৪৮তম বিশেষ বিসিএস [স্বাস্থ্য] ⎯ ডেন্টাল অংশ [Archived]

Diagnosis is not related to irrational use of drug

plasma Half Life 
1)give an idea about
..... Duration of action
......Amount to be administrated 
......Managmemt of drag Overdose 
2) to determine time to achieve steady state concentration 
3) useful for estimating time required for Drug removal from the body

Drugs  act by binding with
enzyme
receptor 
structural protein
career and channel 
Ref - katzung 16th ed.page 20-24

indication of adrenaline 
anaphylactic  shock
status asthmatics 
with local anaesthesia 
cardiac arrest
hypoglycemic shock  
※ ref.  lippincott  2nd edition page 150 to 160

Amoxiciline consider as a safe drug in pregnancy 

in renal failure all antibiotics except azithromycine  required for doses adjustment
Ref. Lange 14th ed. P-911

pregnancy category B
Ref. Katzung 16th, page -1135

ক) atropine- Anti cholinergic Drug  - reduce  respiratory secretion and anaesthetic drug induced hypotension and bradycardia.
Ref. Katzung 16th ed. P 464

গ,ঘ) decrease 

Indomethacin cox1 and Cox's to selective NSAID

penicillin and ceplalosporins are pregnancy safe drugs
Ref. Katzung 16th ed. P -1051

Cholinergic agent increase salivary flow
As Methacholine, pilocarpine

See Table 2.4 Differences between Acute and Chronic Inflammation, pg 29 ( Khaleque sir)

Types of Necrosis (Ref: General Pathology by Dr. Khaleque)

1. Coagulative necrosis
- Cause: ischemia
- Organs: heart, kidney
- Features: preserved outline, protein denaturation

2. Liquefactive necrosis
- Cause: infections, brain infarct
- Organs: brain, abscess
- Features: digestion of tissue, liquid mass

3. Caseous necrosis
- Cause: tuberculosis
- Features: cheese-like appearance, granular debris

4. Fat necrosis
- Cause: acute pancreatitis, trauma
- Features: fat breakdown, saponification with calcium

5. Fibrinoid necrosis
- Cause: immune reactions
- Site: vessel walls
- Features: fibrin and immune complex deposition

6. Gangrenous necrosis
- Dry: ischemia with coagulative necrosis
- Wet: bacterial infection with liquefaction
- Gas: Clostridium infection with gas production

See table 61.6 from Pathology book by Dr. Khaleque

Pathology of HIV Infection
(Reference: General Pathology by Dr. Khaleque – Topic: Immunodeficiency Diseases)

1. Causative Agent
- Human Immunodeficiency Virus (HIV-1 most common, HIV-2 less common)
- Retrovirus with RNA genome and reverse transcriptase enzyme

2. Target Cells
- CD4+ T lymphocytes (main target)
- Also infects macrophages, dendritic cells, microglial cells

3. Mechanism of Entry
- Binds to CD4 receptor and co-receptors (CCR5 or CXCR4)
- Entry via fusion → reverse transcription → integration into host genome

4. Pathological Phases
- Acute Phase: High viral replication, flu-like illness, drop in CD4+ count
- Latent Phase: Clinically silent, slow CD4+ decline
- Crisis Phase (AIDS): CD4+ count <200/mm³, multiple opportunistic infections and tumors

5. Effects on Immune System
- Progressive CD4+ T-cell depletion
- Impaired cell-mediated and humoral immunity
- Reduced macrophage and NK cell function

6. Common Opportunistic Infections
- Oral candidiasis
- Tuberculosis
- Pneumocystis jirovecii pneumonia
- Herpes simplex, CMV
- Oral hairy leukoplakia
- Kaposi’s sarcoma

7. Diagnosis
- ELISA for screening
- Western blot or PCR for confirmation
- CD4 count and viral load for monitoring

8. Clinical Monitoring
- CD4+ count <200/mm³ indicates AIDS
- Appearance of AIDS-defining illnesses confirms progression

Clinical Differentiation of Types of Shock
(Based on Dr. Khaleque's Pathology Textbook)

1. Hypovolemic Shock
*- Cause: Blood or fluid loss
- Pulse: Rapid, weak
- BP: Low
*- Skin: Cold, clammy
- JVP: Low
- CVP: Low
- Urine output: Decreased
*- Common sign: Thirst, pallor

2. Cardiogenic Shock
*- Cause: Myocardial infarction, heart failure
- Pulse: Rapid, weak or irregular
- BP: Very low
*- Skin: Cold, cyanotic
- JVP: Raised
- CVP: Raised
- Urine output: Decreased
*- Other: Pulmonary edema, chest pain

3. Septic Shock
*- Cause: Severe infection (bacterial endotoxins)
- Pulse: Bounding initially, then weak
- BP: Low
*- Skin: Warm in early phase, cold in late
- JVP: Normal or low
- CVP: Variable
- Urine output: Decreased
*- Other: Fever, chills, altered mental state

4. Anaphylactic Shock
*- Cause: Severe allergic reaction
- Pulse: Rapid
- BP: Very low
*- Skin: Warm, flushed, with hives
- JVP: Normal or low
- CVP: Normal
- Urine output: Decreased
*- Other: Bronchospasm, angioedema, wheezing

5. Neurogenic Shock
*- Cause: Spinal cord injury, anesthesia
*- Pulse: Bradycardia
- BP: Low
*- Skin: Warm, dry
- JVP: Low
- CVP: Low
- Urine output: Variable
- Other: Flaccid paralysis below lesion level

Amide vs Ester Local Anesthetics

Amide Group
- Metabolized in liver
- Fewer allergic reactions
- Longer duration of action
- Examples: Lidocaine, Bupivacaine, Mepivacaine, Articaine

Ester Group
- Metabolized by plasma pseudocholinesterase
- Higher risk of allergic reactions due to PABA (para-aminobenzoic acid)
- Shorter duration of action
- Examples: Procaine, Tetracaine, Benzocaine

In hypertensive patients, vasoconstrictors in local anesthetics (like epinephrine) should be used with caution:

Key considerations:

- Limit epinephrine dose:
Maximum 0.04 mg (around 2 cartridges of 2% lidocaine with 1:100,000 epinephrine)

- Use aspiration and slow injection to avoid intravascular delivery

- Avoid if BP is uncontrolled (systolic >180 mmHg or diastolic >110 mmHg)

- Preferred agents:
– Lidocaine with reduced epinephrine concentration
– Plain mepivacaine or prilocaine (without vasoconstrictor) in short procedures

- Monitor vitals before, during and after procedure

Alternative vasoconstrictors:
– Felypressin (caution in ischemic heart disease)

Triple Antibiotic Paste (TAP)

- Metronidazole + Ciprofloxacin + Minocycline
- Used in regenerative endodontics
- Broad-spectrum antimicrobial against anaerobic & aerobic organisms
- Minocycline may cause tooth discoloration (can be replaced with Clindamycin)

CHX is Incompatible with NaOCl (forms brown precipitate – para-chloroaniline.
- So Never mix NaOCl and CHX*
directly in the canal.
- If switching irrigants, flush with saline or EDTA between them to avoid precipitate formation.

Gutta-Percha

Composition:
- Zinc oxide – 59–75% (filler)
- Gutta-percha – 19–22% (matrix)
- Heavy metal salts – 1–17% (radiopacity)
- Waxes/resins – 1–4% (plasticity)

Types:
- Alpha phase (more flowable, used in thermoplasticized techniques)
- Beta phase (rigid, used in conventional cones)

Advantages:
- Biocompatible
- Radiopaque
- Easy to manipulate
- Can be removed if retreatment is needed

Limitations:
- Lacks adhesive properties
- Requires a sealer for complete seal
- Can shrink on cooling (in thermoplastic forms)

Sterilization:
- 1% Sodium hypochlorite immersion for 1 minute

Note on Sodium Hypochlorite (NaOCl)
Reference: Textbook of Endodontics by Nisha Garg (Chapter: Irrigation in Endodontics)

- Concentration used: 0.5% – 5.25%
- Mechanism of Action:
- Dissolves organic tissue (especially necrotic pulp) by saponification, amino acid neutralization, and chloramination reactions
- Antibacterial by releasing hypochlorous acid and free chlorine
- Advantages:
- Strong antimicrobial agent
- Excellent tissue dissolving capacity
- Lubricates canal
- Limitations:
- Toxic if extruded beyond apex
- Unpleasant taste and odor
- Corrosive to instruments
- Precautions:
- Use with side-vented needles
- Avoid excessive pressure during irrigation
- Use rubber dam isolation

Ibuprofen is preferred over paracetamol in dental pain for the following reasons:

- Anti-inflammatory Action: Ibuprofen reduces inflammation at the site of pain (e.g., infected or traumatized pulp), which paracetamol lacks.
- Peripheral and Central Action: Ibuprofen works both peripherally and centrally, making it more effective in conditions like pulpitis or post-extraction pain.
- Longer Duration: Ibuprofen generally provides longer-lasting relief than paracetamol for dental-related pain.
- Better for Swelling: It's more effective in controlling swelling and redness in dental infections.

However, paracetamol is preferred in:
- Patients with gastric issues or ulcers
- Children and pregnant women (in recommended doses)
- Patients with NSAID allergies

So, ibuprofen is more effective when inflammation is a key component of dental pain.

Mechanism of Action of Astringents in Dentistry:

– Protein Precipitation: Astringents cause precipitation of proteins on the superficial layer of mucosa or gingiva, forming a protective layer and reducing permeability.

– Vasoconstriction: They induce contraction of blood vessels, helping to reduce bleeding during procedures like gingival retraction in Gingival retraction cord (GRC)

– Tissue Contraction: Astringents cause shrinkage of tissues, which is useful in creating space for impression making or reducing inflammation.

– Drying Effect: Reduce exudation by tightening epithelial cells, aiding in moisture control during restorative procedures.

Common Astringents in Dentistry:
– Aluminum chloride
– Ferric sulfate
– Tannic acid
– Zinc chloride 

Antiseptics & Disinfectants Used in Dentistry

Antiseptics (Used on Living Tissue):
1. Chlorhexidine

2. Povidone-Iodine
- Iodophore antiseptic
- Used for skin disinfection and oral mucosal application

3. Hydrogen Peroxide (3%)
- Mechanical cleansing action
- Used in minor oral wounds, ulcer cleansing

4. Essential Oils (e.g., Listerine)
- Antimicrobial activity
- Used as commercial mouth rinses

Disinfectants (Used on Inanimate Surfaces):
1. Glutaraldehyde (2%)
- High-level disinfectant
- Used for heat-sensitive instruments
- Long immersion time (10–12 hours)

2. Sodium Hypochlorite (1–5%)
- Used as surface disinfectant
- Also used as an irrigant in endodontics

3. Alcohol (70% Isopropyl or Ethyl Alcohol)
- Rapid-acting disinfectant for surfaces
- Not effective against spores

4. Phenolic Compounds(phenol,cresol)
- Disinfectant for floors, countertops

5. Quaternary Ammonium Compounds (e.g., Benzalkonium chloride)

Primary Use of Potassium Nitrate 
- Dentin desensitizing agent

Mechanism of Action:
- Acts by blocking the nerve transmission in dentinal tubules.
- Increases extracellular potassium concentration, which prevents repolarization of nerve endings, thus reducing pain sensation.

Forms Available:
- Toothpaste (e.g., 5% potassium nitrate)
- Gel formulations
- Mouth rinses (less common)

Indications:
- Relief of dentin hypersensitivity (e.g., in cervical abrasion, exposed dentin)
- Often used in combination with fluoride for enhanced effect

Duration of Use:
- Requires 2–4 weeks of consistent application for noticeable effects.

Types of Hemostatic Agents Used in Dentistry:

1.Mechanical Agents
These provide a physical matrix for clot formation.

- Gelfoam (Absorbable gelatin sponge): Absorbs blood and provides scaffold for platelet aggregation → accelerates clot formation.
- Collagen sponge: Traps platelets, promotes aggregation, and initiates intrinsic coagulation cascade.
- Oxidized regenerated cellulose (e.g., Surgicel, Oxical): Forms a gelatinous mass upon contact with blood → creates mechanical barrier and acidic pH causes vasoconstriction.
- Bone wax: Acts as a mechanical barrier, physically blocking bleeding bone channels without being absorbed.

2. Chemical Agents
These cause protein precipitation or vasoconstriction.

- Ferric sulfate:
- Aluminum chloride:
- Tannic acid:
- Silver nitrate:

3. Biological Agents
These enhance natural coagulation pathways.
- Thrombin,PRF, PRP

4. Pharmacological agents: Adrenaline

Agents Affecting Salivation

1. Sialogogues (Agents that stimulate salivation):

A. Pharmacological Sialogogues:
- Pilocarpine – (most commonly used)
- Cevimeline 
- Bethanechol 
- Neostigmine,Physostigmine – Anticholinesterase (indirectly stimulates salivation)

B. Non-pharmacological Sialogogues:
- Chewing gums
- Citric acid-containing lozenges
- Sugar-free sour candies

2. Anti-sialogogues (Agents that reduce salivation 
Common Anti-sialogogues:
- Atropine 
- Scopolamine (Hyoscine) 
- Glycopyrrolate – Peripheral anticholinergic, fewer CNS effects
- Propantheline – Reduces salivary and gastric secretions

(Remember the names of the drugs only)

Detailed Note on Chlorhexidine (CHX)

1.bisbiguanide antiseptic 

2. Forms Used in Dentistry
- 0.12% or 0.2% mouthwash (Chlorhexidine gluconate)
- 2% gel or varnish
- 2% chlorhexidine solution for root canal irrigation

3. Mechanism of Action
- Disrupts microbial cell membranes by binding to negatively charged bacterial cell walls.
- Causes leakage of intracellular contents, leading to cell death.
- Bacteriostatic at low concentration, bactericidal at higher concentrations.

4. Spectrum of Activity
- Effective against both Gram-positive and Gram-negative bacteria
- Some antiviral and antifungal activity
- Active against Streptococcus mutans and periodontal pathogens

5. Advantages
- Substantivity: Binds to oral tissues and remains active for up to 12 hours

6. Side Effects**
- Brown staining of teeth and tongue
- Altered taste sensation (temporary)
- Oral mucosa irritation
- Parotid swelling (rare)
- Calculus formation with long-term use

8. Contraindications
- Known hypersensitivity
- Should not be used immediately before or after toothpaste (interference with anionic surfactants)

9. Precautions
- Rinse with water before brushing or allow time gap

Ref: Lange medical microbiology, 15th edition 

Disease Corynebacterium diphtheriae causes diphtheria. Other Corynebacterium species (diphtheroids) are implicated in opportunistic infections.
Important Properties Corynebacteria are gram-positive rods that appear club-shaped (wider at one end) and are arranged in palisades or in V- or L-shaped formations. The rods have a beaded appearance. The beads consist of granules of highly polymerized polyphosphate—a storage mechanism for high-energy phosphate bonds. 
Clinical Findings everyone should be aware of its most prominent sign, the thick, gray, adherent pseudomembrane over the tonsils and throat.The other aspects are nonspecific: fever, sore throat, and cervical adenopathy.
There are three prominent complications:
(1) Extension of the membrane into the larynx and trachea, causing airway obstruction.
(2) Myocarditis accompanied by arrhythmias and circulatory collapse.
(3) Nerve weakness or paralysis, especially of the cranial nerves. Paralysis of the muscles of the soft palate and pharynx can lead to regurgitation of fluids through the nose. Peripheral neuritis affecting the muscles of the extremities also occurs.

Ref: Lange microbiology 

সঠিক উত্তর: (ক) ও (গ)
ক)Mycobacterium tuberculosis is relatively resistant to acids and alkalis.
গ)Mycobacterium tuberculosis is an obligate aerobe
অপশনে দ্বৈত উত্তর থাকায় প্রশ্নটি বাতিল করা হলো
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Mycobacteria are aerobic, acid-fast bacilli (rods) (. They are neither gram-positive nor gram-negative (i.e., they are stained poorly by the dyes used in Gram stain).
Important Properties Mycobacterium tuberculosis grows slowly (i.e., it has a doubling time of 18 hours, in contrast to most bacteria, which can double in number in 1 hour or less). Because growth is so slow, cultures of clinical specimens must be held for 6 to 8 weeks before being recorded as negative. Mycobacterium tuberculosis can be cultured on bacteriologic media, whereas M. leprae cannot. Media used for its growth (e.g., Löwenstein-Jensen medium) contain complex nutrients (e.g., egg yolk) and dyes (e.g., malachite green). The dyes inhibit the unwanted normal flora present in sputum samples.

Mycobacterium tuberculosis is an obligate aerobe; this explains its predilection for causing disease in highly oxygenated tissues such as the upper lobe of the lung and the kidney. The acid-fast property of M. tuberculosis (and other mycobacteria) is attributed to long-chain (C78–C90) fatty acids called mycolic acids in the cell wall. Cord factor (trehalose dimycolate) is correlated with virulence of the organism. Virulent strains grow in a characteristic “serpentine” cordlike pattern, whereas avirulent strains do not. The organism also contains several proteins, which, when combined with waxes, elicit delayed hypersensitivity. These proteins are the antigens in the purified protein derivative (PPD) skin test (also known as the tuberculin skin test). A lipid located in the bacterial cell wall called phthiocerol dimycocerosate is required for pathogenesis in the lung. Mycobacterium tuberculosis is relatively resistant to acids and alkalis. NaOH is used to concentrate clinical specimens; it destroys unwanted bacteria, human cells, and mucus but not the organism. M. tuberculosis is resistant to dehydration and therefore survives in dried expectorated sputum; this property may be important in its transmission by aerosol.

Ref: Lange Microbiology

Ref: Lange Microbiology 

Ref: Lange Microbiology 

Coronaviruses These are enveloped viruses with a helical nucleocapsid and a single-stranded, linear, nonsegmented, positive-polarity RNA. The term corona refers to the prominent halo of spikes protruding from the envelope. Coronaviruses cause respiratory tract infections, such as the common cold and severe acute respiratory syndrome (SARS), in humans.

Ref: Lange Microbiology

Dengue is the most common insect-borne viral disease in the world.
Types:
Classic dengue fever (breakbone fever) begins suddenly with an influenzalike syndrome consisting of fever, malaise, retro-orbital pain, and headache. Severe pains in muscles (myalgia) and joints (arthralgia, breakbone) occur. Enlarged lymph nodes, facial flushing, a maculopapular rash, and leukopenia are common. After a week or so, the symptoms regress, but weakness may persist. Although unpleasant, this typical form of dengue is rarely fatal and has few sequelae.
Dengue hemorrhagic fever is a much more severe disease, with a fatality rate that approaches 10%. The initial picture is the same as classic dengue, but then shock and hemorrhage, especially into the gastrointestinal tract and skin, develop. Dengue hemorrhagic fever occurs particularly in southern Asia, whereas the classic form is found in tropical areas worldwide.
Hemorrhagic shock syndrome is due to the production of large amounts of cross-reacting antibody at the time of a second dengue infection. The pathogenesis is as follows: The patient recovers from classic dengue caused by one of the four serotypes, and antibody against that serotype is produced. When the patient is infected with another serotype of dengue virus, an anamnestic, heterotypic response occurs, and large amounts of cross-reacting antibody to the first serotype are produced. There are two hypotheses about what happens next. One is that immune complexes composed of virus and antibody are formed that activate complement, causing increased vascular permeability and thrombocytopenia. The other is that the antibodies increase the entry of virus into monocytes and macrophages, with the consequent liberation of a large amount of cytokines. In either scenario, shock and hemorrhage result. Dengue virus is transmitted by the A. aegypti mosquito, which is also the vector of yellow fever virus. Humans are the reservoir for dengue virus, but a jungle cycle involving monkeys as the reservoir and other Aedes species as vectors is suspected. The diagnosis can be made in the laboratory either by isolation of the virus in cell culture or by serologic tests that demonstrate the presence IgM antibody or a fourfold or greater rise in antibody titer in acute and convalescent sera. A PCR assay that detects virus in the blood is also available. No antiviral therapy or vaccine for dengue is available. Outbreaks are controlled by using insecticides and draining.

Ref- Lange Microbiology