NEET MDS Synopsis
Carbenicillin
Pharmacology
Carbenicillin
Antibiotic that is chemically similar to ampicillin. Active against gram-negative germs. It is well soluble in water and acid-labile.
IMMUNO PATHOLOGY
General Pathology
IMMUNO PATHOLOGY
Abnormalities of immune reactions are of 3 main groups
- Hypersensitivity,
- Immuno deficiency,
- Auto immunity.
Hypersensitivity (ALLERGY)
This is an exaggerated or altered immune response resulting in adverse effects
They are classified into 4 main types.
I. Type I-(reaginic, anaphylactic). This is mediated by cytophylic Ig E antibodies, which get bound to mast cells. On re-exposure, the Ag-Ab reaction occurs on the mast cell surface releasing histamine.
Clinical situations
I. Systemic anaphylaxis, presenting with bronchospasm oedema hypertension, and even death.
2. Local (atopic) allergy.
- Allergic rhinitis (hay fever)
- Asthma
- Urticaria.
- Food allergies.
2. Type II. (cytotoxic). Antibody combines with antigen present on-cell surface. The antigen may be naturally present on the surface or an extrinsic substance (e.g.drug) attached to cell surface.
The cell is then destroyed by complement mediated lysis (C89) or phagocytosis of the antibody coated cell.
Clinical situations
- Haemolytic anemia.
- Transfusion reaction
- Auto immune haemolytic anemia.
- Haemolysis due to some drugs like Alpha methyl dopa
2. Drug induced thrombocytopenia (especially sedormid).
3 Agranulocytosis due to sensitivity to some drugs.
4 Goodpasture’s syndrome-glomermerulonephritis due to anti basement membrane antibodies.
3. Type III. (Immune complex disease). Circulating immune complexes especially small soluble complexes tend to deposit in tissues especially kidney, joints, heart and arteries.
These then cause clumping of platelets with subsequent release of histamine. and serotonin resulting in increased permeability. Also, complement activation occurs which being chemotactic results in aggregation of polymorphs and necrotising vasculitis due to release of lysosmal enzymes
Clinical situations
- Serum sickness.
- Immune complex glomerulonephritis.
- Systemic lupus erythematosus.
- Allergic alveolitis.
- Immune based vasculitis like
o Drug induced vasculitis.
o Henoch – Schonlein purpura
4. Type IV. (Cell mediated). The sensitized lymphocytes may cause damage by cytotoxicity or by lymphokines and secondarily involving macrophages in the reaction.
Clinical situations
I. Caseation necrosis in tuberculosis.
2. Contact dermatitis to
- Metals.
- Rubber.
- Drugs (topical).
- Dinitrochlorbenzene (DNCB).
5. Type V. (stimulatory) This is classed by some workers separately and by other with cytotoxic type (Type II) with a stimulatory instead of toxic effect
Clinical Situations :
LATS (long acting thyroid stimulator) results in thyrotoxicosis (Grave’s disease)
Zones of Periodontal Disease
PeriodontologyZones of Periodontal Disease
Listgarten described four distinct zones that can be observed in periodontal
lesions. These zones may blend with each other and may not be present in every
case.
Zones of Periodontal Disease
Zone 1: Bacterial Zone
Description: This is the most superficial zone,
consisting of a diverse array of bacteria.
Characteristics:
The bacterial zone is primarily composed of various microbial
species, including both pathogenic and non-pathogenic bacteria.
This zone is critical in the initiation and progression of
periodontal disease, as the presence of specific bacteria can
trigger inflammatory responses in the host.
Zone 2: Neutrophil Rich Zone
Description: This zone contains numerous
leukocytes, predominantly neutrophils.
Characteristics:
The neutrophil-rich zone is indicative of the body’s immune
response to the bacterial invasion.
Neutrophils are the first line of defense and play a crucial
role in phagocytosing bacteria and releasing inflammatory mediators.
The presence of a high number of neutrophils suggests an acute
inflammatory response, which is common in active periodontal
disease.
Zone 3: Necrotic Zone
Description: This zone consists of disintegrated
tissue cells, fibrillar material, remnants of collagen fibers, and
spirochetes.
Characteristics:
The necrotic zone reflects tissue destruction and is
characterized by the presence of dead or dying cells.
Fibrillar material and remnants of collagen fibers indicate the
breakdown of the extracellular matrix, which is essential for
maintaining periodontal tissue integrity.
Spirochetes, which are associated with more aggressive forms of
periodontal disease, can also be found in this zone, contributing to
the necrotic process.
Zone 4: Zone of Spirochetal Infiltration
Description: This zone consists of well-preserved
tissue that is infiltrated with large and medium spirochetes.
Characteristics:
The zone of spirochetal infiltration indicates a more chronic
phase of periodontal disease, where spirochetes invade the
connective tissue.
The presence of well-preserved tissue suggests that while
spirochetes are present, the tissue has not yet undergone extensive
necrosis.
This zone is significant as it highlights the role of
spirochetes in the pathogenesis of periodontal disease, particularly
in cases of necrotizing periodontal diseases.
Periodontal ligament development
Dental Anatomy
Periodontal ligament development
Cells from the dental follicle give rise to the periodontal ligaments (PDL).
Formation of the periodontal ligaments begins with ligament fibroblasts from the dental follicle. These fibroblasts secrete collagen, which interacts with fibers on the surfaces of adjacent bone and cementum. This interaction leads to an attachment that develops as the tooth erupts into the mouth. The occlusion, which is the arrangement of teeth and how teeth in opposite arches come in contact with one another, continually affects the formation of periodontal ligaments. This perpetual creation of periodontal ligaments leads to the formation of groups of fibers in different orientations, such as horizontal and oblique fibers.
Hyperparathyroidism
General Pathology
Hyperparathyroidism
Hyperparathyroidism is defined as an elevated secretion of PTH, of which there are three main types:
1. Primary—hypersecretion of PTH by adenoma or hyperplasia of the gland.
2. Secondary—physiological increase in PTH secretions in response to hypocalcaemia of any cause.
3. Tertiary—supervention of an autonomous hypersecreting adenoma in long-standing secondary hyperparathyroidism.
Primary hyperparathyroidism
This is the most common of the parathyroid disorders, with a prevalence of about 1 per 800
It is an important cause of hypercalcaemia.
More than 90% of patients are over 50 years of age and the condition affects females more than males by nearly 3 : 1.
Aetiology
Adenoma 75% -> Orange−brown, well-encapsulated tumour of various size but seldom > 1 cm diameter Tumours are usually solitary, affecting only one of the parathyroids, the others often showing atrophy; they are deep seated and rarely palpable.
Primary hyperplasia 20% -> Diffuse enlargement of all the parathyroid glands
Parathyroid carcinoma 5% -> Usually resembles adenoma but is poorly encapsulated and invasive locally.
Effects of hyperparathyroidism
The clinical effects are the result of hypercalcaemia and bone resorption.
Effects of hypercalcaemia:
- Renal stones due to hypercalcuria.
- Excessive calcification of blood vessels.
- Corneal calcification.
- General muscle weakness and tiredness.
- Exacerbation of hypertension and potential shortening of the QT interval.
- Thirst and polyuria (may be dehydrated due to impaired concentrating ability of kidney).
- Anorexia and constipation
Effects of bone resorption:
- Osteitis fibrosa—increased bone resorption with fibrous replacement in the lacunae.
- ‘Brown tumours’—haemorrhagic and cystic tumour-like areas in the bone, containing large masses of giant osteoclastic cells.
- Osteitis fibrosa cystica (von Recklinghausen disease of bone)—multiple brown tumours combined with osteitis fibrosa.
- Changes may present clinically as bone pain, fracture or deformity.
about 50% of patients with biochemical evidence of primary hyperparathyroidism are asymptomatic.
Investigations are:
- Biochemical—increased PTH and Ca2+ , and decreased PO43- .
- Radiological—90% normal; 10% show evidence of bone resorption, particularly phalangeal erosions.
Management is by rehydration, medical reduction in plasma calcium using bisphosphonates and eventual surgical removal of abnormal parathyroid glands.
Secondary hyperparathyroidism
This is compensatory hyperplasia of the parathyroid glands, occurring in response to diseases of chronic low serum calcium or increased serum phosphate.
Its causes are:
- Chronic renal failure and some renal tubular disorders (most common cause).
- Steatorrhoea and other malabsorption syndromes.
- Osteomalacia and rickets.
- Pregnancy and lactation.
Morphological changes of the parathyroid glands are:
- Hyperplastic enlargement of all parathyroid glands, but to a lesser degree than in primary hyperplasia.
- Increase in ‘water clear’ cells and chief cells of the parathyroid glands, with loss of stromal fat cells.
Clinical manifestations—symptoms of bone resorption are dominant.
Renal osteodystrophy
Skeletal abnormalities, arising as a result of raised PTH secondary to chronic renal disease, are known as renal osteodystrophy.
Pathogenesis
renal Disease + ↓ vit. D activation , ↓ Ca 2+ reabsorption → ↓ serum Ca 2+ → ↑ PTH → ↓ bone absorption
Abnormalities vary widely according to the nature of the renal lesion, its duration and the age of the patient, but include:
- Osteitis fibrosa .
- Rickets or osteomalacia due to reduced activation of vitamin D.
- Osteosclerosis—increased radiodensity of certain bones, particularly the parts of vertebrae adjacent to the intervertebral discs.
The investigations are both biochemical (raised PTH and normal or lowered Ca 2+ ) and radiological (bone changes).
Management is by treatment of the underlying disease and oral calcium supplements to correct hypocalcaemia.
Tertiary hyperparathyroidism
This condition, resulting from chronic overstimulation of the parathyroid glands in renal failure, causes one or more of the glands to become an autonomous hypersecreting adenoma with resultant hypercalcaemia.
Orthodontic MCQ 1
Orthodontics
1. An adult patient with a Class II molar relationship and a cephalometric ANB angle of 2 degrees has which type of malocclusion?
1. Class II dental malocclusion
2. Class II skeletal malocclusion
3. Class I dental malocclusion
4. Class II skeletal malocclusion
ans 1. The molars are Class II but the skeletal relationship described by a normal ANB measurement is normal, so the malocclusion is dental
in origin.
2. Which of the following reactions is least likely to be observed during orthodontic treatment?
1. Root resorption
2. Devitalization of teeth that are moved
3. Mobility of teeth that are moved
4. Development of occlusal interferences
Ans 2. Root resorption is common during orthodontic treatment, although lesions often repair on the root surface. Mobility of teeth is also common as the PDL reorganizes and widens during tooth movement. It is uncommon for teeth to become devitalized as a result of orthodontic movement unless they have also been substantially compromised by injury or infection.
3. A 7-year-old has a 4-mm maxillary midline diastema. Which of the following should be done?
1. Brackets should be placed to close it.
2. A radiograph should be taken to rule out the presence of a supernumerary tooth.
3. Nothing should be done. It will close on its own.
4. Nothing should be done. Treatment should be deferred until the rest of the permanent dentition erupts.
Ans. 2. When a large diastema greater than 2 mm is present, it will probably not close on its own. Diagnostic tests, such as a radiograph, should be accomplished to rule out the presence of a supernumerary tooth, usually a mesiodens.
4. When Class III elastics are used, the maxillary first molars will _____.
1. Move distally and intrude
2. Move mesially and extrude
3. Move mesially and intrude
4. Move only mesially; there will be no movement in the vertical direction
ans 2. Class III elastics are worn from the maxillary first molars to the mandibular canines. The force system created by Class III elastics will produce mesial movement and extrusion of the maxillary first molars.
5. Ideally, Orthodontic traction to pull an impacted tooth to line of arch should begin
1. at 2-3 months post surgically
2. As soon as possible after surgery
3. After a waiting period of at least1.5 months
4. Only the method of traction is critical, not the time
ans 2
Mechanical approaches for aligning unerupted teeth. Orthodontic traction to pull an unerupted tooth toward the line of the arch
should begin as soon as possible after surgery Ideally a fixed orthodontic appliance should already be in place before the unerupted tooth is exposed, so that orthodontic force can be applied immediately. If this is not practical, active orthodontic
movement should being no later than 2 or 3 weeks post-surgically.
Post viral cirrhosis
General Pathology
Post viral (post hepatitic) cirrhosis (15-20%)
Cause:- Viral hepatitis (mostly HBV or HCV)
Acute hepatitis → chronic hepatitis → cirrhosis.
Pathology
Liver is shrunken. Fatty change is absent (except with HCV). Cirrhosis is mixed.
M/E :-
Hepatocytes-show degeneration, necrosis as other types of cirrhosis.
Fibrous septa -They are thick and immature (more cellular and vascular).
- Irregular margins (piece meal necrosis).
- Heavy lymphocytic infiltrate.
Prognosis:- - More rapid course than alcoholic cirrhosis.Hepatocellular carcinoma is more liable to occur
Appendicular Skeleton - Lower extremity
AnatomyHip
Constitutes the pelvic girdle
United with the vertebral column
Union of three parts that is marked by a cup shaped cavity (acetabulum) Ilium
• Prominence of the hip
• Superior border is the crest
• Anterosuperior spine-projection at the anterior tip of the crest
• Corresponding projections on the posterior part are the posterosuperior and posteroinferior iliac spines
• Greater sciatic notch-located beneath the posterior part
• Most is a smooth concavity (iliac fossa)
• Posteriorly it is rough and articulates with the sacrum in the formation of the sacroiliac joint
Pubic bone
Anterior part of the innominate bone
Symphysis pubic-joining of the two pubic bones at the midline
Body and two rami
• Body forms one fifth of the acetabulum
• Superior ramis extends from the body to the median plane: superior border forms the pubic crest
• Inferior ramus extends downward and meets with the ischium
• Pubic arch is formed by the inferior rami of both pubic hones
Ischium
Forms the lower and back part of the innominate bone
Body
• Forms two fifths of the accrabulum
• Ischial tuberosiry-supports the body in a sitting position
• Ramus-passes upward to join the inferior ramus of rhe pubis; known as rhe obturator foramen
Pelvis
Fanned by the right and left hip bones, sacrum, and coccyx
Greater pelvis
o Bounded by the ilia and lower lumbar vertebrae
o Gives support to the abdominal viscera
Lesser pelvis
o Brim of the pelvis corresponds to the sacral promontory
o Inferior outlet is bounded by the tip of the coccyx, ischial tuberosities, and inferior rami of the pubic bones
Female pelvis
o Shows adaptations related to functions as a birth canal Wide outlet
o Angle of the pubic arch is obtuse
Male pelvis
o Shows adaptations that contribute to power and speed
o Heart-shaped outlet
o Angle of the pubic arch is acute
Thigh
Femur-longest and strongest bone of the body
Proximal end has a rounded head that articulates with the acetabulum
Constricted portion-the neck
Greater and lesser trochanters
Slightly arched shaft; is concave posteriorly
o Linea aspera-strengthened by this prominent ridge
o Site of attachment for several muscles
Distal end has two condyles separated on the posterior side by the intercondyloid notch
Knee cap
Patella-sesamoid bone
Embedded in the tendon of the quadriceps muscle
Articulates with the femur
Leg
Tibia-medial bone
o Proximal end has two condyles that articulate with the femur
o Triangular shaft
Anterior-shin
Posterior-soleal line
Distal-medial malleolus that articulates with the latus to form the ankle joint
Fibula-lateral bone
o Articulates with the lateral condyle of the tibia but does not enter the knee joint
o Distal end projects as the lateral malleolus
Ankle, foot, and toes
Adapted for supporting weight but similar in structure to the hand
Talus
o Occupies the uppennost and central position in the tarsus
o Distributes the body weight from the tibia above to the other tarsal bones
Calcaneus (heel)-Iocated beneath the talus
Navicular-located in front of the talus on the medial side; articulates with three cuneifonn bones distally
Cuboid-lies along the lateral border of the navicular bone
Metatarsals
o First, second, and third p1etatarsals lie in front of the three cuneifonn bones
o (2) Fourth and fifth metatarsals lie in front of the cuboid bone
Phalanges
o Distal to the metatarsals
o (2) Two in the great toe; three in each of the other four toes .
Longitudinal arches in the foot (2)
o Lateral-fonned by the calcaneus, talus, cuboid, and fourth and fifth metatarsal bones
o Medial-fonned by the calcaneus, talus, navicular, cuneifonn, and first, second, and third metatarsal bones
Transverse arches-formed by the tarsal and metatarsal bones