NEET MDS Synopsis
SPECIAL SOMATIC AFFERENT (SSA) PATHWAYS
Physiology
SPECIAL SOMATIC AFFERENT (SSA) PATHWAYS
Hearing
The organ of Corti with its sound-sensitive hair cells and basilar membrane are important parts of the sound transducing system for hearing. Mechanical vibrations of the basilar membrane generate membrane potentials in the hair cells which produce impulse patterns in the cochlear portion of the vestibulocochlear nerve (VIII)
Special somatic nerve fibers of cranial nerve VIII relay impulses from the sound receptors (hair cells) in the cochlear nuclei of the brainstem
These are bipolar neurons with cell bodies located in the spiral ganglia of the cochlea.
Vestibular System
The vestibulocochlear nerve serves two quite different functions.
The cochlear portion, conducts sound information to the brain,
The vestibular portion conducts proprioceptive information.
It is the central neural pathways
Special somatic afferent fibers from the hair cells of the macula utriculi and macula sacculi conduct information into the vestibular nuclei on the ipsilateral side of the pons and medulla.
These are bipolar neurons with cell bodies located in the vestibular ganglion.
Some of the fibers project directly into the ipsilateral cerebellum to terminate in the uvula, flocculus, and nodulus, but most enter the vestibular nuclei and synapse there.
Vision
The visual system receptors are the rods and cones of the retina.
Special somatic afferent fibers of the optic nerve (II) conduct visual signals into the brain
Fibers from the lateral (temporal) retina of either eye terminate in the lateral geniculate body on the same side of the brain as that eye.
SSA II fibers from the medial (nasal) retina of each eye cross over in the optic chiasm to terminate in the contralateral lateral geniculate body.
Area 17 is the primary visual area, which receives initial visual signals.
Neurons from this area project into the adjacent occipital cortex (areas 18 and 19) which is known as the secondary visual area. It is here that the visual signal is fully evaluated.
The visual reflex pathway involving the pupillary light reflex - in which the pupils constrict when a light is shined into the eyes and dilate when the light is removed.
Some SSA II fibers leave the optic tract before reaching the lateral geniculates, terminating in the superior colliculi instead.
From here, short neurons project to the EdingerWestphal nucleus (an accessory nucleus of III) in the midbrain, which serves as the origin of the preganglionic parasympathetic fibers of the oculomotor nerve (GVE III).
The GVE III fibers in turn project to the ciliary ganglia, from which arise the postganglionic fibers to the sphincter muscles of the iris, which constrict the pupils.
TEMPOROMANDIBULAR JOINT
Dental Anatomy
TEMPOROMANDIBULAR JOINT
There are three kind of joints:
· Fibrous
Two bones connected with fibrous tissue
Examples
suture (little or no movement)
gomphosis (tooth - PDL - bone)
syndesmosis (fibula & tibia, radius and ulna; interosseous ligament)
· Cartilagenous
Two subtypes:
2a) primary: bone<--->cartilage (costochondral joint)
2b) secondary: bone<-->cartilage<-->FT<-->cartilage<--> bone (pubic symphysis)
· Synovial
Two bones; each articular surface covered with hyaline cartilage in most cases
The bones are united with a capsule (joint cavity)
In the capsule there is presence of synovial fluid
The capsule is lined by a synovial membrane
In many synovial joints there maybe an articular disk
Synovial joints are characterized by the presence of ligaments
Synovial joints are classified according to the number of axes of bone movement: uniaxial, biaxial, multiaxial
the shapes of articulating surfaces: planar, ginglymoid (=hinged), pivot, condyloid
The movement of the joints is controlled by muscles
The temporomandibular joint is a synovial, sliding-ginglymoid joint (humans)
Embryology of the TMJ
Primary TMJ: Meckel's cartilage --> malleus & incal cartilage. It lasts for 4 months.
Secondary TMJ: Starts developing around the third month of gestation
Two blastemas (temporal and condylar); condylar grows toward the temporal (temporal appears and ossifies first)
Formation of two cavities: inferior and upper
Appearance of disk
Bones: glenoid fossa (temporal bone) and condyle (mandible)
Rheumatic Fever - Major and Minor Criteria
Medicine
Rheumatic fever occurs after a streptococcal infection (usually caused by Group A Beta-Hemolytic Strep (GABHS)).
It is an inflammatory condition that affects the joints, skin, heart and brain.
Major criteria are referred to as Jones criteria
J – Joint involvement which is usually migratory and inflammatory joint involvement that starts in the lower joints and ascends to upper joints
O – (“O” Looks like heart shape) – indicating that patients can develop myocarditis or inflammation of the heart
N – Nodules that are subcutaneous
E – Erythema marginatum which is a rash of ring-like lesions that can start in the trunk or arms. When joined with other rings, it can create a snake-like appearance
S – Sydenham chorea is a late feature which is characterized by jerky, uncontrollable, and purposeless movements resembling twitches
Minor criteria include
C – CRP Increased
A – Arthralgia
F – Fever
E – Elevated ESR
P – Prolonged PR Interval
A – Anamesis
L – Leukocytosis
Diagnosis of rheumatic fever is made after a strep infection (indicated by either throat cultures growing GABHS OR elevated anti-streptolysin O titers in the blood) and:
Two major criteria OR
One major criterion and two minor criteria
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
Anemia (Disorder of Hematopoietic System)
General Pathology
Anemia (Disorder of Hematopoietic System) - Probably the most common effect of nutritional deficiency. Any factor that decreases hematopoiesis can cause an anemia.
A. Iron deficiency - Widely recognized as the most important cause of anemia, It is indicated that ½ of all pregnant women and infants are affected, as are ~13% of all adult women.
1. Dietary factors - Availability of iron from different food sources and mixtures.
2. Malabsorption – One third of patients with inflammatory bowel disease (IBD) have recurrent anemia and 30% or more of patients who have had partial gastrectomy will develop iron deficiency anemia.
3. Blood loss - Menses, gastrointestinal bleeding
4. Increased demand - Pregnancy, growth in children.
5. Congenital - Atransferrinemia
6. Importance of multiple factors.
7. Pathophysiology - Initially iron is mobilized from reticuloendothelial stores and increased intestinal absorption occurs. Total iron stores are depleted, serum iron levels fall. In severe cases in peripheral blood, the red cells become smaller (microcytic) and their hemoglobin content is reduced (hypochromic).
B. Megaloblastic anemias- Characterized by the presence of abnormal WBCs and RBCs. In severe cases, megaloblasts (abnormal red cell precursors) may be present. These anemias are a consequence of disordered DNA synthesis.
1. Folate deficiency - Can be caused by:
a. Dietary deficiency
b. Malabsorption (celiac disease)
c. Increased demand (pregnancy & lactation)
d. Drugs - methotrexate, anticonvulsants, oral contraceptives, alcoholism.
e. Liver disease
2. Cobalamin (vitamin B12) deficiency - Almost always a secondary disorder that can be caused by:
a. Intrinsic factor deficiency (pernicious anemia due to autoimmune destruction of the gastric mucosa)
b. Malabsorption
3. Pyridoxine (vitamin B6) deficiency- most commonly associated with alcoholism.
C. Other factors known to be frequently associated with anemia would include protein-calorie malnutrition, vitamin C deficiency, and pyridoxine deficiency (usually associated with alcoholism).
D. Other anemias not particularly associated with nutritional disease would include hemolytic anemia
(decreased red cell life span) and aplastic anemia (failure of marrow to produce new cells).
Formation and Eruption of Deciduous Teeth.
Dental Anatomy
Formation and Eruption of Deciduous Teeth.
-Calcification begins during the fourth month of fetal life. By the end of the sixth month, all of the deciduous teeth have begun calcification.
-By the time the deciduous teeth have fully erupted (two to two and one half years of age), cacification of the crowns of permanent teeth is under way. First permanent molars have begun cacification at the time of birth. -Here are some things to know about eruption patterns:
(1) Teeth tend to erupt in pairs.
(2) Usually, lower deciduous teeth erupt first. Congenitally missing deciduous teeth is infrequent. Usually, the lower deciduous central incisors are thefirst to erupt thus initiating the deciduous dentition. The appearance of the deciduous second molars completes the deciduous dentition by 2 to 2 1/2 years of age.
- Deciduous teeth shed earlier and permanent teeth erupt earlier in girls.
- The orderly pattern of eruption and their orderly replacement by permanent teeth is important.
- order for eruption of the deciduous teeth is as follows:
(1) Central incisor.........Lower 6 ½ months, Upper 7 ½ months
(2) Lateral incisor.........Lower 7 months, Upper 8 months
(3) First deciduous molar...Lower 12-16 months, Upper 12-16 months
(4) Deciduous canine........Lower 16-20 months, Upper 16-20 months
(5) Second deciduous molar..Lower 20-30 months, Upper 20-30 months
CARDIAC GLYCOSIDES
Pharmacology
CARDIAC GLYCOSIDES
Cardiac glycosides (Digitalis)
Digoxin
Digitoxin
Sympathomimetics
Dobutamine
Dopamine
Vasodilators
α-blockers (prazosin)
Nitroprusside
ACE-inhibitors (captopril)
Pharmacology of Cardiac Glycosides
1. Positive inotropic effect (as a result of increase C.O., the symptoms of CHF subside).
2. Effects on other cardiac parameters
1) Excitability
2) Conduction Velocity; slightly increased in atria & ventricle/significantly
reduced in conducting tissue esp. A-V node and His-Purkinje System
3) Refractory Period; slightly ^ in atria & nodal tissue/slightly v in ventricles
4) Automaticity; can be greatly augmented - of particular concern in ventricle
3. Heart Rate
-Decrease due to 1) vagal stimulation and 2) in the situation of CHF, due to improved hemodynamics
4 Blood Pressure
-In CHF, not of much consequence. Changes are generally secondary to improved cardiac performance.
-In the absence of CHF, some evidence for a direct increase in PVR due to vasoconstriction.
5. Diuresis
-Due primarily to increase in renal blood flow as a consequence of positive inotropic effect (increase CO etc.) Possibly some slight direct diuretic effect.
Mechanism of Action of Cardiac Glycosides
Associated with an interaction with membrane-bound Na+-K+ ATPase (Na-K pump).
Clinical ramifications of an interaction of cardiac glycosides with the Na+ K pump.
I. Increase levels of Ca++, Increase therapeutic and toxic effects of cardiac glycosides
II. Decrease levels of K+ , Increase toxic effects of cardiac glycosides
Therapeutic Uses of Cardiac Glycosides
CHF
CHF accompanied by atrial fibrillation
Supraventricular arrhythmias
Lymphocytosis
General Pathology
Lymphocytosis:
Causes
-Infections in children and the neutropenic infections in adults.
-Lymphocytic leukaemia.
-Infectious mononucleosis.
-Toxdplasmosis.
-Myast'henia gravis.