NEET MDS Synopsis
Local anesthetic selection
Pharmacology
Local anesthetic selection
Local anesthetics are typically divided into 3 main categories:
short, intermediate and long acting local anesthetics.
Based on duration of the procedure and the duration of the individual agents
Infiltration
Nerve block
Pulpal
Soft tissue
Pulpal
Soft tissue
Short
30 min
2-3 hrs
45 min
2-3 hrs
Intermediate
60 min
2-3 hrs
75-90 min
3-4 hrs
Long
40 min
5-6 hrs
3-4 hrs
6-8 hrs
Short acting agents
1. Mepivacaine 3 %
2. Lidocaine 2%
Intermediate acting agents
1. Lidocaine 2% 1:100000 epi
2. Lidocaine 2% 1:50000 epi
3. Mepivacaine 2% 1:20000 neocobefrin
4. Prilocaine 4%
5. Articaine 4% 1:100000 epi
Long acting agents
1. Bupivacaine 0.5% 1:200000 epi
Liver cirrhosis
General Pathology
Liver cirrhosis
It is a chronic, progressive diffuse process characterized by
a. Hepatocellular necrosis
b. Replacement by fibrosis and inflammation
c. Hyperplasia of surviving liver cells forming regenerating nodules
d. Vascular derangement.
All these changes lead to loss of the normal liver architecture.
Pathology of cirrhosis
At first the liver is enlarged or of normal size. Late in the disease, it is reduced in size and weight.
Consistency- Firm.
Colour -May be yellow (fatty change), red (congestion), green (cholestaisis), or pale gray (recent nodules due to absence of pigment).
Morphologically According to the size of these nodules, cirrhosis can be classified
Micronodular (regular) cirrhosis. Small nodules 2-3 mm.in diameter.
Macronodular (irregular) cirrhosis, nodules up to one cm in diameter.
Mixed cirrhosis is the end stage of all types of cirrhosis
Microscopic picture
1 Regenerating nodulesn- Proliferated hepatocytes arranged in thick plates and separated by blood sinusoids. Central vein in abnormal sites (eccentric) - Hepatocytes may be small , large , or binucleated
2- Fibrosis- It replaces damaged hepatocytes. It develops at certain sites:-
a-perivenular b -perisinusoidal c -pericellular and d -in relation to portal tracts.
- It may be young, cellular and highly vascular or mature with diminished vasculsarity. It encloses groups of hepatocytes, lobules or regenerating nodules.
-As a result of hepatocyte injury and fibrosis, there’s loss of normal liver architecture including the lobular and acinar pattern as well as the liver cell plates
3- Bile ductular proliferation:- Occurs in the fibrous septa.Focal choestaisis with feathery degeneration of hepatocytes occur at the margins of regenerating nodules. It becomes diffuse terminally.
4- Inflammatory cells:- Lymphocytes, macrophages and plasma cells infiltrate the fibrous septa and regenerating nodules
Etiological classification of cirrhosis
Congenital Occurs at childhood
- congenital syphilis
Hereditary diseases:-
a. Primary idiopathic haemochromatosis b. Thalassemia c. Wilson’s disease d.α 1-antitrypsin deficien e. glycogen storage disease
Acquired
-Cryptogenic (10-50%).
-Alcoholic (30-70%)
-Post viral (15-20%)
- Biliary cirrhosis (16%) primary or secondary.
Dental trauma types in endodontics
EndodonticsIn endodontics, dental trauma often results in the luxation of teeth, which
is the displacement of a tooth from its normal position in the alveolus (the
bone socket that holds the tooth). There are several types of luxation injuries,
each with different endodontic implications. Here are the main types of dental
luxation:
1. Concussion: A tooth is injured but not displaced from its socket. The
periodontal ligament (PDL) is compressed and may experience hemorrhage. The
tooth is usually not loose and does not require repositioning. However, it can
be tender to percussion and may exhibit some mobility. The pulp may remain
vital, but it can become inflamed or necrotic due to the trauma.
2. Subluxation: The tooth is partially displaced but remains in the socket. It
shows increased mobility in all directions but can be repositioned with minimal
resistance. The PDL is stretched and may be damaged, leading to pulpal and
periodontal issues. Endodontic treatment is often not necessary unless symptoms
of pulp damage arise.
3. Lateral luxation: The tooth is displaced in a horizontal direction and may be
pushed towards the adjacent teeth. The PDL is stretched and possibly torn. The
tooth may be pushed out of alignment or into an incorrect position in the arch.
Prompt repositioning and splinting are crucial. The pulp can be injured, and the
likelihood of endodontic treatment may increase.
4. Intrusion: The tooth is pushed into the alveolar bone, either partially or
completely. This can cause significant damage to the PDL and the surrounding
bone tissue. The tooth may appear shorter than its neighbors. The pulp is often
traumatized and can die if not treated quickly. Endodontic treatment is usually
required after repositioning and stabilization.
5. Extrusion: The tooth is partially displaced out of its socket. The PDL is
stretched and sometimes torn. The tooth appears longer than its neighbors. The
pulp is frequently exposed, which increases the risk of infection and necrosis.
Repositioning and endodontic treatment are typically necessary.
6. Avulsion: The tooth is completely knocked out of its socket. The PDL is
completely severed, and the tooth may have associated soft tissue injuries. Time
is of the essence in these cases. If the tooth can be replanted within 30
minutes and properly managed, the chances of saving the pulp are higher.
Endodontic treatment is usually needed, with the possibility of a root canal or
revascularization.
7. Inverse luxation: This is a rare type of luxation where the tooth is
displaced upwards into the alveolar bone. The tooth is pushed into the bone,
which can cause severe damage to the PDL and surrounding tissues. Endodontic
treatment is often necessary.
8. Dystopia: Although not a true luxation, it's worth mentioning that a tooth
can be displaced during eruption. This can cause the tooth to emerge in an
abnormal position. Endodontic treatment may be necessary if the tooth does not
respond to orthodontic treatment or if the displacement causes pain or
infection.
The endodontic management of luxated teeth varies depending on the severity of
the injury and the condition of the pulp. Treatments can range from simple
monitoring to root canal therapy, apicoectomy, or even tooth extraction in
severe cases. The goal is always to preserve the tooth and prevent further
complications.
Alveolar Osteitis
Oral and Maxillofacial SurgeryDry Socket (Alveolar Osteitis)
Dry socket, also known as alveolar osteitis,
is a common complication that can occur after tooth extraction, particularly
after the removal of mandibular molars. It is characterized by delayed
postoperative pain due to the loss of the blood clot that normally forms in the
extraction socket.
Key Features
Pathophysiology:
After a tooth extraction, a blood clot forms in the socket, which is
essential for healing. In dry socket, this clot is either dislodged or
dissolves prematurely, exposing the underlying bone and nerve endings.
The initial appearance of the clot may be dirty gray, and as it
disintegrates, the socket may appear gray or grayish-yellow, indicating
the presence of bare bone without granulation tissue.
Symptoms:
Symptoms of dry socket typically begin 3 to 5 days after
the extraction. Patients may experience:
Severe pain in the extraction site that can radiate to the ear,
eye, or neck.
A foul taste or odor in the mouth due to necrotic tissue.
Visible empty socket with exposed bone.
Local Therapy:
Management of dry socket involves local treatment to alleviate pain
and promote healing:
Irrigation: The socket is irrigated with a warm
sterile isotonic saline solution or a dilute solution of hydrogen
peroxide to remove necrotic material and debris.
Application of Medications: After irrigation,
an obtundent (pain-relieving) agent or a topical anesthetic may be
applied to the socket to provide symptomatic relief.
Prevention:
To reduce the risk of developing dry socket, patients are often
advised to:
Avoid smoking and using straws for a few days post-extraction,
as these can dislodge the clot.
Follow postoperative care instructions provided by the dentist
or oral surgeon.
Verruca vulgaris
General Pathology
Verruca vulgaris
1. Commonly known as warts.
2. Caused by the human papillomavirus (HPV).
3. Warts can be seen on skin or as an oral lesion (vermilion border, oral mucosa, or tongue).
4. Transmitted by contact or autoinoculation.
5. A benign lesion.
Pancreas
Physiology
The bulk of the pancreas is an exocrine gland secreting pancreatic fluid into the duodenum after a meal. However, scattered through the pancreas are several hundred thousand clusters of cells called islets of Langerhans. The islets are endocrine tissue containing four types of cells. In order of abundance, they are the:
beta cells, which secrete insulin and amylin;
alpha cells, which secrete glucagon;
delta cells, which secrete somatostatin, and
gamma cells, which secrete a polypeptide of unknown function.
Beta Cells
Beta cells secrete insulin in response to a rising level of blood sugar
Insulin affects many organs. It
stimulates skeletal muscle fibers to
take up glucose and convert it into glycogen;
take up amino acids from the blood and convert them into protein.
acts on liver cells
stimulating them to take up glucose from the blood and convert it into glycogen while
inhibiting production of the enzymes involved in breaking glycogen back down (glycogenolysis) and
inhibiting gluconeogenesis; that is, the conversion of fats and proteins into glucose.
acts on fat (adipose) cells to stimulate the uptake of glucose and the synthesis of fat.
acts on cells in the hypothalamus to reduce appetite.
Diabetes Mellitus
Diabetes mellitus is an endocrine disorder characterized by many signs and symptoms. Primary among these are:
a failure of the kidney to retain glucose .
a resulting increase in the volume of urine because of the osmotic effect of this glucose (it reduces the return of water to the blood).
There are three categories of diabetes mellitus:
Insulin-Dependent Diabetes Mellitus (IDDM) (Type 1) and
Non Insulin-Dependent Diabetes Mellitus (NIDDM)(Type 2)
Inherited Forms of Diabetes Mellitus
Insulin-Dependent Diabetes Mellitus (IDDM)
IDDM ( Type 1 diabetes)
is characterized by little or no circulating insulin;
most commonly appears in childhood.
It results from destruction of the beta cells of the islets.
The destruction results from a cell-mediated autoimmune attack against the beta cells.
What triggers this attack is still a mystery, although a prior viral infection may be the culprit.
Non Insulin-Dependent Diabetes Mellitus (NIDDM)
Many people develop diabetes mellitus without an accompanying drop in insulin levels In many cases, the problem appears to be a failure to express a sufficient number of glucose transporters in the plasma membrane (and T-system) of their skeletal muscles. Normally when insulin binds to its receptor on the cell surface, it initiates a chain of events that leads to the insertion in the plasma membrane of increased numbers of a transmembrane glucose transporter. This transporter forms a channel that permits the facilitated diffusion of glucose into the cell. Skeletal muscle is the major "sink" for removing excess glucose from the blood (and converting it into glycogen). In NIDDM, the patient's ability to remove glucose from the blood and convert it into glycogen is reduced. This is called insulin resistance. NIDDM (also called Type 2 diabetes mellitus) usually occurs in adults and, particularly often, in overweight people.
Alpha Cells
The alpha cells of the islets secrete glucagon, a polypeptide of 29 amino acids. Glucagon acts principally on the liver where it stimulates the conversion of glycogen into glucose (glycogenolysis) which is deposited in the blood.
Glucagon secretion is
stimulated by low levels of glucose in the blood;
inhibited by high levels, and
inhibited by amylin.
The physiological significance of this is that glucagon functions to maintain a steady level of blood sugar level between meals.
Delta Cells
The delta cells secrete somatostatin. Somatostatin has a variety of functions. Taken together, they work to reduce the rate at which food is absorbed from the contents of the intestine. Somatostatin is also secreted by the hypothalamus and by the intestine.
Gamma Cells
The gamma cells of the islets secrete pancreatic polypeptide. No function has yet been found for this peptide of 36 amino acids.
Skeletal Muscle:
Anatomy
Skeletal Muscle: 1-40 cm long fibres, 10- 60 µm thick, according to myoglobin content there are:
Red fibres: lots of myoglobin, many mitochondriam slow twitching - tire slowly
White fibres: less myoglobin, less mitochondria, fast twitching - tire quickly
Intermediate fibres:
mixture of 2 above
Most muscles have all three - in varying ratios
Structure of skeletal muscle:
Light Microscopy: Many nuclei - 35/mm, Nuclei are oval - situated peripheral, Dark and light bands
Electron Microscopy: Two types of myofilaments
Actin
- 5,6 nm
3 components:
-actin monomers,
-tropomyosin - 7 actin molecules long
- troponin
actin monomers form 2 threats that spiral
- tropomyosin - lie in the groove of the spiral
- troponin - attach every 40 nm
- one end attach to the Z line
- other end goes to the middle of the sarcomere
- Z line consists of á actinin
Myosin:
- 15 nm
- 1,6 µm long
- The molecule has a head and a tail
- tails are parallel
- heads project in a spiral
- in the middle is a thickening
- thin threats bind the myosin at thickening (M line)
Contraction:
A - band stays the same, I - band, H - bands become narrower
Myosin heads ratchet on the actin molecule
Sarcolemma: 9 nm thick, invaginate to form T-tubule,
myofibrils - attach to the sarcolemma
Sarcoplasmic Reticulum:
specialized smooth EPR, Consists of T-tubules, terminal sisternae and sarcotubules
It is speculated that there are gap junctions between the T-tubule and terminal sisterna
An impulse is carried into the fiber by the T-tubule from where it goes to the rest of the sarcoplasmic reticulum
Connective tissue coverings of the muscle
Endomycium around fibres, perimycium around bundles and epimycium around the whole muscle
Blood vessels and nerves in CT
CT goes over into tendon or aponeurosis which attaches to the periosteum
Nerves:
The axon of a motor neuron branches and ends in motor end plates on the fiber
Specialized striated fibres called spindles (stretch receptors) form sensory receptors in muscles telling the brain how far the muscle has stretched
TOXOPLASMOSIS
General Pathology
TOXOPLASMOSIS
Infection with Toxoplasma gondii, causing a spectrum of manifestations ranging from asymptomatic benign lymphadenopathy to life-threatening CNS disease, chorioretinitis, and mental retardation.
Symptomatic infections may present in several ways
Acute toxoplasmosis may mimic infectious mononucleosis with lymphadenopathy, fever, malaise, myalgia, hepatosplenomegaly, and pharyngitis. Atypical lymphocytosis, mild anemia, leukopenia, and slightly abnormal liver function tests are common. The syndrome may persist for weeks or months but is almost always self-limited.
A severe disseminated form characterized by pneumonitis, myocarditis, meningoencephalitis, polymyositis, diffuse maculopapular rash, high fevers, chills, and prostration. Acute fulminating disease is uncommon.
Congenital toxoplasmosis usually results from a primary (and often asymptomatic) acute infection acquired by the mother during pregnancy. The risk of transplacental infection increases from 15% to 30 to 60% for maternal infections acquired in the 1st, 2nd, or 3rd trimester of gestation, respectively