MCQs on NSAIDs and other CNS Drugs - Part 2

#  All of the following statements about pain are correct except: (AIPG-01)
a) Naloxone is a non-competitive antagonist and irreversibly opposes the opioids
b) Analgesia is associated with pi and K receptors
c) Dysphoria is associated with s receptors
d) NSAIDS benefit by preventing prostaglandin synthesis

# Which of the following opioids is not given intrathecally? (AIPG-2011)
a) Sufentanil
b) Morphine
c) Remifentanil
d) Fentanyl

# Which of the following drug is used to counter act the gastric irritation produced by administration of NSAID: (AIIMS-99)
a) Pirenzipine
b) Roxatidine
c) Betaxolol
d) Misoprostol

# All are symptoms of opiate withdrawals except: (AIPG-06)
a) Lacrimation
b) Mydriasis
c) Excessive speech
d) Diarrhea

# Aspirin is contraindicated in: (AP-01)
a) Peptic ulcer
b) Angina
c) Hypertension
d) MI

# Which of the following is a muscle relaxant? (AP-06)
a) Phenylephrine
b) Succinylcholine
c) Hyoscin
d) Pentazocine

# Salicylate administration is contraindicated in pregnancy because:
a) Causes pulmonary hypertension of newborn
b) Readily erases placental barrier
c) Delay onset of labour
d) All of these

# A Hemophiliac patient has rheumatoid arthritis. Which drug might be prescribed to relieve the pain? (KCET-07)
a) Phenylbutazone
b) Acetylsalicylic acid
c) Naproxen
d) Acetaminophen

# Benzodiazepines are true in: (AIIMS-07)
a) After metabolism of other drugs in liver
b) More safe than other sedatives when take in larger amounts
c) Produce distortion in sleep more than other sedatives
d) All have metabolically active substrates

# The rate of injection of intravenous Valium is: (AIPG-05)
a) 2.5 mg / min
b) 2.5 ml / min
c) 1 mg / min
d) 1 ml / min

# Ibuprofen is contraindicated in: (KAR-04)
a) Patients having amoebic dysentery
b) Patients having fever
c) Patients having asthma
d) Patients having bronchitis

# The Ethyl alcohol (Ethanol) is more effective when mixed with water and used as: (KAR-02)
a) 10 to 20 percent
b) 60 to 70 percent
c) 40 to 50 percent
d) 20 to 30 percent

# Which one of the following is NOT an ergot alkaloids? (COMEDK-08)
a) Lysergic acid diethylamide (LSD)
b) Bromocriptine
c) Ketanserin
d) Methysergide

# An antiepileptic drug used in petitmal epilepsy is: (KAR-2K)
a) Diazepam
b) Phenobarbitonse
c) Ethosuximide
d) Dilantoin sodium

# Benzodiazepine antagonist is: (AIIMS-2008)
a) Naltrexone
b) Naloxone
c) Furazolidone
d) Flumazenil

# Which of the following is a short acting barbiturate?
a) Secobarbital
b) Mephobarbital 
c) Diazepam
d) Phenobarbital

# One of the obvious consequences of alcohol (ethanol), ingestion in many individuals is facial flushing and increased heart rate triggered off by alcohol getting metabolized to: (KAR-98)
a) Propanaldehyde
b) Butanaldehyde
c) Acetaldehyde
d) Formaldehyde

# NSAID which undergoes enterohepatic circulation: (AIPG-2010)
a) Ibuprofen
b) Piroxicam
c) Aspirin
d) Phenylbutazone

# Paracetamol is contraindicated in
a) Chronic hepatitis
b) Bleeding disorders
c) Fever
d) Nephritis

# Which of the following is a non-steroidal anti inflammatory agent with a tendency to produce blood dyscrasias? (APPSC-99)
a) Aspirin
b) Indomethacin
c) B & A
d) Ibuprofen

# An untoward effect of that is common to all phenothiazines is
a) A marked increase in blood pressure
b) Rigidity and tremor at rest, particularly with prolonged use
c) Nausea
d) Suppression of Prolactin

# Buprenorphine acts by following mechanism: (KAR-04)
a) Mu receptor partial agonist
b) Kappa receptor antagonist
c) Mu receptor antagonist
d) Kappa receptor partial agonist

# Drugs like barbiturates precipitate symptoms of porphyria because: (COMEDK-07)
a) They inhibit heme oxygenase
b) They depress ALA synthase
c) They inhibit ALA synthase
d) They induce heme oxygenase

# The principal central action of caffeine is on the: (AIIMS-2K)
a) Spinal cord
b) Cerebral cortex
c) Corpus callosum
d) Hypothalamus

# Which one of the following muscle relaxant has the maximum duration of action? (AIPG-06)
a) Rocuronium
b) Atracurium
c) Vecuronium
d) Doxacurium

# Which among the following is a pure antagonist of opioid receptors? (COMEDK-08)
a) Butorphanol
b) Naltrexone
c) Nalbuphine
d) Pentazocine

# Folic acid deficiency occurs in treatment with: (AIIMS-06)
a) Chloramphenicol
b) Phenytoin
c) Cyclosporine
d) Aspirin

# Which among the following may be used as a sedatives-hypnotic? (COMEDK-08)
a) Zolpidem
b) Zolmitriptan
c) Zalcitabine
d) Zileuton

# Which of the following drugs is currently widely used in treating opioid-dependent individuals? (AIPG-03)
a) Pentazocine
b) Methadone
c) Alphaprodine
d) Codeine

# Best and most effective drug to control convulsions in toxicity cases is: (AIPG-97)
a) Phenobarbitone
b) Diazepam
c) Phenytoin
d) Carbamazepine

# Platelet aggregation is inhibited by all except
a) Salicylates
b) Indomethacin
c) Phenobarbitone
d) Dypyradimole

# Respiratory depression is seen with: (PGI-05)
a) Antidepressants
b) Non-barbiturates
c) Synthetic narcotics
d) Tranquilizers

# Barbiturates in pediatrics is: (AIIMS-96)
a) Can be used safely
b) Contraindicated
c) Not much use
d) Low safety

# Which of the following is true about parasympathetic nervous system? (MCET-07)
a) Ach is transmitter at both pre & post synaptic junction
b) It causes dilatation of skeletal muscles
c) Post-ganglionic fibres are longer than pre ganglionic fibres
d) Noradrenalin is the neurotransmitter at post ganglionic junction

# Aspirin is contraindicated in: (AP-2010)
a) Person suffering from chicken pox or small pox
b) Peptic ulcer
c) Hemorrhage
d) All of them

# An anxiolytic, not interacting with GABAergic system and used in generalized anxiety is: (KCET-08)
a) Diazepam
b) Buspiron
c) Alprazolam
d) Phenobarbital

# A patient with grand mal epilepsy would likely be under treatment with: (AIIMS-02)
a) Phenytoin
b) Meprobamate
c) Pentobarbital
d) Trimethadione

# DOPA and 5-Hydroxytryptophan are clinically important because? (AIIMS-2009)
a) They act as neuromodulators
b) They are metabolites of various neurogenic amines
c) They are acidic precursors of Brain amines
d) They cross Blood Brain Barriers

# Gastric irritation is minimum with one of the following non-steroidal anti inflammatory drugs:
a) Indomethacin
b) Meloxicam
c) Tenoxicam
d) Piroxicam

# Acute Barbiturate poisoning results in: (AIIMS-96)
a) Liver failure
b) Renal failure
c) Convulsions
d) Respiratory failure

# The anti-inflammatory analgesic drug the causes least gastrointestinal symptoms is:
a) Phenyl butazone
b) Aspirin
c) Indomethacin
d) Paracetamol

Dental Fluorosis

Dental fluorosis is a common disorder, characterized by hypomineralization of tooth enamel caused by ingestion of excessive fluoride during enamel formation.

It appears as a range of visual changes in enamel causing degrees of intrinsic tooth discoloration, and, in some cases, physical damage to the teeth. The severity of the condition is dependent on the dose, duration, and age of the individual during the exposure. The "very mild" (and most common) form of fluorosis, is characterized by small, opaque, "paper white” areas scattered irregularly over the tooth, covering less than 25% of the tooth surface. In the "mild" form of the disease, these mottled patches can involve up to half of the surface area of the teeth. When fluorosis is moderate, all of the surfaces of the teeth are mottled and teeth may be ground down and brown stains frequently "disfigure" the teeth. Severe fluorosis is characterized by brown discoloration and discrete or confluent pitting; brown stains are widespread and teeth often present a corroded-looking appearance.

People with fluorosis are relatively resistant to dental caries (tooth decay caused by bacteria), although there may be cosmetic concern. In moderate to severe fluorosis, teeth are weakened and suffer permanent physical damage.

The adequate diagnosis of fluorosis can be diagnosed by visual clinical examination. This requires inspection of dry and clean tooth surfaces under a good lighting. There are individual variations in clinical fluorosis manifestation which are highly dependent on the duration, timing, and dosage of fluoride exposure.There are different classifications to diagnose the severity based on the appearances. The clinical manifestation of mild dental fluorosis is mostly characterised a snow flaking appearance that lack a clear border, opaque, white spots, narrow white lines following the perikymata or patches as the opacities may coalesce with an intact, hard and smooth enamel surface on most of the teeth. With increasing severity, the subsurface enamel, all along the tooth becomes more porous. Enamel may appear yellow/ brown discolouration and/ or many and pitted white-brown lesions that look like cavities. They are often described as “mottled teeth”. Fluorosis does not cause discolouration to the enamel directly, as upon eruption into the mouth, affected permanent teeth are not discoloured yet. In dental enamel, fluorosis causes subsurface porosity or hypomineralizations, which extend toward the dentinal-enamel junction as severity increases. Hence, affected teeth are more susceptible to staining. Due to diffusion of exogenous ions (ex, iron and copper), the stains would develop into the abnormally porous enamel.

The differential diagnosis for this condition includes:

  1. Turner's hypoplasia (although this is usually more localized)
  2. Enamel defects caused by an undiagnosed and untreated celiac disease.
  3. Some mild forms of amelogenesis imperfecta and enamel hypoplasia
  4. Enamel defects caused by infection of a primary tooth predecessor
  5. Dental caries: Fluorosis-resembling enamel defects are often misdiagnosed as dental caries.
  6. Dental Trauma: Mechanical trauma to the primary tooth may cause disturbance to the maturation phase of enamel formation, which may result in enamel opacities on the permanent successors.


Severe fluorosis: brown discolored and mottled enamel of an individual from a region with high levels of naturally occurring fluoride.

Severe fluorosis: the enamel is pitted and discolored

The two main classification systems are described below. Others include the tooth surface fluorosis index (Horowitz et al. 1984), which combines Deans index and the TF index; and the fluorosis risk index (Pendrys 1990), which is intended to define the time at which fluoride exposure occurs, and relates fluorosis risk with tooth development stage.

Dean's index
Dean's fluorosis index was first published in 1934 by H. Trendley Dean. The index underwent two changes, appearing in its final form in 1942. An individual's fluorosis score is based on the most severe form of fluorosis found on two or more teeth.

ClassificationCodeCriteria – description of enamel
Normal0The enamel represents the usual translucent semivitriform (glass-like) type of structure. The surface is smooth, glossy and usually of pale creamy white color
Questionable1The enamel discloses slight aberrations from the translucency of normal enamel, ranging from a few white flecks to occasional white spots. This classification is utilised in those instances where a definite diagnosis is not warranted and a classification of ‘normal’ not justified
Very Mild2Small, opaque, paper white areas scattered irregularly over the tooth but not involving as much as approximately 25% of the tooth surface. Frequently included in this classification are teeth showing no more than about 1 – 2mm of white opacity at the tip of the summit of the cusps, of the bicuspids or second molars.
Mild3The white opaque areas in the enamel of the teeth are more extensive but do involve as much as 50% of the tooth.
Moderate4All enamel surfaces of the teeth are affected and surfaces subject to attrition show wear. Brown stain is frequently a disfiguring feature
Severe5All enamel surfaces are affected and hypoplasia is so marked that the general form of the tooth may be affected. The major diagnostic sign of this classification is discrete or confluent pitting. Brown stains are widespread and teeth often present a corroded-like appearance.
TF index
Proposed by Thylstrup and Fejerskov in 1978, the TF index represents a logical extension of Dean's index, incorporating modern understanding of the underlying pathology of fluorosis. It scores the spectrum of fluorotic changes in enamel from 0 to 9, allowing more precise definition of mild and severe cases.

Dental fluorosis is caused by a higher than normal amount of fluoride ingestion whilst teeth are forming. Primary dentine fluorosis and enamel fluorosis can only happen during tooth formation, so fluoride exposure occurs in childhood. Enamel fluorosis has a white opaque appearance which is due to the surface of the enamel being hypomineralised.

The most superficial concern in dental fluorosis is aesthetic changes in the permanent dentition (the adult teeth). The period when these teeth are at highest risk of developing fluorosis is between when the child is born up to 6 years old, though there has been some research which proposes that the most crucial course is during the first 2 years of the child's life. From roughly 7 years old thereafter, most children's permanent teeth would have undergone complete development (except their wisdom teeth), and therefore their susceptibility to fluorosis is greatly reduced, or even insignificant, despite the amount of intake of fluoride. The severity of dental fluorosis depends on the amount of fluoride exposure, the age of the child, individual response, weight, degree of physical activity, nutrition, and bone growth. Individual susceptibility to fluorosis is also influenced by genetic factors.

Many well-known sources of fluoride may contribute to overexposure including dentifrice/fluoridated mouthrinse (which young children may swallow), excessive ingestion of fluoride toothpaste, bottled waters which are not tested for their fluoride content, inappropriate use of fluoride supplements, ingestion of foods especially imported from other countries, and public water fluoridation. The last of these sources is directly or indirectly responsible for 40% of all fluorosis, but the resulting effect due to water fluoridation is largely and typically aesthetic. Severe cases can be caused by exposure to water that is naturally fluoridated to levels above the recommended levels, or by exposure to other fluoride sources such as brick tea or pollution from high fluoride coal.

Dental fluorosis has been growing in the United States concurrent with fluoridation of municipal water supplies, although disproportionately by race. A 2010 CDC report acknowledges an overall incidence of dental fluorosis of 22% from 1986-87 increased to 41% in the early 21st century, with an increase in moderate to severe dental fluorosis from 1% to 4%. The 2011-12 NHANES figures documented another 31% overall increase among American teens since the previous decade, with a total adolescent population impact of 61% afflicted. More than one in five American teens (23%) have moderate to severe dental fluorosis on at least two teeth.

Teeth are the most studied body tissues to examine the impact of fluoride to human health. There are a few possible mechanisms that have been proposed. It is generally believed that the hypomineralization of affected enamel is mainly due to in-situ toxic effects of the fluoride on the ameloblasts in the enamel formation, and not caused by the general effects of fluoride on the calcium metabolism, or by the poisoning effects that suppress the fluoride metabolism. However, despite decades of research and studies, there have yet to be any studies that substantiates the believed mechanism whereby dental fluorosis is a result of alteration in the mineralisation that takes place when fluroide interacts with mineralising tissues.

In the extra-cellular environment of maturing enamel, an excess of fluoride ions alters the rate at which enamel matrix proteins (amelogenin) are enzymatically broken down and the rate at which the subsequent breakdown products are removed. Fluoride may also indirectly alter the action of protease via a decrease in the availability of free calcium ions in the mineralization environment. This results in the formation of enamel with less mineralization. This hypomineralized enamel has altered optical properties and appears opaque and lusterless relative to normal enamel.

Traditionally severe fluorosis has been described as enamel hypoplasia, however, hypoplasia does not occur as a result of fluorosis. The pits, bands, and loss of areas of enamel seen in severe fluorosis are the result of damage to the severely hypomineralized, brittle and fragile enamel which occurs after they erupt into the mouth.

Hydroxyapatite is converted to fluorohydroxyapatite as follows:

Dental fluorosis can be prevented at a population level through defluoridation. It is the downward adjustment of the level of fluoride in drinking water.

Dental fluorosis may or may not be of cosmetic concern. In some cases, there may be varying degrees of negative psychosocial effects. The treatment options are:

  • Mild cases: Tooth bleaching
  • Moderate cases: Micro-abrasion (outer affected layer of enamel is abraded in an acidic environment)
  • Severe cases: Composite fillings, Micro-abrasion, Veneers, Crowns
Fluorosis is extremely common, with 41% of adolescents having definite fluorosis, and another 20% "questionably" having fluorosis according to the Centers for Disease Control. As of 2005 surveys conducted by the National Institute of Dental and Craniofacial Research in the USA between 1986 and 1987 and by the Center of Disease Control between 1999 and 2004 are the only national sources of data concerning the prevalence of dental fluorosis. Before the 1999-2004 study was published, CDC published an interim report covering data from 1999 to 2002.

CDC findings on children and adolescents
Deans Index2002
Questionable fluorosis11.5%
Very mild fluorosis21.68%
Mild fluorosis6.59%
Moderate to severe fluorosis3.26%
Total confirmed fluorosis prevalence31.65%
Total confirmed and questionable fluorosis prevalence43.15%
The U.S. Centers for Disease Control found a 9 percentage point increase in the prevalence of confirmed dental fluorosis in a 1999-2002 study of American children and adolescents than was found in a similar survey from 1986-1987 (from 22.8% in 1986-1987 to 32% in 1999-2002). In addition, the survey provides further evidence that African Americans suffer from higher rates of fluorosis than Caucasian Americans.

The condition is more prevalent in rural areas where drinking water is derived from shallow wells or hand pumps.[citation needed] It is also more likely to occur in areas where the drinking water has a fluoride content greater than 1 ppm (part per million).

Age groupReference weight kg (lb)Adequate intake (mg/day)Tolerable upper intake (mg/day)
Infants 0–6 months7 (16)0.010.7
Infants 7–12 months9 (20)0.50.9
Children 1–3 years13 (29)0.71.3
Children 4–8 years22 (48)1.02.2
Children 9–13 years40 (88)2.010
Boys 14–18 years64
Girls 14–18 years57 (125)3.010
Males 19 years and over76 (166)4.010
Females 19 years and over61 (133)3.010
If the water supply is fluoridated at the level of 1 ppm, one must consume one litre of water in order to take in 1 mg of fluoride. It is thus improbable a person will receive more than the tolerable upper limit from consuming optimally fluoridated water alone.

Fluoride consumption can exceed the tolerable upper limit when someone drinks a lot of fluoride-containing water in combination with other fluoride sources, such as swallowing fluoridated toothpaste, consuming food with a high fluoride content, or consuming fluoride supplements. The use of fluoride supplements as a prevention for tooth decay is rare in areas with water fluoridation, but was recommended by many dentists in the UK until the early 1990s.

In November 2006 the American Dental Association published information stating that water fluoridation is safe, effective and healthy; that enamel fluorosis, usually mild and difficult for anyone except a dental health care professional to see, can result from ingesting more than optimal amounts of fluoride in early childhood; that it is safe to use fluoridated water to mix infant formula; and that the probability of babies developing fluorosis can be reduced by using ready-to-feed infant formula or using water that is either free of fluoride or low in fluoride to prepare powdered or liquid concentrate formula. They go on to say that the way to get the benefits of fluoride but minimize the risk of fluorosis for a child is to get the right amount of fluoride, not too much and not too little. "Your dentist, pediatrician or family physician can help you determine how to optimize your child’s fluoride intake."

Dental fluorosis can be prevented by lowering the amount of fluoride intake to below the tolerable upper limit. The number of cases of dental fluorosis occurring in a population could be reduced by defluoridation drinking water. However, there are other sources of fluoride such as fluoride containing toothpastes. Also, defluoridation of water will not reverse the condiiton in an individual once exposure to excessive levels of fluoride during the years of tooth enamel formation has already occurred.

In ancient times, Galen describes what is thought to be dental fluorosis. However, it was not until the early 20th century that dental fluorosis became increasingly recognized and scientifically studied.

In 1901 Eager published the first description of the "mottled enamel" of immigrants from a small village near Naples, Italy. He writes that the condition is called "Denti di Chiaie" (Chiaie teeth), named after Stefano Chiaie, an Italian professor. In the United States of America, a dentist, Frederick McKay, set up practice in Colorado Springs in 1901 and discovered a high proportion of the residents had stained teeth, locally termed the "Colorado brown stain". He took this information to Greene Vardiman Black, a prominent American dentist of the time. After examining specimens of affected enamel, in 1916 Black described the condition as "[a]n endemic imperfection of the enamel of the teeth, heretofore unknown in the literature of dentistry." They made the interesting observation that although the mottled enamel was hypomineralized, and therefore should be more susceptible to decay, this was not the case.Gradually, they became aware of existing and further reports of a similar condition worldwide.

In 1931, 3 different groups of scientists around the world published their discoveries that this condition was caused by fluoride in drinking water during childhood. The condition then started to become termed "dental fluorosis". Through epidemiological studies in the US, Henry Trendley Dean helped to identify a causal link between high concentrations of fluoride in the drinking water and mottled enamel. He also produced a classification system for dental fluorosis that is still used in modern times, Dean's Index. As research continued, the protective effect of fluoride against dental decay was demonstrated.

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What is Root Canal Treatment (RCT)? Why do I need to Do RCT?

Root canal Treatment, a sophisticated term as it may seem to the general public, is the treatment done to a tooth with severe decay to such an extent that it has already involved the innermost pulpal layer of the tooth. It is not to be feared as many people do and have negative emotions attached to the term as well as the procedure.

The tooth is a mineralized tissue of the body, which once formed completely, doesn't regenerate if it is lost due to caries or is broken. The tooth tissue once lost due to demineralization and cavitation will not be restored unless some inert and biocompatible material is filled into the cavity after removing the decayed portion and the causative bacteria from the lesion.

The tooth decay which begins as a pit and fissure caries at first is reversible and can be arrested if a favorable environment for remineralization is provided. The initial carious lesion involving enamel only or superficial layer of dentin can be restored with Glass Ionomer Cements or Dental Composite Restorative resins by simply preparing a cavity of adequate shape and size for the restorative material to remain there and function properly for a long time. If the decay is to that extent that it involves the pulp, simply filling the cavity  will not eliminate the pain and halt the carious process. So, the pulpal tissue within the crown portion of tooth (the part of tooth that is seen clinically) as well as from the root canal. The canal should be cleaned up to clear all the bacteria and the root canal should be shaped and enlarged such that it can receive an inert filler into it (gutta percha) and then it can be restored to function as a normal tooth.

Root canal treatment is the best option to treat irreversible pulpitis and conserves natural tooth structure because:
- Artificial prostheses are not as good as natural dentition however close they may resemble it
- The patient doesn't have to undergo extraction (invasive procedure much feared  by patients) and the need for prosthesis
- Cost of treatment is cheaper and the tooth becomes functional very early.

Hence, Root canal treatment is the best treatment plan for your severely painful tooth in which the caries has already reached upto pulp but that can be saved via endodontic treatment.

# Gingiva is attached to tooth by:

# Gingiva is attached to tooth by:
A. Epithelial attachment
B. Periodontal Ligament
C. Connective tissue fibers
D. Lamina Propria

Answer: A, Epithelial Attachment

- Gingiva is attached to tooth by Junctional Epithelium which forms a collar around the tooth. It is wider (15-30 cells thick) at the floor of the gingival sulcus and tapers apically to a final thickness of some 3-4 cells. 

- Surface cells of the junctional epithelium provide the actual attachment of gingiva to tooth tissue (the epithelium being sometimes referred to as attachment epithelium)

- The internal basal lamina of Junctional epithelium unites the epithelium to tooth whereas the external basal lamina of junctional epithelium unites the epithelium to the connective tissue of the gingiva. 

- Basal lamina of junctional epithelium is devoid of type IV collagen and type VIII is present.


Types of Cementum / Classification of Cementum

Schroeder has classified Cementum as follows:

A. Acellular Afibrillar Cementum (AAC)
- Contains neither cells nor extrinsic or intrinsic collagen fibers apart from a mineralized ground substance
- It is a product of cementoblasts
- In humans, it is found in the coronal cementum

B. Acellular Extrinsic Fiber Cementum (AEFC)
- It is composed entirely of densely packed bundles of Sharpey's fibers and lacks cells.
- It is a product of fibroblasts and cementoblasts
- In humans, it is found in the cervical 1/3rd of roots but may extend further apically

C. Cellular Mixed Stratified Cementum (CMSC)
- It is composed of extrinsic (Sharpey's) and predominantly intrinsic fibers and contains cells
- It is coproduct of fibroblasts and cementoblasts
- In humans, it appears primarily in the apical third of the roots and the apices and in the furcation areas

D. Cellular Intrinsic Fiber Cementum (CIFC)
- Contains cells but no collagen fibers
- It is formed by cementoblasts.
- In humans, it fills resorption lacunae.

# Width of attached gingiva:

# Width of attached gingiva:
A. Decreases with age
B. Increases with age
C. Remains the same
D. Is not age-related

B. Increases with age

Because the mucogingival junction remains stationary throughout adult life, changes in the width of attached gingiva are caused by the modification in the position of the coronal end.

The width of attached gingiva increases with age and in supraerupted teeth, with the wear of the incisal edge and continued tooth eruption. The gingival margin of the tooth, therefore the entire dentogingival complex, moves coronally with a resulting increase in width of the attached gingiva.


How Long Do Dental Restorations Last?

This is one of the most frequently faced questions by a dentist, "Doctor, How long will my dental restoration last?" In the competitive world of today, people are taken away by the fake promises and guarantees the corporations and manufacturer companies make and expect everything to have a guarantee. But, this question, in particular, is ridiculous because we cannot predict the health or disease of any person or how long will he last!

But, answering the  question, the life of any dental restoration depends principally upon four factors:
- remaining tooth structure
- material with which the tooth is being restored
- clinical technique & expertise of the dentist i.e. how well the restoration is done
- post-restoration environmental challenges the tooth is subjected to

Let's see all these one by one.

i) Remaining tooth structure

"A stitch in time saves nine." This age-old proverb can be well realized in dentistry. We can expect the dental restorations' cost to be cheaper, less time consuming and successful for a long time too if the treatment is done as early as possible. We cannot expect a tooth with cavity extending up to the cervical third of crown involving pulp with almost two-thirds of the crown lost already to have the same prognosis as that of the tooth with cavity extending only up to the enamel layer or superficial dentinal layer.

A restoration may fail due to several reasons:
No 1. - Restoration may fracture if its bulk is too small or its mechanical strength is too low.
No 2. - The tooth may fracture if most of the tooth structure is already lost or excessive occlusal force is applied on the restored tooth.
No. 3 - Failure at the tooth restoration junction: If there is no proper seal at the tooth restoration junction, the food materials, and bacteria can percolate through the breach into the tooth and can cause secondary caries.

Let's see the second factor determining the life of dental restoration.

ii) Material with which the tooth is being restored :

Three major dental restorative materials currently used in dentistry are: 
- Glass ionomer cement
- Dental composite resins
- Amalgams (not used in many countries but still used in some due to the environmental hazard of mercury)

Different types of glass ionomer cement according to their use are available. Glass ionomers are used mostly in the deciduous teeth of children but they can be used adults too and latest GICs with improved properties have been reported to last about 3-5 years too.

Regarding dental composite resins and amalgams, they have similar strength and longevity provided that, the restoration is done meticulously in ideal conditions.

A rule of thumb for clinical service of restoration is that occlusal restorations are stressed an average of one million times per year. And, typically material fails in the range of 10-100 million cycle range during laboratory testing. 

Also, different products from different manufacturers have different mechanical properties. You cannot expect a composite resin from some unknown manufacturer in China to work equally well as that from an internationally renowned brand. 

The third factor determining the longevity of restoration is the clinical technique and expertise. 

iii) How well the dentist has restored the tooth?

Just because the dentist is old and experienced doesn't mean that he will do the restoration well. A dentist who can do well, may not do his best at all times if he is inattentive or is in a hurry. Improper isolation of tooth and contamination by saliva during the procedure also might have compromised the strength. 

And the last and most important factor for the longevity of dental restorations is:

iv) Post-restoration environmental challenges the tooth is subject to

How long would your house last if it were subjected to hot sweet coffee and immediately to freezing cold ice cream? How long would it last if it were struck for about 5000 times daily? What if it is subjected to acidic pH as low as 3 and to alkaline pH as high as 11 within a few minutes? That is what our dental restoration has to sustain. We eat and drink acidic and alkaline foods, hard and soft foods, cold and hot foods, every sort of food without any consideration. How long will it be before the material fatigue occurs in the restoration and breaks down?
By now, you might have understood what I mean to say. But it is a safe bet to say that dental restorations will last about an average of 6-8 years if all the above factors are considered. However, there are cases of restoration failures the very next day as well as some amalgam restorations about 30 years old.

How long has your restoration lasted? What was the material? Please Comment Below for record purpose. Feedback and Suggestions for the article are heartily welcome.

What is Halal Food? - FAO Guidelines for Halal Food


CAC/GL 24-1997[27]

The Codex Alimentarius Commission accepts that there may be minor differences in opinion in the interpretation of lawful and unlawful animals and in the slaughter act, according to the different Islamic Schools of Thought. As such, these general guidelines are subjected to the interpretation of the appropriate authorities of the importing countries. However, the certificates granted by the religious authorities of the exporting country should be accepted in principle by the importing country, except when the latter provides justification for other specific requirements.


1.1 These guidelines recommend measures to be taken on the use of Halal claims in food labeling.

1.2 These guidelines apply to the use of the term halal and equivalent terms in claims as defined in General Standard for the Labelling of Prepackaged Foods and include its use in trademarks, brand names and business names.

1.3 These guidelines are intended to supplement the Codex General Guidelines on Claims and do not supersede any prohibition contained therein.


2.1 Halal Food means food permitted under Islamic Law and should fulfill the following conditions:

2.1.1 does not consist of or contain anything which is considered to be unlawful according to Islamic Law;

MCQs on NSAIDs and Other CNS Drugs Part 1

The correct answers are highlighted in Green. Once you have finished studying these MCQs, Test yourself by watching the video at the bottom of the page.

#  Which of the following drugs is least efficacious in the treatment of temporal lobe epilepsy? (MAN-94, AIIMS-93)
a) Phenobarbitone
b) Phenytoin sodium
c) Primidone
d) Carbamazepine

# All are true of diazepenes except: (MAN-02)
a) Benzodiazepam is used in treatment of status epilepticus
b) Benzodiazepam is used in the long term treatment of psychic disorders
c) Clonazepam is used in the treatment of petit mal epilepsy
d) None of the above

# Morphine is contraindicated in all of the following except (MAN-02)
a) Pulmonary oedema 
b) Emphysema
c) Bronchial asthma 
d) Head injury

# Aspirin produces all of the following effects except: (MAN-02)
a) Frank gastric bleeding
b) Prolonged prothrombin time
c) Platelet dysfunction
d) Constipation

# Which of the following is not a contraindication in the therapy with opioids? (MAN-2K)
a) Use in head injury patient
b) Use in impaired pulmonary function
c) Use of agonist with mixed agonist-antagonist
d) Use in severe constant pain

# Which of the following can be given safely to a patient of congestive heart failure? (MAN-2K)
a) Aspirin 
b) Paracetamol
c) Diclofenac sodium 
d) Ibuprofen

# A common side effect associated with all NSAID drugs is: (MAN-98)
a) Drowsiness 
b) Gastric irritation
c) Xerostomia 
d) Constipation

# Which of the following is an irreversible side effect resulting from long term administration of phenothiazine antipsychotics? (MAN-97)
a) Infertility 
b) Parkinsonism
c) Tardive dyskinesia 
d) B & C

# Verrill's sign is seen in: (MAN-2K, AP-2001)
a) Diazepam administration
b) Digitalis toxicity
c) Paget's disease 
d) Unconscious states

# Which of the following anti inflammatory drug is a COX- 2 inhibitor? (AIPG-01)
a) Rofecoxib
b) Ketoprofen
c) Aspirin
d) Sulidec 

# One of the benzodiazepines (BDZ) comparatively safe in pregnancy is (Category -B): (KAR-2003)
a) Zolpidem
b) Lorazepam
c) Alprazolam
d) None of them

# Morphine a powerful opioid analgesic drug should be avoided in all the following conditions except: (AIPG-01)
a) Bronchial asthma
b) Left ventricular failure
c) Pancreatitis
d) Constipation

# All the following decrease skeletal muscle tone by CNS effects except: (AIPG-99)
a) Diazepam
b) D-tubocurarine
c) Baclofen
d) Mephensin

# Which of the following anti-epileptic agents causes the reversible side-effect of gingival hyperplasia? (MAN-99)
a) Sodium valproate
b) Ethosuximide
c) Phenobarbitone
d) None of them

# NSAID's have adverse effect on: (AIPG-97)
a) Liver
b) Bone
c) Stomach
d) Kidney

# Salicylate overdose in children causes: (AIPG-93)
a) Crystalluria
b) Reye's syndrome
c) Kernicterus
d) None of them

# Carbamazepine is a type of: (AIPG-97)
a) Antiemetic
b) Anti-inflammatory
c) Antidepressant
d) Antibiotic

# Drug which causes gingival hyperplasia: (AIPG-94)
a) Cyclosporin & Nifedipine
b) None of them
c) Aspirin
d) Erythromycin

# All the following statements about opioids is correct except: (AIPG-2001)
a) Pentazocine shows withdrawal symptoms in opioid dependent patients
b) Pentazocine and buprinorphine
c) Ethomorphine is similar to pethidine chemically
d) Partial agonists are free from classic opioid adverse effects

# A patient on 300 mg of aspirin will show all the following except: (AIIMS-94)
a) Prolonged bleeding time
b) Irreversible inhibition of cyclooxygenase path way
c) Inhibition of prostaglandin PGI2
d) Inhibition of thromboxane TXA2

# Thiopentone action is terminated by: (AIPG-99)
a) Metabolism
b) Redistribution
c) Excretion
d) Recycling

# Amyl nitrate is most commonly administered: (MAN-98)
a) Sub lingually
b) Orally
c) Intravenously
d) By inhalation

# Clotting time is most likely to be prolonged by the administration of:
a) Barbiturates
b) Vitamin K
c) Acetaminophen
d) Acetyl salicylic acid

# Aspirin acts on which part of brain? (AIIMS-92)
a) Cortex
b) Medulla
c) Substantia gelatinosa
d) Limbic system

# Antagonist of morphine is: (AIPG-93)
a) Nalpuphine
b) Nalosphine
c) Methadine
d) Naloxone

# Carbamazepine is contraindicated in? (AIPG - 14)
a) Temporal lobe epilepsy
b) Juvenile myoclonus epilepsy
c) None of them
d) Generalized tonic clonic

# Phenytoin is associated with: (AIPG-97, 96)
a) Cushing's syndrome
b) Folic acid deficiency
c) Vitamin C deficiency
d) Alzheimer's disease

# Aspirin causes: (AIPG-97)
a) Hemolytic anemia
b) Aplastic Anaemia
c) Hypoprothrombinemia
d) Agranulocytosis

# Aspirin is used in treatment of Myocardial Infarction: (AIPG-02)
a) It inhibits thromboxanes
b) It helps in reducing inflammatory aggregate
c) It stimulates Prostacyclins
d) It is a vasodilator

# Amitryptyline is a: (AP-03)
a) Tricyclic antidepressant
b) Sedative
c) Antibiotic
d) Diuretic

# Drug which is used to control status epitepticus is: (AP-97, AIPG-93)
a) Glyceryl trinitrite
b) Phero barbital
c) Sodium nitroprusside
d) Diazepam

# Narcotic overdose can be antagonized by: (MAN-99)
a) Nalorphine
b) Naloxone
c) Diphenhydramine
d) Atropine

# An attack of migraine can be easily terminated by: (AIPG-99)
a) Acetylcholine
b) Ergotamine
c) Morphine
d) Ibuprofen

# Which of the following drugs causes extra pyramidal symptoms? (PGI-2K)
a) Antibiotics
b) Barbiturates
c) Salicylates
d) Phenothiazines

# Pregnant patient can be safely given: (AP-2K)
a) Paracetamol
b) Barbiturates
c) Tetracycline
d) Metronidazole

# Aspirin is avoided in children with influenza infection because of association of: (KAR-99)
a) Nausea
b) Diarrhoea
c) Acid-base imbalance
d) Reye's syndrome

# Nausea and vomiting that are associated with administration of opioid analgesic is the result of stimulation of the: (MAN-97)
a) Emetic system
b) Opioid receptors in G.I.T.
c) Limbic system
d) Chemoreceptor trigger zone (CTZ)

# Prolonged use of aspirin causes: (AIPG-98)
a) Hypophosphatasia
b) Hypercalcemia
c) Hyperprothrombinemia
d) Hypoprothrombinemia

# The intramuscular administration of 0.6 mg of atropine sulphate to a 50 kg adult may produce all of the following: effects except: (AIIMS-93)
a) Mydriasis
b) Bradycardia
c) Decreased sweating
d) Decreased salivation

# Prolonged use of aspirin leads to: (AIPG-98)
a) Carcinoma
b) Bleeding defects
c) Peptic ulcer
d) B & C

# Phenothiazines are used to: (AIPG-2003)
a) Suppress coughing
b) Produce muscle relaxation
c) Alter psychotic behaviour
d) Produce analgesia

#  A 50 year old female with end stage renal disease (ESRD), develops pulmonary tuberculosis. Which one of the following drugs should be used in a reduced dose? (KCET-2011)
a) Ethambutol
b) Pyrazamide
c) Isoniazide
d) Rifampicin

# Drug that does not cause sedation: (AIPG-2011)
a) Zopiclone
b) Nitrazepam
c) Buspirone
d) Diazepam

# An attack of bronchial asthma is most likely to be triggered by: (KAR-99)
a) Aspirin
b) Mefenamic acid
c) None of them
d) Diclofenac potassium

MCQs on Skin and Vesiculobullous Diseases - Oral Pathology and Medicine MCQs

The correct answers are highlighted in Green. Once you have finished studying these MCQs, Test yourself by watching the video at the bottom of the page.

# A flat, circumscribed discoloration of skin or mucosa that may vary in size and shape is referred to as: (MAN -94,95; AP- 08)
a) Epulis
b) Macule
c) Nodule
d) Papule

# A twenty-one-year-old woman complains that regular, gentle brushing of her teeth is painful besides causing profuse bleeding. Oral examination reveals the loss of epithelium from the attached gingiva of both arches. Which of the following dermatological problems is this patient most likely to have? (MAN -95)
a) Benign mucous membrane pemphigoid
b) Chronic discoid lupus erythematosus
c) Pemphigus
d) Psoriasis

# Which of the following is an oral manifestation of lichen planus? (MAN -95)
a) Dentinogenesis imperfecta
b) Fordyce spots
c) White, chalky enamel surface
d) White radiating lines on the buccal mucosa

# Antinuclear antibodies are seen in: (MAN -98, KCET -07)
a) SLE
b) Systemic sclerosis
c) Morphea
d) All of the above

# Which of the following diseases of the skin is the most likely to be associated with partial anodontia? (MAN -98, KAR -03)
a) erythema multiforme
b) hereditary ectodermal dysplasia
c) keratosis follicularis
d) lichen planus

# Which of the following is absent in CREST syndrome? (KAR -03, PGI -99, MAN -2K)
a) Calcinosis cutis
b) Raynaud's phenomenon
c) Telangiectasia
d) Endocrine disorders

# Nikolsky's sign is positive in: (KAR -03, COMEDK -03)
a) bullous pemphigus
b) epidermolysis bullosa
c) herpes simplex
d) erythema multiforme

# MONRO's abscess are seen in: (MAN -2K, KAR -97,98)
a) Pemphigus
b) Lichen planus
c) Leukoplakia
d) Psoriasis

#  In lichen planus the basal cells which are shrunken with an eosinophilic cytoplasm and with a pyknotic and fragmented nuclei are called: (MAN -01)
a) Tzanck cells
b) Civatte bodies
c) Donovan bodies
d) Rushton bodies

# Grinspan syndrome is associated with: (COMEDK -03, 06, KAR-04)
a) Hypertension, diabetes, lichen planus
b) Oral, ocular, genital lesions
c) Hypertension with oral lesions
d) Pemphigus, CHF, diabetes

# Ectodermal dysplasia is: (AIPG-05)
a) Autosomal recessive
b) Autosomal dominant
c) X-linked dominant
d) X-linked recessive

# Which sites are characteristically affected in Stevens- Johnson syndrome? (APPSC -99)
a) Conjunctiva, genitalia, oral mucosa
b) Liver, spleen, pancreas
c) Oral mucosa, lacrimal apparatus, ears
d) Parotid gland, palate, conjunctiva

# Which one of the following is NOT a lichenoid reaction? (COMEDK-14)
a) Graft versus Host disease
b) Fixed drug eruption
c) Secondary syphilis
d) Pemphigus vulgaris

# Oral diagnostic features of scleroderma include all of the following, except: (KAR -2K)
a) Pseudo ankylosis of the T.M. Joint
b) Widening of the oral aperture
c) A hard and a rigid tongue
d) Difficulty in swallowing

# A typical example of an immunologically mediated collagen vascular/connective tissue disorder is: (MCET-14)
a) Lichen planus
b) Pemphigus vulgaris
c) Lupus erythematosus
d) Epidermolysis bullosa

# Fine Needle aspiration biopsy is indicated to diagnose: (KAR -98)
a) Necrotic pulp
b) Pemphigus
c) Traumatic ulcer
d) Chronic gingivitis

# Subepithelial vesicles are characteristic all of the following EXCEPT: (KCET-08)
a) Bullous pemphigoid
b) Pemphigus
c) Epidermolysis bullosa acquisita
d) Cicatricial pemphigoid

# Which is a degeneration disorder characterized by atrophic changes of the deeper structures (e.g. fat, muscle, cartilage & bone) involving one side of the face: (AIPG -04, 05)
a) Miescheris syndrome
b) Peutz-Jeghers syndrome
c) Parry Romberg syndrome
d) Scleroderma

# In Cicatrial pemphigoid, which antigen is bound by IgG on the epidermal side of the salt split skin technique: (COMEDK-07)
a) Laminin 5
b) XVII collagen
c) epitigrin
d) BP antigen 1 & 2

# L.E. Cell phenomenon in peripheral blood is seen in: (KAR -2K)
a) Systemic Lupus Erythematosus
b) Ischemic heart disease
c) Infective endocarditis
d) Rheumatic heart disease

#  Erosive lichen planus resembles which of the following: (AIIMS -2K)
a) Monilial gingivitis
b) Acute ulcerative gingivitis
c) Desquamative gingivitis
d) Herpetic gingivitis

# Grinspan syndrome is associated with: (KAR-04)
a) Lichen planus
b) Aphthous ulcer
c) Leukoplakia
d) Oral submucous fibrosis

# Desmoplakin is the target antigen in: (AP-2012)
a) Pemphigus foliaceous
b) Pemphigus Vulgaris
c) Drug-induced pemphigus
d) Paraneoplastic pemphigus

# Unusual extensibility of the tongue is a characteristic feature of: (KAR -03)
a) Syphilis
b) Darier-White disease
c) Ehlers-Danlos syndrome
d) Epidermolysis bullosa

# 60 year old diabetic female presented with burning sensation to spicy food, Intraoral examination revealed multiple periodontal abscess and keratotic area in a lace pattern with occasional erosive areas inside the lace pattern. Syndrome associated with this disease is: (COMEDK-14)
a) Peutz jeghers syndrome
b) Sjogren's syndrome
c) Down's syndrome
d) Grinspan syndrome

# En coup de sabre is most likely to be associated with which type of scleroderma?
a) Linear
b) Radicular
c) Vertical
d) Ovoid

# Histopathologic study of lichen planus shows: (AIIMS-99,94; KAR-98)
a) Antiepithelial antibodies
b) Scattered infiltrate with ill-defined lower border
c) Mixed cellular inflammatory infiltrate
d) Presence of T-lymphocytes predominantly

# Cafe au lait macules are seen in: (KCET-10)
a) Albright's syndrome and Bloom's syndrome
b) Von Reklinghausen's neurofibromatosis
c) None of them
d) All of them

# Psoriasis is associated with: (PGI -95)
a) Lupus erythematosus
b) Lupus vulgaris
c) Benign median rhomboid glossitis
d) Geographic tongue

# White radiating lines can be observed in case of lesions of: (AP -2K, AIIMS MAY -2012)
a) Erythema multiforme
b) Lichen planus
c) Pemphigus
d) Leukoplakia

#  Pemphigus is characterized by: (AIPG -94, 06)
a) Hyperparakeratosis
b) Hyperorthokeratosis
c) Acantholysis
d) Acanthosis

# 60 year old diabetic female presented with burning sensation to spicy food. Intraoral examination revealed multiple periodontal abscess and keratotic area in a lace pattern with occasional erosive areas inside the lace pattern. Histological feature will be: (COMEDK-14)
a) Saw tooth rete ridges
b) Bulbous rete ridges
c) Elongated rete ridges
d) Flattened rete ridges

# Mucocutaneous lesion associated with neoplasia : (COMEDK-2011)
a) Paraneoplastic pemphigus
b) Parapemphigus
c) Pemphigus vegetans
d) Familial benign pemphigus

# ALL the following are inherited disorders of connective tissue EXCEPT: (KAR- 2013)
a) Marfan syndrome
b) McArdle's disease
c) Ehlers-Danlos syndrome
d) Alport syndrome

# Cicatrical pemphigoid is the synonym for: (AP-2012)
a) pemphigus vulgaris
b) mucous membrane pemphigoid
c) paraneoplastic pemphigus
d) Hailey-Hailey disease

# Pathologic calcification is seen in: (COMEDK-09)
a) Scleroderma
b) Lupus erythematosus
c) Dystrophic epidermolysis bullosa
d) Lichen planus

# A 3-year-old patient has extensive vesicles on lip, tongue, oral mucous membrane. After 2-4 days vesicles rupture at followed by pseudomembrane formation and also some dermal lesions seen what will be the diagnosis: 
a) Steven-Johnson syndrome
b) Herpetic stomatitis
d) EM

# Oral, ocular and genital lesions are seen in: (AP -04)
a) Erythema multiforme
b) SLE
c) Stevens-Johnson syndrome
d) None of them

#  Tzanck smear test is used in the diagnosis of: (KAR -02)
a) Pemphigus
c) Lichen planus
d) Apthous disease

# Multiple pulp stones are seen in: (COMEDK-10)
a) Down's syndrome
b) Ehler's Danlos syndrome
c) Apert's syndrome
d) Marfan Syndrome

# Erythema multiforme is: (KAR -97)
a) Bacterial infection
b) An acute self-limiting disease, of skin and oral mucous membrane
c) Painless vesicular self-limiting disease
d) A viral disease

# Target Lesions are observed in case of: (COMEDK -03, 06; AP -2K)
a) Erythema multiforme
b) Psoriasis
c) Lichen planus
d) Pemphigus vulgaris

# Lupus erythematosus is: (KAR -03)
a) Autoimmune disorder
b) Neoplastic condition
c) Degenerative condition
d) Reactive Lesion

# Oral Lesions are not seen in: (AP -04)
a) Psoriasis
b) Pemphigoid
c) Candidiasis
d) Stevens-Johnson syndrome

# False about mucous-membrane pemphigoid: (PGI-2014)
a) Twice in female
b) Disease associated antigen are most frequently present in lamina densa
c) Oral mucosa is most frequently involved
d) Autoantibodies towards basement membrane protein

# The swollen degenerating epithelial cell due to acantholysis is: (KAR-04)
a) Tzanck cell
b) Prickle cell
c) Anitschow cell
d) Ghost cell

# Primary lesion in lichen planus is: (KAR -97)
a) Bulla
b) Vesicle
c) Papule
d) Macule

# Koebner's phenomenon is seen with: (KAR -02)
a) Psoriasis
b) Erythema muLtiforme
c) Impetigo
d) Pemphigoid

# Which of the following is inherited as an autosomal dominant trait? (KAR -98rAIIMS -94)
a) Bullous pemphigoid
b) White sponge nevus
c) Lichen planus
d) Pemphigus vulgaris

# Wickham's striae are seen in: (AP -03}
a) Leukoedema
b) Erythema multiforme
c) Lichen planus
d) Leukoplakia

# In ectodermal dysplasia all of the following structures are affected except: (AIPG -94)
a) Teeth
b) Salivary glands
c) Nails
d) Hair

# Ehlers Danlos syndrome is? (AIPG-09)
a) X-Linked recessive
b) X-Linked Dominant
c) Autosomal recessive
d) Autosomal Dominant

# Butterfly rash is typically seen in: (KCET-10)
a) Systemic lupus erythematosus
b) Herpes simplex
c) Scleroderma
d) None of them

#  Joint erosions are not a feature of:  (AIPG-06)
a) Rheumatoid arthritis
b) Multicentric reticulo-histiocytosis
c) Systemic Lupus eythematosus
d) Psoriasis

# Xeroderma pigmentosum is characterized by: (COMED-2012)
a) Autosomal dominant inheritance
b) Inability to repair sunlight induced damage to DNA
c) Acanthosis of epithelium with elongation of rete ridges
d) Irregular accumulation of melanin in the basal cell layer

# All are diseases of skin except: (AIIMS-09)
a) Keratosis follicularis
b) Erythema multiforme
c) Psoriasis form lesion
d) Erythema migrans

# Intraepithelial vacuolation with formation of vesicle or bulla intraepithelially above the basal layer is characteristically seen in: (AIPG -95)
a) Pemphigus
b) Lichen planus
c) Bullous pemphigoid
d) Candida albicans

# Darier's disease is associated with: (AIPG -04)
a) Vitamin A deficiency and involvement of oral epithelium and skin
b) Diffuse tender ulceration on the palate predominantly
c) Pernicious anaemia
d) Rickets with involvement of teeth and bones

# Which of the following individual show susceptibility to dental caries? (PGI DEC-2013)
a) Down syndrome
b) Pierre robin syndrome
c) Epidermolysis bullosa
d) Hereditary fructose intolerance

# Which of the following is not a type of lichen planus? (KAR -03)
a) Hypertrophic
b) Atrophic
c) Verrucous
d) Erosive

# Autoantibodies Anti Ro and Anti La are completely absent in: (COMEDK-15)
a) Sjogren's syndrome
b) Diffuse Scleroderma
c) Rheumatoid arthritis
d) Systemic lupus erythematosus

# Immunoflourescence is seen at basement membrane as patchy distribution in: (KAR -97)
a) Lichen Planus
b) Pemphigus
c) Pemphigoid
d) Lupus erythematosus

# Histological clefts in lichen planus are: (COMEDK-09)
a) Auspitz's sign
b) Civatte bodies
c) Wickham's Striae
d) Max - Joseph spaces

#  Most common lesion in Mucous membrane pemphigoid is: (COMEDK-14)
a) Esophageal ulcer
b) Ulcer of Soft palate
c) Symblepharon
d) Desquamative gingivitis

# Which of the following are seen in ectodermal dysplasia? (AIIMS -90}
a) Defective or absence of sweat glands
b) Hyperpyrexia
c) Protuberant lips and frontal bossing
d) Any of them

# In which of the following disorders a circulating antibody directed to intercellular cementing substance of stratified squamous epithelium is observed: (AIIMS, KAR -03)
a) Pemphigus vulgaris
b) Bullous pemphigoid
c) Verrucous vulgaris
d) Lichen planus

# Fish Net pattern in pemphigus vulgaris is seen in which of the following tests? (KAR-2013)
a) Tzanck smear
b) Histopathology
c) Direct immunofluorescence

# Intra-epithelial bulla are found in: (AIIMS-98)
a) Pemphigoid
b) Pemphigus
c) Bullous pemphigoid
d) Bullous lichen planus

# A 60-year-old has got severe bulla and target lesion which erythema around halo and genital Lesions: (AIIMS -2K)
a) Herpes zoster
b) Stevens Johnson syndrome
c) Herpes simplex
d) Herpangina

# Bullae formation after striking an intact skin/mucosal surface is known as: (KAR -2K)
a) Chovstek's sign
b) Tinel's sign
c) Babinski's sign
d) Nikolsky's sign

# Hydropic degeneration of the basal cell of the stratum germinativum is a feature of? (PGI-08)
a) Leukoplakia
b) Lichen Planus
c) Pemphigus
d) Syphilis

# Steven-Johnson syndrome involves: (AIPG -98)
a) Type I hypersensitivity reaction
b) Type IV hypersensitivity reaction
c) Type II hypersensitivity reaction
d) Type III hypersensitivity reaction

# Lichen planus: (KAR -02)
a) Must be excised
b) Treated only by medication
c) Can undergo malignant change
d) Is an idiosyncrasy reaction

# Oral lesion associated with ulcerative colitis: (COMEDK-10)
a) Pyostomatitis Vegetans
b) Sarcoidosis
c) Lichen planus
d) Dermatitis herpetiformis

# Immunoflourescence test is positive in: (AIPG -95)
a) Psoriasis
b) Lupus erythematosus
c) Scleroderma
d) Myxoedema

# Formation of multiple pinpoint bleeding spots on scratching the skin is characteristic of: (KAR -2K)
a) Pemphigus vulgaris
b) Lupus erythematosus
c) Psoriasis
d) Herpangina

# Lichenoid reactions are mainly due to: (AP-99)
a) intake of alcohol
b) cigarette smoking
c) betel nut chewing
d) intake of certain drugs