NEET MDS Synopsis
White Blood Cells (leukocytes)
PhysiologyWhite Blood Cells (leukocytes)
White blood cells
are much less numerous than red (the ratio between the two is around 1:700),
have nuclei,
participate in protecting the body from infection,
consist of lymphocytes and monocytes with relatively clear cytoplasm, and three types of granulocytes, whose cytoplasm is filled with granules.
Lymphocytes: There are several kinds of lymphocytes, each with different functions to perform , 25% of wbc The most common types of lymphocytes are
B lymphocytes ("B cells"). These are responsible for making antibodies.
T lymphocytes ("T cells"). There are several subsets of these:
inflammatory T cells that recruit macrophages and neutrophils to the site of infection or other tissue damage
cytotoxic T lymphocytes (CTLs) that kill virus-infected and, perhaps, tumor cells
helper T cells that enhance the production of antibodies by B cells
Although bone marrow is the ultimate source of lymphocytes, the lymphocytes that will become T cells migrate from the bone marrow to the thymus where they mature. Both B cells and T cells also take up residence in lymph nodes, the spleen and other tissues where they
encounter antigens;
continue to divide by mitosis;
mature into fully functional cells.
Monocytes : also originate in marrow, spend up to 20 days in the circulation, then travel to the tissues where they become macrophages. Macrophages are the most important phagocyte outside the circulation. Monocytes are about 9% of normal wbc count
Macrophages are large, phagocytic cells that engulf
foreign material (antigens) that enter the body
dead and dying cells of the body.
Neutrophils
The most abundant of the WBCs. about 65% of normal white count These cells spend 8 to 10 days in the circulation making their way to sites of infection etc Neutrophils squeeze through the capillary walls and into infected tissue where they kill the invaders (e.g., bacteria) and then engulf the remnants by phagocytosis. They have two types of granules: the most numerous are specific granules which contain bactericidal agents such as lysozyme; the azurophilic granules are lysosomes containing peroxidase and other enzymes
Eosinophils : The number of eosinophils in the blood is normally quite low (0–450/µl). However, their numbers increase sharply in certain diseases, especially infections by parasitic worms. Eosinophils are cytotoxic, releasing the contents of their granules on the invader.
Basophils : rare except during infections where these cells mediate inflammation by secreting histamine and heparan sulfate (related to the anticoagulant heparin). Histamine makes blood vessels permeable and heparin inhibits blood clotting. Basophils are functionally related to mast cells. . The mediators released by basophils also play an important part in some allergic responses such as hay fever and an anaphylactic response to insect stings.
Thrombocytes (platelets):
Thrombocytes are cellular derivatives from megakaryocytes which contain factors responsible for the intrinsic clotting mechanism. They represent fragmented cells which contain residual organelles including rough endoplasmic reticulum and Golgi apparati. They are only 2-microns in diameter, are seen in peripheral blood either singly or, often, in clusters, and have a lifespan of 10 days.
Sympatholytics And Alpha Adrenergic Blockers
Pharmacology
Sympatholytics And Alpha Adrenergic Blockers
Types
1. Alpha 1-receptor blockers: prazocin,doxazocin.
2. Centrally acting alpha 2- agonists: methyldopa, clonidine.
3. Peripherally acting adrenergic antagonists: reserpine.
4. Imidazoline receptor agonists: rilmenidine, moxonidine.
Advantages
- Alpha1- receptor blockers and imidazoline receptor agonists improve lipid profile and insulin sensitivity.
- Methyldopa: increases renal blood flow. Drug of choice during pregnancy.
- Reserpine: neutral metabolic effects and cheap.
Indications:
- Diabetes mellitus: alpha1- receptor blockers, imidazoline receptor agonists.
- Dyslipidemia: alpha 1- receptor blockers, imidazoline receptor agonists.
- Prostatic hypertrophy: alpha 1- receptor blockers.
- When there is a need for rapid reduction in blood pressure: clonidine.
Side Effects
- Prazocin: postural hypotension, diarrhea, occasional tachycardia, and tolerance (due to fluid retention).
- Methyldopa: sedation, hepatotoxicity, hemolytic anemia, and tolerance.
- Reserpine: depression, lethargy, weight loss, peptic ulcer, diarrhea, and impotence
- Clonidine: dry mouth, sedation, bradycardia, impotence, and rebound hypertension if stopped suddenly.
Considerations
- Prazocin, methyldopa, and reserpine should be combined with a diuretic because of fluid retention.
Direct Arterial Vasodilators
Types: hydralazine, diazoxide, nitroprusside, and minoxidil
Types and Source of Haemorrhage
Surgery
Types of Haemorrhage
Hemorrhaging is broken down into four classes
Class I Hemorrhage involves up to 15% of blood volume.
There is typically no change in vital signs and fluid resuscitation is not usually necessary.
Class II Hemorrhage involves 15-30% of total blood volume.
A patient is often tachycardic (rapid heart beat) with a reduction in the difference between the systolic and diastolic blood pressures.
The body attempts to compensate with peripheral vasoconstriction. Skin may start to look pale and be cool to the touch.
The patient may exhibit slight changes in behavior.
Volume resuscitation with crystalloids (Saline solution or Lactated Ringer's solution) is all that is typically required. Blood transfusion is not usually required.
Class III Hemorrhage involves loss of 30-40% of circulating blood volume.
The patient's blood pressure drops, the heart rate increases, peripheral hypoperfusion (shock) with diminished capillary refill occurs, and the mental status worsens.
Fluid resuscitation with crystalloid and blood transfusion are usually necessary.
Class IV Hemorrhage involves loss of >40% of circulating blood volume.
The limit of the body's compensation is reached and aggressive resuscitation is required to prevent death.
Source of Haemorrhage
- Extra dural haemorrhage - middle meningeal artery
- Sub dural haemorrhage - bridging or diploic veins
- Sub arachnoid haemorrhage - rupture on berry aneursym
- Tennis bal injury to eye - circulis iridis major
- Epistaxis - Sphenopalantine artery
- During tonsillectomy - para tonsilaar veins, tonsilar and ascending palantine artery
- Tracheostomy - isthemus and inferior thyroid vein
- Heamoptysis-bronchial artery
- Gastric ulcer- left gastric, splenic artery
- Duodenal ulcer - gastroduodenal artery
- Hemmorrhoids - submucous rectal venous plexus formed by superior rectal vein & inferior rectal vein
- Retropubic proastatectomy - dorsal venous plexus
- Hysterectomy - internal illac artery
- Menstruation - spiral arteries
Nephritic syndrome
General Pathology
Nephritic syndrome
Characterized by inflammatory rupture of the glomerular capillaries, leaking blood into the urinary space.
Classic presentation: poststreptococcal glomerulonephritis. It occurs after a group A, β–hemolytic Streptococcus infection (e.g., strep throat.)
Caused by autoantibodies forming immune complexes in the glomerulus.
Clinical manifestations:
oliguria, hematuria, hypertension, edema, and azotemia (increased concentrations of serum urea nitrogen
and creatine).
Casting Alloys
Dental Materials
Casting Alloys
Applications-inlay, onlay, crowns, and bridges
Terms
a. Precious-based on valuable elements
b. Noble or immune-corrosion-resistant element or alloy
c. Base or active-corrosion-prone alloy
d. Passive -corrosion resistant because of surface oxide film
e. Karat (24 karat is 100% gold; 18 karat is 75% gold)
f. Fineness (1000 fineness is I00% gold; 500 fineness is 50% gold)
Classification
High-gold alloys are > 75% gold or other noble metals
Type 1- 83% noble metals (e.g., in simple inlays)
Type II-≥78% noble metals (e.g.,in inlays and onlays)
Type IlI-≥75% noble metals (e.g., in crowns and bridges)
Type IV-≥75% noble metals (e.g., in partial dentures)
Medium-gold alloys are 25% to 75% gold or other noble metals
Low-gold alloys are <25% gold or other noble metals
Gold-substitute alloys arc alloys not containing gold
(1) Palladium-silver alloys-passive .because of mixed oxide film
(2) Cobalt-chromium alloys-passive because of Cr203 oxide film
(3) Iron-chromium alloys-passive because of Cr203 oxide film
Titanium alloys are based on 90% to 100% titanium ; passive because of TiO2 oxide film
Components of gold alloys
- Gold contributes to corrosion resistance
- Copper contributes to hardness and strength
- Silver counteracts orange color of copper
- Palladium increases melting point and hardness
- Platinum increases melting point
- Zinc acts as oxygen scavenger during casting
Manipulation
- Heated to just beyond melting temperature for casting
o Cooling shrinkage causes substantial contraction
Properties
Physical
- Electrical and thermal conductors
- Relatively low coefficient of thermal expansion
Chemical
- Silver content affects susceptibility to tarnish
- Corrosion resistance is attributable to nobility or passivation
Mechanical
- High tensile and compressive strengths but relatively weak in thin sections, such as margins, and can be deformed relatively easily
- Good wear resistance except in contact with Porcelain
GENERAL SOMATIC AFFERENT (GSA) PATHWAYS FROM THE FACE
Physiology
Pain, Temperature, and Crude Touch and Pressure
General somatic nociceptors, thermoreceptors, and mechanoreceptors sensitive to crude touch and pressure from the face conduct signals to the brainstem over GSA fibers of cranial nerves V, VII, IX, and X.
The afferent fibers involved are processes of monopolar neurons with cell bodies in the semilunar, geniculate, petrosal, and nodose ganglia, respectively.
The central processes of these neurons enter the spinal tract of V, where they descend through the brainstem for a short distance before terminating in the spinal nucleus of V.
Second-order neurons then cross over the opposite side of the brainstem at various levels to enter the ventral trigeminothalamic tract, where they ascend to the VPM of the thalamus.
Finally, third-order neurons project to the "face" area of the cerebral cortex in areas 3, 1, and 2 .
Discriminating Touch and Pressure
Signals are conducted from general somatic mechanoreceptors over GSA fibers of the trigeminal nerve into the principal sensory nucleus of V, located in the middle pons.
Second-order neurons then conduct the signals to the opposite side of the brainstem, where they ascend in the medial lemniscus to the VPM of the thalamus.
Thalamic neurons then project to the "face" region of areas 3, I, and 2 of the cerebral cortex.
Kinesthesia and Subconscious Proprioception
Proprioceptive input from the face is primarily conducted over GSA fibers of the trigeminal nerve.
The peripheral endings of these neurons are the general somatic mechanoreceptors sensitive to both conscious (kinesthetic) and subconscious proprioceptive input.
Their central processes extend from the mesencephalic nucleus to the principal sensory nucleus of V in the pons
The subconscious component is conducted to the cerebellum, while the conscious component travels to the cerebral cortex.
Certain second-order neurons from the principal sensory nucleus relay proprioceptive information concerning subconscious evaluation and integration into the ipsilateral cerebellum.
Other second-order neurons project to the opposite side of the pons and ascend to the VPM of the thalamus as the dorsal trigeminothalamic tract.
Thalamic projections terminate in the face area of the cerebral cortex.
COMPOSITE RESINS - Properties
Dental Materials
Properties-improve with filler content
Physical
Radiopacity depends on ions in silicate glass or the addition of barium sulfate (many systems radiolucent)
Coefficient of thermal expansion is 35 to 45 ppm/C and decreases with increasing filler content
Thermal and electrical insulators
Chemical
Water absorption is 0.5 % to 2.5% and increases with polymer level)
Acidulated topical fluorides (e.g., APF) tend to dissolve glass particles, and thus composites should be protected with petroleum jelly (Vaseline) during those procedures
Color changes occur in resin matrix with time because of oxidation, which produces colored by-products
Mechanical
Compressive strength is 45,000 to 60,000 lb/ in2, which is adequate
Wear resistance-improves with higher filler content, higher percentage of conversion in curing, and use of microfiller, but it is not adequate for some posterior applications
Surfaces rough from wear retain plaque and stain more readily
Biologic
Components may be cytotoxic, but cured composite is biocompatible as restorative filling material
HYPERPLASIA
General Pathology
HYPERPLASIA
It is the increase in the size of an organ or tissue due to increase in the number of its constituent cells. This is seen in organs made up of labile and stable cells.
Causes
I. Increased demand:
- Bone marrow in hypoxia and haemolytic states.
- Thyroid gland in puberty
2. Persistant Trauma:
- Acanthosis of the epidermis in chronic inflammations and in warts.
- Hyperplasia of oral mucosa due tooth and denture trauma.
- Mucosa at the edges of a gastric ulcer.
3. Endocrine target organ:
- Pregnancy hyperplasia of breast.
- Prostatic hyperplasia.
4. Compensatory:
Hyperplasia of kidney when the other kidney has been removed.
5. Idiopathic:
Endocrine organs like thyroid, adrenals, pituitary etc. can undergo hyperplasia with no detectable stimulus. .