CHHD Flashcards
1
Q
What is the definition of a:
1) Macule?
2) Papule?
3) Nodule?
A
1) MACULE = Localised area of colour or textural change on skin
2) PAPULE = Small solid elevation of skin (less than 5mm diameter)
3) NODULE = Small solid elevation of skin (more than 5mm diameter)
2
Q
Name 7 Nail Changes…
A
1) Finger Clubbing
2) Splinter Haemorrhages
3) Beau’s Lines
4) Nail Pitting
5) Koilonychia
6) Paronychia
7) Herpetic Whitlow
3
Q
What is Finger Clubbing? How can it be practically measured/detected?
What are 7 diseases it may be seen in?
A
Rounded/Bulbous nails formed by the thickening of tissue beneath the fingertips
Practical: Normal “diamond” shape not seen when Px holds nails together
Possible diseases:
Congenital Heart disease, Lung cancer, Asbestos, Cystic Fibrosis, Inflammatory Bowel Disease (Crohn’s or Ulcerative Colitis), Liver Cirrhosis or GRAVE’S DISEASE
4
Q
What is Koilonychia?
What are 3 possible causes?
A
Spoon-Shaped concavities in the nail
1) Trauma
2) Iron deficiencies - e.g. Microcytic anaemia
3) Haemochromatosis (Iron build up)
5
Q
What are Splinter Haemorrhages?
What are 5 possible causes?
A
Red thin longitudinal lines on nails, caused by capillary leaks in the epidermal ridges. Causes: 1) Trauma - main 2) Infective Endocarditis 3) MI 4) Psoriasis 5) Pregnancy
6
Q
What is meant by Nail pitting?
In what 3 conditions can this be found?
A
Pin-like depressions on nail surface
1) Psoriasis (along with Onycholysis - where nail separates from nail bed and yellows)
2) Reiter’s Syndrome (reactive arthritis - acquired)
3) Lichen Planus
7
Q
What are Beau’s Lines and when may they occur (4)?
A
HORIZONTAL depression lines on the nail caused by disrupted nail growth.
Causes:
- Trauma
- Reduced nutritional intake (diet or during illness)
- High altitude
- Raynaud’s Phenomenon
8
Q
What are the similarities between Lichen Planus and Lichenoid Reaction?
A
1) BOTH are types of “Mucocutaneous Lesion/Disorder” (grouped along with Discoid Lupus Erythematosus)
2) Presentation: Itchy red/purple patches which may have white “Whickham’s Striae” lines present
9
Q
Name 2 drugs involved in the treatment of Psoriasis, what is their dental relevant side effects?
A
1) Methotrexate –> Ulceration
2) Cyclosporin –> Gingival Hyperplasia
10
Q
What are the differences between Lichen Planus and Lichenoid Reaction?
A
1) Lichen Planus = Pre-malignant condition and believed to be Auto-Immune whereas Lichenoid Reaction is Drug or Dental material induced (e.g. Bis-GMA resin or metals) - withdrawal of drug is best diagnosis tool
2) Lichen Planus lesions are often symmetrical, Lichenoid reaction can be asymmetrical if in relation to Dental Material site
3) Lichenoid Reaction usually presents in/around mouth, Lichen Planus present in mouth, on skin or can spread to nasal, oesophageal or genital areas
“Vulvovaginal-Gingival Syndrome” = LP simultaneously in mouth and vagina
11
Q
What are nail changes/effects associated with Lichen Planus?
A
1) Dystrophic - brittle, discoloured and poorly formed
2) Beau’s Lines
3) Pitting + possible blood pooling below nail
12
Q
What is meant by “Koebner’s Phenomenon”?
Name 2 dermatological conditions in which this is evident?
A
Koebner’s Phenomenon = The increased likelihood of a condition to present in sites of trauma (e.g. flexor surfaces)
1) Lichen Planus
2) Psoriasis
13
Q
What are the 5 main presentations (appearance) of Lichen Planus & Lichenoid Reaction?
N.B. Can present as multiple at one time
A
1) Reticular (lines - “Whickham’s Striae)
2) Atrophic/Erythematous (reddening and thinning)
3) Ulcerative/Erosive
4) Papular (flat topped and few mm wide)
5) Bullous (blister-like) - rare
14
Q
What is “Psoriasis”?
How does it appear?
A
“A chronic, non-infectious and relapsing inflammatory condition associated with an increased production of skin/epidermal cells”
Appearance:
Red, flakey patches of skin with silver scaling - mainly associated with sites of trauma (“Koebner’s Phenomenon”)
Nail Changes = Pitting + Onycholysis
15
Q
What are the main tongue, nail (2) and joint changes (3) associated with Psoriasis?
A
Tongue changes:
Geographic tongue!
Nail Changes:
1) Nail pitting
2) Onycholysis - nail comes away from bed and yellowing
Joint Changes:
Associated with the 3 main types of Inflammatory Arthritis - Psoriatic Arthropathy (most common), Rheumatoid + Ankylosing Spondylitis
16
Q
What is “Psoriasis”?
Therefore what are the treatment aims?
What are the 3 main types of treatment?
A
“A chronic, non-infectious and relapsing inflammatory condition associated with an increased production of skin/epidermal cells”
Treatment Aims = Reduce inflammation and slow skin cell production
1) Topical - Coal Tar, Corticosteroids, Dithranol or Vit D
2) Phototherapy (skin exposed to UV light)
3) Systemic - Methotrexate (ulceration risk), Cyclosporin (gingival hyperplasia risk), Retinoids or Hydroxyurea
17
Q
What is Guttate Psoriasis?
A
Psoriasis (“chronic, non-infectious and relapsing inflammatory condition associated with an increased production of skin/epidermal cells”)
that is triggered by Streptococcal throat infection
(psoriasis sores produced are smaller than normal)
18
Q
What is the definition of Eczema?
A
[Form of Dermatitis]
“A pattern of non-infective inflammatory response, characterised by Spongiosis (swelling) of epithelium in the acute stage and Lichenification (scaled, thickened, leathery) in chronic stage”
19
Q
In Blistering conditions, what is the definition of a:
1) Vesicle?
2) Bulla?
A
1) Small fluid-filled blister (less than 5mm diameter)
2) Large fluid-filled blister (more than 5mm diameter)
20
Q
How does Eczema presentation vary from Acute to Chronic stage?
A
Acute = Spongiosis (swelling) Chronic = Lichenification (scaled, thickened and leathery)
21
Q
What are the main treatments for Eczema/Dermatitis? (3)
A
1) Topical emollients (moisturisers)
2) Corticosteroids (reduce swelling and redness)
3) Cyclosporin (Immunosuppressant - increased risk of gingival hyperplasia!)
22
Q
What are 7 general characteristics of a Malignant Swelling?
A
1) Hard
2) Fixed to adjacent structure
3) Indurated
4) Poorly-defined margins
5) Nodular
6) Black/Brown
7) May bleed and crust
23
Q
What is the difference between Basal Cell, Squamous Cell Carcinoma and Malignant Melanomas?
A
Basal Cell Carcinoma = Cancer of Epidermal Basal Cells
Squamous Cell Carcinoma = Cancer of Keratinocytes
Malignant Melanoma = Cancer of Melanocytes (in basement membrane)
24
Q
What are 7 predisposing/risk factors for Basal + Squamous Cell Carcinoma?
(LEARN WELL)
A
1) UV Radiation
2) Ionising Radiation
3) Burn/ Vaccination Scars
4) Type I/2 (Freckles) Skin - Fitzpatrick Scale
5) Arsenic (chemical)
6) Immunesuppression
7) Smoking, Alcohol + Betel Quid Consumption
25
What are the 2 main types of Contact Dermatitis?
1) Contact ALLERGY = Type 4 (Delayed, T Cell mediated) Hypersensitivity reaction - most common is Nickel
2) Contact IRRITANT = Damage to skins barrier function (e.g. chemical)
26
What are the 2 main classifications of Eczema?
| Which is most common? What causes this?
1) ENDOGENOUS
- Atopic (Most common)
- Seborrhoeic - hair follicles involved
- Disocoid
- Venous
- Discoid
- Asteatotic
2) EXOGENOUS
- Contact Allergen
- Contact Irritant
- Infective
27
What is the most common form of Eczema? What causes it and therefore what other conditions are these Px susceptible to (5)?
```
Atopic Eczema (Endogenous)
Caused by high IgE levels --> Type I (Immediate) Hypersensitivity reaction
Atopic Prone skin is susceptible to:
1) Dermatographism
2) Hay Fever
3) Asthma
4) Urticaria (Hives)
5) Oral Allergy Syndrome - allergic reaction in mouth after eating certain foods
```
28
What is "Seborrhoeic Dermatitis"?
Is it Endogenous or Exogenous?
What is the main cause and what are the main treatments?
ENDOGENOUS Dermatitis/Eczema with hair follicle involvement.
Cause: Pityrosporum Ovale yeast (therefore Immunosuppressed Px particularly susceptible)
Treatment: Anti-fungal (e.g. Nystatin) + Corticosteroid (reduce inflammation)
29
What are Basal Cell Carcinomas? How do they initially present?
What are the 2 main forms and how does their presentation differ based on this?
Cancers of the Epidermal Basal Cells.
Initial Presentation: Non-healing lump which ulcerates in centre and may crust or bleed. Most grow slowly and rarely metastasise.
1) NODULAR (Most common) - Pearly papule with rolled edge, spider veins (telangiectasia) and centrally indurated (with or without ulceration)
2) SUPERFICIAL - Slow-growing pink patch (mimics appearance of Psoriasis or Eczema)
30
What is Lupus Erythematosus?
| What are the 2 main forms and which is more severe?
Autoimmune Disease
1) SYSTEMIC LE - most severe
2) DISCOID LE
31
What Drugs can induce Lichenoid Reaction? (9)
1) Beta-Blockers ("-olol")
2) ACE Inhibitors ("-prils")
3) NSAIDs
4) Diuretics (e.g. Furosemide, Chlortalidone, Indapamine etc)
5) Rheumatoid arthritis treatment (Gold Salts or Penicillamine)
6) Oral hypoglycaemics - DM type 2 treatment
7) Anti-malarials
8) Allopurinol - Gout treatment
9) Methyldopa - Hypertension treatment
32
What is Systemic Lupus Erythematosus?
What can be seen for definitive diagnosis?
Using SOAPBRAIN Pnuemonic, what are the possible systemic side effects?
Multi-systemic autoimmune reaction - autoantibodies produced include anti-dsDNA
Diagnosis: Positive detection of anti-nuclear antibodies (ANA) or ANCA
Serositis (inflammation of serious tissue, may lead to pleurisy or pericarditis)
Oral ulcers!!!!!
Arthritis in joints
Photosensitivity - sun exposure triggers acute response (e.g. characteristic facial butterfly red rash)
Blood disorders - vasculitis
Renal
ANA
Immune
Neurological - seizures or psychosis
33
What is Discoid Lupus Erythematosus?
How does it present?
How is it treated (3)?
Lupus Erythematosus (Autoimmune condition) which is defined to the skin and triggered by UV (e.g. Sun exposure!)
Presentation: Red, oval/round, scaly, atrophic plaques on sun exposed areas (mainly face)
Treatment:
1) SUN PROTECTION + AVOIDANCE
2) Anti-malarials
3) Corticosteroids
34
What are the 4 main Autoimmune Blistering conditions?
1) Pemphigus vulgaris
2) Bullous Pemphigoid
3) Mucous membrane Pemphigoid
4) Dermatitis Herpetiformis
35
What is Dermatitis Herpetiformis?
How does it present normally?
Who is susceptible?
Autoimmune blistering condition (Type III Hypersensitivity) Presentation:
- Chronic pruritic (itchy) papulo-vesicular rash on buttocks, elbows and (rarely) knees
- Urticated base (hives) with superficial blisters
Oral presentation = Transient superficial blisters which develop into tender, non-specific ulcers
Susceptible:
Younger Px, Native Irish + Coeliac's (gluten sensitive enteropathy) Treatment = Gluten free diet!
36
What features would you expect in an Alcohol dependent Px (physical, psychological and social)?
In what ways may this affect their dental treatment?
Features:
1) Increased tolerance to alcohol
2) Loss of control and pre-occupation to drink
3) Withdrawal symptoms - Sweating, tachycardia, nausea, hallucinations and seizures
4) Liver problems
5) Social - Family problems and increased accident risk (drink driving or frights)
Dental Relevance:
1) Reduced motivations to attend and upkeep OH
2) Liver problems --> Increased bleeding tendency and reduced drug metabolism
3) DO NOT PRESCRIBE METRANIDAZOLE
4) Maxillo-facial trauma risk (fights)
37
What 2 drugs can be used in the Management of Alcohol Dependency?
(HINT: 2 "Chlor-")
Chlormethiazole + Chlordiazepoxide
38
What type of drug is Warfarin and what is its MOA?
| What are 3 medical conditions it may be prescribed for and how is its use monitored?
Anticoagulant - Vitamin K antagonist
THEREFORE: Affects reversed when Vit K given
1) Atrial fibrillation
2) Prosthetic heart valves
3) Deep vein thrombosis
Monitored using INR (International Normalised Ratio)
39
What Anti-microbials (3 main types) react with Warfarin and therefore cannot be prescribed?
What is an example of a drug that REDUCES the anti-coagulant effect of Warfarin?
Anti-microbials:
1) ANTI-BACTERIAL NITROMIDAZOLES: Metronidazole
2) ANTI-BACTERIAL MACROLIDES: Clarithromycin, Azithromycin + Erythromycin
3) AZOLE ANTI-FUNGALS: Flucoazole + Miconazole
Carbamazepine REDUCES the anticoagulant effect (may be prescribed for Trigeminal Neuralgia)
40
What are 5 oral conditions associated with HIV?
| HINT: HIV --> Immune suppression
1) Kaposi's Sarcoma (HHV8)
2) Hairy Leukoplakia (EBV/HHV4)
3) Non-Hodgkin's Lymphoma
4) Candida infections (e.g. Angular Cheilitis)
5) NUG (Necrotic Ulcerative Gingivitis)
41
What is meant by "Plaque Hypothesis"?
| What are the 3 main types and how do they differ?
Plaque Hypothesis = Theories explaining roles and mechanisms of plaque bacteria in dental caries and periodontal disease
1) SPECIFIC - Specific soley disease-causing bacteria present - absence of which leads to disease absence
2) NON-SPECIFIC - Disease results from overall activity of all microbial flora (certain species predominate)
3) ECOLOGICAL - Disease results from shift in balance of resident microflora due to response to a change in local environment conditions
42
What kind of blistering condition is Dermatitis Herpetiformus?
What is the histological presentation?
Autoimmune (associated with Coeliac): Type III Hypersensitivity reaction
Histological Presentation:
- Localised splitting at basement membrane
- Speckled IgA immunofluorescence on basement membrane
43
What are 2 serological diagnostic markers for Dermatitis Herpetiformis?
1) Presence of antigens to tissue transglutaminase
| 2) Speckled IgA immunofluorescence at basement membrane
44
```
What are the 3 Pemphigus/Pemphigoid blistering conditions to know?
Their treatments (4) are mainly the same, what are these?
```
1) Pemphigus Vulgaris
2) Bullous Pemphigous
3) Mucous Membrane Pemphigus
TREATMENT:
1) Topical Corticosteroids
2) Systemic Corticosteroids (e.g. Prednisolone)
3) Steroid sparing agent (used with above - e.g. Azathioprine, Cyclophosphamide, Cyclosporine, Methotrexate or Mycophenolate mofentil)
4) Tetracycline
45
What are the 2 "Pemphigoid" Blistering conditions and how do they differ?
1) BULLOUS Pemphigoid
2) MUCOUS MEMBRANE Pemphigoid
Differences:
- Mucous Membrane mainly affects middle aged and elderly, whilst Bullous mainly affect elderly
- Mucous Membrane is Type III AI/Hypersensitivity reaction with autoantibodies acting against basement membrane/hemidesmosome proteins
- Mucous Membrane involves formation of blood-filled blisters (leading to chronic painful eruptions)
- Bullous begins as urticarial (itchy hive-like) rash which develops into blistering
- Bullous rarely has oral affects (mainly affects skin) whilst Mucous Membrane affects mucosa (so often oral affects and rarely affects skin)
46
What are 2 difference between "Pemphigoid" and "Pemphigus" conditions?
Name 1 Pemphigus and 2 Pemphigoid conditions you must know...
Both are Autoimmune Blistering conditions with similar appearances (large, tense blisters) BUT..
1) Pemphigus is only one to have "Acantholysis" - loss of connection between skin cells (due to desmosome destruction)
2) Pemphigus vulgaris blistering occurs in the intraepithelial layer, whilst Pemphigoid blistering is subepithelial
1) Pemphigus Vulgaris
2) Bullous Pemphigoid
3) Mucous Membrane Pemphigoid
47
What is Pemphigus vulgaris? Based on this, what are 2 defining features?
How does it appear (oral + cutaneous features)?
Who is most susceptible?
Autoimmune (Type 2) Blistering condition from IgG autoantibodies against desmosomes
Therefore defining feature = "Acantholysis" (loss of connection between skin cells from desmosome destruction) and Nikolsky's Sign (dislodging of intact epidermis upon light pressure, forming a vesicle)
ORAL: Large, shallow, non-healing ulcers (may have short-lived fluid filled blisters) - OFTEN IN MOUTH!
CUTANEOUS: As above (appear 3 months after oral)
Susceptible Px: Middle aged women
48
What is Bullous Pemphigoid?
Who is most susceptible?
Which areas are mainly affected and how does it appear (initially vs. later development)?
Type of Autoimmune blistering condition
Elderly = Most susceptible
ORAL MANIFESTATIONS ARE RARE, USUALLY CUTANEOUS (Mainly affects skin on limbs, trunk and flexures)
1) Initial presentation = Itchy urticaria (hive-like) with white/red lumps
2) Develops to blistering (Tense, large blisters)
49
What is Mucous Membrane Pemphigoid?
Who is most susceptible?
Which areas are mainly affected and how does it present?
Type of Autoimmune blistering condition
Type 3: Autoantibodies against basement membrane (destroy BP180 & BP230 antigens in hemidesmosomes)
Susceptible Px: Middle Aged + Elderly
AFFECTS MUCOSAL tissue (Oral, Genital, Oesophageal, Larynx or Conjunctiva) and rarely affects skin...
Large blood-filled blisters which break down (develop into chronic painful erosions)
Scalp Involvement --> Alopecia
50
What is Erythema Multiforme?
| It has a variable aetiology, what are 4 potential causes?
Type III (Immune-complex) AI/Hypersensitivity blistering condition - excess immune-complex deposition on micro-vasculature of skin
1) Idiopathic (spontaneous) - 50% EM cases!
2) Infection (70% = HSV)
3) Drugs (NSAIDs, Penicillin, Anti-fungals, Anti-epileptics, Barbituates or Allopurinol)
4) Systemic Disease (SLE,Pregnancy or Malignancy)
51
What patients are susceptible to Erythema Multiforme? Which areas are most commonly affected?
```
Younger patients (vs other blistering conditions) - below 30.
Often affects skin extremeties + mucous membranes (li[s commonly affected)
```
52
What is the general presentation of Erythema Multiforme? How does this differ with Oral presentation?
"Target/Iris/Bulls-Eye" lesion with central red (erythematous) blister surrounded by pale banding
Oral Presentation = Lips often affected! Blister can burst to form irregular ulcers that bleed and crust over
53
Name a Corticosteroid.
What are 8 long-term side effects of Corticosteroid use?
How can these effects be minimised?
Prednisolone (systemic corticosteroid)
1) Adrenal gland suppression --> Adrenal Insufficiency (ME)
2) Skin thinning, bruising + slower wound healing
3) Increased vulnerability to infection (oral manifestation: candidal infections etc)
4) Hypertension
5) Weight Gain
6) Hyperglycaemia + Diabetes
7) Cataracts + Glaucoma
8) Osteoporosis (bone fragility)
Minimised when used with Steroid-sparing drugs (e.g. Azathioprine)
54
What is Haemostasis?
| Outline the 2 main types and which defects are associated with both
The stopping of bleeding
1) PRIMARY
Involves blood vessels (vasoconstriction) + platelets (adhesion via vWF)
Defects: Vascular, Platelets or von Willebrand Disease
2) SECONDARY
Involves Clotting factors (Intrinsic, Extrinsic + Common clotting pathways)
Defects: Clotting Factor disorders (Haemophilia A + B) and (rarely von Willebrand Disease as stabilises Factor VIII)
55
What are the 2 main functions of von Willebrand Factor (vWF)?
Therefore, what type of Haemostasis are they involved in (primary/secondary)?
1) Involved in Platelet aggregation
(Therefore involved in PRIMARY Haemostasis)
2) Stabilisation of Clotting Factor VIII (therefore involved in SECONDARY Haemostasis - rare, mainly involved in Primary....)
56
What is meant by a "Haemostatic Disorder"?
| What are 3 congenital causes of them and do they cause issues in Primary or Secondary Haemostasis mechanisms?
Haemostatic Disorder = Disorder in blood coagulation (leading to excess bleeding)
1) Von Willebrand Disease (reduced vWF) - Primary (main) AND Secondary
2) Haemophilia A (reduced Factor VIII) - Secondary
3) Haemophilia B (reduced Factor IX) - Secondary
57
Where are all Clotting Factors produced? What is the one exception to this rule?
All clotting factors are produced in the Liver (circulate in inactive form and are then activated in their extrinsic/intrinsic/common pathways)
EXCEPTION = Factor VIII - produced by blood vessel endothelial cells (along with vWF)
58
What syndrome presents as a more severe version of Erythema Multiforme?
Stevens-Johnson Syndrome
59
What are the 4 clinical features of Von Willebrand Disease?
| In what 3 ways can it be managed?
Clinical features:
1) Prolonged bleeding during surgery
2) Increased bruising
3) Epistaxis (nose bleed)
4) Risk of GIT bleed + Menorrhagia (increased bleeding in menopause)
Management:
1) Give (human) vWF and Factor VIII replacement
2) Desmopressin (DDAVP) - Stimulates vWF and Factor VIII release
3) Anti-fibrinolytics (e.g. Tranexamic Acid or Epsilon-amino caprioc acid/EACA) - Prevent clot breakdown
60
What are 4 Dental considerations for Patients with Haemostatic Disorders?
E.g. Vessel/Platelet Disorder, Von Willebrand Disease or Haemophilia A/B
1) Liase with Hameotological doctor before invasive treatment - INR taken with warfarin
2) Best to avoid regional LA - Give Infiltration
3) Avoid Aspirin/NSAIDs (anti-platelet) - Give Co-Codamol or Acetaminophen
4) All antiplatelets (E.g. Aspirin/Clopidogrel) stopped 7 days before treatment and resumed 1-2 days after
Exception = NSAIDs (stop 24 hours before surgery and resume the next day)
61
What is Osler-Rendu-Weber Syndrome?
Hereditary (Autosomal Dominant) blood vessel disorder --> Haemorrhagic Telangiectasia (Spider veins from small dilated capillaries at the skin surface)
62
How are Haemophilia A and B similar (2) ? What is their main difference?
How can they be classified into: Mild, Moderate & Severe forms?
Similarities:
- Genetic (X-Linked) disorders so only affect Males!!!!!!! (Females act as carriers)
- Haemorrhage often appears to stop immediately but blood oozing follows and results in deep tissue bleeding (therefore Prophylactic Factor VIII may be necessary if H&N injury risk of cranial bleed)
Difference:
Haemophilia A = Deficiency in Clotting Factor VIII (produced by endothelial cells in blood vessel walls)
Haemophilia B = Deficiency in Clotting Factor IX
63
How is Haemophilia classified into:
1) Mild?
2) Moderate?
3) Severe?
Classified based on Clotting Factor (VIII or IX) level in respect to normal levels:
Mild = 5-30% of normal factor level
Moderate = 1-5% of normal factor level
Severe = Less than 1% of normal factor level
64
In what 3 main ways can we treat Haemophilia A + B?
1) Increase Factor VIII (Desmopressin) - Stimulates release of Factor VIII and vWF (used in vWD)
2) Human or Artificial replacement of specific Clotting Factor (VIII or IX)
3) Anti-fibrinolytic agent (E.g. Tranexamic acid or EACA - Epsilon-amino caproic acid)
65
What is Desmopressin?
| What 2 Haemostatic disorders is it therefore used to treat?
Drug that stimulates release of Clotting Factor VIII and von Willebrand Factor (both normally released by endothelial cells of vessel walls)
1) Von Willebrand Disease
2) Haemophilia A/B (main: A as defect in Factor VIII)
66
When is Anti-Coagulation therapy given?
| What are the 3 main types of Anti-Coagulants give?
When Px at risk of Thrombosis (clot formation) e.g. after other heart defects
1) Warfarin - Vit K antagonists, Inhibits Vit K dependent clotting factors (II, VII, IX and X)
2) Heparin - Inhibits clotting factors II and X
3) Novel Oral Anticoagulants (NOACs)
- Rivaroxaban inhibits Factor Xa
- Apixaban inhibits Factor Xa
- Dabigatran inhibits Factor IIa
67
What are the 3 main forms of Novel Oral Anti-Coagulant's (NOACs)? HINT: "RAD"
Which Clotting Factor does each inhibit?
If Px low bleeding risk, they can be taken alongside treatment. If Px at high risk, what changes are made?
1) Rivaroxaban - Inhibits Factor Xa
2) Apixaban - Inhibits Factor Xa
3) Dabigatran - Inhibits Factor IIa
Delay dose/ miss morning dose and take evening dose 4 hours after haemostasis achieved
68
How are the following Anti-coagulants monitored:
1) Warfarin?
2) Heparin?
3) Novel Oral Anti-Coagulants (NOACs)?
1) INR (monitors Extrinsic pathway) - Must be between 1-4 to go ahead with treatment
2) PT/Prothrombin Time (ALSO monitors Extrinsic pathway) - Normal PT = 10-12 secs
3) Don't require routine monitoring... (easier)
69
What 4 factors do we want to look at on a Haemostasis blood test? What does each thing tell us?
1) Full Blood Count (duh) - Tells us platelet count
2) Bleeding Time - Identifies Platelet defects
3) PT (Prothrombin Time) + INR (International Normalised Ratio) - Tells us Extrinsic pathway defects (Only involves Factor VII so increases with Warfarin therapy)
4) APTT (Activated Partial Thromboplastin Time) - Identifies defects in Intrinsic Pathway (e.g. vWD, Haemophilia A/B)
70
What Haematological blood changes (PT/INR, APTT, BT) would you see in the following defects:
1) Haemaphilia A?
2) Haemophilia B?
3) Von Willebrand Disease?
4) Platelet Defects?
1) Reduced Factor VIII --> Increased APTT
2) Reduced Factor IX --> Increased APTT
3) Reduced vWF:
- Reduced stabilisation of Factor VIII-> Increased APTT
- Reduced Platelet aggregation --> Increased BT
4) Platelet defects --> Increased BT
71
What is Leukoplakia?
| Which malignancy does it have the potential to develop into?
Pre-malignant lesion:
White patches that cannot be characterised as any other disease and are not associated with any physical agents EXCEPT tobacco us. They cannot be rubbed off (unlike similar appearing Candida infections)
Potential to develop into SSC
72
What is meant by "Nikolsky's Sign"?
| In what 2 conditions is it associated with? (hint: one blistering and one syndrome)
The dislodging of intact epidermis upon light pressure, resulting in formation of vesicles/urticaria.
1) Pemphigus Vulgaris
2) Stephen-Johnson Syndrome
73
What type of Hepatitis is most likely to form Cirrhosis?
Hepatitis C!
74
What is "Reactive Leucocytosis"? How would you differentiate between potential causes?
```
Leucocytosis (Increased WBC count) secondary to another cause, e.g. infection/malignancy/allergies
FBC used to distinguish
E.g. Increased levels of:
Neutrophils = Acute Bacterial infection
Monocytes = Chronic Bacterial infection
Lymphocytes = Viral infection
```
75
What is meant by the following:
1) Leucocytosis?
2) Leucopenia?
3) Leukaemia?
4) Lymphoma?
1) Increase in WBC count
2) Decrease in WBC count
3) Malignant proliferation of WBCs (so type of Leucocytosis)
4) Solid tumour formed by the malignant proliferation of Lymphocytes in Nodal and Extra-Nodal sites"
76
What are the 4 main types of Leukaemia?
| Which are most common in Children/ Adults?
ACUTE
1) ALL (Acute Lymphoblastic Leukaemia) - children
2) AML (Acute Myeloid Leukaemia) - adults
CHRONIC - all adults
3) CLL (Chronic Lymphocytic Leukaemia)
4) CML (Chronic Myeloid Leukaemia)
77
What are potential causes of Reactive Leucocytosis, if the RBC shows increased levels of:
1) Neutrophils?
2) Monocytes?
3) Lymphocytes?
4) Eosinophils?
5) Basophils?
1) Acute Bacterial infection
2) Chronic Bacterial infection (e.g. TB)
3) Viral infection
4) Allergies, Parasitic infection or Hodgkin's Lymphoma
5) Chronic Myeloid Leukaemia (CML) or Polycythaemia (increased bone marrow production of RBCs)
78
What is Leucocytosis?
| What are 4 potential causes?
Increased WBC levels
Causes:
1) Reactive Leucoytosis (e.g. to Infection)
2) Medications: Prednisolone (corticosteroid) or Heparin
3) Leukaemia
4) Myeloproliferative disease (e.g. CML)
79
What is Leucopenia?
| What are 3 potential causes?
Decreased WBC levels
Causes:
1) Immunosuppression (e.g. Chemotherapy or Radiotherapy)
2) Overwhelming bacterial/viral infection
3) Aplastic Anaemia
80
What is a Lymphoma? What are the 2 main types and what are 5 main ways in which they differ?
Solid tumour formed by the malignant proliferation of Lymphocytes in nodal and extra-nodal areas.
HODGKIN'S LYMPHOMA
NON-HODGKIN'S LYMPHOMA
1) Hodgkin's = B Cell abnormality
Non-Hodgkin's = B AND T Cell abnormality
2) "Reed-Sternberg Cells" seen only in Hodgkin's Lymphoma biopsy (large, malignant and often multi-lobed Lymphocytes)
3) Hodgkins most commonly appears at nodal sites (esp cervical LNs) whereas Non-Hodgkin's most commonly occurs in extra-nodal sites (e.g. GIT + CNS)
4) Non-Hodgkins more common and can occur at any age (though most common over 60s) whereas Hodgkins less common and often presents in Px 15-40 and 50+
5) Non-Hodgkin's Lymphoma linked with HIV
81
What is Burkitt's Lymphoma?
| What are the 2 main sub-divisions?
An aggressive/high-grade form of Non-Hodgkin's Lymphoma associated with EBV infection
1) Endemic (African Children with jaw swelling)
2) Sporadic (Western world, HIV with "starry sky" pattern)
82
What is Amyloidosis?
How does it present on the tongue?
What condition may cause it?
Build up of abnormal Amyloid protein (produced in bone marrow)
Presents as enlarged, swollen and purple crusting tongue
Likely caused by: MULTIPLE MYELOMA (Proliferation of malignant Plasma Cells)
83
What are 5 conditions in which a Px may be taking Bisphosphonates?
What are the potential dental complications with this?
1) Osteoporosis
2) Multiple Myeloma (as causes Osteoporosis)
3) Paget's Disease
4) Osteogenesis Imperfecta
5) Bone metastases (e.g. from Breast Cancer)
Can cause Osteonecrosis of the Jaw (BRONJ)
84
What are the 4 main stages of Hodgkin's Lymphoma and how does treatment differ based on this?
Stage 1 = Single LN involvement
Stage 2 = 2+ LN involvement on same side of diaphragm
Stage 3 = LN involvement on both sides of diaphragm
Stage 4 = Extra-nodal systemic spread (e.g. spleen)
Stage 1-2 = Radiation therapy
Stage 3-4 = Combined Chemotherapy
85
What is Multiple Myeloma?
Proliferation of Malignant Plasma Cells (in bone marrow) resulting in over-production of Monoclonal Paraproteins (abnormal antibodies).
86
Explain the Clinical features of Multiple Myeloma by classifying into 4 main disease mechanisms...
1) Reduced number of normal Ig (abnormal monoclonal paraproteins instead) = Increased infection risk
2) Bone marrow infiltration = Leucopenia (increased infection risk), Anaemia + Thromocytopenia (bleeding risk)
3) Increased Bence-Jones Protein (seen in urine) = Renal failure + Amyloidosis (enlarged tongue)
4) Increased osteoclastic activity (bone resorption) = Hypercalcaemia, Osteoporosis + Bone pain/fracture
87
What are 4 special investigations/diagnostic features of Multiple Myeloma?
1) FBC = Increased monoclonal paraproteins and plasma cells
2) Serum Protein Electrophoresis = Gamma Spike from paraproteins
3) Urine = Increased levels of Bence-Jones Protein
4) Bone CT/MRI Scan = Osteoporosis
88
What is the difference between Leukaemia and Lymphoma?
Leukaemia = Malignancy WBC proliferation
Cancer cells mainly in bone marrow and blood
4 main types: ALL, AML, CLL and CML
Lymphoma = Solid tumour formed by malignant proliferation of LYMPHOCYTES in nodal or extra-nodal sites (Cancer Cells tend to be in LNs + other tissues)
2 main types: Hodgkin's and Non-Hodgkins (e.g. Burketts)
89
The 2 main forms of Lymphoma (Hodgkin's and Non-Hodgkin's) have 6 similar in Clinical Features, what are these?
1) Progressive, painless LN enlargement (most common in cervical LNs in Hodgkins)
2) Fatigue
3) Fever + Night sweats
4) Weight-loss
5) Bone Pain
6) Pruritis (itch)
90
What is Polycythaemia vera? What is a potential complication of this?
OVER production of RBCs
| Complication: Increased clotting/thrombosis
91
What are some causes of the following Anaemias:
1) Microcytic?
2) Normocytic?
3) Macrocytic?
```
1) MICROCYTIC
• Iron deficiency
• Thalassaemia (form of Haemolytic anaemia, abnormal Hb formation)
2) NORMOCYTIC
• Chronic disease (E.g. Renal or Rheumatoid Arthritis)
• Haemolytic Anaemia (E.g. Sickle Cell)
• Acute blood loss/Haemorrhage
• Cancer with bone marrow infiltration
3) MACROCYTIC
• Vit B12 or Folate deficiency
• Aplastic anaemia
• Drugs (e.g. Phenytoin)
• Alcohol
• Cancer (Multiple Myeloma or Myelodysplasia)
```
92
What 4 drugs should be avoided entirely in Kidney Failure?
1) Gentamicin
2) Tetracyclines
3) Cefixime
4) Aminoglycosides
93
What is the difference between Acute and Chronic Renal Failure?
```
Acute = Reversible loss of nephrons
Chronic = Irreversible loss of nephrons
```
Acute = ME → Confusion, Coma or Seizures
Causes: HypOtension, Sepsis, Analgesic overdose, Renal Thrombosis, Nephritis or Obstructed Urine flow
Chronic = diagnosed when GFR below 90ml/min for 3 months, often asymptomatic at first
Causes: HYPERtension, Diabetes ("diabetic nephropathy"), Nephritis, Obstructed Urine flow
Less common causes: SLE, Multiple myeloma, Amyloid or Gout
94
What are the 2 main forms of Renal replacement therapy in cases of renal failure?
1) DIALYSIS
(a) Peritoneal Dialysis - within the body via peritoneal (abdominal) semi-permenant membrane
Simpler + Cheaper but less effective than (b) and risk of Peritonitis infection
(b) Haemodialysis - outside of body via atherovenous shunt
More effective but time consuming and risk of blood-borne viruses (e.g. Hep B or C)
2) RENAL TRANSPLANT
Indications: Child, Diabetic or End-stage Failure
Kidney transplanted into right iliac fossa, usually on immunosuppressants for life (risk of infection)
95
What are 7 Dental Relevance's of Chronic Renal Failure?
| Think of SE's, drugs to avoid, Treatment risks etc
1) Ensure not to describe nephrotoxic drugs (Gentimicin, Tetracycline, Cefixime or Aminoglycosides) - DO NOT PRESCRIBE SYSTEMIC FLUORIDE AS THIS IS RENALLY METABOLISED
2) Avoid Aspirin + NSAIDs (Paracetamol best)
3) SE: Renal Osteodystrophy (weakening of bones)
4) SE: Secondary Hyperparathyroidism (may see brown's tumour on gingiva)
5) SE: Bone marrow toxicity → Anaemia, bleeding risk and increased risk of infection
6) Px on Haemodialysis: Risk of blood-borne viruses (e.g. Hep B/C) and may take Heparin (improve dialysis) so delay treatment to next day
7) Px with Transplant: Immunosuppression medication
96
What is the main difference between Nephrotic and Nephritic Syndrome?
Nephrotic tends to produce greater Proteinuria effect (more protein excreted in urine)
Nephritis can cause Haematuria (blood in urine)
97
[Shanice] What is Nephrotic Syndrome?
| What are 5 clinical features?
Glomerular damage
1) Proteinuria
2) Hypoalbuminaemia
3) Hypercholesterolaemia
4) Facial Oedema + Ascites (fluid in abdomen)
5) Vit D deficiency due to loss of Cholecalciferol binding protein → Secondary Hyperparathyroidism
6) Increased clotting due to
- Hypercholersterolaemia
- Loss of antithrombin III
- Increased circulating clotting factor
98
What is "Ecchymosis"?
Bruising (red-blue in colour) in the mucous membrane of the mouth
Can be caused by trauma or spontaneous (e.g. with anticoagulant warfarin therapy)
