red blood cell (7.5 µm). Although the diameter of a single capillary is quite small, the number of capillaries supplied by a single arteriole is so great that the total cross-sectional area available for the flow of blood is increased. Therefore, the pressure of the blood as it enters the capillaries decreases.
Blood pressure in the veins
When blood leaves the capillaries and enters the venules and veins, little pressure remains to force it along. Blood in the veins below the heart is helped back up to the heart by the muscle pump. This is simply the squeezing effect of contracting muscles on the veins running through them. One-way flow to the heart is achieved by valves within the veins
Exchanges Between Blood and Cells
With rare exceptions, our blood does not come into direct contact with the cells it nourishes. As blood enters the capillaries surrounding a tissue space, a large fraction of it is filtered into the tissue space. It is this interstitial or extracellular fluid (ECF) that brings to cells all of their requirements and takes away their products. The number and distribution of capillaries is such that probably no cell is ever farther away than 50 µm from a capillary.
When blood enters the arteriole end of a capillary, it is still under pressure produced by the contraction of the ventricle. As a result of this pressure, a substantial amount of water and some plasma proteins filter through the walls of the capillaries into the tissue space.
Thus fluid, called interstitial fluid, is simply blood plasma minus most of the proteins. (It has the same composition and is formed in the same way as the nephric filtrate in kidneys.)
Interstitial fluid bathes the cells in the tissue space and substances in it can enter the cells by diffusion or active transport. Substances, like carbon dioxide, can diffuse out of cells and into the interstitial fluid.
Near the venous end of a capillary, the blood pressure is greatly reduced .Here another force comes into play. Although the composition of interstitial fluid is similar to that of blood plasma, it contains a smaller concentration of proteins than plasma and thus a somewhat greater concentration of water. This difference sets up an osmotic pressure. Although the osmotic pressure is small, it is greater than the blood pressure at the venous end of the capillary. Consequently, the fluid reenters the capillary here.
Control of the Capillary Beds
An adult human has been estimated to have some 60,000 miles of capillaries with a total surface area of some 800–1000 m2. The total volume of this system is roughly 5 liters, the same as the total volume of blood. However, if the heart and major vessels are to be kept filled, all the capillaries cannot be filled at once. So a continual redirection of blood from organ to organ takes place in response to the changing needs of the body. During vigorous exercise, for example, capillary beds in the skeletal muscles open at the expense of those in the viscera. The reverse occurs after a heavy meal.
The walls of arterioles are encased in smooth muscle. Constriction of arterioles decreases blood flow into the capillary beds they supply while dilation has the opposite effect. In time of danger or other stress, for example, the arterioles supplying the skeletal muscles will be dilated while the bore of those supplying the digestive organs will decrease. These actions are carried out by
the autonomic nervous system.
local controls in the capillary beds
Alveolar bone (process)
Dental Anatomy
Alveolar bone (process)
1. The bone in the jaws that contains the teeth alveoli (sockets).
2. Three types of bone :
a. Cribriform plate (alveolar bone proper)
(1) Directly lines and forms the tooth socket. It is compact bone that contains many holes, allowing for the passage of blood vessels. It has no periosteum.
(2) Serves as the attachment site for PDL (Sharpey’s) fibers.
(3) The tooth socket is constantly being remodeled in response to occlusal forces. The bone laid down on the cribriform plate, which also provides attachment for PDL fibers, is known as bundle bone.
(4) It is radiographically known as the lamina dura.
b. Cortical (compact) bone
(1) Lines the buccal and lingual surfaces of the mandible and maxilla.
(2) Is typical compact bone with a periosteum and contains Haversian systems.
(3) Is generally thinner in the maxilla and thicker in the mandible, especially around the buccal area of the mandibular premolar and molar.
c. Trabecular (cancellous, spongy) bone
(1) Is typical cancellous bone containing Haversian systems.
(2) Is absent in the maxillary anterior teeth region.
3. Alveolar crest (septa)
a. The height of the alveolar crest is usually 1.5 to 2 mm below the CEJ junction.
b. The width is determined by the shape of adjacent teeth.
(1) Narrow crests—found between teeth with relatively flat surfaces.
(2) Widened crests—found between teeth with convex surfaces or teeth spaced apart.