Warung Bebas

Monday 20 August 2012

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 medical shaman
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
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
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)
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)
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.
Psoriatic erythroderma
Psoriasis Erythrodrmic

Wednesday 15 August 2012

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.

Thursday 9 August 2012

Causative Factors of Psoriasis

Psoriasis Medical Health Shaman
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

Wednesday 8 August 2012

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.

Saturday 4 August 2012

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.

Thursday 2 August 2012

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.

Thursday 26 July 2012

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.



 

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