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Heart Murmurs

Murmurs in valvular heart disease result when there is valvular insufficiency or regurgitation (the valves fail to close completely) or stenosis (narrowing of the valves). The aortic or mitral valves are most commonly involved in valvular disease.

For most of ventricular systole, the mitral valve should be closed and the aortic valve should be open, so that '' common systolic valvular defects '' include mitral insufficiency and aortic stenosis. For most of ventricular diastole, the mitral valve should be open and aortic valve should be closed , so that '' common diastolic valvular defects '' include mitral stenosis and aortic insufficiency.

A heart murmur is heard downstream from the valve. Thus, stenosis is orthograde direction from valve and insufficiency is retrograde direction from valve.

Auscultation sites for mitral and aortic murmurs are shown in figure 

Heart Murmurs

Acne vulgaris


Occurs mostly in teenagers.
Peak: late teenagers but may persist till third decade and beyond especially in females.
  • Etiology:

Elevated sebum excretion:
Sebum excretion is necessary for the development of acne but is not sufficient to cause acne on its own.
The main determinants of sebum excretion are hormonal, which accounts for the onset of acne in the teenagers. 
Androgens and  progestogens increase sebum excretion but estrogens reduce it.

Propionibacterium acnes
It colonises the pilosebaceous ducts and acts on lipids to produce a number of pro-inflammatory factors.

Occlusion or blockage of the pilosebaceous unit.

Clinical features

  • Site: usually limited to the face, shoulders, upper chest and back.
  • Greasy skin
  • Open comedones (blackheads) due to plugging by keratin and sebum of the pilosebaceous orifice, or closed comedones (whiteheads) due to accretions of sebum and keratin deeper in the pilosebaceous ducts are evident.
  • Inflammatory papules, nodules and cysts may occur with some lesion.
  • The lesion may be followed by scarring.
  • Mild form
Dominated by presence of comedones.
May be due to exogenous substances like oily cosmetics, chlorinated hydrocarbons, tars, etc
Pustular rash may also be seen in those treated with steroids, lithium, OCP and anticonvulsants.
  • Moderate or Severe form
May have systemic disorder. E.g- polycystic ovarian disease, Androgen secreting tumors




Blackheads & whiteheads

Clinical variants of Acne:

Conglobate acne: 
severe acne with many abscesses and cysts, marked scaring and sinus formation.

2.      Acne fulminans: 
severe acne accompanied by fever, joint pains and markers of systemic inflammation ( raised ESR)

2.      Acne excoriee: 
effect of scratching or pricking, mostly seen on the face of teenage girls with acne.

3.      Infantile acne: 
Rare. It is due to sebotropic effects of maternal hormones on the infant.

Investigation: Rarely reqd.

It is important to enquire about the details of previous treatments and their duration.

Treatment:

1.Fairly minor disease dominated by comedones:
      Topical benzoyl peroxide or tretinoin is used
2.Mild acne: require antibiotics therapy
                       Local antibiotics: Clindamycin or Erythromycin.
                       Oral antibiotics: Oxytetracycline 1.5g per day on empty stomach. If the response is inadequate: Minocycline ( both must be contiued till 3 mnths to see if the antibiotics have worked or not)
                       If little response after 3 mnths treatment: Erythromycin 1g/day.
In women, oestrogen containing OCP can be used as a adjunct in therapy. ( oral estrogen reduces sebum production)
3. If these systemic and topical agents fails to produce an adequate clinical response within 3-6 months;
 Systemic retinoids—isotretinoin (decreases follicular keratinization, Sebum production, bacterial count)

Physical measures
Cysts incised and drained under LA.
Stubborn cysts: intralesional triamcinolone



Rosacea

It is a chronic disorder affecting the facial convexities, characterized by frequent flushing, persistent erythema and telangiectasia, interspersed by episodes of inflammation during which swelling, papules and pustules are evident.






Clinical features

  • The areas characteristically affected are the central convex areas of the face (nose, forehead, cheeks and chin) . Occasionally, the scalp, upper chest, back and even the limbs may be involved. 
  • In cases of rosacea showing the classical pattern of progression, the onset is most often marked by vascular changes, notably episodic flushing usually unaccompanied by sweating.
  • Erythema, which is often accompanied by a burning sensation, gradually becomes more persistent, is easily triggered by minor irritants, and is associated with increasingly prominent telangiectasia.
  • More advanced cases show follicular and nonfollicular papules and pustules, without comedones, followed by persisting tissue thickening due to oedema, fibrosis and glandular hyperplasia, leading ultimately to a peau d’orange appearance and phymas.
  • Factors which trigger flushing include emotion and stress, hot drinks, alcohol and other vasodilating drugs, and spicy food. 
  • Aggravating factors include the use of topical steroids on those occasions when they are used (usually in error) to treat rosacea.
  • Sun exposure may worsen or improve rosacea.
  • Rhinophyma, with erythema, sebaceous gland hyperplasia  and overgrowth of the soft tissue of the nose, is sometimes associates.
  • There may be complications like blepharitis and conjunctivitis.


Treatment

Oral oxytetracycline can be used for the pustular component of rosacea.

Topical metronidazole can also be used.

Erythema and telangiectasia don’t respond to antibiotic therapy.

Autoimmune skin disorders

  • Pemphigus vulgaris
  • Bullous pemphigoid
  • Dermatitis herpetiformis
  • Pemphigoid gestationis
  • Epidermolysis bullosa acquisita
  • Bullous lupus erythematosus

Pemphigus vulgaris

IgG antibodies against intercellular attachment sites (desmosomes) between Keratinocytes.
Type II hypersensitivity reaction
Vesicles and bullae develop on skin and oral mucosa.
Intraepithelial vesicles are located above the basal layer (suprabasal)
(1) Basal cells resemble a row of tombstones.
(2) Acantholysis of keratinocytcs in the vesicle fluid

Clinical features

Age: 40-60 years
Usually the site of the blisters are the torso & head and there is always an involvement of the mucus membrane.
The blisters are flaccid and fragile & may have many erosions.

Treatment

Corticosteroids and other immunosuppressive agents (e,g., methotrexate, azathioprine


Pemphigus vulgaris: mucus membrane



Pemphigus vulgaris: Torso


Pemphigus vulgaris

Dermatitis herpetiformis


  • IgA-anti-lgA complexes deposit at the tips of the dermal papillae.
  • Produces subepidermal vesicles with neutrophils.
  • Strongly correlated with celiac disease
  • Increase in antireticulin and endomysial antibodies.



Clinical features

Age: young patients associated with coeliac disease.
Sites: Elbow, lower backs, buttocks.
Blisters are often excoriated and not present.

Treatment
(1) Gluten-free diet
(2) Dapsone or sulfapyridine
(3)Nikolsky sign positive




Bullous pemphigoid

IgG antibodies against the basement membrane.
Type II hypersensitivity reaction.
Vesicles are subepidermal 
(1) Develop on the skin and oral mucosa.
(2) No acantholytic cells in vesicle lluid
Disease usually subsides after months or years.


Clinical features

Age: 60 and above
Site: Trunk (especially flexures) and limbs with occassional involvement of the mucous membrene.
The blisters are tense.

Treatment

Disease usually subsides after months or years.
May requires systemic corticosteroid in resistant cases.




Scabies


Scabies is caused by Sarcoptes scabiei.

Spreads in households and environment when there is high frequency of intimate personal contacts.
The main symptom is itch.
Secondary eczema elsewhere in the body ( face and scalp are never involved except in infants)
Involvement of genitalia is pathognomic in boys.
Even after successful treatment the itch can continue and ocassionally nodular lesion persist.
In small children palms and soles can be involved with pustule formation.


Diagnosis:

1.Identifying the scabietic burrows, usually found on the edges of fingers, toes or sides of hands and feet.
2. Extraction of the mite using blunt needle.

1.                                              



2.

Treatment: Aqueous solution of Permethrin or Malathion, two application one week apart to the whole body excluding the head.
Asymptomatic family members are also treated.


In some cases like poor compliance, immunocompromised individuals and heavy infestations( Norwegian scabies) , Oral Ivermectin 200mcg/kg as a single dose is appropriate.

Complications:
Secondary infections
Post streptococcal glomerulonephritis





Psoriasis



- It is  common, chronic, disfiguring, inflammatory and proliferative condition of the skin, in which both genetic and environmental influences have a critical role.

The most characteristic lesions consist of red, scaly, sharply demarcated, indurated plaques, present particularly over extensor surfaces and scalp.

Variable in duration, periodicity of flares and extent.

May start at any age but is unusual before the age of 5 yrs.

In China, psoriasis is estimated to affect 0.3% of the population.




Two patterns:-

HLA unrelated- late onset and usually mild.
HLA associated (particularly HLA-Cw6)- early onset and more likely to be severe.



Aetiology

- Genetic
     Psorias has large familial component. 
     Twin studies shows ~80% heritability.
     In monozygotic twins- 1/3rd of pairs will be concordant for Psoriasis.
     Mode of inheritance is genetically complex.
     Susceptible chromosomal area:- HLA region.

- Environmental risk factors
     Interactions between genes and the environment are important in disease causation. Many environmental factors have been linked to psoriasis, and have been implicated in, for example, initiation of the disease process and exacerbation of pre-existing disease.
       
a) Trauma
            
Psoriasis at the site of an injury is well known (Koebner phenomenon). A wide range of injurious local stimuli, including physical, chemical, electrical, surgical, infective and inflammatory insults, has been recognized to elicit psoriatic lesions.
       
b) Infection
            
Acute guttate psoriasis is strongly associated with preceding or concurrent streptococcal infection, particularly of the throat.
           
Acute episodes of guttate psoriasis are much more common in individuals
with a family history of plaque psoriasis and one-third of cases of guttate psoriasis progress to the chronic plaque form.
          
Guttate and chronic plaque psoriasis share strong HLA associations, particularly with HLA-Cw6. 
          
HIV infection has also been associated with psoriasis.
          
c) Drugs
               
There are many drugs reported to be responsible for the onset or
exacerbation of psoriasis. Important ones are lithium salts, antimalarials,    beta-adrenergic blocking agents, non-steroidal antiinflammatory drugs (NSAIDs), angiotensin-converting enzyme (ACE) inhibitors and the withdrawal of corticosteroids.  
               
Patients with unstable psoriasis should receive appropriate advice before travelling to countries where antimalarial prophylaxis is required.
          
d) Sunlight
                
In minority of patients, psoriasis may be provoked by strong sunlight
and cause summer exacerbations in exposed skin. 
                
Severely photosensitive psoriasis is predominantly female and
strongly associated with HLA-Cw6, family history and very early
age of onset . Photochemotherapy (PUVA) can be helpful in
these patients.
           
e) Metabolic factors
                 
The early onset of psoriasis in women, with a peak around puberty,
changes during pregnancy and provocation of psoriasis by highdose
oestrogen therapy indicates a role for hormonal factors.
              
f) Psychogenic factors:- Stress
                
g) Alcohol and smoking
                      
Alcohol exacerbate pre-existing disease but does not induce psoriasis. M>F. Heavy drinkers have more extensive and inflamed disease.
                      
Smoking also associated with Psoriasis.
                 
h) HIV and acquired Immune deficiency syndrome 
                      
Psoriasis, psoriatic arthropathy and human immunodeficiency virus (HIV) infection are well associated.
                      
The prognosis of acquired immune deficiency syndrome (AIDS) in patients with psoriasis is poor.

Pathogenesis:-

  
a) Keratinocytes hyperproliferation.
      
Grossly increased mitotic index.
      
Abnormal pattern of differentiation which involves the retention of nuclei in the stratum corneum.

  
b) Large inflammatory cell infiltrate comprising polymorphs, T cells and other inflammatory cells.


Gross

  - Common sites:knees, elbows, and scalp
  -Gross: well demarcated erythematousplaques with a silveryscale
  - Auspitz sign: removal of scale results in pinpoint bleeding
  - Nail beds show pitting and discoloration

HPE

  - Dilated, tortuous papillary blood vessels almost touch the undersurface of the thinning epidermis and are surrounded by a mixed mononuclear and neutrophil infiltrate, as well as extravasated erythrocytes
  - Epidermal hyperplasia 
  - Patchy hyperkeratinization with parakeratosis
  - Uniform elongation and thickening of the rete ridges
  - Thinning of the epidermis over the dermal papillae
  - Munro microabscesses formation


C/F

- Stable plaque psoriasis:
    Most common type.
    Individual lesions: few mm to several cms in diameter which are red, dry, silvery white scale.
    Common sites: Elbow, knee and lower back.
    Other sites:
                    Scalp- It is commomly involved.
                               Lesion in the scalp shows well-demarcated easily palpable areas but occasionly shows diffuse, fine scaling making it difficult to distinguish from seborrhoeic dermatitis.
                    Nails-
                                Pittting
                                Oncholysis
                                Subungal hyperkeratosis
                     Flexures:
                                Are not scaly but it is red, shiny and symmetrical.
                                e.g psoriasis found in submammary and axillary folds.
                     Palms:
                                 It is poorly demarcated and doesn’t look erythaematous so difficult to recognise.
                                                      
  
Guttate psoriasis:

This describes the presence of small lesions, appearing generally over the body, particularly in children and young adults, and after acute streptococcal infections. 

In the early stages, there may be little scaling. The lesions are from 2 or 3 mm to 1 cm in diameter, round or slightly oval. They are scattered more or less evenly over the body, particularly on the trunk and proximal part of the limbs, rarely on the soles, not infrequently on the face, ears and scalp. 

Guttate lesions are normally profuse, and in the early stages the colour is not specific.

 The diagnosis is made chiefly on the nature of the scaling, the general distribution and evidence for preceding infection.




Erythrodermic psoriasis:

Skin becomes red or scaly; or occasionly red with little scale.
In some case case of erythoderma, hypo- or hyperthermia may develop d/t problem in temperature regulation.



Pustular psoriasis:

   2 forms


1) Generalised form

       
Sudden onset with numerous small sterile pustules erupting on a red base.
         
Pt may rapidly deteriorate with pyrexia coinciding with appearance of new pustules.

   
2) Localised form
         
More common.
         
Affects pamls and soles.
         
Chronic eruption which comprises small sterile pustules on a red base and which resolve leaving brown macules or scaling.

Pustular psoriasis



- Arthropathy
     
      Onset: 25-40 yrs

      Chronic RF negative inflammatory arthropathy.

      In pt with current or previous psoriasis

      5 main clinical subtypes:
  symmetrical polyarthritis
  asymmetrical oligoarthritis (large joint)
  spondylitic
  distal-interphalangeal
  severe mutilans



-Management

    Explanation, reassurance and instructions.


 


Topical

Topical: - good for single isolated lesions
Tar - based preparations
Vitamin D-analogues
Steroids (rebound)
Dithranol (inhibits mitochondrial DNA)



UV and PUVA therapy:
 
   - UVR
      For mild to moderate Psoriasis (UVB)

    - PUVA = Psoralen + UV light
      For chronic plaque Psoriasis

Systemic:

    - Useful for multiple lesions, erythrodermic psoriasis, pustular psoriasis
    - methotrexate (hepatic fibrosis, cirrhosis + myelosuppression)
    - cyclosporin (hypertension, renal impairment, immunosuppression)
    - retinoids (good for pustular psoriasis)