how to pass medicine exams2

Cardiac dicussion2
Case3/atrial fibrillation
1-history
*palpitation
*syncope
*tiredness
*dyspnea
*history of[ischamic heart disease---hypertension---rheumatic heart disease---congenital heart disease---valvular heart dsisease---thyrotoxicosis]
*history of caffien/digitals/theophylin consumption
2-examination
*irregular irregular pulse
look for * malar flash,mitral valvotomy scar[mitral stenosis]
*warm hands,goitre,pretibial myxedema[thyrotoxicosis]
*check for blood pressure [hypertension]


Q1.what are the commenest causes of atrial fibrillation?
A1.(1)mitral valvular disease in middle and young age
(2)ischaemic heart disease and hypertension in old age
(3)thyrotoxicosis (atrial fibrilltion may be the only clinical feature in old age)
(4)constrictive pericarditis
(5)chronic pulmonary disease


Q2.what are the commenest sites of systemic embolisation?
A2.legs, brain,kideny,spleen , coronary artery , superior mesenteric artery


Q3.how would you investigate this patient?
A3. ECG / echocardiography / thyroid function test


Q4.what are the other causes of irregular irregular pulse?
A4. multiple ventricular ectopics / atrial flutter / complete heart block


Q5.how would you treat such a patient?
1-Attempt to restore ventricular rate
*in hypertensive patient use Ca blockers
*in thyroid patient use beta blockers
*in ischeamic heart patient use beta blockers or Ca blockers
*in heart failure use digoxin or Ca blockers
2-attempt to restore sinus rhythm by cardioversion and drugs
*drugs restore the sinus rhythm are[quinidine/procainamide/amidarone]
3-anticoagulation with warfarin is advised in some patient



case4/aortic stenosis
1-history
*most of patient are asymptomatic
*dyspnea is a common symptom suggest left ventricular dysfunction
*fatigue
*angina in 70%
*syncope in 25%

2-examination
*low volume pulse
*heaving non displaced heart apex
*palpable systolic vibration over the primary aortic area with the patient in sitting position
*systolic thrill over the aortic area
*second soft heart sound
*ejection systolic murmur+ejection click after 1st heart sound
*third heart sound indicate left ventricular dysfunction.

Q1.mention some causes of aortic stenosis?
A1.-under the age of 60[rheumatic,congenital]
-between 60 to 75[cacified bicuspid aortic valve]
-more than 75 [degenerative cacification]


Q2.what do you understand by the term ejection systolic murmur?
A2.it is a crescendo-decrescendo murmur which begins after the 1st heart sound and ends before the second.

Q3.what are the complication of aortic stenosis?
A3.(1)left ventricular failure
(2)arrythmias
(3)systemic embolization
(4)infective endocarditis 10% of cases
(5)heamolytic anemia
(6)sudden death 10-20%


Q4.how would you manage this patient?
A4.valve replacement even in asymptomatic patients
*if the patient presents with signs and symptoms of aortic stenosis with normal aortic valve in echocardigraphy,this cauld be supravalvular or subvalvular aortic stenosis.

Q5.if this patient had a bleeding per rectum what is the unusual cause come to mind?
A5.angiodyplasia of the colon

Q6. if the patient was icteric and had a heamolytic anemia what is the cause?
A6.sever cacified aortic stenosis cause sever heamolysis and jaundice.



Case5/myocardial infarction
1-history
*dyspnea
*palpitation
*syncope
*post infarct angina
*family history of[cardiovascular diease/hyperlipidemia/gout]
*smoking
*past medical history of [DM/hypertension/stroke/myocardial infarction /hyperlipidemia]
*history of cotraceptives in youn women


2-examination
*hands:nicotine staining of the fingers
*pulse:check the rate(keeping in your mind tackycardia or bradycardia),check the rhythm (keeping in your mind atrial fibrillation or ventricular arrythmias)
*check blood pressure
*JVP may be raised
*eyes:look for arcus senilis or xanthelasma
*apex beat: double apical impulse
*auscultate: 4th heart sound,pericardial rub,pansystolic murmur


Q1.what is levien's sign?
A1. in acute myocardial infarction the patient often descibes the pain as cleching fist

Q2.what are the major risk factors for MI ?
A2.*DM
*HTN
*hyperlipidemia
*smoking


Q3.how would you manage a patient with acute MI?
A3.*immediatly(1)chewable non coated aspirin 160-325mg
(2)pain relif
*within 30min after hospital admission:--thrombolysis
*within 12hours from the infarction:--beta blockers if there is no contraindications
*within the 1st 24hours :--ACE inhibitors

Q4. what are the complication of MI?
A4.*arrythmias[early and late complication]
*thromboembolism[early and late complication] *heart failure[early complication]
*circulatory failure:cardiogenic shock:heart block [early complication]
*pericarditis[early complication]
*mitral regurgitation[late complication]
*rupture of ventricular septum[late complication]
*dresseler's syndrome(pyrexia+pericarditis 2 to 12 weeks after the infarction) [late complication]
*ventricular aneurysm[late complication]

Q5.what is a silent MI?
A5.it is a painless infarction ,common in diabetics and in elderly,they may be presents with complication.

reference:Davidson's clinical cases

Cardiac discission1
cardiac symptoms(DOP CSTC)
1-dyspnea:there are 4 types
(1)dyspnea on exertion ---in all CVS diseases-anemia-respiratory diseases
(2)dyspnea at night or nocturnal dyspnea----in left side heart failure-aortic valve disease-cardiac arrythmias-bronchial asthma
(3)dyspnea on lying flat or orthopnea----persistent pulmonary odema – advanced heart disease
(4)periodic dyspnea in old people


2-odema:
*it's a fluid retention leading to accumulation of fluid under the skin causing pitting or non pitting odema.
*odema of cardiac origin usually starts to accumulate in the lower limb[in bedriddin patient it accumulate in the back,buttocks,thighs and abdomen]
*odema of renal origin usually begins to accumulate in the face causing puffness and periorbital odema.
*the most common causes of odema are---cardiac failure – renal dieases – chronic venous insuffiency – hypoalbunemia – drugs


3-palpitation:
*it's an awarenace of heart beats which is in the most cases have no relation to heart diseases
*if it's from cardiac origin it will be associated with arrythmias such as [regular paraxosmol tackycardia-irregular fibrillation – in hyperkientic circulatory state such as arteriovenous shunts , cor pulmonale and beriberi
*other causes [anemia-thyrotoxicosis-anxiety-smoking-coffee-kola over use-asthma medication-digitalis]

4-chest pain:
*features of cardiac chest pain are-----central and retrosternal pain radiated to left shoulder , or diffuse heavy pain increase by exertion and decrease by rest.
*non cardiac causes ----febrile episodes-anxiety-pnumothorax-pleurisy
*cardiac causes----myocardial infarction-angina-pericarditis-cardiac ischamia- aortic aneurysm.

5-syncope:
*it's fainting due to decrease cerebral perfusion causesd by
(1)cardiac arrythmias
(2)impaired venous return[hypovolemia-diabetis melitus-hemorrhage-cough]
(3)excessive vasodilatation[antihypertensive drugs]
(4)vasovagal
(5)acute heart failure[pulmonary embolism-myxoma-aortic stensis]

6-tirdness:occurs mainly in low cardiac output cases and anemias

7-cough:
*more commonlly associated with respiratory than cardiac diseases.
*cough of cardiac origin manifested by frothy sputum pricpitated by exertion.


Case1=mitral stenosis

1-history[to obtain symptoms] * symptoms of left side heart failure
-decrease cardiac output:---pallor,syncope,tirdness,decrease blood pressure,palpitation and cold periphry
-increase atrial pressure---pulmonary odema which will cause persistent dyspnea and basal crepitation
*more specific symptoms for mitral stenosis[heamoptysis-hoarsness of voice-symptoms of right side heart failure-palpitation]

2-examination[to obtain signs]
*regular or irregular pulse due to atrial fibrillation.
*raised jugular venous pressure.
*malar facies or malar rash.
*tapping apex beat in the 5th intercostal space.
*left retrosternal heave indicate right ventricular enlargment.
*loud 1st heart sound.
*opening snap best heard at the apex with the patient in the lateral decubitus position.
*Low pitched mid diastolic murmur best heard with the patient in the left lateral position on expiration.


Q1.what is the commenest cause of mitral stenosis?
A1.rheumatic heart disease

Q2.what are the other rarer causes of mitral stenosis?
A2.-rheumatoid arthritis
-systemic lupus erythromatosis
-congenital stenosis
-malignant calcinoid


Q3.what is the mechanism of tapping apex beat?
A3.it is due to accentuated 1st heart sound.


Q4.what does opening snap indicate?
A4.indicate the opening of stenosed non calcified mitral valve, because if calcified will be absent.

Q5.what is the mechanism of loud 1st heart sound?
A5.the valve open during diastole and suddenly slammed shut by contraction in systole.

Q6.what are the complication of mitral stenosis?
A6. 1)systemic embolisation
2)left atrial enlargment and atrial fibrillation
3)pulmonary hypertension
4)tricispid regurgitation
5)right side heart failure


Q7.what are the investigation?
A7. 1)ECG:broad P wave[P mitrale]
2)chest x ray
3)echocardiography:the investigation of choice
4)cardiac catheterization


Q8.how would you manage this patient?
A8.- asymptomatic patient:--only prophylaxis aganist infective endocarditis - mild sypmtoms:--diuretics to reduce atrial pressure - atrial fibrillation:---(1)to control atrial rate[digitalis-beta blockers or channel calcium blockers,(2) anticogulants - moderate to sever symptoms or pulmonary hypertension----(1)ballon valvotomy or percutanous mitral ballon valvoplasty,(2)surgery


Q9.what is ortner's syndrome?
A9.refers to the hoarsness of voice caused by left vocal cord paralysis associated with atrial enlargment




case2/hypertension
1.history
*chest pain/dyspnea
*intermittent claudication
*headaches/visual disturbance
*family history of hypertension
*ask about hypertension in pregnancy
*medications

2-examination
look for aetiology:
-cashingoid face
-radiofemoral delay
-examine blood pressure in both arms
-listen for renal bruit of renal stenosis,feel for polycystic kidney

look for organ damage:
-examine the heart for left ventricular hypertrophy
-look for signs of heart failure
-examine the fundus for hypertensive retinopathy
-check the urine for evidence of renal failure[protein or sugar

Q1. what are the causes of hypertension?
A1.- unknown or idiopathic 90% - renal cause :diabetic nephropathy , renal artery stenosis , glomerulonephritis , pyelonephritis. - endocrine cause :cushing syndrome, pheochromocytoma , steriod therapy - others:coaraction of aorta , toxemia of pregnancy , contraceptives


Q2.what are the causes of blood pressure discrepancy between the arms or between the arms and legs?
A2.- coaraction of aorta -dissecting aortic aneurysm
-atrial occlusion or stenosis
-patent ductus arteriosis
-thoracic outlet syndrome



Q3.how you would you investigate a patient wth hypertension?
A3.CBC – serum urea and electrolyte – serum creatinine – fasting lipids – fasting blood sugar – serum uric acid – ECG – chest x ray – 24 hour urine collection to measure vanillylmandelic acid


Q4. what spcial investigation would you perform to screen for the underlying cause ?
A4. - renal digital subtraction angiography
-24 hour collection urinary catecholamines
-dexamethasones suppression test

Q5.which drugs should be used as 1st line treatment?
A5.- the older 1st line [beta blockers/thiaziades]
- the newer 1st line [Ca blockers/ACE inhibitors]


Q6.what is the appropriate interval before assessing the response to therapy?
A6. most of the antihypertensive drugs have their maximum blood pressure lowering affect 2 to 4 weeks although thiazide diuretics may take slightly longer [most physcians take around 6 weeks before assesing the efficasy.


Q7.what drug combination are effective?
A7. step1: monotherapy
step2: A or B + C or D
step3: consider 2ry hypertension and specialist refer
A=ACE inhibitors B= beta blockers
C= Ca blockers D=thiazides


Q8.what are the indication,adverse effects and contrindications for thiazides ?
A8.- there is no specific indication
-the contraindications are [gout/renal impairment/sever hepatic impairment/pregnancy]
-the adverse effects are[gout/ rashes/hyponatremia/hypotension]


Q9.what are the contraindication and adverse effects for beta blockers?
A9.-the contraindication[asthma/COPD/heart failure]
-the adverse effects [signs of central effect---tiredness/nightmares/insomnia/sexual dysfunction]


Q10.what are the drug of choice for each of the following:-
uncomplicated HTN------ diuretics(hydrothiazides-furosemide-spirolactone)
diabetes melitus and proteinuria----ACE inhibitors(captopril-enalopril)
heart failure------ACE inhibitors/diuretics
mycardial infarction----ACE inhibitors /beta blockers
angina-----beta blockers / Ca blockers
renal insuffeciency----ACE inhibitors
benign prostatic enlargment[BPE]---- alph blockers

Reference::250 cases in clinical medicine

battle aganist cancer

*in these days the commonest cause of death is heart diseases but still we panic from cancer and we may be avoid to name it and called CA or the Bicc.

*after a thousands of researches all scientists agree on what ancient scientists say “the cure in your food” . And the food are
1-garlic
2-cabbage
3-ginger
4-soybean
5-carrots
6-onion,green tea,
7-brown rice,spices,tomatoes
8-oat,mint,cucumber,potatoes
9-melon,thyme

*all those plants are rich in natural material for example:antioxidants =polyphenols,carotenoids,flavinoids,coumarins,phenolic acid,lignans and indoles.

*although taking additional antioxidants from minerals and multivitamins which does not contain iron is a part of aging delay plan.

*recently researches approve that diet rich in olive oil may reduce the incidence of getting colon cancer and this research say that “the percentage of colon cancer incidence in whom taking plenty of olive oil is less than people who are using other types of oils “ because it regulate the levels of cholestrol between bad[LDL] and useful cholestrol[HDL].


*many of us thought that our minds are the biggest force in cancer battle but there is no scientific approve about this ,but an American research last for 3 years revealed that cancer patient who received relaxation training their white blood cells are reinforced to kill the cancer cells and those patients are lived longer than others so conclusion we have to know that the positive thinking will not cure the cancer but if definitely help to improve the condition and increase life survival rate.

Thiamin:do we realy need to take it

*thiamin is also known as vitamin B1

*what are the benefit of B1?......1-the first benefit is enhancement of normal body growth 2-protect the nervous,muscular,and the cardiovascular system
3-have an important role in producing energy by consumption of the sugar that we eat
4-help to reduce fatigue ,depression and nausea

*where we could find it?..... in grilled potatoes-meat-baking powder-orange juice-fruits[pears,raisin,peaches]-and the products of the hole grains.

*do we need B1?.... vitaminB1 accelerate metabolism so we need it especially who suffers from liver diseases,hyperthyroidism,chronic diarrhea,pregnant women,lactating women,alcoholism and elderly people.

*there are no contraindication except for hypersensitivity to B vitamin.

Simple notes on skin infestation

1.SCABIES
Clinical Features
Symptom occurs 3 to 4 weeks after the acquire of the infection. This latency period may not occur if an individual has had a previous infestation. Itchiness is the most obvious symptom of scabies. It is worst at night time when the patient is warm.
The pathognomonic sign of scabies is a burrow; it is a short, wavy, dirty-appearing line crossing skin lines. They may occur on the wrists, the borders of the hands, the sides of the fingers and the finger web-spaces, the feet particularly the instep and in male the genitalia and nodules on scrotum. Burrows are uncommon on the trunk in adult but they may be found in elderly and infants. Pruritic papules which accompany hypersensitivity reaction occur around axillae, peri-areolar regions, peri-umbilical regions, buttock and thighs. The lesions do not occur above the neck-line. Secondary change like eczematous change frequently give confusion to the clinical picture. Inappropriate use of topical steroid may change the clinical picture to mimic other dermatoses.
1.4. Diagnosis
Absolute confirmation can only be made by the discovery of the burrows and microscopic examination. A burrow is gently scraped off the skin with a blunt scalpel, and the material placed in a drop of mineral oil on a microscopic slide. Oil mounting of the specimen sharpens the microscopic image and does not kill the mites which may be present (as potassium hydroxide would). Presence of mites, eggs or fragments of egg-shells confirms the diagnosis. Other diagnostic tests include needle extraction of mite, epidermal shave biopsy and punch biopsy.
1.5. Treatment
It is important that all members of the household and all close contacts should be treated simultaneously. Elderly members of the family often resent for treatment but they can be asymptomatic reservoirs of infection.
Treatment must be given on two consecutive nights but not for longer. Anti-scabies preparations are primary irritants which will eventually cause eczema, patients should be warned about over-use. The patient should first take a bath, and this is followed by a brisk toweling to open the hydrated burrows. Hot bath increases the percutaneous absorption of the drug and may cause toxicity. Benzyl benzoate employed as a 25% emulsion should remain on the skin for 24 hours. The emulsion is most conveniently applied with a 2" paint brush applied to the whole body from the neck down including the genitalia and the soles of the feet. This anointing is repeated on the following morning. On the following evening the patient should take a bath again and has the bed-linen and clothing changed which are then laundered in the usual way.
After the scabicidal treatment, pruritus may persist for a further 2 weeks. A topical antipruritic such as crotamiton cream may be applied on residual itchy areas. Postscabetic eczema can be treated with topic steroid.
Secondary infection should be treated with a systemic antibiotic. If eczematisation is severe, a non-irritant scabicide, preferably in an aqueous base, should be used.
Treatment of neonates - 6.25% benzyl benzoate emulsion may be used. Other alternatives include 10% crotamiton cream (applied nightly for 2 nights and washed off after the second application), 10% sulphur in petrolatum (applied nightly for 3 nights and washed off 24 hours after the last application) and 5% permethrin cream.
Other drugs used:
1) 1% gamma benzene hexachloride (Lindane) - a single application wash off after 12-24 hours is usually recommended. It is not recommended to be used in young children, pregnant and nursing women, and those with neurological diseases.
2) malathion - malathion 0.5% in aqueous base has been used as scabicide. It should be left on the skin for 24 hours. The advantage over BBE is that it is much less stinging and acceptable.
3) permethrin - 5% dermal cream employed as a single application, wash off 8-12 hours. It is of low toxicity, and a single application which is removed in 8-10 hours is adequate. The disadvantage is that it is much more expensive than BBE or malathion.
4) monosulfiram - 25% solution diluted with 2-3 parts of water to be applied daily for 2 or 3 days.
5) crotamiton - 10% crotamiton cream is not highly effective and should not be a first line treatment for scabies. It is at best an adjunctive treatment for post-treatment pruritus and an alternative for BBE in infants and pregnant ladies.
6) topical sulphur e.g. 10% sulphur in petrolatum.

2. CRUSTED SCABIES (NORWEGIAN SCABIES)
Crusted scabies is an infestation with Sarcoptes scabiei hominis in which huge number of mites were present. The grossly thickened horny layer is honeycombed with cavities which contain large number of mites, and these are shed into the environment of the patient. Crusted scabies is highly contagious; an undiagnosed case of crusted scabies may lead to large outbreak of common scabies.
2.1. Aetiology and Pathogenesis
In common scabies there are few mites probably because of scratching destroys the burrows. In some patients skin anaesthesia secondary to neuropathy or spinal injury obviously do not perceive itch and do not scratch crusted scabies is likely to develop.
Crusted scabies has a predilection for patients with physical debilitation, mental retardation, sensory impairment and immunosuppression.
2.2. Clinical Features
Masses of horny debris accumulate beneath thickened and discoloured nails. Large warty crusts form on the hands and feet, and the palms and soles may be irregularly thickened and fissured. Itching is often absent or slight. It may present as exfoliative dermatitis. Differential diagnoses include hyperkeratotic eczema, psoriasis, Darier's disease and contact dermatitis.
2.3. Treatment
There is no single treatment for crusted scabies. The general principle is that multiple treatment is needed and sequential use of several agents may be necessary. The following regimen is suggested with the use of 25% benzyl benzoate emulsion (BBE), which is the most commonly used agent in public hospitals in Hong Kong. Ivermectin, given in a single oral dose, is found to be effective in healthy and HIV subjects in a small study.
Equipment to prepare: Soft brushes to apply the BBE, tooth brushes to rub away the scales, nail clipper to trim the nails.
Treatment is intensive and should be given by nurses well informed and dedicated to give the treatment.
BBE is applied from neck include behind the ear down to the toes.
Application to the face and scalp is necessary. BBE may also apply to those area but may be too stinging. 0.5% Malathion is a good alternative which is also effective and causing less irritation. Crotamiton is an alternative to malathion to the area, but is much less effective.
Nails should be cut short. BBE should be scrubbed into the area under the nail.
Scales, which are usually thick under the nail and on flexural area should be gently rubbed away with brushes.
Repeat the above steps for 4 consecutive days at least.
Repeat examination and isolation for mite on day 5. Continue treatment until identification is negative.
Give oral antibiotics which are effective against staphylococcus and streptococcus unless contraindicated, for 7-10 days.
Change clothing and bed linen daily and these are treated in method mentioned below.
Isolation can be stopped when treatment is completed (e.g. day 5 when identification is negative).
Repeat identification procedure one week after treatment is stopped. Repeat scrapings for identification each week as long as the patient is still in ward.
While BBE is cheap and safe, its use in crusted scabies is less reported in the literature. It causes irritant contact dermatitis especially in areas infected or eczematised. The local profile of resistance to BBE is not reported, but since BBE is the most commonly used scabicide locally, resistance to the agent is not surprising. Physician should be prepared for this possibility and ready to use other agents if clinical response is not satisfactory. The microbiologist،¦s opinion is invaluable.
Management of Contacts:
Adequate treatment of contacts is as important as adequate management of the target patient. Success of treatment depends on an all-inclusive approach: all individuals in the ward and their family members should be treated, and treated simultaneously, no matter whether they are symptomatic or asymptomatic.

3. PEDICULOSIS CAPITIS
3.1. Epidemiology
The infection rate was higher in urban than in rural areas. In the early 1980s, there was a resurgence of infection due to the emergence of the so-called 'super-louse' which was resistant to DDT powder.
Lice are more common on children than on adults, and female of all ages are more frequently infected than males. There does not appear to be any direct correlation between hair length and louse infection rates, and it has been suggested that large masses of hair may, in fact, impede transmission of lice from scalp to scalp. The vast majority of head louse infections are acquired by direct head-to-head contact. Spread of lice is encouraged by poverty, ignorance, poor hygiene and overcrowding. Overcrowding is perhaps the most important factor. Transmission of head lice by sharing personal articles such as hair brushes, combs and towels is possible.
3.2. Clinical Features
These occur in the long hair of the scalp, but may also invade eyebrows and eyelashes. The characteristic manifestation of head louse infection is scalp pruritus. Secondary bacterial infection may occur as a result of scratching, and concomitant head louse infection must always be considered in cases of scalp impetigo. Pruritic papular lesions may occur on the nape of the neck, and occasionally a generalized non-specific pruritic eruption develops. In severe, neglected cases pus and exudate may produce matting of the hair.
Nits are egg-cases. They occur in greatest density on the occipital and parietal regions. Most of the unhatched nits are within 5 mm of the scalp surface. The eggs can be distinguished from dandruff by the fact that they are firmly attached to the hair. Moreover, if the affected hair is cut off and observed under microscope, the oval egg capsule can be easily identified. Adult lice and nymphs may be seen in heavy infestation.
3.3. Treatment
Treatment of pediculosis of the scalp aims at the destruction of the lice and the ova. Other members of the family and the whole class of school children should be examined, otherwise re-infestation will occur.
Malathion is effective and has good ovicidal activity. It is adsorbed onto keratin, a process which takes approximately 6 hours, and has a residual protective effect against re-infection for about 6 weeks. Malathion should be left on the scalp for 12 hours before washed off. The insecticide is degraded by heat, and a hot-air dryer should not be used. Treatment should be repeated 2 weeks later when the larvae have hatched out. Lotions are preferable to shampoos, as the latter expose the insects to relatively low concentrations of insecticide which will favour the development of resistance.
Empty egg-cases are difficult to dislodge, they persist for some time until they are gradually worn away by repeated washing. They may be removed with a fine-tooth comb or forceps. A cream rinse containing formic acid may facilitate the removal.

4. PEDICULOSIS CORPORIS
4.1. Incidence and Epidemiology
Pediculosis corporis is now uncommon in developed countries. It mainly affects the poor and neglect and flourishes in overcrowded, dirty situations where individuals seldom change their clothes. There is great variation in the number of eggs and lice on the clothing. In most cases the number of lice is small but in some thousand of lice may be present. Transmission is mainly by direct close body contact or by sharing infested clothing. Lice on a cooling dead body will look for alternate lodgings, and doctors asked to certify death in a vagrant should be aware of this.
4.2. Clinical Features
Intense pruritus is the chief complaint. It is due to sensitization to salivary antigens of the lice. Excoriation with secondary bacterial infection and hyperpigmented changes are common physical findings.
When the lice are not feeding, they stay in the clothing. Therefore, it is important to examine the inner lining of clothing including the seams of underpants.
Hands and feet are usually not involved and there is a predilection for the upper back. The characteristic distribution helps to distinguish it from scabies. The principal louse-borne diseases are epidemic typhus, trench fever and louse borne relapsing fever.
4.3. Treatment
It is the clothing rather than the patients which require treatment. Destruction of the lice is accomplished by laundering or boiling the clothing and bedding. High temperature laundering of underpants and dry-cleaning of outer clothing are also effective. Tumble-drying is the most effective means of killing both lice and eggs.
The patient should bath thoroughly with soap and water. Theoretically, this is sufficient. However, many dermatologists would prescribe gamma benzene hexachloride to treat the body as well. Mass delousing of large number of persons can be carried out successfully by simply blowing DDT powder under the clothing with a hand dust gun.

Simple notes on alopecia

1. DEFINITION
Alopecia is defined as excessive or abnormal loss of hairs.
2. PHYSIOLOGY
Natural hair loss is a physiological phenomenon. It is not a disease. Only when the loss is excessive or when the pattern of loss is abnormal, then it is pathological. Before one talks about the causes of alopecia, one has to understand the physiology of hair growth (Diagram 1).
Diagram 1: Hair Cycle
2-6 years
Anagen ---------------------------------------» Catagen
| |
Hair shedding «---------------------------------Telogen
100 days
90% of our terminal hairs are at anagen phase which is the growing phase. It lasts for 2-6 years. The scalp hair on average grows at the rate of 0.37 mm per day.
Catagen is a transient period. Hair matrix cells stop dividing. As a result, there is no hair growth.
Less than 10% of our hairs should be in telogen phase which lasts for 100 days (about 3 months). Since on average, each person has about 100,000 hairs. Therefore, less than 10,000 should be in telogen phase and on each day less than 100 hairs fall off physiologically.

3. SPECIAL POINTS TO LOOK FOR
When examining patients with alopecia the following points are worth paying attention to:
1) Pattern of alopecia
a) Diffuse alopecia is usually due to telogen effluvium, systemic disorder (e.g. hypothyroidism, Fe deficiency, secondary syphilis), drugs.
b) Patchy alopecia is typically seen in alopecia areata, scarring alopecia.
c) Marginal alopecia affects the hair margin only. It occurs in alopecia areata or due to hair styling.
d) Frontal and bitemporal alopecia is typical of male-type baldness.
2) Sign of scalp inflammation indicates alopecia may be secondary to inflammatory dermatosis (e.g. tinea capitis)
3) Presence of scarring together with alopecia will switch the differential diagnosis towards the cause of scarring alopecia (e.g. DLE, Lichen Planus).
4) Other than the scalp, see if hairs in other areas are also affected (e.g. axillary, pubic regions, eyebrow, eyelashes etc.).
5) Detailed drug history and history of past health are important.
4. CAUSES OF DIFFUSE ALOPECIA WITH NO SIGN OF INFLAMMATION NOR SCARRING
1) Telogen Effluvium
a) Post-Partum
b) Severe Illness
c) Major Operations
d) Malnutrition
2) Anagen Effluvium e.g. chemotherapy
3) Male Pattern Baldness
4) Female Pattern Baldness
5) Diffuse Alopecia Areata
6) Drugs e.g. heparin, antithyroid drugs, etretinate, isotretinoin
7) Systemic Disease e.g. Fe deficiency, thyroid disease, secondary syphilis, SLE
8) Ageing: usually causes thinning of hairs
4.1. Telogen Effluvium
When a severe insult striking our bodies (severe infection, delivery, major operation) the anagen hairs (> 90% of hair population) will all simultaneously shift to telogen phase. As a result, about 3 months after the insult, more than 90% of the hairs will fall off at the same time giving rise to the condition which is called telogen effluvium.
The diagnosis can be made from a detailed history of the past health. In case when the diagnosis is in doubt, it can be confirmed by the telogen hair count test. It is done by plucking a bundle of hairs and counting for the percentage of telogen hairs present. Normally, the telogen hair count should not exceed 10% of the total hair count. Unfortunately, this test is not available in most centres.
For telogen effluvium, no specific treatment is needed since spontaneous remission is the rule.

4.2. Anagen Effluvium
Chemotherapy attacks the rapidly dividing cells i.e. anagen hairs. As a result, more than 90% of hairs fall off soon after chemotherapy. Usually, there is no problem with the diagnosis since it is obvious from the history.
4.3. Male Pattern Baldness (Androgenetic Alopecia)
4.3.1. Pathogenesis
Even though the exact aetiology is unknown, there are proofs that genetic factor, as evidenced by frequent positive family history, and androgen play an important role in the development of the disease. Eunuchs and castrated males never develop baldness. Under the influence of androgen in a genetically predisposed person, the terminal hairs are gradually transforming into vellus hairs and they eventually fall off.
4.3.2. Clinical Features
Typically, it starts off with bitemporal recession and subsequently, thinning or complete loss of hair at the crown. Hair on the occiput and around the sides of the scalp is seldom affected and it seems that hair in those areas are more resistant to the effect of androgen. The diagnosis can often be made by the characteristic pattern of hair loss and the frequently presence of a positive family history.
4.3.3. Treatment
1.No good treatment is available at present.
2.Topical minoxidil may be useful in minority of cases but the effect disappears soon after stopping the treatment and yet it is expensive. It is the only FDA approved drug at presence for the treatment of androgenetic alopecia.
3.Topical ether-in-spirit: the effect is no better than placebo.
4.Hair Transplant: based on donor dominance theory which states that hairs from growing areas will survive and grow when transplanted to bald areas. The operation is tedious and requires expertise.
5.Wigs: quite practical if it is acceptable by the patient.
4.4. Female Pattern Baldness
It is characterized by thinning of hairs at the crown or a diffuse hair loss. Unlike male pattern baldness, there is no bitemporal and frontal recession. If female pattern baldness occurring in a young female, especially with the presence of menstrual disturbance, signs of hirsutism or virilization, excessive androgen activity needs to be excluded e.g. androgen-secreting tumour. Treatment is difficult but one may try cyproterone acetate which is an anti-androgen.
5. CAUSES OF PATCHY ALOPECIA WITHOUT SCARRING
Alopecia areata/totalis/universalis
Trichotillomania
Traction alopecia
Tinea capitis (excluding favus)
5.1. Alopecia Areata/Totalis/Universalis
These 3 conditions all belong to a spectrum of the same disease. They only differ in the degree of severity. When all the scalp hair is lost, it is called alopecia totalis. If both scalp and body hair are involved, it becomes alopecia universalis.
Alopecia areata is the commonest cause of patchy alopecia.
5.1.1. Aetiology
The exact aetiology is unknown. Genetic factor and atopy play some role as some patients may have positive family history or history of atopy. It is considered as a kind of autoimmune disease since it has an association with other organ-specific autoimmune disease (e.g. Vitiligo, Hashimoto thyroiditis). The incidence of alopecia areata is high in patients with Down's syndrome and those who are under stress.
5.1.2. Clinical Features
The disease affects male and female equally at all age. It is presented as discrete patches of baldness with no scarring and no sign of inflammation. Broken hairs with tapering shafts (i.e. exclamation mark hairs) are diagnostic. Nail pitting may also be present.
5.1.3. Treatment
1.Local Steroid
a) Topical Steroid e.g. 0.025% fluocinolone, halometasone
b) Intralesional Steroid e.g. triamcinolone
These treatment modalities may be useful in dealing with localized disease.
2.Irritants or Contact Sensitizers e.g. dithranol, diphencyprone. DNCB is no longer recommended because of its carcinogenic potential.
3.PUVA/UVB: May show response in some cases but need many treatment sessions. The actual beneficial effect is controversial.
4.Topical minoxidil: effect is doubtful.
5.Oral prednisolone: it is effective in some cases but has to be reserved for resistant or severe cases (e.g. alopecia universalis or alopecia totalis) because of its potential side effects.
6.Wigs wearing: last solution.
5.1.4. Prognosis
The prognosis is usually good since 75% of patients with alopecia areata have spontaneous remission eventually.
Signs of Poor Prognosis:
Multiple patches
Ophiasis (extensive hair loss at occipital area)
Eyebrows and eyelashes involvement
Alopecia totalis/universalis
Young age of onset
Presence of atopic disease
Frequent recurrent attacks
Nail involvement
Down's syndrome
5.2. Trichotillomania
5.2.1. Cause
The hair loss is due to self-induced twisting and pulling of hairs. It usually occurs in children or adolescents. It may be due to a bad habit, attention seeking or a manifestation of psychological problem.
5.2.2. Clinical Features
Patches of alopecia with no sign of inflammation are seen. Unlike alopecia areata, the margin of the lesion is less well defined and there is no exclamation mark hairs. The hair loss is never complete. Short broken hairs of varying length are characteristic.
5.2.3. Diagnosis
The disease can be diagnosed clinically. A detailed social and psychological history are essential.
5.2.4. Treatment
Often, the disease is self-limiting upon reassurance. Parents have to be interviewed so that the problem can be addressed. Sometimes, referring patient to clinical psychologist or psychiatrist may be helpful.
5.3. Traction Alopecia
Alopecia secondary to hair styling, hot-combing to straighten kinky hair.
It is rare in Hong Kong.
5.4. Tinea Capitis
Tinea capitis must be considered as one of differential diagnosis as a cause of patchy alopecia in children. The infected hair are brittle and are easily broken. It is associated with inflammation i.e. redness, scaling. Even though for most of the time, the lesion heal without scarring, in severe cases (e.g. kerion), scarring alopecia can occur. Please refer to the chapter on skin infection for details.
6. CAUSES OF DISCRETE PATCHY ALOPECIA WITH SCARRING
1.Congenital e.g. aplasia cutis, naevus sebaceus
2.Post-trauma e.g. burn, injury, radiotherapy
3.Post-infection e.g. kerion, herpes zoster
4.Inflammatory dermatosis e.g. DLE, lichen planus, morphoea: common cause of scarring alopecia
5.Neoplasm e.g. squamous cell carcinoma of skin
6.Idiopathic
6.1. Aplasia Cutis
This is a very rare congenital disease and the alopecia is present since birth.
6.2. Naevus Sebaceus
It is a kind of epidermal naevus which presents at birth as a yellowish hairless plaque on the scalp. It becomes more warty after puberty. The diagnosis can be confirmed by skin biopsy. It has potential of undergoing malignant change (e.g. basal cell carcinoma). For this reason, excision of the lesion after puberty is recommended.
6.3. Inflammatory Dermatosis Causing Alopecia
DLE, lichen planus and morphoea are common causes of patchy scarring alopecia. Sometimes, clinically, it is difficult to differentiate them one from another. One should examine the rest of the body to look for any sign that are related to each of these 3 diseases. Of course, skin biopsy of the lesion on scalp is usually helpful.
6.4. Idiopathic Scarring Alopecia (Pseudopelade)
Occasionally, despite thorough examination and investigation, no cause can be attributed to patient's scarring alopecia. If the disease is still active, topical steroid can be tried.

(Social Hygiene Handbook - 2nd Edition )

Simple notes in fungal infection of the skin

Pityriasis Versicolor
It is caused by yeasts (Pityrosporum orbiculare and P. ovale) providing widespread fine scaly macules on the upper trunk and back. The colour of the lesions varies. The lesions are pale in dark skin and darker in fair skin. Recurrent attacks are common. The diagnosis is established clinically and can be supported by the faint yellow fluorescence under Wood's light in the affected areas.
Treatment
1) Topical treatment
a) Imidazoles cream e.g. clotrimazole, miconazole, isoconazole
b) Ketoconazole shampoo
c) 2.5% selenium sulphide shampoo
d) 3% salicylic acid in spirit
e) 20% sodium thiosulphate in spirit
2) Systemic treatment
a) Oral ketoconazole 200 mg daily for 5 days
b) Oral itraconazole 100 mg daily for 5 days
Tinea Pedis
It is a fungal infection of the toe webspaces and the soles. Trichophyton rubrum (T. rubrum), T. Mentagrophytes Var. interdigitale and Epidermophyton floccosum are the commonest causative organisms. There are 3 main clinical patterns.
1) Chronic Plantar Scaling
It presents as a "Moccasin" distribution, on plantar surface and the edges of feet. Peeling of skin and scales are common. Hyperkeratosis may develop on weight-bearing areas.
2) Acute Vesicular Tinea Pedis
Sudden eruption of pruritic or painful vesicles develop on the soles. The eruption is usually unilateral. This pattern may give rise to Id reaction presenting as symmetrical, vesicular pompholyx at sites distant from the site of active fungal infection.
3) Interdigital Tinea Pedis
Peeling, maceration and fissuring occurs frequently in the lateral toe clefts. It is usually very itchy and is more common in people with sweaty feet or occlusive foot-wear.
Tinea Manuum
T. rubrum is the commonest cause. There is unilateral scaling particularly in the skin creases and the nails are usually involved.


Tinea Unguium
Infection of nail and/or the nail bed with dermatophyte fungi is usually due to T. rubrum. It presents as distal nail edge onycholysis with subungual tan crumbly debris, subungual hyperkeratosis and brownish discolouration from secondary colonization by non-pathogenic fungi e.g. Aspergillus.


. Tinea Cruris
Tinea cruris presents as itchy advancing red, sharply demarcated skin rashes enlarging from inguinal folds down inner thigh or into pubic area. Central healing followed by post-inflammatory hypopigmentation is its characteristic. It is usually caused by Trichophyton rubrum, Epidermophyton floccosum and T. mentagrophytes var. interdigitale.


Tinea Capitis
Scalp ringworm is uncommon in H.K. nowadays. It appears as scattered scaly patches containing broken hairs. The lesions may be asymptomatic or mildly itchy. In general, the pattern of involvement can be classified as ectothrix, endothrix, kerion and favus respectively. In severe situation, boggy mass of inflamed and purulent skin known as kerion may occur especially by animal infections. Usually human infections produce minor degrees of erythema and scaling while animal infections cause considerable inflammation.

. Tinea Corporis
It refers to the dermatophyte infection of smooth skin. The lesion is identical to that of tinea cruris but occurs on the trunk and limbs. It is easily misdiagnosed as discoid eczema or pityriasis rosea.

Tinea Faciei
It presents as an amorphous, asymptomatic reddish patch, which may be photosensitive. The skin lesion may be mistaken for polymorphic light eruption, lupus erythematosus and contact dermatitis. It is commonly caused by Trichophyton rubrum, T. mentagrophytes and Microsporum species. Outbreak of zoophilic species induced tinea faciei has been found in Hong Kong.
Diagnosis
1) Wood's light (more useful in Tinea capitis)
2) Microscopic examination of scrapings and clippings in 10% - 30% KOH
3) Culture
Treatment of Tinea infection
1) Topical treatment
Imidazole e.g. miconazole (Daktarin), clotrimazole (Canesten, Lotremin), Tionazole (Trosyd), Ketoconazole (Nizoral), Isoconazole (Travogen), Bifonazole (Mycospor)
Allylamine e.g. Terbinafine (Lamisil), Natifine (Exoderil)
Others e.g. Tolciclate (Tolmicen), whitfield's ointment, mycota, Castellani's paint, Ciclo-piroxolamine (Batrafen), Tolnaftate (Tinaderm), Zinc Undecenoate (Tineafax)
2) Systemic treatment
Griseofulvin, ketoconazole, Itraconazole, Terbinafine
Candidiasis
Candida infections caused by yeast-like fungi Candida albicans commonly occur in moist, flexural sites. It is more common at the extremes of age and during pregnancy. Predisposing factors include diabetes mellitus, pregnancy, broad-spectrum antibiotics, obesity, Cushing disease, uraemia, malignant disease and immunodeficiency. It can present as 10 clinical patterns, depending on the site of involvement. They are the oral thrush, angular cheilitis, genital candidiasis (vulvovaginitis), candida balanitis, candida intertrigo, chronic paronychia, chronic onychia, pruritus ani, erosio interdigitalis and candida granuloma. The diagnosis is arrived clinically and confirmed by fungal culture.
Treatment
1) Topical treatment
Nystatin, imidazole cream, amphotericin lozenges (in oral candidiasis)
2) Systemic treatment
Oral fluconazole, itraconazole, ketoconazol

Simple notes on herpes zoster infection

Herpes Zoster (HZ)
The varicella-zoster virus causes the characteristic herpetic lesion similar to herpes simplex. Whereas varicella represents a primary lesion, herpes zoster (shingles) represents reactivation of the virus from the dorsal root ganglion and results in the classic dermatomic distribution. Herpes zoster is a common condition. There is a correlation between age and incidence of the condition. The disease usually affects the elderly and the immunocompromised patients. Constitutional symptoms are followed by tingling and pain, erythema, and vesicle formation in a dermatomic distribution
Major complications of herpes zoster
1) Acute phase
a) Ocular involvement-Herpes ophthalmitis
b) Secondary infection
c) Cutaneous or visceral dissemination
2) Chronic phase
a) Post-herpetic neuralgia
b) Scarring
c) Motor neuropathy, post-infection encephalomyelitis, paralysis
Treatment
1) Topical agents
a) Acyclovir cream
b) Topical antibiotic cream may be useful in lesions with secondary infection
2) Systemic agents
a) Oral acyclovir 800 mg 5 times daily for 1 week
b) Oral Famciclovir 250 mg 3 times daily for 1 week
c) Oral Valaciclovir 1 gram 3 times daily for 1 week
In immunocompromised patient, IV acyclovir treatment is indicated.
Indications of systemic anti-viral treatment.
a) Patients get skin rashes within 3 days of onset, especially for the elderly group.
b) Patients suffer from ophthalmopathy within 3 days of onset.
c) Immunocompromised patient whenever vesicles present.

Simple notes in STDs (sexually transmitted diseases)

they are a group of diseases that trnsmitted sexually and they are of many causes:

1-bacterial:gonorrhea , syphilis , chlamydia

2-fungal: candidiasis

3-viral:herpes zoster virus , herpes simplex virus , HIV

4-parasite: trichomanis vaginalis , scabies , pediculosis pubis.




Gonorrhea...:

definition:

it's a purulent inflammation of mucous membrane surfaces caused by Neisseria gonorrhea


incubation period:

5 days in men , 2 weeks in females.


Clinical presentation:

in males.... urethral discomfort , dysuria , discharge.

In females... discharge from endocervicitis is the most common presenting symptom, the discharge is discribed as thin , purulent and mildy odorous .

In neonates... ophthalmia neonatorum.


Investigations:

gram stain culture


treatment

1-ceftriaxone(Rocephin)-- 125-250mg IM once

2-ciprofloxacin(Cipro)--- 500mg PO once for uncomplicated urogenital or rectal infections.

3-spectinomycin 2g IM once

4-doxycyclin (vibramycine)200 mg/day for 7 days






Syphilis....:

definition:

it's achronic systemic veneral disease with multiple clinical presentations and charactrized by episodes in active disease( 1ry,2ry,3ry stages) caused by a spirochete called treponema pallidum , and syphilis transmitted by 3 ways from intimate contact and blood transfusion transplacentally from infected mother to her fetus.


INCUBATION PERIOD :

It varies from 9 to 90 days (usually 2-4 weeks)



CLINICAL FEATURES:

1-Primary syphilis

The characteristic feature is the chancre which is usually a solitary and painless ulcer with indurated base. It can occur at penis, vulva esp. fourchette, cervix, and extragenital areas like anus or lip. Inguinal lymphadenopathy is also common. The enlarged lymph nodes are usually discrete, non-tender and rubbery in consistency.

2-Secondary syphilis

This stage usually occurs 6-8 weeks after chancre. The characteristic features include:

1) generalized, symmetrical and non-pruritic papulosquamous rash characteristically affecting palms and soles

2) generalized lymphadenopathy

3) mucosal ulcerations (mucosal patches, snail-track ulcer) over genitalia and mouth

4) condylomata lata at perianal area and mouth

5) patchy alopecia

6) systemic: fever, malaise, anorexia, weight loss and anaemia

3-Tertiary syphilis

1) Cardiovascular syphilis (3A) - It usually occurs after a latent period of 10-20 or more years.

a) Angina pectoris due to coronal ostial stenosis

b) Aortic incompetence

c) Aortic aneurysm (ascending aorta is the commonest site)

2) Neurosyphilis

a) Asymptomatic neurosyphilis

There is no clinical abnormality but abnormal CSF.

b) Meningovascular neurosypilis

It usually occurs 3-7 years after infection, affecting cerebral and/or spinal meninges.

c) General paralysis of insane (GPI)

This usually occurs 10-20 years or more after infection. The clinical features include dementia with recent memory loss, loss of insight, euphoria with delusion of grandeur, tremor, spastic paraparesis, convulsions, incontinence and finally bedridden.

d) Tabes dorsalis

Similarly this occurs 10-20 years or more after infection. The clinical features include lightning pain in legs, paraesthesia, sensory ataxia (positive rombergism and ataxic gait), sensory loss in proprioception and vibration, deep pain in Achilles tendon, absent reflexes, overflow incontinence, Argyll Robertson pupils, optic atrophy, Charcot's joints and visceral crises.

e) Ocular syphilis

The typical features are ocular atrophy, optic neuritis, chorioretinitis with pepper and salt fundus.

3) Gummatous syphilis (benign tertiary syphilis)

This is due to granulomatous lesions affecting skin, bone and mucosae (mouth, palate, pharynx, nasal septum). Rarely liver, brain and spinal cord are involved as well.

4-Congenital Syphilis

Congenital syphilis is transmitted in utero after the first 16 weeks of pregnancy, therefore it is usually not a cause of abortion during the first trimester. The infected child born later in a family usually has less severe syphilis. Again, it has been divided according to the arbitrary dividing line of two years into early and late types.



INVESTIGATIONS:

1-Dark Ground Examination (DGE) (dark field elemnation test)

2-Serological Tests

3-Lumbar Puncture

4-Others (depends on clinical suspicion)

Chest X-Ray, Electrocardiography, Echocardiography, Cardiac catheterization, biopsy of gumma



TREATMENT:

Primary, Secondary & Early Latent Syphilis

1) Procaine penicillin (Servipen)

1.2 megaunit IMI qd x 10 days
Before holidays: Benzathine penicillin 1.2 to 2.4 megaunit is to be given (i.e. 0.6 megaunit/day according to length of holiday) to cover the holiday.

2) Benzathine penicillin (Penadur)

2.4 megaunit IMI weekly x 3 weeks (half into each side of buttock)

For patient who is sensitive to penicillin:

3) Tetracycline 500 mg qid x 2 weeks

4) Erythromycin 500 mg qid x 2 weeks

5) Doxycycline 100 mg bd x 2 weeks

Pregnant woman with syphilis:

1) Penicillin or erythromycin, No tetracycline
(Probenecid, if used, requires special precaution)

2) Reply letter to MCH from SYPSH head-office

3) After treatment, quantitative measure of VDRL monthly till delivery

4) Retreat the patient if there is serological evidence of reinfection or relapse

5) Follow-up three weeks after delivery together with her baby

Precautions in Treatment

1) Risk of anaphylaxis

a) ask for history of penicillin allergy

b) resuscitation facilities should be available

c) Penicillin test

500 ml N.S. + one megaunit soluble penicillin
Inject 0.1 ml hypodermal (200 units)
Read 15 minutes later, wheal >5 mm positive

This test has limited value as a negative test does not exclude the chance of anaphylactic reaction. It is still done in Social Hygiene Service for medicolegal reason.

d) After injection, observe the patient in the clinic for at least 30 minutes.

2) Jarisch-Herxheimer reaction

This reaction usually occurs within 12 hours after the first dose of treatment. It is believed to be due to hypersensitivity reaction to killed treponeme and their liberated toxins. In early syphilis, this reaction is common but harmless. Patient usually has flu-like symptoms, feverishness, chills and malaise. However, patient should be warned beforehand and symptomatic treatment like paracetamol may be necessary. In late syphilis, this reaction is uncommon but dangerous, causing morbidity and even death. Steroid cover before treatment is therefore important.


HEALTH EDUCATION

Health education is given to patients in the anti-VD office in Social Hygiene Clinic. Preventive measures are taught as well.


CONTACT TRACING

Again this is done by the health visitors of anti-VD office.

Examination and treatment of sexual contacts are important steps in the control of spread of sexually transmitted diseases. In early syphilis, contacts of preceding three to six months should be traced. Those who have contact within three months should be treated even without symptom and sign. In late syphilis, spouse or regular sex partners should be screened, and in mother, her children as well. However, they should be treated only when the diagnosis has been established. It must be emphasized again that the screening of all these contacts should be voluntary and confidential.







Refrence: :Dr. L.Y. CHONG



(Social Hygiene Handbook - 2nd Edition )

HIV....:

what are the stages of HIV ?

Stage one: subclinical a symptomatic infections

stage two: Aids related complex(ARC)

weight loss + lymphodenopathy +cutanous

lesions

stage three: full blown Aids



what are skin manifestation of Aids?

1- hairy oral leukoplakia

2- herpes simplex virus

3-recurrent candidiasis

4-seborrheac dermatitis

5- acute onset psoriasis

6- kapsois sarcoma



INVESTIGATIONS

1) HIV antibody test

Methods used locally:

a) ELISA (enzyme linked immunosorbent assay)

This is a very sensitive test for screening purpose, but it may sometimes give a false positive result.

b) Western Blot

In this test, there is electrophoretic separation of viral proteins into a characteristic profile. It is used for confirmatory purpose.

There is cross reactivity between HIV-1 and HIV-2 infection, therefore specific test for HIV-2 antibody for patient from west Africa would be needed. Seroconversion usually occurs within three weeks to three months after infection. However, a small proportion (<5%) of HIV-infected patients may remain seronegative.

2) Tests for immune function

a) T lymphocyte subsets test

T-helper cell (T4/CD4), T-suppressor cell (T8/CD8)

b) p24 antigen, anti-p24 antibody

c) Immunoglobulin level

d) Delayed cutaneous hypersensitivity test

3) Tests for other systems: depend on the clinical suspicion


MANAGEMENT

Both the preventive measures and the specific therapies are equally important in the management of HIV infection.

1) Prevention

Health education
Practice of safe sex
Precautions when dealing with patients' body fluid
Screening of blood or blood products for transfusion, organs for transplantation
Screening for high risk group

2) Counselling and education

Precautions to prevent further spread
Psychological support

3) Specific and supportive treatment

Specific anti-HIV therapy: AZT, ddI, ddC, Ribavirin
Treatment of opportunistic infections
Treatment of malignancy
Symptomatic relief
Nursing care
Immunotherapy (potential HIV vaccine)
Social support


Practice in Social Hygiene Clinic concerning HIV infection:

1) All patients who attend Social Hygiene Clinics (except skin cases) would have screening for HIV antibody. Informed consent would be obtained before the test. Acceptance or refusal of the test must be documented in the record.

2) Strict confidentiality is emphasized. Only consultant, medical officer in-charge and nursing officer in-charge of the clinic could have access to the records of the HIV-positive patients. Staffs who involved in handling the patient would be informed to take adequate precautions and keep strict confidentiality.

3) Counselling (including pretest counselling) and health education in the anti-VD office.

4) All HIV-positive patients would be referred to AIDS unit of Special Preventive Programme of Department of Health for further management. Doctor's referral letter would be given to the patient directly, and nursing officer in-charge would arrange appointment with the staff of AIDS unit in Yaumatei Clinic.


Precautions when perform minor operations in HIV-positive patients and disinfection procedures in Social Hygiene Service:

1) Protective barriers during minor operations: gloves, masks, protective goggles, gowns and aprons.

2) Used needles should be recapped with recapping device. Disposed the used needles in a puncture resistant sharp box which should be labelled "Blood Precaution" before sending to incineration.

3) Laboratory specimens should be kept in leak-proof containers with secure lids and "biohazard" label.

4) Surfaces contaminated by blood or body fluid should be mopped up using disposable towels with gloved hands. The area should than be cleaned with sodium hypochlorite (household bleach) (1,000-10,000 ppm).

5) Laundry items should be double bagged and labelled to warn cleaning staff.

6) Instruments or reusable items should be totally immersed in water and sent for autoclave (80-100o C x 10 minutes) or decontamination by chemical disinfectants. For heat-sensitive device, used 2% glutaraldehyde (Cidex) x 10 minutes.


Procedure for management of needlestick injury:

1) First aid is important. Express blood from the wound, wash immediately and thoroughly with soap and water.

2) Injured staff should report to his/her officer-in-charge or unit head.

3) Measure the HIV-Ab and hepatitis-Ag and Ab of the injured and the patient (with consent).

4) The injured staff should preferably attend the Accident & Emergency Department or the Viral Hepatitis Preventive Service in Yaumatei Clinic, especially when post-exposure prophylaxis for hepatitis-B and HIV infection are considered.

Counselling and education in anti-VD office to patients who attend Social Hygiene Clinic:

To prevent sexual transmission of HIV infection, the following advice would be given by the health nurses in this office:

1) Avoid promiscuity, decrease number of sexual partners, avoid casual sexual partners.

2) Advised on safe sex such as avoiding exchange of body fluid during sexual activity with potential HIV carriers, avoiding anal sex, and proper use of condom.

3) Encourage the prostitutes to come for regular check up in female Social Hygiene Clinics.

4) Trace the HIV-positive cases for follow up and refer to Special Medical Consultation Clinic.


AIDS programs in Hong Kong:

1) Special Preventive Program of Department of Health

2) Screening program in Social Hygiene Service

3) Various programs are planned and implemented through the advice of Advisory Council on AIDS (Committee on Education and Publicity on AIDS + Scientific Working Group on AIDS) e.g. Unlinked anonymous urine screening for patient in various selected population

4) Screening for blood donors in the Hong Kong Red Cross Blood Transfusion Service

5) Screening for semen donors in the Family Planning Association.

6) Various programs are planned and run by the government assisted or non-government organization e.g. The Hong Kong AIDS Foundation and the AIDS Concern.

Simple notes of leprosy

defintion...:
it is a chronic granulomatous disease which affects pricipally the skin and peripheral nervous system , caused by acid fast stained bacilli called mycobactreium leprae or hansen's bacilli.

Types...:
1]low immunity patients develop lepromatous leprosy(LL)
2]moderate immunity patients develpe tuberculoid leprosy(TL)
3] mixed or border line leprosy.




Clinical manifestation...:
a]tuberculoid leprosy
*show hypopigmented macules which charactrized by loss of hair , loss of sensation and diminshed sweating.
*hypopigmented macules in white skin patient is present as erythamatous or brown discolouration .
B] lepramatous leprosy
it is serious lesion affecting many organs [liver, eye , spleen , glands.
When affect the nose wil cause epistaxis.
The lesion varies from papules , paques and subcutanous nodules .
Sensory nerve sensation are lost 1st then motor nerves are lost resulting in :[claw hand, drop foot ,resorptin of digits, and deformity of extremitis].





Diffrential diagnosis...:
1- vitiligo
2- post inflammatory hypopigmentaion
3- localized scleroderma[morphea]


Treatment...:

1-dapsone:* dialy 100mg
*used also in dermatitis herpatiformis
*contraindicated in cardiac disease ,pulmonary disease or anemia
*side effects: hemolysis- methmoglubenimia- allergic dapsone syndrome
2-rifampicin 600mg per month
3-clofazamine 300mg per month
-tuberculoid leprosy requires 6 months up to 2 years treatment.
-lepramatous leprosy requires about 3 to 5 years treatment.

Simple notes of cutenous leshmania

definition....
it's a parasitic infection caused by species of protozoa called leshmania .

Etiology...:
1-old world cutaneous leshmaniasis
1]leshmania tropica major
2]leshmania tropica minor
2-new world cutaneous leshmaniasis
1]leshmania maxican
2]leshmania amazonesis
3]leshmania colobiensis
Reservoir...
mainly dogs in the mediteranean area.

Vector...: female sand fly

season...:
*summer in leshmania trpoica major
*any time in leshmania trpoica minor

incubation period...:
*1-4 weeks in leshmania major
*2-8 weeks in leshmania minor

clinical description...:
*single or multiple localized or diffuse sores mainly on the arm or the face with multiple papules and nodules surrounded by depressed scar of healed papules and nodules *special signs :volcano sign,ice berg sign and satellite lesions.




Differential diagnosis ....:
1-pyoderma gangrenosum
2-deep fungal infection
3-mycobacterium infections
4-sarcoidosis
5-psoriasis
6-squamous cell carcinoma


investigations...:
1)skin scraping:
slit and smear giemsa or leshmania stain,scraping from the edge of the ulcer not from the centr because it healed by scar and not contain amastigoits.
2)serology and PCR[polymerase chain reaction] reveal lack of specifity
3)culture:NNNmedia(Novy Mac Neal Nicolle media)reveal a motile promastigoites.
4)dermatopatholgy:reveal macrophages filled with amastigoits mixed with lymphocytes ,plasma cells and other infiltrating cells.
5)needle aspiration:to visualize amastigoites.


Treatment...:
1- no specific threapy for traveler exist
2-specific treatment is delaed until ulceration occurs to allow the immunity to develop but if the lesin disfiguing or persists more than 6 months the treatment should be started.
3-small isolated lesions of leshmaniasis may be self limited and does not need a treatment.
4- the modules of treatment are :
a))local therapy for small lesions :-intralesional injection of antimonial
drug.[0.3-0.8ml]
-currtage, crysurgery, surgical excision
b))systemic therapy used for multiple lesions , facial lesions & visceral lesions,Using pentavalent antimonial [20mg/kg/day for 20 days IV or IM].
c))the antimonial drugs are :sodium stibogluconate(pentostam)--and meglumine antimonate.
The side effects of antimonial drugs are [chemical pacreatitis – arthralgia -elavetated serum transaminases – leukopenia – thrombocytopenia – peripheral neuropathy – cardiac conduction abnormality]

Simple Wart note

definition...
warts are acommon benign proliferation of skin and mucosa due to viral infection.
Causative organisms...
human papilloma virus[ there are more than 150 types of HPV], children and young adults are most commnly affected.

Types of warts....
1-common wart:found mainly in the hand[palm or around the nails ] , treated mainly with salicylic acid [but liquid nitrogen is contraindicated for a fear of defomity]
2-plane wart:found manily in the back of the hands ,face and limbs, treated mainly with liquid nitrogen or retonic acid .
3-plantar wart:found in pressure exposed areas of foot more common in females , treated mainly by electro cautry- salicylic acid-liquid nitrogen-podphylin.
4-ano genital wart=inversus wart=condyloma accuminata:
treated mainly with podophylin or cryotherapy.
Other types[filiform wart-epidermodysplasia]


Clinical description to the common lesions:
1)common wart:disecrte fleshy coloured papule multiple or single.
2)plane wart:well defined flat topped surface papules.
3)plantar wart:disecete red or black raised papules.


Diffrential diagnosis of wart:
1- malignant melanoma[sharp scalpel to remove the tumor which will reveal vascular tissue in melanoma but, in wart it's thickned epidermis underlying.
2-condyloma latum( serological test for confirmation).


General treatment:
a-topical agents
1]salicylic acid: is a1st line treatment,acting by removing surface keratin[keratolytic agents]...(a combination of salicylic acid 16.7%+ actic acid 16.7%=salactol).
2]trichloroactic acid is a caustic compound that causes immediate superficial tissue necrosis, it may require weekly applications.
3]Podophylin is a plant that contains cytotoxic compounds it has a powerful irritant effect,contraindicated in a pregnant women.
b-systemic agents( 2 agents are used)
1]cimitidine 2]retinoids
c-surgical care
1]cryosurgery:liquid nitrogen is contraindicated in case of
common wart because its very painful & also can cause
deformity to the nail. otherwise it can be used in any type.
2]laser:carbon dioxide lasers have successfully treated
resistant warts.
3]electrodesiccation and curettage
4]surgical excision:avoid using surgical excision in most circumstances because of the risks of scarring and recurrence .

Simple notes in vitilgo

definition....
acquired areas of depigmentation

Causes....[actually no known causes but hypothesis]
1-)autoimmune hypothesis:
*autoimmune destruction of cutanous melanocytes with total loss of melanocytes on the affected area of skin.
*lymphocytic infiltration on skin biopsy indicate involvement of lymphocytes in the destruction process.
*may associated with other autoimmune diseases [alopecia areata, thyroid dysfunction, Addison disease, adrenal disease, atrophic gastritis, perncious anemia].
*serum autoimmune antibody against melanocytes , thyroid, adrenal, gastric parital cell or intrinsic factor.


2-)self destruct hypothesis:
*defect in the natural protect mechanism of melanocytes.
*this defect will cause accumulation of toxins procusers which destroy melanocytes.


3-)neurgenic hypothesis:
*caused from released compound at the peripheral nerve endings in the skin which is toxic to the melancytes.
*the affected areas shows sympathatic nreve dysfunction.

Note:[vitilgo also may be caused as a result of truma , cauld be familial etheir]


Clinical presentation:

+distribution:
-localized disease in---
*sun exposed areas[dorsal of hands]
*normal hyperpigmented areas[axilla,groin,
nipple, flexures]
*sites of friction[bony promenince]

-generilized--- widspread disease.
+lesions:
*typical presentation=white milky colouration ,sharp
margin ,no scales , normal texture & intact sensation
*Atypical presentation=
-trichome\\ tan colour naturally evolves typical area
-quadrichrome\\perifollicular macules or repigmented
vitiligo.
-inflammatory\\erythomatous .
+differential diagnosis of vitiligo:
*generalized hypomelanosis[albinism-hypopitutrism]
*patchy hypomelanosis[vitiligo-sclerosis]
*inflammed patchy hypomelanosis[tinea versicolor-leprosy-
pityriasis alba].
*atrophied patchy hypomelanosis[morphea-post inflamm.-
lichen planus].
+investagation:
-skin biopsy:absent melanocytes.
-wood's lamp:ivory white skin lesions.

Treatment:

1)sun screens[spf more than 30]
what for?..1.vitiligous ares are more suscptable for sunburn.
2.sunburn to normal skin may turn into vitiligo[kobner phenomena]
3.in vitiligous area sun induced darkening of the surrounding
normal skin cause accentuation of cosmatic disfigurment.

2)camouflage=covermark=dermablend
what for?... it's a tanning preperation contain Dihydroxy acetone.

3)Repigmentation therpies for localized vitiligo
1-topical corticosteroid=sicorten[0.5% halometasone]
*twice dialy to 6-12months[should stoped if no improvement]
*once dialy in flexural area.
*shouldn't applied to eyelids or periorbital areas for risk of
cataract or glucoma.
2-PUVA(psoralen ultraviolet radiation A)
*the treatment 2 times per week & it needs to avoid sunlight 2 days
after each session with using of sunsceens outdoor.
*ultraviolt A radiation for 30 minutes after application of
meladinine[methoxasalen]
*the PUVA cotinued for 1 year [100-200session]
*contraindication for PUVA:
-pregnant women
-children below 12
-photosensetivity
-cardiac diseases
-hepatic diseases
-renal diseases
-visual problem[aphakia- cataract]
-skin cancer
4)depigmentation therapy
*by using bleaching agents 20% hydroqunine(benzoquine) one or
twice daily when the vitiligo is extensive or universal.
*side effect: dermatitis-albinoid skin



the fate of vitilgo:
stasis ~ spread ~ re pigmentation spontaneously

How to get control of your life and your time:....

*many people go through life without finding any satisfaction in the simple fact of being alive .

*yet this lifetime is the only time we will have -we had better make the most of it . Few of us do of course .

*we act as if this time were just a practice run for the next , fortunately however we live in an age when people have developed methods to help us -if we choose- to use our time wisely.

*most of people on our time waste all minutes of times , nor do they think in terms of their whole life , they operate in the mid-range of hours or days . So they start over again every week and spend an other chunk unrelated to their lifetime goals. They are doing a random walk through life , moving without getting anywhere.

*the real question is : what do we really want to do ? If we don't know sooner or later we will realize that whatever it was there just isn't enough time left to do it , our lifetime isn't entirely our own and yet it is all we have, and it's absurd to spend that time in constant reaction and accommodation to someone else's plan -whether that plan in imagined as god's the boss's or a spouse's . distinctions must be made , if it is the boss's time , then we must do his thing , done properly this should leave us time of our own to do our thing .


*it takes organization and concentration to carve out your own time ,but most important of all it takes self-knowledge to know what you want to do with it.

*without goals and motivation the time will evaporate. “A typical best use of time is to plan , some people don't even make lists , much less imagine that today is connected with next week and five years from now.

*but you can't effectively plan the next few days without deciding on the next ten years , and so we begin asking to sort out our priorities:
-what are your life goals?
Write down every thing you can think of, including money , career physical, family, social, community, spiritual and personal goals.
Try to fill up an entire sheet of paper, now place an “A” in front of three goals that are most important to you , on an other sheet of paper ,be specific about each of the three: identify sub goals , logical next steps and immediate plans.
Then from each A goal select one “next step” to take next week. And now you have an action program!! the list should be redone once a month to keep up a continuous and evolving spiral of improvement.


-how would you like to spend the next five years?
Not how will you or how should you , but how would you like to?
If you have just written down as a lifetime goal a desire to be rich , and now find yourself answering “ i would like to be building birdhouses,for example” you have not been honest in the question , the point to discover your own goals not the ones you have been taught .
We do too many things because of some atavistic sense that we have to, but do we?even if the action was originally ,is it sensible now?


-How would you like to live if you knew you would be dead six months from today?
Many people have never consciously thought out the answers , and once they recognize their own feelings they can begin to set firm policies to see that their lives are arranged to make them happier more often while reducing guilt and frustration and that is the point of the process :to meet the stranger that is often ourselves, and to establish priorities that take that person on to account.

Simple notes in Psoriasis lecture

defintion...
it's chronic relapsing & remitting skin diseases
where red raised plaques covered by white scales.


Precpitating factors:
1-truma 2-infection 3-AIDS
4-hormonal factors[pregnancy,contraceptive pills]
5-cold weather 6-smoking & alchol
7-emotional psoriasis


Pathological features ....
1)acanthosis= hyperkeratosis =marked thickning of the epidermis
2)abscence of the granular cell layer.
3)parakeratosis = retention of nuclei in the horny layer.
4)monro microabscess= accumulation of leucocytes.
5)dilated capillary loops.


General features....

*exposure to sunlight and UV radiation improve psoriasis.
*drugs aggrevate the condition of psoriasis [beta blockers-antimalarial-lithium].
*the disease has a kobner phenomena [other diseases that have the same feature like lichen planus, vitiligo and wart.




Types of psoriasis....
1)classical type=psoriasis valguris
*involve extonsersurfac of elbow, knee joints,hands &
sacral areas
*there is no consistent laboratory finding but may be
raised uric acid level.
*treated with :-dithranol (anthrolin)
-topical steriod with or without tar and
salicylic acid.
-UV radiation
-PUVA,retinoids or cytotoxic drugs may
used in a serious psoriasis.
2)Guttate or rain drop psoriasis
*multiple small psoriatic lesions like drops mainly on the trunk proceeded by streptococcal throat infection.
*involve the abdomen and trunk.
*Can be miss diagnosed or mistaken with pityriasis roscea
*easly treated with UV radiation and mild tar based ontiment

3)scalp psoriasis
*it's difficult to diffrentiate between scalp psoriasis and seborrheic dermatitis but psoriasis is generally thicker ,sever dandrof and temporary alopecia.
*treated with : tar shampoo- topical combination of tar and salicylic acid – topical steriods with or without salicylic acid.

4)nail psoriasis
*the finding are painful pitting & oncholysis[liftting of the nail plate or seperate of a part of nail bed.
*long standing psoriasis cause nail changes.
*treatment:nail changes not respod to topical treatment so systemic therapies may be helpful.

Other types:
5)psoriasis inversus 6)psoriatic arthropathy
7)palmoplantar psoriasis 8)napkin psoriasis
9)erythrodermic psoriasis



which type of psoriasis is dangerous?
Erythrodermic psoriasis is the dangerous type because it may cause electrolyte imbalance,heart failure,infection and hyponatremia.

What sites should be examined in a case of psoriasis?
Extonser surface of the knee and elbow,back, hands, sacral area, nail, scalp and feet.

Diffrential diagnosis of psoriasis....
1]discoid eczema 2]sebarrhoic eczema
3]pityriasis roscea 4]2ry syphilis
5]cutaneous T-cell lymphoma 6]tinea unguium



investigation...
1)biopsy[rarely needed] : will reveal pathological features
2)throat soap for streptococcal culture.
3)skin scraping to exclude tinea
4)rheumatoid factor to exclude psoriatic arthropathy
5)serological tests to exclude 2ry syphilis


treatment....
a-topical treatment:
1-emollients
2-tar:-it's a crude tar in a form of
an alcholic solution inhibits
DNA synthesis.
-side effects are:stain the cloths
smelly and can leads to folliculitis.
3-dithranol:-single most effective topical antipsoriatic treatment ,may cause staining and burning.
4-topical steriods
5-calcipotriol:(dovenex) not more than 100gm/week , act by inhibiting orthine decaeboxylase so decrease scale formation &erythema.
b- systemic treatment
1)PUVA[psoralen UVA]
*psoralen is taken 2-3 hrs before exposure to UVA
*psoralen is hepatotoxic so liver function test is lmportant
*long term exposure to radiation carry high risk of developing skin cancer.
*side effects of PUVA[erythema , itching and cataract].
2)retinoids
*it's a vitamin A derivatives
*may cause dry lips ,hair loss, teratogenic,hyperlipidemia ,liver impairment and renal impairment.
*liver function test,renal function test and lipid profile must be considered before beginning the treatment with retenoids.
3)cytotoxic drugs
liver function test and bone marrow function must be done before giving cytotoxic drugs.
4)cyclosporin
it's nephrotoxic and may cause high blood pressure.
5)systemic steroids.

Simple notes of acne

definition....
it's a disorder of pilosebaceous follicles.
Types of acne....
1-acne vulgaris..this is the typical type
2-juvenile acne
3-occupational acne
4-drug acne
5-cosmetic acne

6-acne fulmines

Pathogenesis...
1-androgens[quantitively&qualitatively normal]stimulate sebaceous glands to produce large amounts of sebum .
2-corynebacterium acne cotains lipase enzyme that acts on lipids of sebum to form free fatty acids , which acts as chemotactic factor for neutrophils.
3-both increase in sebum &free fatty acids which cause sterile inflammation of pilosebaceous gland leading to hyperproliferation of upper portion of sebaceous duct & hyperkeratinization of the lining of the follicle resultingin pulgging.
4-the enlarged follicular lumen containing inspassted keratin & lipid debris resulting in white heads or white comedones.
5-if the folicle has open a portal of entry to the skin the plugg will protrude & the tyrosine contained in the keratin will be oxidized to melanin in the follicle orifice [black heads=black comedons].
6- the distended follicular wall may break dawn, the contents[sebum-lipids-free fatty acids-&keratin]enter the dermis result in forigen body response which make[papules,pastules& nodules]
7-rupture of these lesions+intense inflammation cause post inflammatory hyperpigmentation & scarring.

Causes of acne....
1- body androgens[especially in females because of androgen receptor sensitivity]
2-bacterial infections[propionobacterium acne-staphylococcus epidermis-microsporum ovale]
3-physiological factors[stress- humidity-menstrual cycle].

Clinical description to the acne lesion....
multiple maculopapular rash over the [chin,face,forehead& upper back] with multiple black or white comedones with or without scar or post inflammatory hyperpigmentation spots of a previos healed lesions with greasy skin.



Diffrential diagnosis....
Roscea: looks like acne but it occur in elderly with no comedones ,papules or pastules only associated erythema.

What is the date in which the acne excpected to end..?
most of the cases resolve at age 23-25years but about 5% of cases in females & 1% of cases in males persists up to 25-40years.

What is the 1ry acne..?
it's the non inflammatory acne in which are known as comedones, they take 1-2 weeks to heal.
What is the 2ry acne..?
it's the inflammotory acne which may occur on top of non inflammatory comedones or start DE novo , they present as:
-superficial:papules or pastules[take 2-4 weeks to heal]
-deep: deep pastules,nodules or even cysts[take months to heal].


General treatment:
a-topical treatment---
1)Benzoyal peroxide;it's acomedolytic agent.
2)Retinoic acid;it' a vitamine A derivatives , used as an alternative to benzoyl peroxide so also has a comedolytic affect.
3)topical antiseptics;it's a washes like chlorhexidine but have a little value.
4)topical antibiotics;tetracycline,erythromycin, fucidine & clindamycin.
b-systemic therapies
1)antibiotics;
*must be fat soluble to be effective.
*antibiotics reduce bacterial counts.
*the most effective for acne are
tetracyclines and erythromycin .
*most tetracycline should be taken on an
empty stomach.
*contraindication of tetracyclines are age
under 12,in pregnancy or laction.
2)cyproterone acetate;it's effective anti androgen and can only be given to women.and must be combined with oestrogen to prevent menorrhagia and to ensure contraceptive cover(it will feminize male fetus).
3)retinoic acid
4)steriods;used in cases of sever acne.
5)sugical intervention.


Management of acne patient:
mild acne;
*this is an acne in which only comedones are present only restricted to the face.
*topical treatment alone may control mild acne begining with [benzoyl peroide+retionic acid] with or without aniseptics or topical antibiotics.

Moderate acne;
*this is an acne in which more papulopustular lesions are present on the face or over a wider area .
*1st line treatment of moderate acne should combine topical benzoyl peroxide with tetracycline or erythromycin .
*this treatment taken in a dose of 500mg twice dialy for at least 3 to 6 months before consider any failure.

Sever acne;
1-girls may be treated with cyproterone acetate combined with an oestrogen for a period of at least 6 months.
2-men require retionic acid for at least 4 months.
3- intralesional steriods rarely used in suppressing acute inflammatory lesions.