PSORIASIS CLINICAL FORMS

1. Psoriasis Vulgaris
This form is prevalent because it called psoriasis vulgaris. Named as well as lesions of plaque-type lesions are generally shaped plaque. Place predileksinya namely the scalp, scalp border with the face, extremities, especially the extensor ie knees, elbows and lumbosacral region.

Psoriasis Vulgaris

2. Psoriasis guttate
Diameter abnormalities are usually less than 1 cm. Sudden onset and disseminated, is generally after Streptococcus infection in the upper respiratory tract after influenza or morbili especially in children and young adults. It also can occur after other infections both bacterial and viral.

Psoriasis Guttate

3. Inversa Psoriasis (Psoriasis Flexural)
Psoriasis has a place in the flexor predilection to its name.

Psoriasis Flexura

4. Psoriasis Exudative
This form is very rare. Usually abnormalities in psoriasis it in dry form, but in this type  such as exudative dermatitis is acute.

5. Psoriasis Seborrhoeic
The clinical features of psoriasis seborrheic a combination of psoriasis and seborrheic dermatitis, which is usually dried squama be a bit oily and somewhat soft. Apart is a location commonly, also found in place seborrheic.

Psoriasis Seborrhoeic

6. Psoriasis pustulosa
There are 2 opinions about psoriasis pustulosa, first considered as a separate disease, both regarded as a variant of psoriasis. There are 2 forms of psoriasis pustulosa namely:
a. Pustulosa palmoplantar psoriasis (Barber)
Pustulosa palmoplantar psoriasis are chronic and residif, the palms of the hands or soles of the feet or both. Abnormalities of the skin in the form of small groups of sterile pustules and deep, over an erythematous skin, accompanied by itching.

Pustulosa palmoplantar psoriasis (Barber)

b. Pustulosa Acute Generalized Psoriasis (Von Zumbusch)
Psoriasis pustulata acute generalized (von Zumbusch) can be caused by a variety of provocative factors, such as the most common drug for systemic corticosteroid discontinuation. Other drugs for example, penicillin and its derivatives, as well as other antibiotic Betalaktam, hidroklorokuin, potassium iodide, morphine, sulfapiridine, sulfonamide, codeine, Fenilbutason, and salicylates. Factors other than the drug is hypocalcemia, sunlight, alcohol, emotional stress, as well as bacterial and viral infections. This disease can occur in people who are or have got psoriasis. Can also appear in people who have never suffered from psoriasis. Symptoms initially are skin pain, hyperalgesia accompanied by general symptoms such as fever, malaise, nausea, anorexia. Plaque psoriasis who have been there more erythematous. After a few hours raised edematous and erythematous plaques much on normal skin. Within a few hours many pustules arise billion in these plaques. In a day-pustules pustules confluences lake of pus forming sized some cm great Pustule . Spongioform occurred due to migration of neutrophils into the Malpighian stratum, in which these neutrophil aggregate in between keratinocytes and degenerates. Thinning disorders such will continue and can be erythroderma. Laboratory tests showed leukocytosis, culture of pus from sterile pustules.

Pustulosa Acute Generalized Psoriasis (Von Zumbusch)

7. Psoriatic erythroderma
Erythrodermic psoriasis can be caused by topical treatment that is too strong or widespread as the disease itself. Usually the lesions were typical for psoriasis not looked back since there is erythema and thick squama universal. Sometimes psoriasis lesions still loomed over erythematous and the skin is rising.

Psoriasis Erythrodrmic

Clinical Symptoms of Psoriasis

General condition is not affected, except in the erythrodermic psoriasis. Some patients complained of mild itching. Predilection spot on scalp, face scalp border, extremity, especially the extensors at the elbow and knee and lumbo sacral region.

 

     Skin abnormalities consist of patchy erythema raised (plaque) with squama thereon. Circumscripta erythema and patchy, but the healing period in the middle is often erythema disappeared and exist only on the edge. Squama layered, rough and white as well as transparent mica. Of the abnormalities varies, can lenticular, nummular, plaque and can confluented. If all or most of the so-called psoriasis guttate lenticular shaped, usually in children, young adults and occurs after infection by Streptococcus.

        Primary lesion in patients with skin psoriasis is bright red, papules and develop into reddish, demarcated plaques. Location of the plaque is generally found on the elbows, knees, scalp, umbilicus, and intergluteal. In psoriasis patients with dark skin, the distribution is almost the same, but the purple papules and plaques primarily to gray scales. The palms and soles of the feet, demarcated and containing sterile pustules and thickened at the same time.

      In psoriasis there is a phenomenon of wax droplets, Auspitz and Kobner (isomorphic). The second phenomenon and Auspitz wax droplets are considered typical, while Kobner considered typical, only approximately 47% of the positive and is found also in other diseases., For example, Lichen Planus and juvenile Plana verruca. The phenomenon is squama wax droplets that change color to white on a scratched scratches like a candle, caused by changes in refractive index. Way to the edge of the glass can scratch pad. In the Auspitz phenomenon of serum or blood appears mottled due to papilomatosis. How to do this is by way of a multi-layered squama is scraped with the tip of a glass pedestal. Having exhausted the scrapping squama be done slowly because if it does not look too in the form of bleeding, but bleeding spots are evenly distributed. Trauma to the skin such as psoriasis sufferers of trauma due to scratching can cause a skin disorder called psoriasis and similar to the Kobner phenomena arising approximately after 3 weeks.

       Psoriasis can also cause abnormalities of the nail as much as approximately 50% which is rather typical of the so-called nail or nail pitting pit in the form of curves billion. Abnormalities are not typical of the nail that is cloudy, thick, raised distal parts as there are below the stratum corneum (subungual hyperkeratosis) and onikolysis. Besides causing skin and nail disorders, the disease can also cause abnormalities in the joints. Polyarticular generally, where predilected place is interfalangs distal joints and most are at the age of 30-50 years. Enlarged joints then place ankylosis and subcortical cystic lesions. Mucosal abnormalities are uncommon.

Causative Factors of Psoriasis

Psoriasis

For several decades, psoriasis is a disease characterized by hyperplasia of epidermal and dermal inflammation. Additional characteristics based on histopathological changes were found in psoriatic plaques and laboratory data describing the cell cycle and transit time of cells in the epidermis. Thickened epidermis in psoriasis plaques and hyperplastic, and there are incomplete maturation of epidermal cells over the cell area germinatif. Rapid replication of cells germinatif very easily recognized, and there is a reduction in transit time for cells through the epidermal cells thick.   

Cutaneous vascular abnormalities characterized by increased amounts of inflammatory mediators, namely lymphocytes, polymorphonuclear, leukocytes, and macrophages, accumulate in the dermis and epidermis. These cells can induce changes in the structure of the dermis well insial and advanced-stage disease.

There are several factors that act as the etiology of psoriasis, include the following:
1. Genetic Factors
Approximately 1/3 of people affected by psoriasis report a family history of disease who also suffer from psoriasis. At the risk of monozygotic twins suffering from psoriasis was 70% when one of his suffering from psoriasis. If parents do not suffer from psoriasis then the risk of having psoriasis by 12%, whereas if one parent has psoriasis the risk of psoriasis increased to 34-39%. Based on the onset of the disease are two types, namely:
a. Psoriasis type I with early onset, and  familial
b. Type II psoriasis with late onset and  non-familial
Another thing that supports the existence of genetic factors that psoriasi adalag associated with HLA. Psoriasis type I associated with HLA-B13, B17, Bw57 and Cw6. Type II psoriasis associated with HLA-B27 and Cw2, whereas psoriasis pustulosa associated with HLA-B27.

2. Immunologic factors
        Genetic defect in psoriasis may be expressed in one of the three types of cells are T lymphocytes, antigen presenter cells (dermal) or keratinocytes. Keratinocytes in psoriasis require stimuli for activation. Lesions of psoriasis is generally full of mature T lymphocytes in the dermis which mainly consisted of CD4 T lymphocytes with little lymphocytic sebukan the epidermis. While new lesions are generally more dominated by CD8 T cells limphocyte. In the psoriasis lesions contained about 17 cytokine production increases. Langerhans cells also play a role in psoriasis imunopathogenesis. Epidermal proliferation begins with the movement of both endogenous and exogenous antigen by Langerhans cells. In psoriasis epidermis formation (turnover time) is faster, only 3-4 days, whereas in normal skin of 27 days duration.
      Nickoloff (1998) concluded that psoriasis is an autoimmune disease. Over 90% can be in remission after being treated with immunosuppressive. Berbaga trigger factor in psoriasis are mentioned in the literature include psychological stress, focal infection, trauma (Fenomenan Kobner), endocrine, metabolic disorders, drugs, alcohol and smoking. Psychological stress is a major trigger factor. Hunungan focal infection has close links with one type of psoriasis is guttate psoriasis, while psoriasis vulgaris with no apparent. Guttate psoriasis has been reported recovery after tonsillectomy. Generally, the infection caused by Streptococcus. Endocrine factors generally affect the course of the disease. The peak incidence of psoriasis, especially during puberty and menopause. At the time of pregnancy generally improves while in the postpartum period is generally worse. Metabolic disorders such as dialysis and hypocalcemia were reported to be one trigger factor. Generally, drugs that can cause residif are beta adrenergic blocking agents, lithium, anti-malaria and the sudden cessation of systemic steroids.

         There are several predisposing factors that can cause this disease, namely:
1. Hereditary factors are dominant autosomal with incomplete penetration.
2. Psychological factors, such as stress and disruption emotion. The study mentions that 68% of patients with psoriasis express stress, and anxiety caused more severe and severe disease.
3. Focal infection. Chronic infection in the nose and ears, pulmonary tuberculosis, dermatomycosis, arthritis and chronic inflammation of the kidneys.
4. Metabolic diseases, such as latent diabetes mellitus.
5. Digestive disorders, such as obstipate.
Weather factors. Some cases showed a tendency to heal in the summer, while in the rainy season will relapse and more severe

Psoarias

Psoriasis is probably one of the diseases that have long been found in humans and is a disease that also raises many question marks in the diagnosis. Some researchers believe that psoriasis had existed long ago and known as "Tzaraat" in the Bible. At the time of dahalu psoriasis included in category one variation of leprosy.

In the 18th century, British dermatologist, Robert Willan and Thomas Bateman distinguish psoriasis with other skin diseases. It is said that the abnormalities in the skin of leprosy efloresensi a regular, circular macula is always temporary in psoriasis in an irregular entuk. With all the confusion that exists, then in 1841, the condition of the skin disorder called psoriasis by experts from Vienis dermatolgis, German named Ferdinand von Hebra. It took its name from the Greek word "psora" meaning "itch".

    Psoriasis is an autoimmune disease that causes, are chronic and residif, characterized by patches of erythema skuama demarcated with a rugged, multi-layered and transparent, with the phenomenon of wax droplets, Auspitz, and Kobner.

      Psoriasis is a chronic inflammatory disease hiperproliferatif and on the skin with clinical manifestations similar to each ethnicity. The disease is associated with skin diseases hiperproliferatif mild to severe degree and joint inflammation. Disease onset and degree of illness is influenced by age and genetics, and is triggered by various internal and external factors, such as physical injury to the skin, systemic treatment, infection, and emotional stress. More frequently encountered cases of psoriasis. Although the disease is not fatal but causes cosmetic disturbance, the more so given that chronic and residif journey. The incidence of psoriasis spread throughout the world, but its prevalence varies in ethnic and geographical dareah. Psoriasis therapies have minimal variation in each ethnicity.

     Cases of psoriasis more frequently found. Although the disease is not fatal but causes cosmetic problems mainly due to the disease course is chronic and residif. Incidence in whites is higher than the colored population. In Europe, reported to be between 3-7%, 1-2% in the United States while in Japan 0.6%. On black people, for example in Africa as well as the rarely reported in the American Indian tribes. Psoriasis can be affected in men and women. Slightly higher incidence of men than women. Psoriasis is found in all age groups but generally in adults between the ages of 15-25 years.

       Age of psoriasis onset in early type with the peak age of 22.5 years (in children, the average onset age of 8 years). For the slow type, appeared at the age of 55 years. Early onset of disease and predict the degree of chronic diseases, and is usually accompanied by a family history of psoriasis. No difference in incidence between men and women. Psoriasis affects 1.5 - 2% of the population of western countries. In the United States, there are 3 to 5 million people suffer from psoriasis. Most of them suffer from psoriasis locally, but around 300,000 people suffer from generalized psoriasis.

Treatment and Therapy of Paronychia

Acute paronychia is generally caused by bacteria, the treatment of choice preparations flucloxacilin 4 x 250 mg / day; generally worked well. When formed pus drainage done, without neglecting the five principles of treatment of hand infections are:
1. Administration of antibiotics
2. Rest and elevation of the affected part of the infection
3. Early recognition of pus and the pus is right
4. Remove the pus, if necessary debridement in space abscess
5. Adequate treatment after action

        In the superficial paronychia is generally localized and pussy clearly visible: it can be done with incision drainage or bayonet forms a sharp pointy scalpel which inserted into the sulcus with an oblique angle, should be done parallel to the nail plate. After the drainage then compressed with warm physiological saline solution to stimulate wound drainage; in some cases simply do compresses and topical antibiotic Neosporin. The position of the infected finger was rested in a position of flexion for accelerating wound healing.

       At paronychia deep, often found clinical symptoms of swelling, pus erythematous without clear point; can be given antibiotics as sensitive as cloxacillin or erythromycin. Having given antibiotics and warm compresses will happen to localized pus, and drainage occurs via the spontaneous folding nail indentations, or it can be done as paronychia superficial incision.

       For sub ungual paronychia which not responsive to antibiotics after 2 days, needed surgery to remove 1/3 proximal nail plate; tranversal cut the nail plate with nail scissors under local anesthesia without adrenaline, you can also ethylchloride spray or liquid nitrogen.

Widespread infection in sub ungual distal, 40% of cases occur in the pus under the nail plate. In the area of ​​the hospital performed the penetration of the nail plate, so that the pus can be removed and further handling compress finger with antiseptic solution such as: khlorheksidin 2x a day, and made wet compresses will speed healing.

       Treatment of chronic paronychia requires patience doctors and patients. At this state of chronic bacterial infections must be prevented so that the compressing, while the compress would prolong and worsen the course of the disease state. A common treatment is: reduce exposure to water. When doing work related to the water should wear protective gloves, better wear gloves of cotton and coated with rubber gloves made of vinyl: If the gloves are wet should be replaced.

       The use of drying agents after doing work related to the water with a solution of aluminum chloride or chloroform dalarn 6-20% alcohol; if irritation can be recommended granting corticosteroid lotion or cream.

       Given the chronic paronychia infection causes most of the Candida albicans antifungal use in tincture form used 2x a day that is: the solution klotrimoksasol, haloprigin or miconazole. The use of combination antifungal faster lotrisone topically.

     If there is a sign of inflammation, redness, heat, swelling and pain, is recommended oral erythromycin administration, because it is always found staphylococcus in the wound that is still sensitive to these antibiotics. Other antibiotics is Sulfasetamid 15% solution in 50% methylated spirit or alcohol and the use of paint castelani is still effective.

        Paronychia in patients who also suffer from diabetes is the most important aspects of treatment: in particular the control of blood sugar levels. Toe paronychia often followed unguis incarnatus, surgery can be performed after paronychia controlled, and carried out a radical removal of the nail.

Dose of radiotherapy treatment for chronic cases of 75 rad / week with 43-50 KM (Dermopan Siemens) to a maximum dose of 450 rad (total 6x administration) often helps healing.

        Chronic paronychia which not responsive to any treatment should receive treatment with surgical excision of the crescent shape of the proximal nail fold 5-6 mm. At the widest part extends into the lateral nail fold

       Wound healing by secondary intention occurs, could be 2 months. It may take 2-3 months for the re-establishment of damaged cuticles as in the original state of chronic paronychia. Nail growth dystrophy takes medication for 6 months, the patient should guard against exposure to water during the treatment of paronychia is an infection.

Paronychia

Paronychia or CANTENGAN is an inflammatory reaction of the folds of skin and tissue around the nail. Acute paronychia most often caused by bacterial infection, usually Staphylococcus aureus or Pseudomonas aeruginosa, whereas chronic paronychia caused by the fungus Candida albicans.

Paronychia is characterized by nail into soft tissue, and swelling and can secrete pus (pus), nails grow thicker, discolored, and forming the back line, the transverse. When the infection was chronic, then there is a bright horizontal at the base of the finger nails usually affects 1-3.

       This disease develops in people who are old hands submerged in water, when the finger was injured only slightly, the bacilli or fungi will damage the tissue around the nail. People with diabetes or malnutrition more easily attacked.

More common in women, the disease sometimes appears in children, especially those fond of sucking her fingers. Each finger can be affected, but more often is the ring finger and little finger

CLINICAL MANIFESTATIONS

A. Acute paronychia

       Frequent cause of acute paronychia is Staphylococcus aureus, (80%) while the rest are Streptococcus and other gram-negative bacteria. Superficial paronychia appears as an area of ​​redness, tenderness around the nail fold, swelling, presence of abscess or intra kutikular sub kutikular and also on the lateral nail fold. Paronychia is in providing a picture of tender swelling and cellulitis in almost all tissues proximal to the nail, most often in eponikium. At the beginning before the antibiotic treatment, no visible pus and after treatment of localized pus will form. Bacterial infection of the nail fold often occur secondary to trauma such as sucking and nail biting, nail kesusuban or punctured, the old wounds and nail care is wrong with the use of unsterilized equipment that may lead to tearing of the cuticle

B. Chronic paronychia

     Based on the etiology divided into primary and secondary. In the primary state of pain and swelling of existing lateral and posterior nail fold, erythematous looks shiny. The cuticle is usually separated from the nail plate which is an important diagnostic picture.

      In the early stages of the nail plate still looked normal; to further process the plate in the proximal and lateral nail discoloration even dystrophy. The disease is more common in women, especially at the age of 30-60 years. Sometimes occurs in children who love to suck his fingers.

    Etiology associated with hand immersion in water for long. The disease is more common in housewives, cooks, nurses, people with jobs related to fishing such as fishermen, fish sellers, workers canteen (catering), which is a predisposing systemic disease such as diabetes (DM).

      Mild inflammation that persists in the nail fold is often followed by acute attacks of spots formed pus that can be known with an emphasis nail fold tissue will exit the material are like cheese. Pus is formed in a bag under the nail fold; no visible abscess in perinychium.

     Acute attacks and chronic repeated cause discoloration of the nail plate and the lateral proximal part such as yellow, brown or blackish. This discoloration is caused by an organism resulting dihydroxy acetone in the nail fold. Pseudomonas gives a special color of green or blue depending on the species of Pseudomonas. Pseudomonas pyocyanea give a green color because the pigment piosianin, while the green color of Pseudomonas aeruginosa.

Candida paronychia have the following signs:

1. Painless.

2. In the palpability less warm, compared with bacterial paronychia.

3. The absence of pus or pus.

4. Chronically runs.

5. Often accompanied onikolisis

        On Candida paronychia, the nail plate is affected secondarily. Darker the nail plate, convex, sometimes thinner, there is rarely a sub ungual hyperkeratosis. While the clinical nail candidiasis is characterized by sub-ungual hyperkeratosis. Clinical picture of nail candidiasis is difficult to distinguish from tinea unguium.

        The differences can be detected by culture in the presence of the fungus Candida fungus and treatment response is not well with griseofulvin. Whereas in tinea unguium, the cause of dermatophyte fungi growing culture, improving the response to treatment with griseofulvin.

      In the secondary paronychia, nail infections are usually caused by: Hendersonula toruloidea or Scytalidium hyalinum. The mechanism of chronic paronychia Secondary paronychia is similar to the primary. The first interruption of eponikium loss of the nail plate due to immersion in water for long. Exposure causes the cuticles soft and finally escape, resulting in the invasion of bacteria and fungi.

How to Prevent Coronary Heart Disease

No old motto better than "Prevention is better than cure". This goes for anyone, especially in people who have high risk factors.
Priority of prevention, performed mainly on:
a. Patients with CHD, peripheral arterial disease, and cerebrovascular atherosclerosis.
b. Patients without symptoms but considered high risk because of:

- Many risk factors and the magnitude of the 10-year risk ≥ 5% (or by more than 60 years of age) to have a fatal cardiovascular disease.
- The increase of one component of risk factors: cholesterol ≥ 8 mmol / l (320 mg / dl), low density lipoprotein (LDL) cholesterol ≥ 6 mmol / l (240 mg / dl), BP ≥ 180/110 mmHg.
- Patients with diabetes type 2 and type 1 with microalbuminuria.
c. Close family, with:
- Patients with atherosclerotic cardiovascular disease earlier
- Patients with high risk but without symptoms.
d. People who regularly perform a clinical examination.


1. Guidelines for Primary Prevention of Cardiovascular Disease and Stroke
     It has been a lot of evidence that suggests that CHD can be prevented, and research for this continues. From the results of long-term prospective study, showed that people with low risk factors have a smaller risk for developing CHD and stroke.
    ACC / AHA recommends directions for prevention of cardiovascular disease risk factors determined from the existing
a. Risk factors:
 Search for risk factors -> Destination: adults know the extent and importance of risk factors checked routinely.
Recommendation: Examination of risk factors should begin at the age of 20 years. Family history of CHD should be routinely monitored. Smoking, diet, alcohol, physical activity should be evaluated regularly. Blood pressure, body mass index, waist circumference, should be examined interval of 2 years. Cholesterol checks and blood sugar levels must still be monitored as well.

b. Estimation of risk factors in general -> All adults over the age of 40 should know their risk factors for CHD disease. Objectives: reducing the risk factors as much as possible.
Recommendation: Every 5 years (or more if there are changes in risk factors), particularly those with ≥ 40 years of age or a person with more than 2 risk factors, should be able to identify the risk factors based on a count of 10-year risk factor. Risk factor is smoking seen in blood pressure, cholesterol checks, blood sugar levels, age, gender, and diabetes. Patients with diabetes or a 10-year risk> 20% is considered as CHD patients (CHD risk equivalent).


Intervention efforts by non-pharmacologic and various pharmacologic and clinical trials show a beneficial thing.
a. Smoking:
-> Stop total. Not exposed, the environment smokers.
b. Blood Pressure Control
-> Destinations TD <140/90 mm Hg; <130/80 in renal impairment or heart failure, or <130/80 mm Hg in diabetes.
c. Diet
-> Objective: Eat a healthy diet.
d. Giving Aspirin
-> Objective: Low-dose aspirin in patients with high cardiovascular risk (in particular patients with a 10-year risk of cardiovascular events ≥ 10%).
e. Lipid arrangements in the Body
-> Primary goal: LDL - C <160 mg / dl if ≤ 1 risk factor, LDL-C <130 mg / dl if they have ≥ 2 risk factors and CHD risk 20%, or LDL-C <100 mg / dl if ≥ 2 risk factors and 10% had CHD risk ≥ 20% or if the patient is also affected by diabetes.
-> Secondary Objectives (if LDL-C is a prime target): if triglycerides> 200 mg / dl, and then used non-HDL-C as the second goal; non HDL-C <190 mg / dl to ≤ 1 risk factor; non -HDL-C <160 mg / dl to ≤ 2 risk factors and CHD risk ≤ 10 years at 20%, non-HDL-C <130 mg / dl for diabetes or with ≥ 2 risk factors and risk of CHD 10 years> 20 %.
-> Target else therapy: triglycerides> 150 mg / dl; HDL-C <40mg/dl in men and <50 mg / dl in women.
f. Physical Activity
-> Objective: at least 30 minutes of physical activity or physical activity of moderate intensity every day within 1 week.
g. Weight regulation
-> Objective: Achieve danmempertahankan weight (BMI 18.5 to 24.9 kg/m2). When BMI ≥ 25 kg/m2, waist circumference ≤ 40 inches in men and ≤ 35 inches in women.
h. Management of Diabetes
-> Objective: fasting blood sugar levels (<110 mg / dl) and HbA1c (<7%).
i. Chronic Atrial Fibrillation
-> Objective: Achieving sinus rhythm or chronic atrial fibrillation if it appears, the anticoagulant
with INR 2.0 to 3.0 (target 2.5).


2. Secondary Prevention of Coronary Heart Disease
Secondary prevention in individuals suffering from CHD has been proven, is an attempt to prevent recurrent CHD was no longer
a. Smoke
-> Objective: Stop the total, are not exposed to environmental smoke
b. Blood Pressure Control
-> Objective: BP <140/90 mmHg or <130/80 mmHg in patients with diabetes or chronic kidney disease
c. Lipid Management
-> Goal: LDL-C <100 mg / dl If Triglserid ≥ 200 mg / dl, non-HDL-C should be <130 mg / dl
d. Physical activity
-> Objective: 30 minutes, 7 days a week (at least 5 days per week)
e. Weight regulation
-> Objective: BMI: 18.5 to 24.9 kg/m2. Waist circumference: men <40 inches, women <35 inches.
f. Management of Diabetes
-> Objective: HbA1c <7%
Antiplatelet drug use / Anticoagulants: Aspirin, clopidogrel, warfarin as indicated.
Use of Renin-Angiotensin-Aldosterone System Blockers: replace with ARB if intolerant.
The use of Beta-Blockers: unless there are contraindications.
Influenza vaccination in patients with cardiovascular disorders.


Secondary prevention is very necessary to remember:
- Individuals who have ever been, or has been proven to suffer from coronary heart disease, heart disease tend to have longer, more likely than those who had never hurt the heart.
- The process of atherosclerosis is the underlying CHD, it can affect other organs of blood vessels in the brain that lead to cerebrovascular disease (stroke), the aorta or carotid arteries, peripheral arteries, etc.. Therefore, secondary prevention for CHD may also be the primary prevention of atherosclerotic disease to others.
Secondary prevention has not been fully received attention (underutilized) of medical practitioners, as reported by WHO in 2004, particularly in countries with per capita income, low and medium.

Treatments and Theraphy of Coronary Heart Disease

The goal of treatment are:
a. Improve prognosis by preventing myocardial infarction and death. Efforts is how to reduce the occurrence of acute thrombotic and left ventricular dysfunction. This goal can be achieved by lifestyle modification or pharmacologic interventions that will:

(i) subtracting the progressive plaque

(ii) stabilize the plaque, by reducing inflammation and improving endothelial function, and finally

(iii) to prevent thrombosis or endothelial dysfunction in the event of plaque rupture.

Drugs used: antithrombotic drugs: a low-dose aspirin, ADP receptor antagonists (thienopyridin) that clopidogrel and ticlopidine; cholesterol-lowering drugs (statins), ACE-Inhibitors: Beta-blockers: Calcium channel blockers (CCBs).

b. To cope with symptoms and ischemia: the drug used. Nitric working short and long term, beta-blockers, CCBs.

General Procedures

       To patients suffering from CHD and their families, need to be briefed about the course of the disease and the choice of drugs available. Patients should be reassured that most cases of angina can be improved with medication and lifestyle modifications so that the quality of life better. Comorbid disorders such as hypertension, diabetes, dyslipidemia, etc..

CHD treatments, consisting of pharmacological treatment and myocardial revascularization. Keep in mind that none of the above nature cure. In other words it is necessary lifestyle modifications and addressing the causes that disease progression can be slowed.

Pharmacologic treatment

* Low-dose aspirin

From various studies have clearly shown that aspirin is still the main drug for the prevention of thrombosis. Meta-analysis showed that a dose of 75-150 mg equal effectiveness compared with larger doses. Therefore, aspirin is recommended in all patients with CHD were given unless contraindicated encountered. In addition to aspirin is also recommended that given the long-term side effects but it should be noted gastrointestinal irritation and bleeding, and allergies. Cardioaspirin provide a more minimal side effects other than aspirin.

* Inhibits platelet aggregation

Thienopyridine Clopidogrel and ticlopidine are antagonists of ADP and inhibits platelet aggregation. Clopidogrel is more indicated in patients with resistance or intolerance to aspirin.

AHA / ACC guidelines update the 2006 include a combination of aspirin and clopidogrel should be given to patients with PCI with stent implantation, over 1 month for bare metal stent, 3 months for sirolimus eluting stent and 6 months for paclitaxel-eluting stent.

* Cholesterol-lowering drugs

Treatment with statin use to reduce risk in both primary prevention and secondary prevention. Various studies have shown that statins can reduce complications by 39% (Heart Protection Study), Ascott-LLA atorvastatin for primary prevention of CHD in post-hypertension.

Than as a cholesterol-lowering statins, also have other mechanisms (pleiotropic effect) which can act as an anti-inflammatory, anti-thrombotic etc.. Provision of atorvastatin 40 mg one week prior to PCI may reduce myocardial damage due to the action. Target reduction in LDL cholesterol is <100 mg / dl and in high risk patients, DM, CHD patients is recommended lowering LDL cholesterol <70 mg / dl.

* ACE-Inhibitor/ARB
The role of ACE-I as secondary prevention for Cardioprotection in patients with CHD has been demonstrated from various studies, among others., HOPE study, etc. EUROPA study. If intolerance to ACE-I may be replaced by the ARB.
* Nitrate is generally recommended, because nitrate has an effect so venodilator myocardial preload and left ventricular end volume and thus decreases myocardial oxygen consumption also decreases. Nitrates also dilate blood vessels of normal and atherosclerotic experiencing. Raise collateral blood flow, and inhibits platelet aggregation. When an attack of angina does not respond to short-term nitrate, then be wary of myocardial infarction. Drug side effects are headaches, and flushing.
* Beta blockers 

Beta Blockers are also a standard drug. Beta blockers block the effects of catecholamines on the circulation and Beta-1 receptors which can cause a decrease in myocardial oxygen consumption. Beta blockers do with the provision of a target heart rate 50-60 per minute. The most important  contraindication to beta blocker administration is history of bronchial asthma, and acute left ventricular dysfunction.
* Calcium antagonists 

 have the effect of vasodilatation. Calcium antagonists can reduce complaints in patients who had received nitrates or beta blockers; but it is also useful in patients whoose contraindications to the use of Beta blockers. Calcium antagonists is not recommended if there is a decrease in left ventricular function or conduction disturbances atrioventricular. 

Treatment recommendations to improve the prognosis of patients with unstable angina according to the ESC 2006 as follows.:
1. Giving aspirin 75 mg per day in all patients without specific contraindications (ex. active gastric bleeding, aspirin allergy, or a history of aspirin intolerance) (level of evidence A).
2. Statin treatment for all patients with coronary heart disease (evidence level A).
3. The provision of ACE inhibitors in patients with an indication of the provision of ACE inhibitors, such as hypertension, left ventricular dysfunction, history of myocardial infarction with left ventricular dysfunction, or diabetes (level of evidence A).
4. Provision of oral beta-blockers in patients with heart failure or myocardial infarction who had received (evidence level A).

Myocardial revascularization
      There are two ways that have proven good revascularization in stable CHD is caused by atherosclerotic coronary revascularization act of surgery, coronary bypass surgery (coronary artery bypass surgery = CABG) and percutaneous intervention (PCI = percutneous coronary intervention).
Lately, both methods have progressed rapidly in the introduction of action, off pump with minimally invasive surgery and drug eluting stent (DES). Revascularization goal is to improve survival or prevent infarction or for relief of symptoms. Where the action is chosen, depending on the risk and patient complaints.
Indications for Revascularization
In general, patients who have indications for coronary arteriography and actions performed catheterization showed narrowing of the coronary arteries is a potential candidate for myocardial revascularization action. In addition, the act of revascularization performed on the patient, if:
a. Treatment failed to control the patient's complaints.
b. Non-invasive test results indicate a risk of infarction.
c. Found a high risk for the incidence and mortality.
d. Patients prefer the intervention compared with usual treatment and fully understand the risks of the treatment given to them.


Actions CABG Surgery
Surgery is better to do than with medication, in the circumstances:
a. Significant stenosis (≥ 50%) in the left main (LM).
b. Significant stenosis (≥ 70%) in the region proximal to the 3 major coronary arteries.
c. Significant stenosis in two main areas, including coronary artery stenosis is high enough levels in the proximal region of the left anterior descending coronary artery.


PCI acts
        In the first act of percutaneous transluminal angioplasty is only performed on the blood vessels only, now it has grown more rapidly both because of the experience, equipment, especially stents and drug investigations. In patients with stable CHD with appropriate coronary anatomy of the PCI can be performed on one or more blood vessels (multi-vessel) with a good (successful PCI). The risk of death by about 0.3-1% of this action. Action PCI in patients with stable CHD compared with medical drugs, not add to survival and it is different than CABG.


Installation of Elective Stent and Drug-eluting stents (DES)
      Stenting can reduce restenosis and repeat PCI compared with balloon angioplasty actions. Currently available drug-coated stent (drug-eluting stent = DES) as serolimus, paclitaxel, etc.. Compared with bare-metal stents, the use of DES may reduce restenosis. RAVEL study showed restenosis can be reduced to 0%. Direct stenting (stent without balloon pre-dilatation with the first) is a feasible action in patients with coronary artery stenosis without calcification is a specific, single lesion, without angulation or severe turtoasitas. Direct action stenting can reduce the time the action / ischemic time, reduce radiation, the use of contrast, to reduce costs.


Primary Percutaneous Coronary Intervention actions (Primary PCI)
        Stable CHD patients had complications and had a heart attack (ACS), mortality is very high (> 90%). With advances in technology have now been able to do primary percutaneous coronary intervention (primary PCI) is a technique to remove thrombi and dilate the narrowed coronary arteries with balloon catheters and stent insertion is often done. This action can remove the blockage immediately, so that blood flow can be normal again, so the heart muscle damage can be avoided. Primary PCI is the treatment of acute cardiac infarction are best at this, because it can stop the attack of acute cardiac infarction and reduce mortality to below 2%.



 

How to Diagnose Coronary Heart Disease

The first step in the management of Coronary Heart Disease (CHD) is the designation of a definite diagnosis. Correct diagnosis is important, because if a diagnosis of CHD has been made, in which are likely to have the sense that people will be able to experience cardiac infarction or sudden death. Diagnosis is wrong always have bad consequences on quality of life of patients ..

In addition, their opportunities for employment, may be reduced. If this happens to older people, then they probably should have retired too early, to be repeatedly hospitalized to eat excessively or drugs of potential toxins for a long time. On the other hand, fatal consequences can occur when the presence of CHD is unknown or if the presence of other cardiovascular diseases that cause angina pectoris missed and go undetected.

Diagnostic Method
      Here, the most important diagnostic methods of CHD, either currently existing or in the foreseeable future, will potentially have a major role. Physicians should choose whatever checks that need to be made to the patient to achieve the accuracy
maximum diagnostic risks and costs to a minimum. Stages of the evaluation conducted in patients with angina pain:

Diagnostic Steps
1 Anamnesis
2. physical examination
3. laboratory
4. Photos of the chest
5. Non-invasive cardiac examination
- Resting ECG
- Test of physical exercise (treadmill)
- A combination of physical exercise testing imaging:
- Physical exercise testing echocardiography (Stress Eko)
- Physical exercise testing Myocardial Perfusion Scintigraphy
- Physical exercise testing pharmacologic Combination Imaging Technique
- Echocardiography break
- Monitoring ECG ambulatoir
- Non-invasive technique of determining the classification of the coronary and coronary anatomy:
- Computed Tomography
- Magnetic Resonanse arteriography
6. Invasive testing to determine coronary anatomy
- Coronary arteriography
- Intra-vascular ultrasound (IVUS)

        Any patient with chest pain needs to be done a thorough anamnesis, the determination of risk factors, physical examination and ECG. In patients with mild symptoms of angina pectoris, fairly non-invasive examination. When patients with severe complaints and takes action and the possibility of revascularization, the action was an indication of angiography.
        On the dubious circumstances to do the treadmill test. The treadmill test is more sensitive and specific compared with resting ECG and a test of choice for detecting patients with angina pectoris and the possibility of this examination the ingredients are easy and affordable cost. In certain circumstances, it is difficult to interpret the results of the treadmill as in patients with resting ECG abnormalities, among others.: LBBB, repolarization abnormalities, LVH and so on.
          Another alternative tests, which can be done is to echocardiography and non-invasive technique of determining coronary calcification and coronary anatomy, Computed Tomography, Magnetic Resonanse arteriography, the sensitivity and specificity is higher. In addition the test is also suitable for patients who can not do excercise, where the exercise test can be done by using drugs dipyridamole or dobutamine

Evaluate Algorithm of Patient with Angina

Translate this article to Indonesian language Click Here