NEET MDS Synopsis
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.
HAEMORRHAGIC DISORDERS
General Pathology
HAEMORRHAGIC DISORDERS
Normal homeostasis depends on
-Capillary integrity and tissue support.
- Platelets; number and function
(a) For integrity of capillary endothelium and platelet plug by adhesion and aggregation
(b) Vasoactive substances for vasoconstriction
(c) Platelet factor for coagulation.
(d) clot retraction.
- Fibrinolytic system(mainly Plasmin) : which keeps the coagulation system in check.
Coagulation disorders
These may be factors :
Deficiency .of factors
Genetic.
Vitamin K deficiency.
Liver disease.
Secondary to disseminated intravascular coagulation.or defibrinatian
Overactive fibrinolytic system.
Inhibitors of the factors (immune, acquired).
Anticoagulant therapy as in myocardial infarction.
Haemophilia. Genetic disease transmitted as X linked recessive trait. Common in Europe. Defect in fcatorVII Haemophilia A .or in fact .or IX-Haemaphilia B (rarer).
Features:
May manifest in infancy or later.
Severity depends on degree of deficiency.
Persistant wound bleeding.
Easy Bruising with Hematoma formation
Nose bleed , arthrosis, abdominal pain with fever and leukocytosis
Prognosis is good with prevention of trauma and-transfusion of Fresh blood or fTesh plasma except for danger of developing immune inhibitors.
Von Willebrand's disease. Capillary fragility and decreased factor VIII (due to deficient stimulatory factor). It is transmitted in an autosomal dominant manner both. Sexes affected equally
Vitamin K Deficiency. Vitamin K is needed for synthesis of factor II,VII,IX and X.
Deficiency maybe due to:
Obstructive jaundice.
Steatorrhoea.
Gut sterilisation by antibiotics.
Liver disease results in :
Deficient synthesis of factor I II, V, Vll, IX and X Incseased fibrinolysis (as liver is the site of detoxification of activators ).
Defibrination syndrome. occurs when factors are depleted due to disseminated .intravascular coagulation (DIC). It is initiated by endothelial damage or tissue factor entering the circulation.
Causes
Obstetric accidents, especially amniotic fluid embolism. Septicaemia. .
Hypersensitivity reactions.
Disseminated malignancy.
Snake bite.
Vascular defects : (Non thrombocytopenic purpura).
Acquired :
Simple purpura a seen in women. It is probably endocrinal
Senile parpura in old people due to reduced tissue support to vessels
Allergic or toxic damage to endothelium due to Infections like Typhoid Septicemia
Col!agen diseases.
Scurvy
Uraemia damage to endothelium (platelet defects).
Drugs like aspirin. tranquillisers, Streptomvcin pencillin etc.
Henoc schonlien purpura Widespeard vasculitis due to hypersensitivity to bacteria or foodstuff
It manifests as :
Pulrpurric rashes.
Arthralgia.
Abdominal pain.
Nephritis and haematuria.
Hereditary :
(a) Haemhoragic telangieclasia. Spider like tortous vessels which bleed easily. There are disseminated lesions in skin, mucosa and viscera.
(b) Hereditary capillary fragilily similar to the vascular component of von Willbrand’s disease
.(c) Ehler Danlos Syndrome which is a connective tissue defect with skin, vascular and joint manifestations.
Platelet defects
These may be :
(I) Qualitative thromboasthenia and thrombocytopathy.
(2) Thrombocytopenia :Reduction in number.
(a) Primary or idiopathic thrombocytopenic purpura.
(b) Secondary to :
(i) Drugs especially sedormid
(ii) Leukaemias
(iii) Aplastic-anaemia.
Idiopathic thrombocytopenic purpura (ITP). Commoner in young females.
Manifests as :
Acute self limiting type.
Chronic recurring type.
Features:
(i) Spontaneous bleeding and easy bruisability
(ii)Skin (petechiae), mucus membrane (epistaxis) lesions and sometimes visceral lesions involving any organ.
Thrombocytopenia with abnormal forms of platelets.
Marrow shows increased megakaryocytes with immature forms, vacuolation, and lack of platelet budding.
Pathogenesis:
hypersensitivity to infective agent in acute type.
Plasma thrombocytopenic factor ( Antibody in nature) in chronic type
Jaundice
General Pathology
Jaundice, or icterus
a. Characterized by yellowness of tissues, including skin, eyes, and mucous membranes.
b. Caused by excess conjugated and/or unconjugated serum bilirubin. (increased levels of bilirubin in the blood)
lcterus is visible when the serum bilirubin exceeds 2 mg/dl. In unconjugated hyperbilirubinemia, bilirubin is not excreted into the urine because of tight protein binding in serum. In conjugated hyperbilirubinemia, small amounts of bilirubin are excreted in the urine because
it is less tightly protein bound.
NOTE: Concentration of bilirubin in blood plasma does not normally exceed 1 mg/dL (>17µmol/L). A concentration higher than 1.8 mg/dL (>30µmol/L) leads to jaundice.
The conjunctiva of the eye are one of the first tissues to change color as bilirubin levels rise in jaundice. This is sometimes referred to as scleral icterus.
c. Types and causes include:
(1) Hepatocellular jaundice—caused by liver diseases such as cirrhosis and hepatitis.
(2) Hemolytic jaundice—caused by hemolytic anemias.
(3) Obstructive jaundice—caused by blockage of the common bile duct either by gallstones (cholelithiasis) or carcinomas involving the head of
the pancreas.
Differential diagnosis
Jaundice is classified into three categories, depending on which part of the physiological mechanism the pathology affects. The three categories are:
Pre-hepatic → The pathology is occurring prior to the liver.
Hepatic → The pathology is located within the liver.
Post-Hepatic → The pathology is located after the conjugation of bilirubin in the liver.
Pre-hepatic
Pre-hepatic jaundice is caused by anything which causes an increased rate of hemolysis (breakdown of red blood cells).
Certain genetic diseases, such as sickle cell anemia, spherocytosis, thalassemia and glucose 6-phosphate dehydrogenase deficiency can lead to increased red cell lysis and therefore hemolytic jaundice.
Commonly, diseases of the kidney, such as hemolytic uremic syndrome, can also lead to coloration. Defects in bilirubin metabolism also
present as jaundice, as in Gilbert's syndrome (a genetic disorder of bilirubin metabolism which can result in mild jaundice, which is found in about 5% of the population) and Crigler-Najjar syndrome.
In jaundice secondary to hemolysis, the increased production of bilirubin, leads to the increased production of urine-urobilinogen. Bilirubin is not usually found in the urine because unconjugated bilirubin is not water-soluble, so, the combination of increased urine-urobilinogen with no bilirubin (since, unconjugated) in urine is suggestive of hemolytic jaundice.
Laboratory findings include:
• Urine: no bilirubin present, urobilinogen > 2 units (i.e., hemolytic anemia causes increased heme metabolism; exception: infants where gut flora has not developed).
• Serum: increased unconjugated bilirubin.
• Kernicterus is associated with increased unconjugated bilirubin.
Hepatocellular
Hepatocellular (hepatic) jaundice can be caused by acute or chronic hepatitis, hepatotoxicity, cirrhosis, drug induced hepatitis and alcoholic liver disease. Cell necrosis reduces the liver's ability to metabolize and excrete bilirubin leading to a buildup of unconjugated bilirubin in the blood.
Laboratory findings depend on the cause of jaundice.
• Urine: Conjugated bilirubin present, urobilirubin > 2 units but variable (except in children). Kernicterus is a condition not associated with increased conjugated bilirubin.
• Plasma protein show characteristic changes.
• Plasma albumin level is low but plasma globulins are raised due to an increased formation of antibodies.
Bilirubin transport across the hepatocyte may be impaired at any point between the uptake of unconjugated bilirubin into the cell and transport of conjugated bilirubin into biliary canaliculi.
Post-hepatic
Post-hepatic jaundice, also called obstructive jaundice, is caused by an interruption to the drainage of bile in the biliary system. The most common causes are gallstones in the common bile duct, and pancreatic cancer in the head of the pancreas. Also, a group of parasites known as "liver flukes" can live in the common bile duct, causing obstructive jaundice. Other causes include strictures of the common bile duct, biliary atresia, cholangiocarcinoma, pancreatitis and pancreatic pseudocysts. A rare cause of obstructive jaundice is Mirizzi's syndrome.
Pathophysiology
When RBCs are damaged, their membranes become fragile and prone to rupture. As each RBC traverses through the reticuloendothelial system, its cell membrane ruptures when its membrane is fragile enough to allow this.
Hemoglobin, are released into the blood. The hemoglobin is phagocytosed by macrophages, and split into its heme and globin portions. The globin portion, a protein, is degraded into amino acids and plays no role in jaundice.
Two reactions then take place with the heme molecule.
The first oxidation reaction is catalyzed by the microsomal enzyme heme oxygenase and results in biliverdin (green color pigment), iron
and carbon monoxide.
The next step is the reduction of biliverdin to a yellow color tetrapyrol pigment called bilirubin by cytosolic enzyme biliverdin reductase.
This bilirubin is "unconjugated," "free" or "indirect" bilirubin. Approximately 4 mg of bilirubin per kg of blood is produced each day.[11] The majority of this bilirubin comes from the breakdown of heme from expired red blood cells in the process just described.
However approximately 20 percent comes from other heme sources, including ineffective erythropoiesis, and the breakdown of other heme-containing proteins, such as muscle myoglobin and cytochromes.
Hepatic events
The unconjugated bilirubin then travels to the liver through the bloodstream. Because bilirubin is not soluble, however, it is transported through the blood bound to serum albumin.
In Liver, it is conjugated with glucuronic acid (to form bilirubin diglucuronide, or just "conjugated bilirubin") to become more water soluble.
The reaction is catalyzed by the enzyme UDP-glucuronyl transferase.
This conjugated bilirubin is excreted from the liver into the biliary and cystic ducts as part of bile. Intestinal bacteria convert the bilirubin into urobilinogen.
Urobilinogen can take two pathways. It can either be further converted into stercobilinogen, which is then oxidized to stercobilin and passed out in the feces, or it can be reabsorbed by the intestinal cells, transported in the blood to the kidneys, and passed out in the urine as the oxidised product urobilin.
Stercobilin and urobilin are the products responsible for the coloration of feces and urine, respectively.
General structure of amino acids
Biochemistry
General structure of amino acids
All organisms use same 20 amino acids.
Variation in order of amino acids in polypeptides allow limitless variation.
All amino acids made up of a chiral carbon attached to 4 different groups
- hydrogen
- amino group
- carboxyl
- R group: varies between different amino acids
Two stereoisomers (mirror images of one another) can exist for each amino acid. Such stereoisomers are called enantiomers. All amino acids found in proteins are in the L configuration.
Amino acids are zwitterions at physiological pH 7.4. ( i.e. dipolar ions). Some side chains can also be ionized
Structures of the 20 common amino acids
Side chains of the 20 amino acids vary. Properties of side chains greatly influence overall conformation of protein. E.g. hydrophobic side chains in water-soluble proteins fold into interior of protein
Some side chains are nonpolar (hydrophobic), others are polar or ionizable at physiological pH (hydrophilic).
Side chains fall into several chemical classes: aliphatic, aromatic, sulfur-containing, alcohols, bases, acids, and amides. Also catagorized as to hydrophobic vs hydrophilic.
Must know 3-letter code for each amino acid.
Aliphatic R Groups
Glycine: least complex structure. Not chiral. Side chain small enough to fit into niches too small for other amino acids.
Alanine, Valine, Leucine, Isoleucine
no reactive functional groups
highly hydrophobic: play important role in maintaining 3-D structures of proteins because of their tendency to cluster away from water
Proline has cyclic side chain called a pyrolidine ring. Restricts geometry of polypeptides, sometimes introducing abrupt changes in direction of polypeptide chain.
Aromatic R Groups
Phenylalanine, Tyrosine, Tryptophan
Phe has benzene ring therefore hydrophobic.
Tyr and Trp have side chains with polar groups, therefore less hydrophobic than Phe.
Absorb UV 280 nm. Therefore used to estimate concentration of proteins.
Sulfur-containing R Groups
Methionine and Cysteine)
Met is hydrophobic. Sulfur atom is nucleophilic.
Cys somewhat hydrophobic. Highly reactive. Form disulfide bridges and may stabilize 3-D structure of proteins by cross-linking Cys residues in peptide chains.
Side Chains with Alcohol Groups
Serine and Threonine
have uncharged polar side chains. Alcohol groups give hydrophilic character.
weakly ionizable.
Basic R Groups
Histidine, Lysine, and Arginine.
have hydrophilic side chains that are nitrogenous bases and positively charged at physiological pH.
Arg is most basic a.a., and contribute positive charges to proteins.
Acidic R Groups and their Amide derivatives
Aspartate, Glutamate
are dicarboxylic acids, ionizable at physiological pH. Confer a negative charge on proteins.
Asparagine, Glutamine
amides of Asp and Glu rspectively
highly polar and often found on surface of proteins
polar amide groups can form H-bonds with atoms in other amino acids with polar side chains.
Modified Widman Flap
PeriodontologyModified Widman Flap Procedure
The modified Widman flap procedure is a surgical technique used in
periodontal therapy to treat periodontal pockets while preserving the
surrounding tissues and promoting healing. This lecture will discuss the
advantages and disadvantages of the modified Widman flap, its indications, and
the procedural steps involved.
Advantages of the Modified Widman Flap Procedure
Intimate Postoperative Adaptation:
The main advantage of the modified Widman flap procedure is the
ability to establish a close adaptation of healthy collagenous
connective tissues and normal epithelium to all tooth surfaces. This
promotes better healing and integration of tissues post-surgery
Feasibility for Bone Implantation:
The modified Widman flap procedure is advantageous over curettage,
particularly when the implantation of bone and other substances is
planned. This allows for better access and preparation of the surgical
site for grafting .
Conservation of Bone and Optimal Coverage:
Compared to conventional reverse bevel flap surgery, the modified
Widman flap conserves bone and provides optimal coverage of root
surfaces by soft tissues. This results in:
A more aesthetically pleasing outcome.
A favorable environment for oral hygiene.
Potentially less root sensitivity and reduced risk of root
caries.
More effective pocket closure compared to pocket elimination
procedures .
Minimized Gingival Recession:
When reattachment or minimal gingival recession is desired, the
modified Widman flap is preferred over subgingival curettage, making it
a suitable choice for treating deeper pockets (greater than 5 mm) and
other complex periodontal conditions.
Disadvantages of the Modified Widman Flap Procedure
Interproximal Architecture:
One apparent disadvantage is the potential for flat or concave
interproximal architecture immediately following the removal of the
surgical dressing, particularly in areas with interproximal bony
craters. This can affect the aesthetic outcome and may require further
management .
Indications for the Modified Widman Flap Procedure
Deep Pockets: Pockets greater than 5 mm, especially in
the anterior and buccal maxillary posterior regions.
Intrabony Pockets and Craters: Effective for treating
pockets with vertical bone loss.
Furcation Involvement: Suitable for managing
periodontal disease in multi-rooted teeth.
Bone Grafts: Facilitates the placement of bone grafts
during surgery.
Severe Root Sensitivity: Indicated when root
sensitivity is a significant concern.
Procedure Overview
Incisions and Flap Reflection:
Vertical Incisions: Made to access the periodontal
pocket.
Crevicular Incision: A horizontal incision along
the gingival margin.
Horizontal Incision: Undermines and removes the
collar of tissue around the teeth.
Conservative Debridement:
Flap is reflected just beyond the alveolar crest.
Careful removal of all plaque and calculus while preserving the root
surface.
Frequent sterile saline irrigation is used to maintain a clean
surgical field.
Preservation of Proximal Bone Surface:
The proximal bone surface is preserved and not curetted, allowing
for better healing and adaptation of the flap.
Exact flap adaptation is achieved with full coverage of the bone.
Suturing:
Suturing is aimed at achieving primary union of the proximal flap
projections, ensuring proper healing and tissue integration.
Postoperative Care
Antibiotic Ointment and Periodontal Dressing:
Traditionally, antibiotic ointment was applied over sutures, and a
periodontal dressing was placed. However, these practices are often omitted
today.
Current Recommendations: Patients are advised not to
disturb the surgical area and to use a chlorhexidine mouth rinse every 12
hours for effective plaque control and to promote healing.
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Neutrophil Disorders Associated with Periodontal Diseases
Neutrophils play a crucial role in the immune response, particularly in
combating infections, including those associated with periodontal diseases.
Various neutrophil disorders can significantly impact periodontal health,
leading to increased susceptibility to periodontal diseases. This lecture will
explore the relationship between neutrophil disorders and specific periodontal
diseases.
Neutrophil Disorders
Diabetes Mellitus
Description: A metabolic disorder characterized by
high blood sugar levels due to insulin resistance or deficiency.
Impact on Neutrophils: Diabetes can impair
neutrophil function, including chemotaxis, phagocytosis, and the
oxidative burst, leading to an increased risk of periodontal infections.
Papillon-Lefevre Syndrome
Description: A rare genetic disorder characterized
by palmoplantar keratoderma and severe periodontitis.
Impact on Neutrophils: Patients exhibit neutrophil
dysfunction, leading to early onset and rapid progression of periodontal
disease.
Down’s Syndrome
Description: A genetic disorder caused by the
presence of an extra chromosome 21, leading to various developmental and
health issues.
Impact on Neutrophils: Individuals with Down’s
syndrome often have impaired neutrophil function, which contributes to
an increased prevalence of periodontal disease.
Chediak-Higashi Syndrome
Description: A rare genetic disorder characterized
by immunodeficiency, partial oculocutaneous albinism, and neurological
problems.
Impact on Neutrophils: This syndrome results in
defective neutrophil chemotaxis and phagocytosis, leading to increased
susceptibility to infections, including periodontal diseases.
Drug-Induced Agranulocytosis
Description: A condition characterized by a
dangerously low level of neutrophils due to certain medications.
Impact on Neutrophils: The reduction in neutrophil
count compromises the immune response, increasing the risk of
periodontal infections.
Cyclic Neutropenia
Description: A rare genetic disorder characterized
by recurrent episodes of neutropenia (low neutrophil count) occurring
every 21 days.
Impact on Neutrophils: During neutropenic episodes,
patients are at a heightened risk for infections, including periodontal
disease.
NEUROHISTOLOGY
Anatomy
NEUROHISTOLOGY
The nervous system develops embryologically from ectoderm, which forms the neural plate
Successive growth and folding of the plate results in the formation of the primitive neural tube.
The neuroblasts in the wall of the tube differentiates into 3 cell types:
Neurons: conduction of impulses
Neuroglial cells: connective tissue and support of CNS
Ependymal cells: Lines the lumen of the tube.
- Specialized neuro-ectodermal cells which lines the ventricles of the adult brain
- Essentially also a neuroglial cell
Basic Unit = neuron
Exhibits irritability (excitability) and conductivity
A typical neurons consists of:
Cell body : Has nucleus (karyon) and surrounding cytoplasm (perikaryon) which contains organelles cell's vitality
Dendrites: Several short processes
Axon:One large process
Terminates in twig like branches (telodendrons)
May also have collateral branches projecting along its course. These exit at nodes of Ranvier
Axon enveloped in a sheath, and together forms the nerve fiber
Classification:
May be done in different ways, i.e.
Functional = afferent, efferent, preganglionic, postganglionic, etc.
Morphological = shape, processes, etc
A typical morphological classification is as follows
a. Unipolar: Has one process only Not found in man
b. Bipolar (so-called ganglion cell):Has two processes Found in sensory systems, e.g. retina olfactory system
c. Multipolar: Has several process Most common in CNS
Cell bodies vary in shape, e.g. stellate (star) , pyramidal
d. Pseudo-unipolar: Essentially bipolar neurons, but processes have swung around cb and fused with each other. They therefore enter and leave at one pole of the cell.
Typical neuron:
- Has 2 or more dendrites
Close to the cb the cytoplasm of dendrites has Nissl granules as well as mitochondria
Only one axon Arises from axon hillock, Devoid of Nissl granules, Encased in myelin sheath
No additional covering except for occasional foot processes of neuroglial cells
May branch at right angles
Branches at a node of Ranvier is known as a collateral
Ends of axons break up into tree-like branches, known as telodendria
Axons may be short (Golgi Type II) e.g. internuncial long (Golgi Type I) e.g. pyramidal neuron
Nucleus Central position Large and spherical
Chromatin is extended and thus not seen in LM. This allows the nucleolus to be prominent
Cytoplasm (perikaryon)
Surrounds nucleus May be large or small, shape may be round, oval, flattened, pyramidal, etc
Contains aggregates Nissl granules(Bodies) which is also sometimes referred to as rhomboid flakes
aggregation of membranes and cisternae of rough endoplasmic reticulum (RER)
numerous ribosomes and polyribosomes scattered between cisternae
(Polyribosome = aggregate of free ribosomes clumped together)
responsible for ongoing synthesis of new cytoplasm and cytoplasmic substances
needed for conduction of impulses
highly active in cell protein synthesis
resultant loss of power to divide which is characteristic of neurons
- Golgi network surrounding nucleus (seen in EM only)
- Fibrils made up of:
- neurofilaments
- microtubules
Tubules involved in:
1. plasmic transport
2. maintenance of cell shape
3. essential for growth and elongation of axons and dendrites
Neurofilament:
1. provide skeletal framework
2. maintenance of cell shape
3. possible role in axonal transport
(Axonal [axoplasmic; plasmic] transport may be antero- or retrograde. Anterograde transport via neurotubules is fast and moves neurotransmitters. Retrograde transport is slow and is the reason why viruses and bacteria can attack and destroy cell bodies. E.g. polio in the ventral columns and syphilis in the dorsal columns).
- Numerous mitochondria
- Neurons lack ability to store glycogen and are dependent for energy on circulating glucose
Impulses are conducted in one direction only
Dendrites conduct towards the cb
Axons conduct away from cb
Synapses:
- Neurons interconnect by way of synapses
- Normally the telodendria of an axon synapse with the dendrites of a succeeding axon
axo-dendritic synapse
This is usually excitatory
- Other types of synapses are:
axo-axonic
May be excitatory and/or inhibitory
axo-somatic
May be excitatory and/or inhibitory
dendrodendritic
Usually inhibitory
- Synapses are not tight junctions but maintain a narrow space the so-called synaptic cleft
- The end of an telodendron is usually enlarged (bouton) and contains many synaptic vesicles,
mitochondrion, etc. Its edge that takes part in the synapse is known as the postsynaptic membrane and no
vesicles are seen in this area
- Synapses may be chemical (as above) or electrical as in the ANS supplying smooth muscle cells subjacent to adjacent fibres
Gray and White Matter of Spinal Cord:
- Gray matter contains:
- cb's (somas) of neurons
- neuroglial cells
- White matter contains:
- vast number of axons
- no cb's
- colour of white matter due to myelin that ensheathes axons
Myelin:
- Non-viable fatty material contains phospholipids, cholesterol and some proteins
- Soluble and not seen in H&E-sections because it has become dissolved in the process, thus leaving empty spaces around the axons
- Osmium tetroxide (OsO4) fixes myelin and makes it visible by staining it black. Seen as concentric rings in cross section
- Myelin sheath (neurolemma) is formed by two types of cells
- Within the CNS by Oligodendrocytes
- On the peripheral neurons system by Schwann cells
- Sheath is formed by being wrapped around the axon in a circular fashion by both types of cells
Neuroglial Cells:
- Forms roughly 40% of CNS volume
- May function as: 1. support
2. nurture ("feeding")
3. maintain
Types of glial cells:
Oligodendrocytes:
- Small dark stained dense nucleus
- Analogue of Schwann cell in peripheral nervous system
- Has several processes which forms internodal segments of several fibres (one cell ensheathes more than one axon)
- Provides myelin sheaths in CNS
- Role in nurturing (feeding) of cells
Astrocytes:
Protoplasmic astrocytes:
- found in gray matter
- round cell body
- large oval nucleus with prominent nucleolus
- large thick processes
- processes are short but profusely branched
- perivascular and perineurial foot processes
- sometimes referred to as mossy fibres
Fibrous Astrocytes:
- found in white matter
- polymorphic cells body
- large oval nucleus
- long thin processes
Microglia:
- Neural macrophages
- smallest of the glial cells
- intense dark stained nucleus
- conspicuously fine processes which has numerous short branches
Cerebral Cortex:
Consists of six layers which are best observed in the cortex of the hippocampus
From superficial to deep:
- Molecular layer:
- Has few cells and many fibres of underlying cells
- Outer granular layer:
- Many small nerve cells
- Pyramidal layer:
- Pyramidally-shaped cells bodies
- Inner granular layer:
- Smaller cells and nerve fibres
- Internal (inner) pyramidal layer:
- Pyramidal cells bodies
- Very large in the motor cortex and known as Betz-cells
- Polymorphic layer:
- Cells with many shapes
Cerebellar Cortex:
Consists of three layers
Connections are mainly inhibitory
From superficial to deep
- Outer molecular layer:
- Few cells and many fibres
- Purkinje layer:
- Huge flask-shaped cells that are arranged next to one another
- Inner granular layer:
- Many small nerve cells
Motor endplate:
Seen in periphery on striated muscle fibres
- known as boutons
- has no continuous myelin covering from the Schwann cells
- passes through perimysium of muscle fiber to "synapse"
- multiple synaptic gutter (fold) in sarcoplasma of muscle fiber beneath bouton
- contains numerous synaptic vesicles and mitochondria
Ganglia:
- Sensory Ganglia:
(e.g. trigeminal nerve, ganglia and dorsal root ganglia)
- No synapse (trophic unit)
- pseudo-unipolar neurons
- centrally located nucleus
- spherical smooth border
- conspicuous axon hillock
- Surrounded by cuboidal satellite cells (Schwann cells)
- Covered by spindle shaped capsular cells of delicate collagen which forms the endoneurium
- Visceral and Motor Ganglia (Sympathetic and Parasympathetic):
- Synapse present
- Ratio of preganglionic: postganglionic fibres
1. Sympathetic 1:30
Therefore excitatory and catabolic
2. Parasympathetic 1:2
Therefore anabolic
Except in Meissner and Auerbach's plexuses where ratio is 1:1000 '2 because of parasympathetic component's involvement in digestion
- Preganglionic axons are myelinated (e.g. white communicating rami)
- Postganglionic axon are non-myelinated (e.g. gray communicating rami)
- small multipolar cell body
- excentrally located nucleus
- Inconspicuous axon hillock
- satellite cells few or absent
- few capsular cells
Behavioral Classification
PedodonticsBehavioral Classification Systems in Pediatric Dentistry
Understanding children's behavior in the dental environment is crucial for
effective treatment and management. Various classification systems have been
developed to categorize these behaviors, which can assist dentists in guiding
their approach, systematically recording behaviors, and evaluating research
validity.
Importance of Behavioral Classification
Behavior Guidance: Knowledge of behavioral
classification systems helps dentists tailor their behavior guidance
strategies to individual children.
Systematic Recording: These systems provide a
structured way to document children's behaviors during dental visits,
facilitating better communication and understanding among dental
professionals.
Research Evaluation: Behavioral classifications can aid
in assessing the validity of current research and practices in pediatric
dentistry.
Wright’s Clinical Classification
Wright’s clinical classification categorizes children into three main groups
based on their cooperative abilities:
Cooperative:
Children in this category exhibit positive behavior and are
generally relaxed during dental visits. They may show enthusiasm and can
be treated using straightforward behavior-shaping approaches. These
children typically follow established guidelines and perform well within
the framework provided.
Lacking in Cooperative Ability:
This group includes children who demonstrate significant
difficulties in cooperating during dental procedures. They may require
additional support and alternative strategies to facilitate treatment.
Potentially Cooperative:
Children in this category may show some willingness to cooperate but
may also exhibit signs of apprehension or reluctance. They may need
encouragement and reassurance to engage positively in the dental
environment.
Frankl Behavioral Rating Scale
The Frankl behavioral rating scale is a widely used tool that divides
observed behavior into four categories, ranging from definitely positive to
definitely negative. The scale is as follows:
Rating 1: Definitely Negative:
Characteristics: Refusal of treatment, forceful crying, fearfulness,
or any other overt evidence of extreme negativity.
Rating 2: Negative:
Characteristics: Reluctance to accept treatment, uncooperativeness,
and some evidence of a negative attitude (e.g., sullen or withdrawn
behavior).
Rating 3: Positive:
Characteristics: Acceptance of treatment with cautious behavior at
times; willingness to comply with the dentist, albeit with some
reservations. The patient generally follows the dentist’s directions
cooperatively.
Rating 4: Definitely Positive:
Characteristics: Good rapport with the dentist, interest in dental
procedures, and expressions of enjoyment (e.g., laughter).
Application of the Frankl Scale
Research Tool: The Frankl method is popular in research
settings for assessing children's behavior in dental contexts.
Shorthand Recording: Dentists can use shorthand
notations (e.g., “+” for positive behavior, “-” for negative behavior) to
quickly document children's responses during visits.
Limitations: While the scale is useful, it may not
provide sufficient clinical information regarding uncooperative children.
For example, simply recording “-” does not convey the nuances of a child's
behavior. A more descriptive notation, such as “- tearful,” offers better
insight into the clinical problem.
Application of agglutination reactions
General Microbiology
Application of agglutination reactions
Agglutination reaction Example
Tube agglutination -> Widal test, Weil Felix reaction, Standard tube test for brucellosis
Slide agglutination -> Typing of pneumococci,Diagnosis of Salmonella,Diagnosis of Shigella
Agglutination Absorption test -> Salmonella diagnosis
Coagglutination -> Grouping of streptococci, Identification of gonococci, Detection of Haemophilus, Antigen in CSF
Passive agglutination
Latex agglutination Detection of HBs Ag, ASO, CRP