1
Q
List the 8 conditions that maybe found in pateitns coming from Sub-Saharan Africa.
A
- Malaria
- HIV
- Rickettsiae
- Schistosomiasis
- Dengue
- Enteric fever
- Brucellosis
- Amoebiasis
2
Q
Write the history you would take from a returned traveller.
A
Detailed travel iteniary history:
- Where –> detailed geopgtaphy of travel, including setting (rural/urban)
- When –> dates of travel, time of symptom onset, duration of symptoms
- Risk and activities:
1. bites?
2. diet?
3. fresh-water exposure (schistomiasis)
4. dust exposure
5. sexual activity
6. game parks
7. farms
8. caves (rabies, ebola)
9. unwell contact
10. visting friends or family
3
Q
Detailed symptom review for infectious disease (4).
A
- neck stiffness and sensitivity to light (meningitis)
- severe muscle or joint pain (dengue, chikungunya)
- nausea, diarrhoea, or abdominal pain (typhoid, gastroenteritis)
- rash or unusual bleeding (dengue, meningococcus, typhoid “rose spots”)
4
Q
Investigations done in a traveler returning with fever?
A
- must exlude malaria 1st –> thick and thing blood smear and/or malaria rpaid diagnsotic test (RDT)
- baseline bloods (CBC, U+E, LFTs, CRP/ESR, Glucose)
- blood cultures x2 (before antibiotics)
- HIV tests
- Viral serology (guided by hx) –> hepatitis, dengue
- stool culture
- urinalaysis and urine culture
- consider PCR (if severe or unclear diagnosis) and pregnancy test (if woman of childbearing age)
5
Q
List the test used in latent TB testing
A
- Tubercilin skin test (TST) = Mantoux test:
≥5 mm = Positive in high-risk patients
(e.g. HIV, recent TB contact, immunosuppressed, transplant, anti-TNF)
≥10 mm = Positive in moderate-risk patients
(e.g. healthcare workers, recent immigrants from high-prevalence countries, IV drug users, prisoners, homeless, children <5 years)
≥15 mm = Positive in NO risk factors - Interferon-gamma release assay (IGRA)
NOTE:
- neither test can diagnose or exclude active disease
- immune suppressed status reduce the sensitivity of both tests
6
Q
List the investigations used in active pulmonary TB testing.
A
- CXR : -
- fibronodular/linear opacities in upper lobe (typical), lower/middle lobe (atypical)
- cavitations
- calcification
- effusion - Sputum sample –> 3 early morning specimens. Stained for presence of acid fast bacilli (AFB). All mycobacteriuj, including Mycobacterium TB, are acid fast-fast
- Sputum culture –> can detect drug sensitivity
- Nucleic acid amplification test (NAAT) –> rapid diagnosis (<8h). Can detect blood sensitivity
7
Q
What test should be done in all patients with TB or suspected TB?
A
HIV test
Suspected pulmonary TB requires airborne isolation in a negative-pressure room to prevent transmission.
8
Q
Treatment of TB with the duration.
A
RIPE:
- Rifampicin – 2months intesive and 4months continuation
- Isoniazid – 2months intesive and 4months continuation
- Pyranzimide – 2months intesive
- Ethambutamol – 2months intensive
9
Q
SE of rifampicin?
A
- cytochrome P450 enzymes inducer thus cautioun when used with warfarin, oestrogen
- causes organge-red coloured body secretions and altered LFTs
10
Q
SE of isoniazid?
A
- inhibits pyridoxine (vitamin B6) which causes a peripheral nephropathy (high risk with DM, CKD, HIV, malbsorption
Therefore, give with prophylactic pyridoxine
11
Q
SE of pyrazinmaide?
A
Idiosyncratic hepatotoxicity
12
Q
SE of ethambutol?
A
Colour blindess, decreased visual acuity, optic neuritis. Check visual acuity at start of treatment, monitor for symptoms. Monthly visual check if treatment >2months. Moniyot lvls if eGFR <30
13
Q
Name the 2 most prevalent parasites causing malaria?
A
- Plasmodium falciparum
- Plasmodium vivax
14
Q
List the symptoms of malaria.
A
Symptoms are non-specific: -
fever, headache, malaise, myalgia, diarrhoea, cough.
15
Q
What is the most characteristic feature of malaria?
A
The high fever which spikes every 48 hours
16
Q
Which parasites of malaria can live up to 4 year?
A
P. Vivax and P. Ovale
Thus even exposure several years ago maybe relevant
17
Q
Explain how malaria can result in hemolytic anemia?
A
The plasmodium infect and multiply within RBCs. These infected RBCs tupture to release parasities (intravascular hemolysis). The spleen clear infected and damaged RBCs, and may clear uninfected RBCs (extravascular hemolysis). Repeated cycles of this process exceeds the bone marrow’s replacement of RBCs, leading to hemolytic anemia.
18
Q
List the complications of malaria (8)
A
- Cerebral malaria
- Seizures
- Severe hemolytic anemia
- Multi-organ failure and death
- AKI
- DIC
- Pulmonary oedema
- Decreased consciousness
19
Q
What should you do if malaria suspected but blood film is -ve?
A
Repeat blood film at 12-24 hours and after further 24 hours.
Malaria is unlikely if 3 expert serial blood films are -ve
20
Q
Uncomplicated malaria treatment?
A
- artemether with lumefantrine (usual 1st choice)
- quinine plus doxycycline
- quinine plus clindamycin
- progunail with atovaquone (malarone)
- chloroquine (these have high rates of resistance)
- primaquine (can cause hemolysis in G6PD deficiency)
21
Q
Severe or complicated malaria IV options treatment?
A
- Artesunate —> usual 1st choice (causes hemolytic anemia as a SE)
- Quinine dihydrocholride
Often requires admission to ICU.
22
Q
List the 4 main anti-malarial medications: -
A
- Proguanil with atovaquone (Malarone)
- Doxycycline
- Mefloquine
- Chloroquine with Proguanil
23
Q
DDx of peticeal rash?
A
- Meningitis
- Vasculitis
- Acute leukemia
- Thrombocytopenia (eg. ITP)
- Severe vitamin deficinecy (B12 folate)
- Drugs (carbamazepine, valproate)
24
Q
DDx of meningitis (without rash)?
A
- Malaria
- Encephalitis
- Subarachnoid hemorrhage
- Dengue
- Tetanus
25
List the early features of meningitis.
1. Headache
2. Fever
3. Cold peripheries
4. Abnormal skin color
26
List the late features of meningitis.
1. Meningisim: neck stiffness, photophobia, Kernig's sign (pain + resistance on passive knee extension with hip fully extended)
2. Non-blanching peticheal rash (maybe 1 or 2 spots)
3. Low GCS, coma
4. Seziures
5. Septic shock
6. Brudzinski sign (meningitis):
Passive flexion of the neck causes involuntary flexion of the hips and knees, indicating meningeal irritation.
27
Treatment and management of meningitis spetcemia.
28
List 5 bacteria causes of meningitis.
1. Neisseria meningitis
2. Strep pneumonia (pneumococcus)
3. Haemophilius influnezae
4. Group B Strep (GBS)
5. Listeria monocytogenes
29
List the main clinical findings in scabies.
1. Severe nocturnal pruritis
2. Papular/scaly rash, burrows maybe visible which are tiny, raised, linear lesions on the skin
3. severe crusted scabies if immunocompromised
30
Name the 2 topical treatments used in scabies and write advice for the patient.
Permethrin 5% or Malathion 0.5% or Crotamiton cream (for night symptoms)
- This needs to be applied to the whole body, completely covering skin. It is best to do this when the skin is cool (i.e. not after a bath or shower) so that a layer of cream remains on top of the skin and does not get absorbed. The cream should be left on for 8 – 12 hours and then washed off. This should be repeated a week later to kill all the eggs that survived the first treatment and have now hatched.
- Scabies is contagious to all household and close contacts. When one person is diagnosed, all household and close contacts should also be treated in exactly the same way, even if asymptomatic. This is because they may be infected and not yet have symptoms.
- All clothes, bedclothes, towels and other materials in contact with scabies need to be washed on a hot wash to destroy the mites. Thorough hoovering of carpets and furniture is also essential.
31
One oral treatment for scabies and when is it indicated?
Oral ivermectin.
As a single dose that can be repeated a week later is an option for difficult to treated or crusted rabies.
32
Diagnostic tool of scabies?
- clinical diagnosis
- skin scraping (for mites/eggs/faeces)
- dermascopy may reveal delta wing or mini triabgle sign
- burrow ink test may reveal zig-zag
- adhesive tape test
- used to transfer a sample from a suspicious lesion directly to a microscope slide.
- Skin biopsy (rarely necessary)
33
What abnormality would you expect to find if you did a sex hormone profile on a teenager with acne vulgaris?
Raised androgens (eg. testosterone or DHEA-S)
34
Lifestyle management of acne vulgaris.
1. avoid chocolate and high glycmeic index foods to decrease insulin/IGF-1-mediated sebaceous and keratinocyte overactivity
2. cleansing twice daily using non-comedogenic cleanser
3. avoid squeezing or picking the skin lesions
4. avoid makeup or use non-comedogenic products
5. manage stress and regular sleep
6. stick to therapy for more than 6-8 weeks
35
List the different pharmacological therapies for acne (topical and oral).
Treatment is initiated in a step-wise fashion based on the severity and response to treatment:
1. no treatment is acceptable for mild acne
2. topical benzyl peroxide (is toxic to C.acne bacteria aswell)
3. topical retinoids (chemicals related to vitamin A + women of childbearing age need effective contraception)
4. topical antibiotics such as clindamycin (prescribed with bezyl peroxide to reduce bacterial resistance)
5. oral antibiotics such as lymecycline
6. oral contraceptive pill (cab stabilize female hormones)
7. Oral retinoids (isotretinoin) is an effectibr last-line option, although it is only prescribed after other methods fail.
36
T/F: The lesions of scabies are usually symmetrical.
True
Scabies typically presents with symmetrical lesions due to the distribution of mites, favouring areas like the wrists, elbows, and web spaces
37
Which body areas are mainly affected by scabies?
mainly affect the hands, wrists, axillae , thighs, buttocks, waist, soles of the feet, areola and vulva in females and penis and scrotum in males. The neck and above are usually spared, except in cases of crusted scabies and in infections occurring in infants, the elderly, and the immunocompromised.
38
T/F: In scabies, eczematous changes may mask the typical features of the rash.
True
39
Describe the appearance or nature of the rash in atypical or generalised scabies.
Papular/scaly rash, burrows maybe visible which are tiny, raised, linear lesions on the skin
40
Write the features of an basal cell carcinoma. (6)
1. slowly growing plaque or nodule
2. skin coloured, pink or pigmented lesions
3. spontaneous bleeding or ulceration
4. shiny or pearly nodule with smoth surface
5. may have central depression or ulceration, so its edges appear rolled
6. blood vessels cross its surface
41
Where does BCC commonly occur and why?
BCC predominantly occurs on the face, but other sun-exposed sites, hair-bearing scalp, behind the ear, and the trunk can be affected aswell.
BCC is multifactorial: most often, there are DNA mutations in the PTCH tumor suppressor gene. These maybe triggered by UV radiation. Various spontaneous and inherited gene defects predisopse to BCC.
42
Types of BCC (4).
1. Nodular BCC (most common on face)
2. Superficial BCC
3. Morpheoic BCC
4. Basosquamous carcinoma
43
Primary treatment of BCC?
Depends on size and location, the number to be treated, patient factors, and the preferance of doctor. Most BCCs are treated surgically (eg. excision, mohs microgtaphically controlled excision, superfical skin surgery)
44
Alternative for superficial/early/small BCC?
1. cryotherapy
2. photodynamic surgery
3. imiquimod cream
4. flurouracil cream
45
how can BCC be prevented?
Avoid sun burn. Especially imp in fair skinned and family hx individuals. Protect skin from sun-exposure daily, year-round, and lifelong.
1. stay indoors inder the shade in the middle of the day
2. wear covering clothing
3. apply high protection factor SPF50+ borad specturm sunscreen genoursly to exposed skin if outdoors
4. avoid indoor tanning (sunbeds, solaria)
46
What can reduce number and severity of BCC?
Oral nicotinamide (vitamin B3) 500mg twice daily.
47
List bedside and lab investigations for tinea capitis.
Bedside:
1. Wood lamp --> detects microsporum species
2. Dermoscopy of scalp (trichoscopy)
Lab tests:
1. Microscopy of scalp scrapings in KOH preparation
2. Fungal culture
3. Skin biopsy
4. PCR
5. Endothrix and ectothrix
48
Describe apperance of molluscum contagiosum.
Mainly presents in childhood as clusters of small, round, soft umblicated papules, which range in size from 1-6mm and maybe white, pink, or brown. Thick white material can be expressed from the middle of papules. It frequently induces dermatitis around them and affected skin becomes pink, dry, and itchy. They mostly arise in moist places, such as armpit, behind the knees, groin, and genital area.
49
What is the Koebnar phenomenon and what is another name for it?
Also known as isomorphic phenomenon. Is a flare of a pre-existing inflammatory skin condition involving a site of skin trauma such as scratch or burn.
50
Describe the apperance of a legs with venous eczema.
1. Itchy, red, blistered and crusted plaques; or fissured and scaly plaques on both or one LL.
2. Atrophie blanchie (white irregular scars surrounded by red spots)
3. Champagne bottle apperance - narrowing at the ankles with induration (lipodermatosclerosis)
4. Orange-brown macular pigmentation - hemosiderin deposition
51
List the subjective symptoms of venous eczema.
- heaviness, itching, throwing, aching, swelling of lower limb
- pain on prolonged standing
- alleviation of pain by elevation of leg
52
Management of venous eczema.
Reduce swelling:
1. Dont stand for long periods
2. Take regular walks
3. Elevate your feet when sitting
4. During acute phase of eczema, bandaing is important to reduce swelling
5. When eczema has settled, wear compression stockings.
Reduce eczema:
1. Dry up oozing patches with Condy's solution (K+ permanganate) or diltue vinegar on gauze as compresses
2. Oral antibiotics luke flucloxacillin if 2ndry infection
3. Apply prescribed topical steroid: start with patent steroid cream (eg. betnovate or dermovate) applied daily to the patches until they have flattened out. After a few days, switch to a mild topical steroids (hydrocortisone) until itchy patches have resolved
4. Mostiuring cream. Use urea cream if scaly
5. Protect skin from injury: this can result in infection or ulceration that maybe difficult to treat
53
What are the complications of venous eczema?
1. Impetiginisation — secondary infection with Staphylococcus aureus resulting in yellowish crusts
2. Cellulitis — infection with Streptococcus pyogenes: there may be redness, swelling, pain, fever, a red streak up the leg, and swollen nodes in the groin
3. Secondary eczema — eczema spreads to other areas on the body
4. Contact allergy to one or more components of the ointments or creams used
54
Management of acute flare of contact dermatitis?
1. Emollient creams (prescribe in large amounts and use liberally 3-4x daily)
2. topical steroids (hydrocortisone) or potent steroids (betnovate) maybe needed - step up or down using the weakest steroid which is fully effective
3. topical or oral antibiotics for secondary infection
4. oral steorids (prednisolone), usually short courses, for severe cases
5. phototherapy or photo chemotherapy
6. azathioprine, ciclosporin or another immunosuppressive agent
7. calcineurin inhibitors
- Most importantly is to identify and avoid causative irritant/allergen.
- Oral antihistamines for symptomatic relieft, especially nocturnal pruritus
55
What is the difference between atopic and contact dermatitis?
Atopic is endogenous, caused by genetic skin barrier defects and immune dysregulation (Th2/IgE mediated). Contact is exogenous, a tupe 4 or delayed hypersensitivityreaction and occurs 48-72 hours after exposure to allergen.
56
Why might hx of atopy predispose to eczema?
Atopic individuals have an impaired skin barrier (filaggrin mutation), making the skin more permeable to irritants and allergens.
Chronic dryness and microfissures facilitate allergen penetration and sensitization.
57
Main sign of pemphigus vulgaris.
Flaccid superficial blisters which rupture easily to leave widespread erosions. Oral mucosa affected early often.
58
Why can pemphegus vulgaris present with hoarseness?
Due to the involvement of the larynx and pharynx, which dysphagia and hoarse voice
59
Management of Pemphigus vulgaris
1. Topical steroids (eg. betnovate) and emollients (for localized skin disease and symptomatic relief)
2. Prednisolone (40-60mg/day PO, and taper gradually) --Core treatment
3. Pulsed IV methylprednisolone (for severe cases)
4. Steroid sparing agents: azathioprine and mycophenolate
5. Rituximab and IV immuniglobulin in resistant cases
60
Investigations for pemphigous vulgaris?
1. Skin biopsy from skin adjacent to a lesion with direct immunofluoresence
2. Indirect immunofluoresence blood test (may reflect effectivness of treatment).
3. anti-DSG3 in blood or saliva by ELISA ( Enzyme-Linked Immunosorbent Assay)
61
Complications of pemphigous vulgaris?
1. very extensive life-threathening erosions
2. secondary bacterial infection
3. fungal infections, especially candida
4. nutritional deficinecies due to difficulty eating
5. Complications of systemic steroids, especially infections and osteoporosis
62
T/F: Seborrhoeic keratoses appear everywhere on the body
False
Seborrhoeic keratoses can arise on any area of skin, covered or uncovered, with the exception of palms and soles. They do not arise from mucous membranes.
63
T or F: Seborrhoeic keratoses are not associated with grease
True
nor are they formed from sebaceous glands, as is the case with sebaceous hyperplasia, nor are they associated with sebum — which is greasy.
64
T or F: Seborrhoeic keratoses are considered degenerative
True
Seborrhoeic keratoses are considered degenerative in nature. As time goes by, seborrhoeic keratoses become more numerous. Some people inherit a tendency to develop a very large number of them.
65
What is the most common form of autoimmune subepidermal blistering disease?
Bullous pemphegoid
66
In whar age group does bullous pemphegoid commonly present in?
Bullous pemphigoid often presents in people over 80 years of age, and mostly affects people over 50. It can occur in younger adults, but bullous pemphigoid in infants and children is rare.
67
In what conditions is bullous pemphegoid more prevalent?
1. Neurological conditions (eg. Stroke and Parkinson's)
2. Psoriasis and it can be precipitated by treatment of psoriasis with phototherapy.
68
T/F: People with 5 or more clinically atypical naevi have a higher risk than the general population of developing melanoma
True
the relative risk is reported to be six times that of people without atypical naevi. People with FAMM syndrome have an extremely high risk of developing melanoma.
69
T/F: melanoma are rare in darker skin
True (HOWEVER)
Acral and nail melanoma can occur in all types of skin color
70
What does macule mean?
Area of discolouration
71
List the 11 different types of tinea infections
w1. Tinea barbae – beard area
2. Tinea capitis – scalp
3. Tinea corporis – body (trunk and limbs)
4. Tinea cruris – groin (“jock itch”)
5. Tinea faciei – face
6. Tinea manuum – hand
7. Tinea pedis – foot (“athlete’s foot”)
8. Tinea unguium (onychomycosis) – nail infection
9.Tinea versicolor – yeast infection (Malassezia species; causes hypo/hyperpigmented macules)
10. Tinea incognito – fungal infection modified by topical steroid use
11. Tinea nigra – superficial mould infection causing dark patches on palms/soles
72
What is the group of fungus causing Pityriasis versicolor?
Malassezia, which are part of the normal flora and survive on lipids. They usually grow on the suborrheoic areas (scalp, face, chest) without causing a rash.
73
What pattern does Pityriasis versicolor follow?
Pityriasis often dissapears in the winter and recuts when in the summer when the weather becomes warm and humid again. Regular use of topical treatment minimizes this risk.
74
What are dermatophyte infections?
keratinophilic fungi (Trichophyton, Microsporum, Epidermophyton) that infect skin, hair, and nails, producing tinea (ringworm) infections.
They digest keratin, remain superficial, and are treated with antifungal agents.
NOTE --> Pityriasis vesicolor is not a dermatophyte and thus Terbinafine, an antifungal agent, is NOT effective for yeast infections such as pityriasis vesicolor.
75
Give 3 oral antifungal medications.
1. itraconazole
2. fluconazole
3. terbinafine (NOT effective for pityriasis vesicolor)
76
3 Topical antifungal agents?
1. Selenium sulfide shampoo
2. Topical azole cream/shampoo (ketoconazole/ecoconazole)
3. Terbinafine gel
77
List the most common causes of acute DIC?
Acute DIC is a bleeding disorder caused by a number of conditions. The most common are infections, including:
1. Gram positive and Gram negative septeciema (sepsis)
2. Meningocoocaemia
3. Tyohoid fever
4. Rocky Mountain spotted fever
5. Viraemia
6. Parasites
- Obstetrics patients (abrupto placentae, amniotic fluid embolism, theraputic abortions, eclampsia
- Acute tissue injuries such as certain snakebites, necrotising rnterocolitis, freshwater drowning, heat stroke, and crush injury, renal homograft rejection
78
T/F: BCC commonly metastasizes
False
Rarely metastasizes
79
List the clinical features of SCC?
1. Presents as enlarging scaly or crusted lumps
2. Usually aruse within pre-existing acitnic keratoses or intraepidernal carcinoma
3. Grows over weeks to months
4. May ulcerate
5. Located on sun-exposed sites
80
Types of SCC?
81
T/F: Keratocanthoma is a rapidly growing keratinising nodule that may resolve without treatment
True
82
What is the most common metastases site of SCC?
Regional lymph nodes (80%), lungs, liver, brain, bones and skin.
83
List the clincal features of alopecia aeata.
1. Focal hair loss
2. Well demarcated (defined borders) single or several round/oval patches of normal-appearing skin
3. Exclamation point hairs, particularly in the periphery of bold patches (thick distal and thin proximal portions)
4. Localized tingling or itching preceding hair loss (trichodynia)
5. Nail changes (nail pitting) can be seen in 10-40% of patients
84
Risk factors of alopecia areata?
1. Chromosomal disorders (drown's syndrome)
2. polyglandular autoimmune syndrome type 1
3. Other autoimmune conditions such as vitiligo and thyroid disease
4. family hx
85
Management of alopecia areata?
There is NO cure for alopecia areata. The hair loss of alopecia areata is associated with minimal harmful physical effects and resolution may occur. However, the psychological impact can be significant, therefore warranting treatment. Numerous therapies have been used with variable effects and high quality evidence is lacking:
1. Intralesional corticosteroid injections (triamcinolone)
2. Topical steroids:
- potent corticosteroid
- minoxidil solution
- anthralin
3. education, counselling, and camoflagoue
86
When is the onset peak of psoriasis?
15-25 years and 50-60 years.
It persists lifelong, fluctuating in extent and severity.
87
Define psoriasis.
A chronic inflammatory skin condition characterized by symmetrically distributed and clearly defined, scaly and erythematous plaques, which typically follows a relaping/remitting course. The epidermis in psoriatic plaques is hyperproliferative.
88
T/F: The epidermis in psoriasis plaques are hyperproliferative
True.
There is proliferation and dilation of BVs in the dermis + infultration of inflammatory cells.
89
What is the most common type of psoriasis?
Plaque psoraisis (vulgaris) (90%)
90
Clinical features of psoriasis?
1. Symmetrically distributed scaly, erythematous plaques with well defined borders.
2. The scale is typically silvery white, except in skin folds where plaques often appear shiny with moist peeling surface
3. Usually on the scalp, elbows, and knees but any part of skin can be involved
4. Itch is mostly mild but maybe severe, leading to scratching and lichenification
5. Koebnar phenomenon (isomorphic phenomenon)
91
T/F: Psoriasis is typically symmetrical
True
It presents as well-circumscribed, shiny, red, scaly plaques that can appear on both sides of the body. Commonly affected areas include the scalp, elbows, knees, and nails. Family history is often a factor in the occurrence of psoriasis.
92
Tell me about Guttate psoriasis.
- Post-step guttate psoriasis
- widespread small plaques
- often resolves after several months
93
Tell me about Chronic plaque psorasis
- Persistent and treatment resistant
- Most common type.
- >3cm plaques
- Most often on knees, elbows, lower back
- Ranges from mild to extensive
94
Tell me about small plaque psoriasis
- <3cm plaques
- often late age onset
95
Tell me about unstable psoriasis
- Rapid extension of existing or new plaques
- Induced by infection, stress, drug, or drug withdrawal
- Koebnar phenomenon; new plaques at site of injury
96
Tell me about flexural psoriasis.
- Affects the body folds or genitals
- Smooth and well-defined patches
- Colonized by candida or yeast
97
Tell me about scalp psoriasis
Often the first or only site of psoriasis
98
Tell me about Sebopsoriasis
- Overlap of dermatitis and psoriasis
- Affects scalp, ears, chest
- Colonized by Malassezia (same yeast causing pityriasis versicolor)
99
Tell me about palmoplantar psoriasis
1. Affects palms and/or feet
2. Keratoderma
3. Painful fissuring
100
Tell me about nail psoriasis
- associated with inflammatory arthritis
- piiting, onycholysis, yellowing, ridging
101
Tell me about erythrodermic psoriasis
- erythrodermic psoriasis is rare
- may or may not be preceded with by another form of arthritis
- acute or chronic forms
- may result in systemic illness with temprature dysregulation, electrolyte imabalance, or cardiac failure
102
Managemenr for psoriasis?
Education is vital; control not cure is realistic. Consider phototherapy or systemic therapy (ciclosporin/MTX) if >10% of body affected. Emollients help reduce scale and relieve irritation.
1. Use topical steroids (betnovate) each morning + topical vitamin D analogue (calcipotriol) at night
2. Review after 4 weeks; stop if skin is clear
3. If good response, continue until clear or nearly clear
Potent steroids 1) should NOT be used for more than 8 weeks continously 2) require a 4 week treatment break before restarting 3) during a break, vitamin D analouges maybe continued
- 1% coal tar lotion: useful for widespread thin plaque disease
- Monitor CBC, LFTs, U+E, glucose, lipids
- Consider phototherapy for guttate or plaque psoriasis that can not be controlled with topical or is widespread
103
What areas does hidradenitis suppurativa (HS) affect?
The apocrine gland bearing skin, like the axilla, groin, perianal region, burrcoks, and inframammary folds.
104
T/F: Hidradenitis suppurativa is caused by poor hygiene.
False
It is NOT caused by poor hygeine
105
T/F: Hidradenitis suppurtiva is contagious
False
It is NOT contagious
106
List the clinical features of hidradenetis suppurtiva.
1. Affects the intertriginous (skin folds), apocrine gland bearing skin like the axilla, breast folds, groin, and perineum
2. Open and closed comedones
3. Painful firm nodules and papules
4. Abscesses and draining sinuses
5. Pustules and fluctant pseudocytes
6. Hypertropic and atrophic scarring with deformity
107
On what criteria is hidradenitis supportiva diagnosed?
Modified Dessau Criteria
108
Give me an example of instralesional steroid injection
Triamcinolone
109
Management of HS?
1. Lifestyle changes: weight loss, smoking cessation, loose clothing
2. Topical treatment (alone for mild cases or in adjunctive for severe): topical clindamycin 1%, topical antiseptics (chlorehexidine), Mg2+ sulphate paste
3. Antibiotics (tetracyclines): prolonged courses (3-6m) and can be used in combination wih other antibiotics (clindamycin + rifampicin)
4. Consider short courses of antibiotics (IV) for superimposed infections or for severe flares
110
Give me the different types of melanoma.
1. Superfical spreading melanoma (most common about 50-60% of all melanomas)
2. Nodular melanoma
3. Lentigo melanoma
4. Acral melanoma (can occur in black people)
111
What is the most common type of melanoma?
Superfical spreading melanoma
112
T/F: Melanoma is always epithelial in origin
False
Melanoma is usually epithelial in orgin (strating in skin), or less often mucous membranes. However, very rarely, melanoma can strat in an internal tissue such as the brain or back of the eye.
113
List the criteria used for melanoma assessment.
ABCDEFG assessment:
- Aysemmetry outline of the lesion
- Border irregularity or blurring
- Colour variation and change (with shades of black, brown, pink, blue)
- Diameter >6mm (can not be covered by end of pencil)
- Evolution (all changing moles - in size, elevation, and/or colour are suspect)
- Funny looking mole which stands out or is different from others -"ugly duckling sign"
For nodular melanoma, also consider EFG:
- Elevated
- Firm to touch
- Growing
114
Describe the process of treating an suspicious looking lesion or a melanoma
Surgery is the only curative tretment. For any unusal, growing, or changing pigmented lesion, excision biopsy of the whole lesion must be considered (with a 2mm margin of normal skin around the lesion + a cuff of subcutaneous fat). This allows for histological diagnosis and measurement of tumor depth (Breslow thickness). If malugnant melanoma is confirmed, a wider excision margin is taken (up to 3mm) to ensure complete removal.
115
Superficial spreading melanoma accounts for about 70% of all melanomas.
True
116
Superficial spreading melanoma grows initially in the vertical plane before spreading radially.
False
It grows initially in the radial plane (spreads outwards), then later may invade vertically.
117
Superficial spreading melanoma commonly occurs on the trunks of men and the legs of women.
True
118
Nodular melanoma is the most aggressive type of melanoma.
True
Nodular melanoma is the most aggressive type due to its rapid deep invasion and early metastasis
119
Nodular melanoma has both a radial and vertical growth phase.
False
Nodular melanoma has NO radial growth phase; it grows directly vertically, making it more dangerous
120
Nodular melanoma lesions grow rapidly, invade deeply, and metastasize early.
True
121
Nodular melanomas are always darkly pigmented.
False
Nodular melanoma mostly are darkly pigmented but about 5% can be amelanotic (non-pigmented)
122
Acral lentiginous melanoma occurs on the palms, soles, and under the nails (subungual areas).
True
Acral lentiginous melanoma occurs on palms, soles, and subungual (under-nail)
123
Acral lentiginous melanoma is the most common type of melanoma in people with fair skin.
False
It is most common type in black and asian skin, not in fair skin (where superfical spreading is more common)
124
Hutchinson’s nail sign refers to pigmentation extending from the nailbed to the nailfold.
Huntchinson's nail sign = pigmentation spreading from the nailbed to the nail fold - highly suspicious for melanoma
125
Lentigo maligna melanoma arises within a pre-existing lentigo maligna, usually on chronically sun-damaged skin.
True
This includes face and neck
126
Rosacea clinical features.
1. Central facial rash (usually symmetrical)
2. Erythema
3. Telangiectasia
4. Papules
5. Pustules (without comedones)
6. Inflammatory nodules
In some may see:
- facial lymphoedema
- rhinophyma
127
Management of Roseaca
General measures:
- Use soap substitutes (gentle cleansers)
- Avoid excessive sun exposure, use broad spectrum sun block (eg. SPF)
- Identify and avoid triggers (eg. spicy food, alcohol, stress, heat)
Mild measures:
- topical metronidazole gel or cream
- topical azeliac acid
- topical ivermectin for papulopustular roseacea
Modreate to severe measures:
- Oral tetracycline
- Doxycline low dose
- Oral isotretinoin (for severe or refractory cases)
- Laser therapy
128
What organs are mostly affected in leptospirosis?
Liver and kidney, thus hepatorenal syndrome is a hallmark sign.
129
T/F: Leptospirosis can affect the CSF
True
130
What are the 2 types of leptospirosis and their difference?
1) Anicteric leptospirosis:
- most cases are mild or aysmptomatic
- some are severe and potentially fatal
2) Weil's syndrome:
- more severe (fatal disease of leptospirosis)
- hepatorenal failure
- pulmonary hemorrhage (+/- pleural effusion)
131
Preliminary labs and specific labs for leptospirosis?
Preliminary labs:
1- abnormal urine --> proteinurea, wbc, rbc, hyaline, granular casts
2- Bloods: CBC (high wbc, low plt), U+E (renal insufficiency), LFTs (high bilirubin), ESR, glucose, coagulation
3- creatinine kinase (high)
Specific investigations:
1. days 1-7 --> PCR (blood +/- CSF)
2. after day 7 --> PCR (urine)
3. after 1 week --> serology (paired sera)
132
List the clinical features of leptospirosis.
1. conjuctival suffusion
2. myalgia (high CK)
3. jaundice (hepatosplenomeagly)
4. meningitis
5. uveitis
6. AKI
7. pulmonary haemorrhage
133
How is leptospirosis transmitted?
from rodent, dogs, and other domestic animals.
direct contact with their urine/fluids of an acutely infected animal or exposure to fresh water contaminated with urine of chronic carrier.
134
What is the treatment options for leptospirosis?
Mild treatment:
- doxycycline
- /amoxycillin
Moderate/severe:
- benzylpenecillin (IV) 1.2mg
- /amoxycillin IV
- /ceftriaxone
135
What is the chemoprophylaxis for leptospirosis?
doxycycline 200mg PO ince weekly
136
What is the prevention of leptospirosis?
avoiding potential sources of infection such as stagnant water and animal farm water runoff, rodent control, and protection of food from animal contamination.
137
What is the most common healthcare associated pathogen?
Clostoridum difficile (C.diff)
138
Antibiotics that cause Clostridium Difficile?
Start with the letter C: -
- Cephalosporins
- Clindamycin
- Ciprofloxacin (and other fluroquinolones)
- Carbapenems (eg. meropenem)
139
Presentation of clostiridum in its different phases?
Colonisation --> aysmptomatic
Infection --> diarrhoea and abdo pain
Severe infection --> colitis + dehydration and systemic symptoms (hypertension and tachycardia)
140
How is the diagnosis of Clostridium difficile made?
Based on stool samples, which can be tested for:
- Clostiridum antigens (glutamate dehydrogenase) --> detects all strains
- A and B toxins by PCR or enzyme immunoassay --> distinguish infection from carriage
NOTE: the antigen test shows whether C.difficile is present but not whether it is producing toxins. The antigen is the inital screening test and is followed up for toxins if C.difficile is identified.
141
Treatment of C.difficile?
- SIGHT: suspect, isolate within 48 hours, gloves and aprons, hand wash with soap, test immediately
1. oral vanomycin (1st line)
2. oral fidoxomicin
- patients needs to be isolated until 48 hours after the last episode of diarrhoea. There is high recurrence rate.
- Faecal microbiota transplanation is an option for recurrent cases. The stool microbiome from a donor is transferred via capsules, endoscopy, or enema.
142
What is infectious mononucleosis and what virus causes it?
Infectious mononucleosis is a clinical syndrome caused by infection with the Epstein–Barr virus (EBV).
143
List two alternative names for infectious mononucleosis.
Glandular fever
Kissing disease
(Also acceptable: “mono”)
144
How is Epstein–Barr virus transmitted between individuals?
EBV is transmitted through saliva, most commonly by kissing or sharing items such as cups or toothbrushes.
145
In which bodily fluid is EBV primarily found?
Saliva
146
Why is infectious mononucleosis more severe when acquired in adolescence or young adulthood?
Because primary EBV infection in adolescents and young adults triggers a more pronounced immune response, leading to symptomatic disease.
147
What are the three most common symptoms of infectious mononucleosis?
Fever
Sore throat (pharyngitis)
Fatigue
148
Why do most EBV infections in childhood cause few or no symptoms?
Because the immune response in childhood is less intense, resulting in mild or asymptomatic infection.
149
For how long can an infected individual shed EBV in saliva?
EBV can be shed in saliva for weeks before symptom onset and intermittently for life.
150
What characteristic rash may develop if a patient with infectious mononucleosis is treated with amoxicillin or cephalosporins?
An intensely itchy, generalised maculopapular rash.
151
Why should an itchy maculopapular rash after amoxicillin in an adolescent with sore throat raise suspicion of infectious mononucleosis?
Because EBV infection commonly causes a characteristic rash following exposure to amoxicillin or cephalosporins, even in the absence of penicillin allergy.
152
Why does amoxicillin cause a rash in patients with infectious mononucleosis despite no true penicillin allergy?
Because the rash is an immune-mediated reaction related to EBV infection, not an IgE-mediated penicillin allergy.
153
Investigations for infectious mononucleosis?
1) initial blood tests: CBC, Blood film --> lymphocytosis, atypical lymphocytes (suggestive NOT specific)
2) screening test: hetrophile antibody test (monospot/paul-bunnell) --> becomes +ve from 2nd week (85% +ve)
3) confirmatory tests: EBV serology --> anti-VCA IgM (acute infection), anti-VCA IgG (past infection) --> use if monopost -ve or immunocompromised
4) special situations: EBV PCR --> used rarely, helpful in immunocompromised
154
Management of IM?
- Supportive care: IM is usually self-limiting. Acute illness lasts 2-3 weeks, however, it can leave the patient with fatigue for several months once cleared.
- education, advice to avoid alcohol and contact sports (splenic rupture risk)
- consider antivirals and steroids (seek expert help)
155
Complications of IM?
- Splenic rupture
- Glomerulonephritis
- Hemolytic anemia
- Thrombocytopenia
- Chronic fatigue
156
What is a notable cancer that infectious mononucleosis (IM)?
Burkitt's lymphoma
157
List the AIDS-defining illnesses associated with end-stage HIV.
These occur when the CD4 count has dropped to a level that allows for unusual opportunitic infections and malignancies to appear: -
1. Kaposi's sarcoma
2. Pneumocystis jirovecii penumonia (PCP)
3. Cystomegalovirus infection (CMV)
4. Candidiasis (oesophageal or bronchial)
5. Lymphomas
6. Tuberculosis
158
Investigations done for HIV?
1. ELISA for HIV antibody and antigen (p24) - screening test
2. confirmatory HIV assay - required after +ve screening
3. rapid point of care testing (finger prick or mouth swab) - gives quick results but requires confirmation with serology
4. viral tests: HIV viral load / PCR - monitor response to ART, measures amount of virus
5. CD4 count - NOT diagnostic, monitor diseases progression and immune function
159
Investigations for pneumocytis jirovecci pneumonia?
- CXR
- SpO2 (compare rest and exertion)
- sputum induction or bronchoalveolar lavage (BAL)
- LDH
160
Management of pneumocysitis jirovecci pneumonia?
- ART is part of treatment of all opportunistic infections
1. Co-trimoxazoleIV 1st line (switch to oral if favourable response) - 21 day course
2. Steroids in moderate-severe disease
3. Pentamidine (2nd line)
161
What is the prophylaxis given for pneumocystis jieovecci pneumonia (PCP) and when is it given?
Co-trimoxazole given if CD4 count <200cells/microlite
162
ART treatment?
Use local guidelines. Get expert help. There are several classes:
1) protease inhibitor (PI)
2) intergrase inhibitor (IH)
3) nucleoside reverse transcriptase inhibitors (NRTI)
4) non-nucleoside reverse transciptase inhibitor (NNRTI)
5) entry inhibitors (ET)
- Usual starting regime --> 2 NRTI + third agent
- check for medication interaction
163
Investigations for Chlamydia?
164
Presentation of chlamydia in women?
Most are aysmptomatic
- abnormal vaginal discharge
- pelvic pain
- abnormal vaginal bleeding (intermenstrual or postcoital)
- dyspareunia
- dysuria
165
How does chlamydia present in men?
1. urethral discharge or discomfort
2. dysuria
3. epididymo-orchitis
4. reactive arthritis
166
Management of chlymadia?
- Doxycyxline 100mg BD for 7 days (1st line)
- Azithromycin 1g PO single dose then 500mg BD for 2 days
167
Investigations for Gonorrhoea?
- NAAT: endocervical in woman, first catch urine in men
- Charcol swab for microscopy, culture, and sensitivity to guide treatement (required in Gonorrhoea, unlike chlyamidia)
- HIV and syphilos serology
168
Managemenr of gonorrhoea?
1- Ceftriaxone 1g IM single dose if sensitivities are unknown
2- Ciprofloxacin PO 500mg single dose if sensitivites are known
3- Complicated disease: add doxycycline +/- metronidazole
169
What family of viruses does HIV belong to?
Retroviridae (a retrovirus).
170
Is HIV Gram-positive or Gram-negative? Explain why or why not.
HIV is neither Gram-positive nor Gram-negative because it is a virus and lacks a bacterial cell wall.
171
What enzyme allows HIV to integrate into host DNA?
Reverse transcriptase
172
What component is detected in 4th-generation HIV tests besides antibodies?
p24 antigen
173
What is the gram stain apperance of N.Gonorrhoea?
Gram-negative diplococci.
174
Why is culture important in gonorrhoea but not in chlamydia?
Because gonorrhoea has significant antibiotic resistance and requires sensitivity testing, whereas chlamydia does not.
175
Which of the following is a virus, a Gram-negative diplococcus, and an obligate intracellular bacterium: HIV, gonorrhoea, chlamydia?
Virus: HIV
Gram-negative diplococcus: Gonorrhoea
Obligate intracellular bacterium: Chlamydia
176
Which STI cannot be visualised on Gram stain and why?
Chlamydia, because it is intracellular and lacks a typical cell wall.
177
What bacteria causes syphilis?
Treponema pallidum
178
Investigations for syphilis?
1. dark field microscopy
2. PCR
3. RPR and VDRL --> non-specific but sensitive tests
179
Management of syphilis?
Single seep IM benzylpenicillin; duration depends on stage (atleast 7 days)
180
Complications of syphilis?
- aortic regurgitations
- aneurysms
- gumma lesions
- neurosyphilis
- tobes dorsalis
- blindness
- death
181
What conditions are caused by herpes simplex virus (HSV)?
- cold sores (herpes labialis)
- genital herpes
- apthous ulcers (small painful oral sores in the mouth)
- herpes keratitis (inflammation of the cornea of the eye)
- hepetic whitlow (painful skin lesion on a finger or thumb)
182
Where does HSV remain latent after the initial infection?
Sensory nerve ganglia.
Typicaly rhis is the trigeminal nerve gangliom (CN:V) with cold sores and the sacral nerve ganglia with genital herpes
183
Where does HSV remain latent after the initial infection?
trigeminal nerve (CN:V)
184
T/F: HSV is only transmissable when symptomatic
False
It is transmissted when aysmptomatic aswell via asymptomatic viral shedding
185
What is the difference between HSV-1 and HSV-2?
HSV-1 is most commonly associated with oral herpes (cold sores). It is usually acquired in childhood through non-sexual oral contact such as kissing or exposure to saliva. After primary infection, it remains latent in the trigeminal nerve ganglion and may reactivate later in life. HSV-1 can also cause genital herpes, usually via oral–genital contact.
HSV-2 is most commonly associated with genital herpes and is transmitted primarily through sexual contact. It becomes latent in the sacral nerve ganglia and tends to cause more frequent genital recurrences than HSV-1, although it can occasionally infect the oral region.
186
Why does HSV infection recur?
The virus remains latent in the sensory ganglia and periodically reactivates
187
Name two triggers for HSV reactivation.
Stress
Illness / immunosuppression
(Also acceptable: fatigue, sunlight)
188
Investigations for HSV?
PCR
189
Management of HSV?
- GUM referral
- Antivirals (within 5 days): aciclovir, valaclovir, famiciclov
- Additional measures, including symtom management: paracetemol, topical lidocaine, topical vaseline, wear loose clothing, avoiding intercourse with symptoms, additional oral fluids
190
How is malaria transmitted?
It is transmitted through the bite of an infected female anopheles mosquito, which injects plasmodium sporozoites into the bloodstream suring feeding
191
What is mumps?
an acute viral infection (RNA virus) chatacterized by parotid gland swelling, fever, and malasie
192
How is mumps transmitted?
By respiratory droplets and direct contact with saliva from infected individuals.
193
What are the typical clinical features of mumps?
Patients experience an initial period of flu-like symptoms known as the prodrome. These occur a few days before the parotid swelling:
Fever
Muscle aches
Lethargy
Reduced appetite
Headache
Dry mouth
194
Why does mumps cause jaw pain when eating?
because inflammed parotid glands cause pain during salivation
195
Complications of mumps ?
pancreatitis
epididymo-orchitis
meningitis
deafness
196
Why does mumps cause jaw pain when eating?
It may lead to testicular atrophy and subfertility, particularly in post-pubertal males.
197
What is the management of mumps?
- isolate and notify public health (notifiable disease)
- supportive care (fluids, analgesioa, manage complications)
-
198
CIs to the MMR vaccine?
pregnancy
severe immunosuppressed
allergy
199
why is mumps increasing
due to increased hesitancy to take the MMR vaccine
200
Sites swabed during MRSA infection?
Nasal swab (anterior nares)
Throat swab
Perineal / groin swab
(Also acceptable: wounds or catheter sites if present)
201
T/F: Scabies causes a delayed hypersensitivity reaction (type IV)
True
resulting intense itching which is worse at night
202
T/F: Repeated use of disinfectants during the treatment of scabies can lead to irritant dermatitis
True
Excessive or repeated use of disinfectants damages the skin barrier and causes irritant contact dermatitis, leading to ongoing itch and erythema. This persistent irritation can be incorrectly interpreted as treatment failure or continued scabies infestation, prompting further disinfectant use. In reality, symptoms are due to skin irritation or post-scabetic itch, not active mites, creating a self-perpetuating cycle of dermatitis.
203
Why does acne vulgaris improve with anti-androgenic hormonal contraception?
Because it occurs as a result of increased androgens (eg. testosterone and DHEA-S)
204
Where is acne vulgaris found?
Acne vulgaris is found in areas with a high density of pilosebaceous units, classically:
- Face (especially forehead, cheeks, chin)
- Chest
- Upper back
- Shoulders
205
Pathophysiology of acne (4 key steps — very exam-high yield):
1. Increased sebum production (androgens)
2. Follicular hyperkeratinisation → blocked follicle (comedone)
3. Cutibacterium acnes proliferation in the trapped sebum
4. Inflammation → papules, pustules, nodules
➡️ Acne therefore occurs only where pilosebaceous units exist.
206
T/F: Acne vulgaris commonly affects the face and upper trunk
True
207
T/F: Acne occurs in areas rich in sebaceous glands
True
208
T/F: Acne affects palms and soles
False
because there is no pilosebaceous units there
209
T/F: Sebaceous glands open directly onto the skin surface in acne
False
they open into hair follicles
210
T/F: An elderly fair-skinned man with long-term sun exposure presenting with a slowly growing indurated ulcer on the nasal bridge that bleeds on contact is most likely to have squamous cell carcinoma.
False
Basal cell carcinoma classically occurs in elderly, fair-skinned individuals with chronic sun exposure, commonly on sun-exposed areas of the face such as the nose. It is slow-growing, often presents as an indurated or pearly ulcer (“rodent ulcer”), and bleeds easily on contact. Although locally invasive, BCC rarely metastasizes, which distinguishes it from squamous cell carcinoma.
211
T/F: Basal cell carcinoma is the most common skin cancer
True
212
T/F: A rapidly growing painful ulcer suggests BCC
False
Think SCC
213
What are other names for BCC?
Rodent ulcer and basalioma.
214
T/F: Patients with BCC often develop multiple. primary tumors overtime
True
This is because:
Field cancerisation (main reason)
- Chronic UV exposure damages large areas of skin, not just one spot
- This creates a “field” of genetically damaged keratinocytes
- Each damaged area can independently give rise to a new primary BCC
215
T/F: BCC recurrence after inital treatment if NOT uncommon
True
216
A 9-year-old boy was treated for presumed alopecia areata after developing a patch of hair loss on the scalp. He was prescribed topical corticosteroids, but over the next few weeks the area became swollen, boggy, and tender, with some pustules and crusting. There was no improvement with topical antibiotics.
1) What did the child develop and why (name of boggy mass)?
2) Why was topical corticosteroids ineffective and topical antibiotics?
1) The child developed a kerion due to untreated or misdiagnosed tinea capitis, which was initially mistaken for alopecia areata. Use of topical corticosteroids suppressed local immunity, allowing dermatophyte infection to worsen and provoke a severe inflammatory (hypersensitivity) reaction, resulting in a kerion.
2) Topical corticosteroids mask fungal infection and worsen tinea capitis by reducing immune response. Topical antibiotics are ineffective because kerion is caused by a fungal infection, not bacteria. Effective treatment requires systemic antifungal therapy.
217
What is a kerion? (brief exam definition)
A kerion is a severe inflammatory form of tinea capitis, caused by a delayed hypersensitivity (type IV) reaction to dermatophyte fungi, presenting as a boggy, tender, pustular scalp mass and may result in scarring alopecia if not treated promptly.
218
What is the causative organism of molloscum contagoisum?
poxvirus, the molloscum conatgosium poxivirus
219
MD4 Semster 1
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