NEET MDS Synopsis
Acute leukaemia
General Pathology
Acute leukaemia
Lympheblastic is commoner in children and myeloblastic in adults .
Features:
- Anaemia.
- Fever and infections especially oral and respiratory.
- Haemorrhagic tendencies.
- Bone pains and tenderness (sternal).
- Lymphnode enlargement especially in lymphocytic.
- Gum hypertrophy especially in monocytic.
Blood picture:
- Anaemia and thrombocytopenia.
- Leucocyte count usually 20,-50,000/cu.mm. It may be less in subleukaemic leukaemia (even leucopenic levels may be seen).
- Blast cells form 30-90% of cells. Smudge cells and basket cells are seen .The type of balst cell may be recognised by the associated more mature forms or by special cytochemical stains
- Blasts may be few in peripheral blood in the aleukamic stage
Bone Marrow
- May be a dry tap , necessitating a trephine biopsy
- Hypercellular with 70-90% blasts
- Reduction in megakaryocytes and erythroid cells
Appendicular Skeleton -Upper extremity
AnatomyAppendicular Skeleton
Upper extremity
• Shoulder-clavicle and scapula
Clavicle
Articulates with the manubrium at the sternal end
Articulates with the scapula at the lateral end
Slender S-shaped bone that extends horizontally across the upper part of the thorax
Scapula
Triangular bone with the base upward and the apex downward
Lateral aspect contains the glenoid cavity that articulates with the head of the humerus
Spine extends across the upper part of the posterior surface; expands laterally and
forms the acromion (forms point of shoulder)
Coracoid process projects anteriorly from the upper part of the neck of the scapula
Arm (humerus)
Consists of a shaft (diaphysis) and two ends (epiphyses)
Proximal end has a head that articulates with the glenoid fossa of the scapula
Greater and lesser tubercles lie below the head
Intertubercular groove is located between them; long tendon of the biceps attaches here
Surgical neck is located below the tubercles
o Radial groove runs obliquely on the posterior surface; radial nerve is located here
o Deltoid muscles attaches in a V-shaped area in the middle of the shaft. called the deltoid tuberosity
Distal end has two projections. the medial and lateral epicondyles
Capitulum-articulates with the radius
Trochlea-articulates with the ulqa
Forearm
Radius
Lateral bone of the forearm
Radial tuberosity is located below the head on the medial side
Distal end is broad for articulation with the wrist: has a styloid process on its lateral side
Ulna
Medial side of the forearm
Conspicuous part of the elbow joint (olecranon)
Curved surface that articulates with the trochlea of the humerus is the trochlearnotch
Lateral ide is concave (radial notch); articulates with the head of the radius Distal end contains the styloid process
Distal end contains the styloid process
Hand
Carpal bones (8)
Aranged in two rows of four
Scaphoid. lunate. triquetral. and pisiform proximal row); trapezium. trapezoid.
capitate. and hamate (distal row)
Metacarpal bones (5)
Framework of the hand
Numbered 1 to 5 beginning on the lateral side
Phalanges (14)
Fingers
Three phalanges in each finger; two phalanges in the thumb
Nerves of the Tongue
Anatomy
Anterior 2/3 of tongue
Posterior 1/3 of tongue
Motor Innervation
All muscles by hypoglossal nerve (CN XII) except palatoglossus muscle (by the pharyngeal plexus)
General Sensory Innervation
Lingual nerve (branch of mandibular nerve CN V3)
Glossopharyngeal nerve (CN IX)
Special Sensory Innervation
Chorda tympani nerve (branch of facial nerve)
Glossopharyngeal nerve (CN IX)
Adrenocortical Hyperfunction
General Pathology
Adrenocortical Hyperfunction (Hyperadrenalism)
Hypercortisolism (Cushing Syndrome) is caused by any condition that produces an elevation in glucocorticoid levels. The causes of this syndrome are
A. Exogenous through administration of exogenous glucocorticoids; the most common causeB. Endogenous
1. Hypothalamic-pituitary diseases causing hypersecretion of ACTH (Cushing disease)
2. Adrenocortical hyperplasia or neoplasia
3. Ectopic ACTH secretion by nonendocrine neoplasms (paraneoplastic)
Pathological features
- The main lesions of Cushing syndrome are found in the pituitary and adrenal glands.
- The most common change in the pituitary, results from high levels of endogenous or exogenous glucocorticoids, is termed Crooke hyaline change. In this condition, the normal granular, basophilic cytoplasm of the ACTH-producing cells in the anterior pituitary is replaced by homogeneous, lightly basophilic material. This is due to accumulation of intermediate keratin filaments in the cytoplasm.
- There is one of four changes in the adrenal glands, which depends on the cause.
1. Cortical atrophy
2. Diffuse hyperplasia
3. Nodular hyperplasia
4. Adenoma, rarely a carcinoma
1. In patients in whom the syndrome results from exogenous glucocorticoids, suppression of endogenous ACTH results in bilateral cortical atrophy, due to a lack of stimulation of the cortex by ACTH. In cases of endogenous hypercortisolism, in contrast, the adrenals either are hyperplastic or contain a cortical neoplasm.
2. In Diffuse hyperplasia the adrenal cortex is diffusely thickened and yellow, as a result of an increase in the size and number of lipid-rich cells in the zonae fasciculata and reticularis.
3. Nodular hyperplasia, which takes the form of bilateral, up to 2.0-cm, yellow nodules scattered throughout the cortex.
4. Primary adrenocortical neoplasms causing Cushing syndrome may be benign or malignant. The adrenocortical adenomas are yellow tumors surrounded by capsules, and most weigh < 30 gm .
Fermentation
Biochemistry
Anaerobic organisms lack a respiratory chain. They must reoxidize NADH produced in Glycolysis through some other reaction, because NAD+ is needed for the Glyceraldehyde-3-phosphate Dehydrogenase reaction (see above). Usually NADH is reoxidized as pyruvate is converted to a more reduced compound, that may be excreted.
The complete pathway, including Glycolysis and the re-oxidation of NADH, is called fermentation.
For example, Lactate Dehydrogenase catalyzes reduction of the keto group in pyruvate to a hydroxyl, yielding lactate, as NADH is oxidized to NAD+.
Skeletal muscles ferment glucose to lactate during exercise, when aerobic metabolism cannot keep up with energy needs. Lactate released to the blood may be taken up by other tissues, or by muscle after exercise, and converted via the reversible Lactate Dehydrogenase back to pyruvate
Fermentation Pathway, from glucose to lactate (omitting H+):
glucose + 2 ADP + 2 Pi → 2 lactate + 2 ATP
Anaerobic catabolism of glucose yields only 2 “high energy” bonds of ATP.
Oxygen Transport
PhysiologyOxygen Transport
In adult humans the hemoglobin (Hb) molecule
consists of four polypeptides:
two alpha (α) chains of 141 amino acids and
two beta (β) chains of 146 amino acids
Each of these is attached the prosthetic group heme.
There is one atom of iron at the center of each heme.
One molecule of oxygen can bind to each heme.
The reaction is reversible.
Under the conditions of lower temperature, higher pH, and increased oxygen pressure in the capillaries of the lungs, the reaction proceeds to the right. The purple-red deoxygenated hemoglobin of the venous blood becomes the bright-red oxyhemoglobin of the arterial blood.
Under the conditions of higher temperature, lower pH, and lower oxygen pressure in the tissues, the reverse reaction is promoted and oxyhemoglobin gives up its oxygen.
Role of Coenzymes
Biochemistry
Role of Coenzymes
The functional role of coenzymes is to act as transporters of chemical groups from one reactant to another.
Ex. The hydride ion (H+ + 2e-) carried by NAD or the mole of hydrogen carried by FAD;
The amine (-NH2) carried by pyridoxal phosphate
Endodontic Microbiology
EndodonticsBacterial portals to pulp: caries (most common source), exposed dentinal tubules (tubule permeability ↓ by dentinal fluid, live odontoblastic processes, tertiary and peritubular dentin)
1. Vital pulp is very resistant to microbial invasion but necrotic pulps are rapidly colonized
2. Rarely does periodontal disease → pulp necrosis
3. Anachoresis: microbes carried in blood to area of inflammation where they establish infection
Caries → pulp disease: infecting bacteria are immobile, carried to pulp by binary fission, dentinal fluid movement
1. Smooth surface and pit and fissure caries: S. mutans (important in early caries) and S. sobrinus
2. Root caries: Actinomyces spp.
3. Mostly anaerobes in deep caries.
4. Once pulp exposed by caries, many opportunists enter (e.g., yeast, viruses) → polymicrobial infection
Pulp reaction to bacteria: non-specific inflammation and specific immunologic reactions
1. Initially inflammation is a chronic cellular response (lymphocytes, plasma cells, macrophages) → formation of peritubular dentin (↓ permeability of tubules) and often tertiary dentin (irregular, less tubular, barrier)
2. Carious pulp exposure → acute inflammation (PMN infiltration → abscess formation). Pulp may remain inflamed for a long time or become necrotic (depends on virulence, host response, circulation, drainage, etc.)
Endodontic infections: most commonly Prevotella nigrescens; also many Prevotella & Porphyromonas sp.
1. Actinomyces and Propionibacterium species can persist in periradicular tissues in presence of chronic inflammation; they respond to RCT but need surgery or abx to resolve infection
2. Streptococcus faecalis is commonly found in root canals requiring retreatment due to persistent inflammation
Root canal ecosystem: lack of circulation in pulp → compromised host defense
1. Favors growth of anaerobes that metabolize peptides and amino acids rather than carbohydrates
2. Bacteriocins: antibiotic-like proteins made by one species of bacteria that inhibit growth of another species
Virulence factors: fimbriae, capsules, enzymes (neutralize Ig and complement), polyamines (↑ # in infected canals)
1. LPS: G(-), → periradicular pathosis; when released from cell wall = endotoxin (can diffuse across dentin)
2. Extracellular vesicles: may → hemagglutination, hemolysis, bacterial adhesion, proteolysis
3. Short-chain fatty acids: affect PMN chemotaxis, degranulation, etc.; butyric acid → IL-1 production (→ bone resorption and periradicular pathosis)
Pathosis and treatment:
1. Acute apical periodontitis (AAP): pulpal inflammation extends to periradicular tissues; initial response
2. Chronic apical periodontitis (CAP): can be asymptomatic (controversial whether bacteria can colonize)
3. Acute apical abscess (AAA), phoenix abscesses (acute exacerbation of CAP), and suppurative apical periodontitis: all characterized by many PMNs, necrotic tissue, and bacteria
Treatment of endodontic infections: must remove reservoir of infection by thorough debridement
1. Debridement: removal of substrates that support microorganisms; use sodium hypochlorite (NaOCl) to irrigate canals (dissolves some organic debris in areas that can’t be reached by instruments); creates smear layer
2. Intracanal medication: recommend calcium hydroxide (greatest antimicrobial effect between appointments) inserted into pulp chamber then driven into canals (lentulo spiral, plugger, or counterclockwise rotation of files) and covered with sterile cotton pellet and temporary restoration (at least 3mm thick)
3. Drainage: for severe infections to ↓ pressure (improve circulation), release bacteria and products; consider abx
4. Culturing: rarely needed but if so, sterilize tissue with chlorhexidine and obtain submucosal sample via aspiration with a 16- to 20-gauge needle