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Adverse Drug Reactions And Orofacial Tissues Flashcards

1
Q

How often do oral adverse effects by medicines occur?

A

Oral adverse effects by medicines are rare but their impact signifixant

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2
Q

How can an adverse drug reaction present in the oral cavity

A 
Oral ulceration or blistering
Lichenoid reaction/ lupus like eruptions
Erythema multiforme
Discoloration of mucosa or teeth
Altered taste or sensation
Reduced or increased salivary flow
Salivary Gland or gingival swelling
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3
Q

When may an adverse reaction involve oropharyngeal candidosis

A

Following broad spectrum antibiotic use

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4
Q

What effect may bisphosphonate use have?

A

Osteonecrotic lesion in the bone of the Jaws may occur

Spontaneously or following tooth xla

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5
Q

Can adverse drug reactions have a genetic element? Give an example

A

Reaction seen with carbamazepine in individuals of Chinese descent

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6
Q

What is an adverse effect if the vasodilator antihypertensive drug hydralazine

A

Can predispose to symptoms that are almost indistinguishable from sjogrens syndrome.
Therefore may not be recognised as an adverse effect
Instead being misdiagnosed as a systemic disease

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7
Q

How can a hydralazine drug reaction be distinguished from sjogrens disease?

A

If the pt is suffering from a hydralazine drug reaction then normal histological findings in labial Gland biopsy will confirm this

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8
Q

What is hydralazine

A

An antihypertensive drug vasodilator
Can predispose to symptoms that are almost indistinguishable from sjogrens syndrome.
Therefore may not be recognised as an adverse effect
Instead being misdiagnosed as a systemic disease

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9
Q

When do clinical signs and symptoms of an adverse drug reaction present

A

The pt could be taking the medication for moths before clinical signs and symptoms become apparent

It’s quite rare for the pt to start a new drug and attend clinic the next week with symptoms of adverse drug reaction

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10
Q

What can help the clinician in diagnosing an adverse drug reaction

A

Ask the pt to bring in a print out of their current medication

This is particularly the case for pts who have been on the same medication for years

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11
Q

How is type 2 diabetes now controlled compared with the past and why is this important to clinical practice

A

Insulin is now also used to control type 2 diabetes mellitus in pts who previously were largely controlled with diet combined with oral hypoglycaemic age ts

The likelihood of a hypoglycaemic attack is much more in a type 2 diabetes who is controlled using insulin

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12
Q

Who is responsible for monitoring drug safety in clinical practice in the uk

A

The commission on human medicine CHM

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13
Q

What does the CHM encourage?

A

Using the yellow card system to report suspected adverse drug interactions

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14
Q

What does the yellow card do

A

Records details of the pt
Suspected drug
Pt details
Other concurrent medication

Can either be submitted by post or online

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15
Q

When regulatory authorities are considering advice on possible adverse drug reactions what clinical questions related to the drug therapy need to be considered

A

What are the manifestations of the adverse event
What proportion of pts taking a suspected drug will suffer symptoms
Are symptoms dose related
How long after taking the drug do symptoms appear
How long after cessation of drug therapy will the symptoms appear

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16
Q

How are sidee effects or adverse events usually listed?

A 
Very common: greater than 1 in 10
Common: 1 in 100 to 1 in 10
Uncommon: 1 in 1000 to 1 in 100
Rare: 1 in 10000 to 1 in 1000
Very rare: less than 1 in. 10000
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17
Q

What are the stages of drug development, who is involved

A

Synthetic chemist’s structure activity studies, novel compounds
Analytical chemist’s (confirm purity)
Pharmacologists (detect activity, toxicological studies)

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18
Q

What are adverse drug reactions to dental mineralised tissues? Give an example

A

The visual and structural changes that can be induced by tetracycline therapy during mineralisation of the developing teeth

A clinically identical phenomenon can occur in adults given prolonged tetracycline therapy

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19
Q

Is tetracycline staining only developed in children taking the drug?

A

No. A clinically identical phenomenon can occur in adults given prolonged tetracycline therapy

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20
Q

How is the staining thought to occur following tetracycline therapy?

A

Tetracycline section into saliva

Surface remineralisation and demineralisation

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21
Q

What other antibiotic has an adverse effect on dental mineralised tissues? Can this be treated

A

Rifampicin
Teeth can be yellowed
Removed by polishing

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22
Q

Can drugs precipitate various orofacial changes in an unexpected manner that closely mimic naturally occurring diseases?

A

Yes
In this way drugs act as “precipitating factors’
When they produce an orofacial adverse reaction in a relatively predictable manner

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23
Q

What is an example of drugs as precipitating factors

A

Candidiasis following systemic antibiotic therapy or corticosteroid therapy either topically or systemically

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24
Q

What is the characteristic manifestation of systemic antibiotic therapy in the mouth

A

Pseudomembranous oral candidosis in the soft palate

The erythematous (painful form) may also occur

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25
Q

If a female suffers from candidosis where is it also likely to occur

A

Vagina

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26
Q

How can this Vaginal candidosis be prevented

A

Concomitant systemic use of antifungal fluconazole

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27
Q

If the pt is takinf antibiotic therapy what else may present apart from candidosis on the palate

A

A localised form of oral erythematous candidosis identical to median rhomboid glossotis

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28
Q

What should the pt be instructed to od at home to avoid median rhomboid glossotis and palatal candidosis

A

Pts should be instructed to rinse or gargle with water after inhaler use to clear residual drug
Since up to 80% of the steroid can remain in the oral cavity

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29
Q

How much of the steroid can remain the mouth if the pt doesn’t gargle after use

A

up to 80% of the steroid can remain in the oral cavity

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30
Q

What can using a spacer and gargling with water after steroid use prevent?

A

Palatal candidosis and median rhomboid glossotis potentially

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31
Q

What are bisphosphonates prescribed for

A

Osteoporosis mainly

Pagets disease, metastatic cancer affecting bone and hypocalcaemia of malignancy

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32
Q

How many groups of bisphosphonates exist

A

Three groups of bisphosphonates are recognised

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33
Q

How do bisphosphonates work

A

Two of the bisphonates inhibit the enzyme farnesyl pyrophosphate synthetase (important factor in osteoclast function)
The third bisphosphonate is incorporated into adenosine triphosphate leading to osteoclast apoptosis

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34
Q

How are bisphosphonates administered

A

Intravenously or orally

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35
Q

Who is most likely to develop BRONJ

A

Cancer pts receiving these drugs at high doses intravenously

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36
Q

Which appears to have less risk of adverse event oral or intravenous administration of bisphosphonates

A

Oral

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37
Q

How in bronj treated

A

Maybe

  1. Antibiotic therapy (clindamycin penetrates bone well) either as treatment or preventive capacity
  2. Local measures
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38
Q

Which antibiotic is used to treat Bronj why?

A

Clindamycin

Penetrates bone well

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39
Q

In what ways may drug therapy affect salivary Gland

A

There are 4 main ways in which drug therapy can affect salivary Gland structure or function

  1. Sialosis
  2. Sialorhea
  3. Salivary gland pain
  4. Xerostomia
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40
Q

What is sialosis

A

Non neoplastic
Non inflammatory
Persistent swelling of the salivary tissues
Usually of both the parotid glands

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41
Q

What salivary glands does sialosis affect

A

One or both parotid glands

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42
Q

What drugs are associated with sialosis

A

Phenylbutazone
Anti thyroid drug propylthiouracil
Isoprenaline

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43
Q

What do isoprenaline, anti thyroid drug propylthiouracil have in common

A

They can all cause sialosis

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44
Q

In clinical practice what is the commonets drug to cause sialosis

A

Alcohol

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45
Q

What is the prevalence of sialosis recorded in diabetic pts

A

25%

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46
Q

What mouthwash has been rarely reported as causing salivary swelling

A

Chlorhexidine

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47
Q

What is xerostomia

A

Dry mouth

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48
Q

True or false

There is no compelling evidence that increasing age of the pt results in reduced salivary function and xerostomia

A

True

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49
Q

True or false

The scientific basis linking a particular drug to causing xerostomia is sometimes lacking

A

True

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50
Q

What drugs are linked to xerostomia anecdotally

A

Tricyclic agents Eg amitriptyline and dosulepin

Given for depression anxiety muscle tension headache fibromyalgia

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51
Q

In clinical practice what drug most commonly causes xerostomia

A

Omeprazole

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52
Q

What is omeprazole

A

Proton pump inhibitor
Prescribed to inhibit gastric secretion
Leads to dry mouth (process unclear)

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53
Q

Why does polypharmacy make the diagnosis difficult

A

Taking multiple drugs makes it extremely difficult to attribute the onset of the dry mouth to one medicine

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54
Q

What is sialorrhoea

A

CO too much saliva

In many cases pts Co of too much saliva. Have underlying hypochondriasis

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55
Q

True or false

In many cases pts Co of too much saliva. Have underlying hypochondriasis

A

True

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56
Q

What may the cause of sialorrhoea be apart from hyoichindriasis

A

Use of drugs with cholinergic activity Eg tetrabenazine and cloazopine

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57
Q

What oral symptoms may a pt taking tetrabenazine and cloazopine have?

A

Siolorrhoea
These are cholinergic drugs
Stimulate salivary glands

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58
Q

What else may increase saliva production

A

Radioactive iodine

Possibly related to the agent being secreted in saliva and tears

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59
Q

What do amitriptyline, dosulepin and muscle relaxants have in common

A

Cause xerostomia

60
Q

What is dosulepin

A

An antidepressant

61
Q

What effects may drugs have on oral mucosa and skin?

A 
Contact Hypersensitivity
Connective tissue changes
Pigmentary changes
Vascular changes
Lichenoid drug reaction
Erythema multiforme
Bullous type reactions
Epithelial keratinisation changes
Neurological changes
62
Q

Can drugs have direct chemical changes on the oral mucosa? Give an example

A

Mucosal erosion due to placement of aspirin tablet adjacent to a painful carious tooth
Direct chemical effects occur as a result of direct exposure of an agent to the oral mucosa or skin it is not Uncommon to see a localised sloughing erosion at an intra oral site where. Pt has placed an aspirin tablet adjacent to a painful tooth
Sometimes pts hold an aspiring tablet directly in the mouth to relief the pain of oral ulceration

63
Q

What is the pathophysiology of a mucosal aspirin burn

A

Dissolution of aspirin in saliva produces a low pH and the net result is effectively a chemical burn

64
Q

What are drugs may cause an aspirin like burn?

A

Over the counter preparations of choline salicylate gel on the fitting surface of an upper denture to relive discomfort leads to palatal mucosa burn

Chronic acid, phenol, paraquat all produce usually more extensive burns

65
Q

What is contact Hypersensitivity how may it affect the oral cavity

A

A range of commercial dental care preparations including mouthwashes gels toothpastes can cause mucosal changes due to Hypersensitivity reaction.
A frequently documented adverse oral reaction to toothpaste involves cinnamon which is often used as a flavouring agent

66
Q

How can contact Hypersensitivity be treated

A

Patch testing points out the allergens (often delayed Hypersensitivity reaction occurs)

67
Q

How can drugs cause connective tissue changes

A

Systemic drug therapy produces a proliferative response in the connective tissues which usually manifests as gingival hyperplasia

The mechanism of the drug induced effect is still not clear but appears to involve fibroblast proliferation and reduced fibroblast turnover

68
Q

What drugs are associated with fibroblast proliferation and reduced fibroblast turnover

A

Phenytoin antiepileptic drug
Nifedipine calcium channel blocker antihypertensive
Ciclosporin immunosuppressant
And combined oral contraceptive

69
Q

What is phenytoin

A

Anti epileptic drug
Causes fibroblast proliferation reduced fibroblast turnover
Manifests as gingival hyperasia

70
Q

How does a Nifedipine adverse drug reaction manifest

A

Gingival hyperplasia

71
Q

What is nifedipine

A

Calcium channel blocker antihypertensive

72
Q

What is Ciclosporin

A

Immunosuppressant

73
Q

What % of pts taking phenytoin will suffer some degree of hyperplasia within the first 3 months of starting medication

A

50%

74
Q

What is the incidence of swelling associated with ciclosporin

A

30%

75
Q

What is the incidence of swelling associated with nifidepine

A

15%

76
Q

WHAT MAY CONTRIBUTE TO THE GINGIVAL HYPERPLASIA ASSOCIATED WITH PHENYTOIN

A

poor oral hygiene
Dose of drug
Duration of drug therapy

77
Q

What may allow clinical resolution of the problem of gingival hyperplasia

A

Improved oh
Gingival surgery
Change in drug therapy

78
Q

What does oral pigmentation as a result of drug therapy usually look like?

A

Bluish or blue grey appearance

79
Q

How does drug induced pigmentation present

A

Symmetrical

On the hard palate

80
Q

What are the drugs most frequently involved in drug induced pigmentation

A

Antimalarials

Antibiotics

81
Q

If the pt hasn’t travelled abroad should you then discount anti malarial drugs

A

No
The pt may still have been prescribed anti malarial therapy since the same drugs can also be used as a second line treatment for rheumatoid arthritis

82
Q

What is required to be safe when diagnosing Pigmentary changes

A

Biopsy to discount malignant melanoma

83
Q

What is the main feature of histopathological exam of tissues involved in a drug induced oral pigmentation

A

Pigmentary incontenance

84
Q

What is a fixed drug reaction

A

Appearance of a localised lesion at the same site each time a drug is taken
Reaction usually involves a drug that is taken intermittently such as fluconazole doxycycline fluconazole

85
Q

What drugs may be involved in a fixed drug reaction

A

fluconazole doxycycline fluconazole

86
Q

What elements can cause oral pigmentation

A

Metals Eg silver gold bismuth

Almgam tattoo

87
Q

What is the most frequent pigementary lesion caused by metal

A

Amlagma tattoo

88
Q

What is seen on biopsy of a suspected amalgam tattoo why is this surprising

A

A v small number of amalgam particles visible in the biopsy tissue
When compared to the depth of the dark clinical colour of the lesion

89
Q

Can vascular changes occur in the mouth due to adverse drug reaction?

A

They’re not usually reported by pts unless they have taken to examining their oral mucosa
Even for experienced clinicians the changes observed are subjective and there are no recognized diagnostic criteria

90
Q

If vascular changes do occur what is the medical history of this pt likely to be

A

Cancer pt

Secretion of an acidic drug Eg methotrexate into parotid saliva

91
Q

What drugs are most frequently implicated in a Lichenoid reaction

A 
NSAIDS
Ace inhibitors
Beta blockers
Hypoglycaemic agents
Anti malarials
92
Q

What are Lichenoid drug reactions

A

Where drugs such as NSAIDS Ace inhibitors and Beta blockers cause lesions in the mouth resembling lichen planus

93
Q

What is cephelaxin

A

Cefalexin, also spelled cephalexin, is an antibiotic that can treat a number of bacterial infections. It kills gram-positive and some gram-negative bacteria by disrupting the growth of the bacterial cell wall. Cefalexin is a beta-lactam antibiotic within the class of first-generation cephalosporins

94
Q

What drugs cause pemphigus

A

Drugsthatcause pemphigusinclude: Thioldrugs, including penicillamine, captopril. Antibiotics: penicillins, cephalosporins, vancomycin. Antihypertensivedrugs: other angiotensin-converting enzyme inhibitors such as cilazapril, lisinopril, enalapril.

95
Q

What is nicotinic stomatitis where does it present

A

Nicotine stomatitis, also often called smoker’s palate, is a reaction seen on the roof of the mouth caused by extreme heat in the mouth, most commonly from smoking. It is known by many other names includingnicotinic stomatitis,stomatitisnicotina and smoker’s keratosis.

96
Q

What is erythema multiforme

A

Erythema multiforme(EM) is a skin condition of unknown cause; it is a type oferythemapossibly mediated by deposition of immune complexes (mostly IgM-bound complexes) in the superficial microvasculature of the skin and oral mucous membrane that usually follows an infection or drug exposure.

97
Q

What drugs cause erythema multiforme

A

Manydrugshave been reported to triggererythema multiforme, including barbiturates, non-steroidal anti-inflammatorydrugs, penicillins, sulphonamides, nitrofurantoin, phenothiazines, and anticonvulsants

98
Q

What skin condition presents with “target lesions”

A

EM erythema multiforme

99
Q

What is another term for Lichenoid drug reaction

A

drug-induced lichen planus. If thereactionoccurs inside your mouth, it’s called orallichenoiddrug eruption. The rash can take some time to develop.

100
Q

What is nicorandil

A

Nicorandil is a vasodilatory drug used to treat angina. Angina is chest pain that results from episodes of transient myocardial ischemia. This can be caused by diseases such as atherosclerosis, coronary artery disease and aortic stenosis. Angina commonly arises from vasospasm of the coronary arteries

101
Q

What are the oral adverse effects of nicorandil

A

Nicorandilinducedulcersare very painful and distressing for patients. Clinically they appear as large, deep, persistentulcersthat have punched out edges. …Nicorandil, a nicotinamide ester, is a potassium channel activator used in the prevention and long term treatment of angina pectoris.

102
Q

Define bulla

A

A large blister containing serous fluid

103
Q

Define bollous

A

characterized by blisters or bullae on the skin.

104
Q

What is grinspan syndrome

A

Grinspan syndromeis asyndromecharacterized by presence of the triad: essential hypertension, diabetes mellitus, and oral lichen planus. Oral lichen planus is thought to be a result of the drugs used for treatment of hypertension and diabetes mellitus but this is not confirmed.

105
Q

What is the triad of grinspan syndrome

A

Essential hypertension
Oral lichen planus
Type 2 diabetes

106
Q 
What does the presentation of
Essential hypertension
Oral lichen planus
Type 2 diabetes
In a pt mean?
A

Grinspan syndrome

107
Q

What is the aetiology of lichen planus

A

Unknown

108
Q

How is lichen planus LP treated compared with Lichenoid reaction LR

A

The treatment of LP comprises mainly the utilization of corticosteroids and the LR

109
Q

What is the cause of LR (how is this different from LP)

A

etiology of LRs is related to the contact with specific agents, such as metallic restorative materials, resins, and drugs, allowing the establishment of a cause-effect relationship. In this case, the disease is caused by the antigen fixation in the epithelial cells, which are destructed by the immune system

110
Q

What is indirect immunofluorescence

A

Indirect immunofluorescenceassay: A laboratory test used to detect antibodies in serum or other body fluid. The specific antibodies are labeled with a compound that makes them glow an apple-green color when observed microscopically under ultraviolet light.

111
Q

What is the homunculus theory

A

The termhomunculusis Latin for “little man.” It is used in neurology today to describe the map in the brain of sensory neurons in each part of the body (the somatosensoryhomunculus).

112
Q

What two clinical features help to differentiate Lichenoid reaction from lichen planus

A
  1. Lack of symmetry

2. Tendency to affect the hard palate and floor of the mouth

113
Q

When should Lichenoid reaction be considered as a DDx

A

If a pt reports onset after starting a new medication even if their relationship is many months later

114
Q

What test can help differentiate LR from LP

A

Indirect immunofluorescence using a blood same from the pt

115
Q

What indirect immunofluorescence of LR demonstrate

A

Circulating igG against the basal cell membrane

116
Q

Is the indirect immunofluorescence test considered valid

A

Controversial

117
Q

In grinspan syndrome what is the evidence of the oral lichen planus in the triad? Why is the syndrome questioned or deemed irrelevant by some

A

It is more likely to be a Lichenoid reaction related to antihypertensive medication
Therefore the true basis of the syndrome is under question

118
Q

How does nicorandil work

A

It is a potassium channel activator

Used for prevention and long term treatment of angina

119
Q

Where does nicorandil ulceration usually occur

A

Tongue and buccal mucosa

120
Q

What is the onset of erythema multiforme

A

Rapid onset extensive oral ulcers

AND blood crusted lips

121
Q

What drug is associated with inducing erythema multiforme

A

Co trimoxazole

122
Q

Why is the use of Co trimoxazole limited to those situations where biological studies deem it necessary

A

Some evidence Co trimoxazole is associated with the onset of erythema multiforme

123
Q

How should EM be treated

A

If the history reveals a close association with a medicine that the pt has commenced then this should be discontinued
Prescribe benzoate free preparations of drugs

124
Q

What should be excluded in the diagnosis and tx of EM

A

Sensitivity to benzoic acid E210

And benzoate E211 E219

125
Q

What is Glibenclamide

A

Glibenclamide, also known as glyburide, is a medication used to treat diabetes mellitus type 2. It is recommended that it be taken together with diet and exercise. It may be used with other antidiabetic medication. It is not recommended for use by itself in diabetes mellitus type 1. It is taken by mouth.

126
Q

What sulphonylurea drug administered to pts with diabetes mellitus type 2 to augment insulin secretion may cause bullous type reactions

A

Glibenclamide

127
Q

How can drug therapy precipitate a disease in susceptible individuals which is clinically and pathologically identical to the iatrogenic disease process

A

Eg a pt taking Glibenclamide to treat his diabetes presented with pemphigus vulgaris

128
Q

What is pemphigus vulgaris

A

Pemphigus vulgaris (PV) is a rare and serious (potentially life-threatening) condition that causes painful blisters to develop on theskin and lining of the mouth, nose, throat and genitals.

Theblistersare fragile and can easily burst open, leaving areas of raw unhealed skin that are very painful and can put you at risk of infections.

There’s currently no cure for pemphigus vulgaris, but treatment can help keep the symptoms under control.

The conditioncan affect people of all ages, including children, but most cases develop in older adults between the ages of50 and 60.It isn’t contagious and can’t be passed from one person to another.

Symptoms of pemphigus vulgaris

Theblisters usually develop in the mouth first, before affecting the skin a few weeks or months later.



There may be times when the blisters are severe (flare-ups), followed by periods when they heal and fade (remission). It’s impossible to predict when this might happen and how severethe flare-upswill be.

Blisters in the mouth often turn into painful sores, which can make eating, drinking and brushing teeth very difficult.The voice can become hoarse if the blisters spread to the voice box (larynx).

Sores on the skin canjoin together to form large areas of painful, raw-looking skin, before crusting over and forming scabs.They don’t usually leave anyscars, althoughaffected skin canoccasionally become permanently discoloured.

As well as getting blisters in the mouth, they can also develop in other areas of the digestive system’s soft tissue lining, including the nose, throat, anus, genitals and vagina. The thin membrane that covers the front of the eye and inside of the eyelids (conjunctiva) can also be affected.

129
Q

What is the most common form of pemphigus

A

Vulgaris

130
Q

What type of Hypersensitivity reaction is pemphigus

A

Type II

131
Q

What are the antibodies found in pemphigus against

A

The antibodies are formed againstdesmosomes, the cell adhesion proteins. As desmosomes are attacked, the layers of skin separate = a blister. These blisters are due to acantholysis, or breaking apart of intercellular connections through an autoantibody-mediated response. Over time the condition inevitably progresses without treatment: lesions increase in size and distribution throughout the body, behaving physiologically like a severe burn.

132
Q

What is Rituximab

A

Monoclonal antibody used to treat autoimmune disorders It is used fornon-Hodgkin’s lymphoma,chronic lymphocytic leukemia,rheumatoid arthritis,granulomatosis with polyangiitis,idiopathic thrombocytopenic purpura,pemphigus vulgaris,myasthenia gravisandEpstein-Barr virus-positivemucocutaneous ulcers. It is given byslow injection into a vein.

133
Q

How is pemphigus treated

A

Corticosteroids

134
Q

How is pemphigoid different from pemphigus

A

pemphigoid does not featureacantholysis, a loss of connections between skin cells.

135
Q

Which is more common pemphigoid or pemphigus

A

Pemphigoid

136
Q

What is pemphigoid? What is it mediated by

A

Pemphigoidis a group of rareautoimmuneblisteringskin diseases
Usuqlly igG mediated

137
Q

What is the pathophysiology of pemphigoid

A

The pathophysiology of bullous pemphigoid consists of two major components, which are immunologic and inflammatory. In the immunologic component, autoantibodies act against the hemidesmosomal bullous pemphigoid antigens BP230 (BPAg1) and BP 180(BPAg2 or type XVII collagen) which are located at the lamina lucida of the basement membrane zone. These antigens play an important role in the adhesion complexes that promote epithelial-stromal adhesion.[8]The predominant subclass of antibodies that acts against the antigens is IgG4. IgG1 and IgG2 antibodies are less frequently detected compared to IgG4 antibodies, while IgG3 antibodies are usually absent.[14]When the autoantibodies bind specifically to the target antigens, the complement system and mast cells are activated, thereby representing the inflammatory component. Inflammatory cells such as neutrophils and eosinophils are then attracted to the affected area. They are postulated to release proteolytic enzymes which degrade the hemidesmosomal proteins, resulting in blister formation.[8]

Other potential contributory factors including genetic factors, environmental exposures to infections and drugs as well as the phenomenon of epitope spreading are also known to cause bullous pemphigoid

138
Q

What is the histopathology of pemphigoid

A

Lesional tissue, preferably of an intact vesicle or the edge of an intact bulla is obtained using punch biopsy for Haemotoxylin and Eosin (H&E)staining.

Typical histopathologic findings include:[17][18]

Sub-epidermal split with numerous eosinophils within the cleft.

A superficial dermal inflammatory cell infiltrate of variable intensity with lymphocytes, eosinophils, and neutrophils.

Eosinophlic spongiosis (Specifically in early lesion or may be seen in clinically erythematous skin surrounding the blister)

139
Q

How direct immunofluorescence differ from indirect immunofluorescence

A

Direct immunofluorescenceEdit

Direct immunofluorescence (DIF) studies involves directly detecting tissue bound antibodies. Biopsy specimens for DIF should be taken from perilesional skin instead of lesional skin for H&E histopathologic evaluation.

DIF of bullous pemphigoid will show the presence of fine, continuous and linear deposits of IgG and/or C3 along the epidermal basement membrane. Other classes of immunoglobulins such as IgM and IgA are present in approximately 20% of cases and usually are less intense. In some cases with the deposits of IgA, patient may have oral lesion. At early stages of the disease, only C3 may be present.[18]

Indirect immunofluorescenceEdit

Indirect immunofluorescence is used to detect circulating antibodies targeting the antigens at the basement membrane zone in patients with pemphigoid. In this procedure, patient’s serum is collected and overlaid on salt-split normal human skin and incubated. Following this, the specimen will be stained for fluorescent detection of antibodies.

In bullous pemphigoid, circulating IgG targeting the basement membrane, mainly BP180 and BP230 hemidesmosomal proteins are detectable in 60-80% of patients. IgA and IgE classes can also be detected, but less frequently.[18]

140
Q

What is hyperkeratinisation

A

is adisorderof the cells lining the inside of ahair follicle. It is the normal function of these cells to detach or slough off (desquamate) from the skin lining at normal intervals. The dead cells are then forced out of the follicle (primarily by the growing hair). However, in hyperkeratinization, this process is interrupted and a number of these dead skin cells do not leave the follicle because of an excess ofkeratin, a natural protein found in the skin. This excess of keratin, which is influenced by genetics, results in an increased adherence/bonding of dead skin cells together.

141
Q

What drug most frequently induces hyperkeratinization

A

Nicotine

142
Q

Apart from the nicotine what else has vee. Suggested to chase smoker’s keratosis/ smoker’s palate

A

The heat from smoke itself is also involved since similar appearance in the palate has been reported in jndividus who drink hot tea or coffee

143
Q

What drugs may cause circumoral paraesthesia?

A

Topical polymyxinB
Acetaomine
Colistin

144
Q

What do the following drugs have in common
Polymyxin b
Acetaomine
Colistin
What adverse drug reaction can they cause

A

Circumoral paraesthesia

145
Q

What is the function of hydralazine and labetalol

A

Control blood pressure

146
Q

What is labetalol

A

Labetalolis a medication used to treat high blood pressure and in long term management of angina. This includes essential hypertension, hypertensive emergencies, and hypertension of pregnancy. In essential hypertension it is generally less preferred than a number of other blood pressure medications.

147
Q

What is hydralazine

A

Hydralazine, sold under the brand name Apresoline among others, is a medication used to treat high blood pressure and heart failure. This includes high blood pressure in pregnancy and very high blood pressure resulting in symptoms

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