NEET MDS Synopsis
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
Autoimmune Diseases
General Pathology
Autoimmune Diseases
These are a group of disease where antibodies (or CMI) are produced against self antigens, causing disease process.
Normally one's immune competent cells do not react against one's own tissues.
This is due to self tolerance acquired during embryogenesis. Any antigen encountered at
that stage is recognized as self and the clone of cells capable of forming the corresponding antibody is suppressed.
Mechanism of autoimmunity
(1) Alteration of antigen
-Physicochemical denaturation by UV light, drugs etc. e.g. SLE.
- Native protein may turn antigenic when a foreign hapten combines with it, e.g. Haemolytic anemia with Alpha methyl dopa.
(2) Cross reaction: Antibody produced against foreign antigen may cross react with native protein because of partial similarity e.g. Rheumatic fever.
(3) Exposure of sequestered antigens: Antigens not normally exposed to immune competent cells are not accepted as self as tolerance has not been developed to them. e.g. thyroglobulin, lens protein, sperms.
(4) Breakdown of tolerance :
- Emergence of forbidden clones (due to neoplasia of immune system as in lymphomas and lymphocytic leukaemia)
- Loss of suppressor T cells as in old age and CMI defects
Autoimmunity may be
- Organ specific.
- Non organ specific (multisystemic)
I. Organ specific.
(I) Hemolytic anaemia:
- Warm or cold antibodies (active at 37° C or at colder temperature)
- They may lyse the RBC by complement activation or coat them and make them vulnerable to phagocytosis
(ii) Hashimoto's thyroiditis:
- Antibodies to thyroglobulin and microsomal antigens.
- Cell mediated immunity.
- Leads to chronic. destructive thyroiditis.
(3) Pernicious anemia
Antibodies to gastric parietal cells and to intrinsic factor.
2. Non organ specific.
Lesions are seen in more than one system but principally affect blood vessels and connective tissue (collagen diseases).
(I) Systemic lupus erythematosus (SLE). Antibodies to varied antigens are seen. Hence it is possible that there is abnormal reactivity of the immune system in self recognition.
Antibodies have been demonstrated against:
- Nuclear material (antinuclear I antibodies) including DNA. nucleoprotein etc. Anti nuclear antibodies are demonstrated by LE cell test.
- Cytoplasmic organelles- mitochondria, rib osomes, Iysosomes.
- Blood constituents like RBC, WBC. platelets, coagulation factors.
Mechanism. Immune complexes of body proteins and auto antibodies deposit in various organs and cause damage as in type III hypersensitivity
Organs involved
- Skin- basal dissolution and collagen degeneration with fibrinoid vasculitis.
- Heart- pancarditis.
- Kidneys- glomerulonephritis of focal, diffuse or membranous type
- Joints- arthritis.
- Spleen- perisplenitis and vascular thickening (onion skin).
- Lymph nodes- focal necrosis and follicular hyperplasia.
- Vasculitis in other organs like liver, central or peripheral nervous system etc,
2. Polyarteritis nodosa. Remittant .disseminated necrotising vasculitis of small and medium sized arteries
Mechanism :- Not definitely known. Proposed immune reaction to exogenous or auto antigens
Lesion : Focal panarteritis- a segment of vessel is involved. There is fibrinoid necrosis with initially acute and later chronic inflammatory cells. This may result in haemorrhage and aneurysm.
Organs involved. No organ or tissue is exempt but commonly involved organs are :
- Kidneys.
- Heart.
- Spleen.
- GIT.
3. Rheumatoid arthritis. A disease primarily of females in young adult life.
Antibodies
- Rheumatoid factor (An IgM antibody to self IgG)
- Antinuclear antibodies in 20% patients.
Lesions
- Arthritis which may progress on to a crippling deformity.
- Arteritis in various organs- heart, GIT, muscles.
- Pleuritis and fibrosing alveolitis.
- Amyloidosis is an important complication.
4. Sjogren's Syndrome. This is constituted by
- Kerato conjunctivitis sicca
- Xerostomia
- Rheumatoid arthritis.
Antibodies
- Rheumatoid factor
- Antinuclear factors (70%).
- Other antibodies like antithyroid, complement fixing Ab etc
- Functional defects in lymphocytes. There is a higher incidence of lymphoma
5. Scleroderma (Progressive systemic sclerosis)
Inflammation and progressive sclerosis of connective tissue of skin and viscera.
Antibodies
- Antinuclear antibodies.
- Rheumatoid factor. .
- Defect is cell mediated.
lesions
- Skin- depigmentation, sclerotic atrophy followed by cakinosis-claw fingers and mask face.
- Joints-synovitis with fibrosis
- Muscles- myositis.
- GIT- diffuse fibrous replacement of muscularis resulting in hypomotility and malabsorption
- Kidneys changes as in SLE and necrotising vasculitis.
- Lungs – fibrosing alveolitis.
- Vasculitis in any organ or tissue.
6.Wegener’s granulomatosis. A complex of:
- Necrotising lesions in upper respiratory tract.
- Disseminated necrotising vasculitis.
- Focal or diffuse glomerulitis.
Mechanism. Not known. It is classed with autoimmune diseases because of the vasculitis resembling other immune based disorders.
Ampholytes, Polyampholytes, pI and Zwitterion
Biochemistry
Ampholytes, Polyampholytes, pI and Zwitterion
Many substances in nature contain both acidic and basic groups as well as many different types of these groups in the same molecule. (e.g. proteins). These are called ampholytes (one acidic and one basic group) or polyampholytes (many acidic and basic groups). Proteins contains many different amino acids some of which contain ionizable side groups, both acidic and basic. Therefore, a useful term for dealing with the titration of ampholytes and polyampholytes (e.g. proteins) is the isoelectric point, pI. This is described as the pH at which the effective net charge on a molecule is zero.
For the case of a simple ampholyte like the amino acid glycine the pI, when calculated from the Henderson-Hasselbalch equation, is shown to be the average of the pK for the a-COOH group and the pK for the a-NH2 group:
pI = [pKa-(COOH) + pKa-(NH3+)]/2
For more complex molecules such as polyampholytes the pI is the average of the pKa values that represent the boundaries of the zwitterionic form of the molecule. The pI value, like that of pK, is very informative as to the nature of different molecules. A molecule with a low pI would contain a predominance of acidic groups, whereas a high pI indicates predominance of basic groups.
INNATE (NON-SPECIFIC) IMMUNITY
General Microbiology
INNATE (NON-SPECIFIC) IMMUNITY
The elements of the innate (non-specific) immune system include anatomical barriers, secretory molecules and cellular components.
Among the mechanical anatomical barriers are the skin and internal epithelial layers, the movement of the intestines and the oscillation of broncho-pulmonary cilia.
Associated with these protective surfaces are chemical and biological agents.
A. Anatomical barriers to infections
1. Mechanical factors
The epithelial surfaces form a physical barrier that is very impermeable to most infectious agents. Thus, the skin acts as our first line of defense against invading organisms. The desquamation of skin epithelium also helps remove bacteria and other infectious agents that have adhered to the epithelial surfaces.
2. Chemical factors
Fatty acids in sweat inhibit the growth of bacteria. Lysozyme and phospholipase found in tears, saliva and nasal secretions can breakdown the cell wall of bacteria and destabilize bacterial membranes. The low pH of sweat and gastric secretions prevents growth of bacteria. Defensins (low molecular weight proteins) found in the lung and gastrointestinal tract have antimicrobial activity. Surfactants in the lung act as opsonins (substances that promote phagocytosis of particles by phagocytic cells).
3. Biological factors
The normal flora of the skin and in the gastrointestinal tract can prevent the colonization of pathogenic bacteria by secreting toxic substances or by competing with pathogenic bacteria for nutrients or attachment to cell surfaces.
B. Humoral barriers to infection
Humoral factors play an important role in inflammation, which is characterized by edema and the recruitment of phagocytic cells. These humoral factors are found in serum or they are formed at the site of infection.
1. Complement system – The complement system is the major humoral non-specific defense mechanism (see complement chapter). Once activated complement can lead to increased vascular permeability, recruitment of phagocytic cells, and lysis and opsonization of bacteria.
2. Coagulation system – Depending on the severity of the tissue injury, the coagulation system may or may not be activated. Some products of the coagulation system can contribute to the non-specific defenses because of their ability to increase vascular permeability and act as chemotactic agents for phagocytic cells. In addition, some of the products of the coagulation system are directly antimicrobial. For example, beta-lysin, a protein produced by platelets during coagulation can lyse many Gram positive bacteria by acting as a cationic detergent.
3. Lactoferrin and transferrin – By binding iron, an essential nutrient for bacteria, these proteins limit bacterial growth.
4. Interferons – Interferons are proteins that can limit virus replication in cells.
5. Lysozyme – Lysozyme breaks down the cell wall of bacteria.
6. Interleukin -1 – Il-1 induces fever and the production of acute phase proteins, some of which are antimicrobial because they can opsonize bacteria.
C. Cellular barriers to infection
Part of the inflammatory response is the recruitment of polymorphonuclear eosinophiles and macrophages to sites of infection. These cells are the main line of defense in the non-specific immune system.
1. Neutrophils – Polymorphonuclear cells are recruited to the site of infection where they phagocytose invading organisms and kill them intracellularly. In addition, PMNs contribute to collateral tissue damage that occurs during inflammation.
2. Macrophages – Tissue macrophages and newly recruited monocytes , which differentiate into macrophages, also function in phagocytosis and intracellular killing of microorganisms. In addition, macrophages are capable of extracellular killing of infected or altered self target cells. Furthermore, macrophages contribute to tissue repair and act as antigen-presenting cells, which are required for the induction of specific immune responses.
3. Natural killer (NK) and lymphokine activated killer (LAK) cells – NK and LAK cells can nonspecifically kill virus infected and tumor cells. These cells are not part of the inflammatory response but they are important in nonspecific immunity to viral infections and tumor surveillance.
4. Eosinophils – Eosinophils have proteins in granules that are effective in killing certain parasites.
Factors Affecting Heart Rate
Physiology
A heart rate that is persistently greater than 100bpm is termed tachycardia. A heart rate that is persistantly lower than 60 pulse per min is termed bradycardia. Let's examine some factors that could cause a change in heart rate:
Increased heart rate can be caused by:
Increased output of the cardioacceleratory center. In other words, greater activity of sympathetic nerves running to the heart and a greater release of norepinephrine on the heart.
Decreased output of the cardioinhibitory center. In other words, less vagus nerve activity and a decrease in the release of acetylcholine on the heart.
Increased release of the hormone epinephrine by the adrenal glands.
Nicotine.
Caffeine.
Hyperthyroidism - i.e., an overactive thyroid gland. This would lead to an increased amount of the hormone thyroxine in the blood.
Decreased heart rate can be caused by:
Decreased activity of the cardioacceleratory center.
Increased activity of the cardioinhibitory center.
Many others.
Wedging Techniques
Conservative DentistryWedging Techniques
Various wedging methods are employed to achieve optimal results,
especially in cases involving gingival recession or wide proximal boxes. Below
are descriptions of different wedging techniques, including "piggy back"
wedging, double wedging, and wedge wedging.
1. Piggy Back Wedging
A. Description
Technique: In piggy back wedging, a second smaller
wedge is placed on top of the first wedge.
Indication: This technique is particularly useful
in patients with gingival recession, where there is a risk of overhanging
restoration margins that could irritate the gingiva.
B. Purpose
Prevention of Gingival Overhang: The additional
wedge helps to ensure that the restoration does not extend beyond the tooth
surface into the gingival area, thereby preventing potential irritation and
maintaining periodontal health.
2. Double Wedging
A. Description
Technique: In double wedging, wedges are placed
from both the lingual and facial surfaces of the tooth.
Indication: This method is beneficial in cases
where the proximal box is wide, providing better adaptation of the matrix
band and ensuring a tighter seal.
B. Purpose
Enhanced Stability: By using wedges from both
sides, the matrix band is held securely in place, reducing the risk of
material leakage and improving the overall quality of the restoration.
3. Wedge Wedging
A. Description
Technique: In wedge wedging, a second wedge is
inserted between the first wedge and the matrix band, particularly in
specific anatomical situations.
Indication: This technique is commonly used in the
maxillary first premolar, where a mesial concavity may complicate the
placement of the matrix band.
B. Purpose
Improved Adaptation: The additional wedge helps to
fill the space created by the mesial concavity, ensuring that the matrix
band conforms closely to the tooth surface and providing a better seal for
the restorative material.
Clinical and biologic death
General Pathology
Clinical & biologic death
Clinical death
Clinical death is the reversible transmission between life and biologic death. Clinical death is defined as the period of respiratory, circulatory and brain arrest during which initiation of resuscitation can lead to recovery.
Signs indicating clinical death are
• The patient is without pulse or blood pressure and is completely unresponsive to the most painful stimulus.
• The pupils are widely dilated
• Some reflex reactions to external stimulation are preserved. For example, during intubations, respiration may be restored in response to stimulation of the receptors of the superior laryngeal nerve, the nucleus of which is located in the medulla oblongata near the respiratory center.
• Recovery can occur with resuscitation.
Biological Death
Biological death (sure sign of death), which sets in after clinical death, is an irreversible state
of cellular destruction. It manifests with irreversible cessation of circulatory and respiratory
functions, or irreversible cessation of all functions of the entire brain, including brain stem.
Tooth Deformation Under Load
Conservative DentistryTooth Deformation Under Load
Biomechanical Properties of Teeth
Deformation (Strain): Teeth are not rigid structures;
they undergo deformation (strain) during normal loading. This deformation is
a natural response to the forces applied during chewing and other functional
activities.
Intraoral Loads: The loads experienced by teeth can
vary widely, with reported forces ranging from 10 to 431 N (1 N = 0.225 lb
of force). A functional load of approximately 70 N is considered clinically
normal.
Factors Influencing Load Distribution
Number of Teeth: The total number of teeth in the arch
affects how forces are distributed. More teeth can share the load, reducing
the stress on individual teeth.
Type of Occlusion: The occlusal relationship (how the
upper and lower teeth come together) influences how forces are transmitted
through the dental arch.
Occlusal Habits: Habits such as bruxism (teeth
grinding) can significantly increase the forces applied to individual teeth,
leading to greater strain and potential damage.
Clinical Implications
Restorative Considerations: Understanding the
biomechanical behavior of teeth under load is essential for designing
restorations that can withstand functional forces without failure.
Patient Management: Awareness of occlusal habits, such
as bruxism, can guide clinicians in developing appropriate treatment plans,
including the use of occlusal splints or other interventions to protect
teeth from excessive forces.