NEET MDS Synopsis
The Body Regulates pH in Several Ways
PhysiologyThe Body Regulates pH in Several Ways
Buffers are weak acid mixtures (such as bicarbonate/CO2) which minimize pH change
Buffer is always a mixture of 2 compounds
One compound takes up H ions if there are too many (H acceptor)
The second compound releases H ions if there are not enough (H donor)
The strength of a buffer is given by the buffer capacity
Buffer capacity is proportional to the buffer concentration and to a parameter known as the pK
Mouth bacteria produce acids which attack teeth, producing caries (cavities). People with low buffer capacities in their saliva have more caries than those with high buffer capacities.
CO2 gas (a potential acid) is eliminated by the lungs
Other acids and bases are eliminated by the kidneys
Anemia (Disorder of Hematopoietic System)
General Pathology
Anemia (Disorder of Hematopoietic System) - Probably the most common effect of nutritional deficiency. Any factor that decreases hematopoiesis can cause an anemia.
A. Iron deficiency - Widely recognized as the most important cause of anemia, It is indicated that ½ of all pregnant women and infants are affected, as are ~13% of all adult women.
1. Dietary factors - Availability of iron from different food sources and mixtures.
2. Malabsorption – One third of patients with inflammatory bowel disease (IBD) have recurrent anemia and 30% or more of patients who have had partial gastrectomy will develop iron deficiency anemia.
3. Blood loss - Menses, gastrointestinal bleeding
4. Increased demand - Pregnancy, growth in children.
5. Congenital - Atransferrinemia
6. Importance of multiple factors.
7. Pathophysiology - Initially iron is mobilized from reticuloendothelial stores and increased intestinal absorption occurs. Total iron stores are depleted, serum iron levels fall. In severe cases in peripheral blood, the red cells become smaller (microcytic) and their hemoglobin content is reduced (hypochromic).
B. Megaloblastic anemias- Characterized by the presence of abnormal WBCs and RBCs. In severe cases, megaloblasts (abnormal red cell precursors) may be present. These anemias are a consequence of disordered DNA synthesis.
1. Folate deficiency - Can be caused by:
a. Dietary deficiency
b. Malabsorption (celiac disease)
c. Increased demand (pregnancy & lactation)
d. Drugs - methotrexate, anticonvulsants, oral contraceptives, alcoholism.
e. Liver disease
2. Cobalamin (vitamin B12) deficiency - Almost always a secondary disorder that can be caused by:
a. Intrinsic factor deficiency (pernicious anemia due to autoimmune destruction of the gastric mucosa)
b. Malabsorption
3. Pyridoxine (vitamin B6) deficiency- most commonly associated with alcoholism.
C. Other factors known to be frequently associated with anemia would include protein-calorie malnutrition, vitamin C deficiency, and pyridoxine deficiency (usually associated with alcoholism).
D. Other anemias not particularly associated with nutritional disease would include hemolytic anemia
(decreased red cell life span) and aplastic anemia (failure of marrow to produce new cells).
Multiple myeloma
General Pathology
Multiple myeloma.
Blood picture:
- Marked rouleaux formation.
- Normpcytic normochromic anaemia.
- There may be leucopenia or leucoery!hrohlastic reaction.
- Atypical plasma cells may be seen in some patients
- Raised ESR
- Monoclonal hypergammaglobulinaemia
- If light chains are produced in excess, they are excreted in urine as bence jones protein
Bone marrow
- Hyper cellular
- Plasma cells from at least 15 – 30% atypical forms and myeloma cells are seen.
Sickle Cell Disease
General Pathology
Sickle Cell Disease
Sickle cell anemia is a autosomal recessive genetic disorder. It affects the BETA GLOBIN gene on the CHROMOSOME 16. In sickle cell anemia, the hemoglobin abnormality consists of a point mutation in the beta chain gene for hemoglobin; the resulting abnormal gene product is denoted HbS. If you are heterozygous for the HbS gene you will have what is called sickle trait, which is asymptomatic .
If you are homozygous for the HbS gene you will get sickle cell disease, which is symptomatic in most patients.
The problem with HbS is that as it releases oxygen, it polymerizes and aggregates with other HbS molecules, making the red cell stiff and distorted. These distorted, sickle-shaped red cells are fragile so the patient can end up with a hemolytic anemia.
This can occur as pure disease (homozygous) or trait (heterozygous) or with other haemoglobinopathies. It is common. in Negroes. It is due to Hb-s which is much less soluble than Hb-A hence deoxygenation insoluble form sickling of RBC.
This causes:
• Removal by RE system.
• Blockage of microvessels causing ischaemia.
Selective serotonin reuptake inhibitors
Pharmacology
Selective serotonin reuptake inhibitors (SSRIs)
e.g. fluoxetine, paroxetine, citalopram, and sertraline
- Most commonly used antidepressant category
- Less likely to cause anticholinergic side effects
- Relatively safest antidepressant group in overdose
- Selectively inhibits reuptake of serotonin(5-HT)
Mode of Action;
- Well absorbed when given orally
- Plasma half-lives of 18-24 h allowing once daily dosagedaily dosage
- Metabolised through CYP450 system and most SSRIs inhibit some CYP isoforms
- Therapeutic effect is delayed for 2-4 weeks
ADVERSE DRUG REACTIONS
- Insomnia, increased anxiety, irritability
- Decreased libido
- Erectile dysfunction, anorgasmia, and ejaculatory delay
- Bleeding disorders
- Withdrawal syndrome
Osteoradionecrosis
Oral and Maxillofacial SurgeryOsteoradionecrosis
Osteoradionecrosis (ORN) is a condition that can occur following radiation
therapy, particularly in the head and neck region, leading to the death of bone
tissue due to compromised blood supply. The management of ORN is complex and
requires a multidisciplinary approach. Below is a comprehensive overview of the
treatment strategies for osteoradionecrosis.
1. Debridement
Purpose: Surgical debridement involves the removal of
necrotic and infected tissue to promote healing and prevent the spread of
infection.
Procedure: This may include the excision of necrotic
bone and soft tissue, allowing for better access to healthy tissue.
2. Control of Infection
Antibiotic Therapy: Broad-spectrum antibiotics are
administered to control any acute infections present. However, it is
important to note that antibiotics may not penetrate necrotic bone
effectively due to poor circulation.
Monitoring: Regular assessment of infection status is
crucial to adjust antibiotic therapy as needed.
3. Hospitalization
Indication: Patients with severe ORN or those requiring
surgical intervention may need hospitalization for close monitoring and
management.
4. Supportive Treatment
Hydration: Fluid therapy is essential to maintain
hydration and support overall health.
Nutritional Support: A high-protein and vitamin-rich
diet is recommended to promote healing and recovery.
5. Pain Management
Analgesics: Both narcotic and non-narcotic analgesics
are used to manage pain effectively.
Regional Anesthesia: Techniques such as bupivacaine
(Marcaine) injections, alcohol nerve blocks, nerve avulsion, and rhizotomy
may be employed for more effective pain control.
6. Good Oral Hygiene
Oral Rinses: Regular use of oral rinses, such as 1%
sodium fluoride gel, 1% chlorhexidine gluconate, and plain water, helps
prevent radiation-induced caries and manage xerostomia and mucositis. These
rinses can enhance local immune responses and antimicrobial activity.
7. Frequent Irrigations of Wounds
Purpose: Regular irrigation of the affected areas helps
to keep the wound clean and free from debris, promoting healing.
8. Management of Exposed Dead Bone
Removal of Loose Bone: Small pieces of necrotic bone
that become loose can be removed easily to reduce the risk of infection and
promote healing.
9. Sequestration Techniques
Drilling: As recommended by Hahn and Corgill (1967),
drilling multiple holes into vital bone can encourage the sequestration of
necrotic bone, facilitating its removal.
10. Sequestrectomy
Indication: Sequestrectomy involves the surgical
removal of necrotic bone (sequestrum) and is preferably performed
intraorally to minimize complications associated with skin and vascular
damage from radiation.
11. Management of Pathological Fractures
Fracture Treatment: Although pathological fractures are
not common, they may occur from minor injuries and do not heal readily. The
best treatment involves:
Excision of necrotic ends of both bone fragments.
Replacement with a large graft.
Major soft tissue flap revascularization may be necessary to support
reconstruction.
12. Bone Resection
Indication: Bone resection is performed if there is
persistent pain, infection, or pathological fracture. It is preferably done
intraorally to avoid the risk of orocutaneous fistula in
radiation-compromised skin.
13. Hyperbaric Oxygen (HBO) Therapy
Adjunctive Treatment: HBO therapy can be a useful
adjunct in the management of ORN. While it may not be sufficient alone to
support bone graft healing, it can aid in soft tissue graft healing and
minimize compartmentalization.
Radiographic films used in Dentistry
Radiology
Radiographic films used in Dentistry
1. Intraoral Periapical (IOPA) Film
Size 0:
Dimensions: 22 x 35 mm
For: Small children
MPD (Maximum Permissible Dose) for whole body: 0.1 Rem in 1 year
Size 1:
MPD for gonads/bone marrow: 0.5 Rem in 1 year
Size 2:
Dimensions: 24 x 40 mm or 32 x 41 mm
For: Anterior projections and adults
MPD for gestation period in relation to the fetus: 5 Rem
MPD for skin: 0.5 Rem in 1 year
Radiation Exposure:
Mean exposure from one IOPA: 300 mR
Mean exposure from improved dental X-ray techniques: as low as 110
mR
2. Bitewing Film
Size 0:
For: Very small children
Size 1:
For: Children
Size 2:
For: Adults
3. Occlusal Film
Size:
3 times larger than size 2 film (57 x 76 mm)
Used for capturing larger areas of the dental arch.
4. Screen Film
Size:
8 x 10 inches
Used for extraoral projections in conjunction with an intensifying
screen.
Additional Information
Erythema Dose: The amount of radiation necessary to
produce a noticeable skin reaction, typically 300-400 R.
ALARA Principle: Stands for "As Low As Reasonably
Achievable," emphasizing the importance of minimizing radiation exposure.
Immunoglobulins.
General Pathology
Immunoglobulins. (Ig)
These are made up of polypeptide chains. Each molecule is constituted by two heavy and two light chains, linked by disulfide (S-S) bonds. The h~ chains are of 5 types, with corresponding, types or immunoglobulin. IgG (gamma), IgM (mu µ ), IgA(alpha α), IgD(delta ), IgE(epsilon)
Each of these can have light chains of either kappa (k) or lambda type.Each chain has a constant portion (constant for the subtype) land a variable portion (antigen specific).
Enzyme digestion can split the Ig molecule into.2 Fab (antibody binding) fragments and one Fc (crystallisable, complement binding ) fragment.
Characteristics of Immunoglobulin subclasses
I. Ig G:
(i) Predominant portion (80%) of Ig.
(ii) Molecular weight 150, 000
(iii) Sedimentation coefficient of 7S.
(iv) Crosses placental barrier and to extra cellular fluid.
(v) Mostly neutralising effect. May be complement fixing.
(vi) Half life of 23 days.
2.IgM :
(i) Pentamer of Ig.
(ii) Molecular weight 900, 000
(iii) 19S.
(iv) More effective complement fixation and cells lysis
(v) Earliest to be produced in infections.
(vi) Does not cross placental barrier.
(vii) Halflife of 5 days.
3. Ig A :
Secretory antibody. Found in intestinal, respiratory secretions tears, saliva and urine also.
Secreted usually as a dinner with secretory piece.
Mol. weight variable (160,000+)
7 S to 14 S.
Half life of 6 days.
4.Ig D :
Found in traces.
7 S.
Does not cross placenta.
5. Ig E
Normally not traceable
7-8 S (MoL weight 200,000)
Cytophilic antibody, responsible for some hypersensitivity states,