ATHEROSCLEROSIS

 

Atherosclerosis 

 

 Atherosclerosis is a thickening and hardening of large and medium-sized muscular arteries, primarily due to involvement of tunica intimae and is characterized by fibrous fatty plaques or atheromas.

The term atherosclerosis derived from athero-(meaning porridge) referring to the soft lipid rich material in the center of atheroma and sclerosis (scarring) referring to connective tissues in the plaques.

Etiology 

Cardiovascular disease, mostly related to atherosclerotic coronary heart disease or ischemic heart disease (IHD) is the most common cause of the premature death in the developed countries of the world.

#Major risk factors

(a)           Modifiable

-         Dyslipidemia

-         Hypertension

-         Diabetes mellitus

-         Smoking

(b)           Constitutional

-         age

-         gender

-         genetic factors

-         familial and racial factors

 

# Emergency risk factors

-          obesity

-         Hormones –estrogen deficiency

-         Physical inactivity

-         Prothrombotic factors

 

Pathogenesis

 

The pathogenesis of atherosclerosis consists of 4 stages :

1.   Firstly endothelial injury is the initial triggering event in the development of lesions of atherosclerosis.

2.    Endothelial injury causes adherence, aggregation and platelet release reaction at the site of exposed sub endothelial connective tissue and infiltration by inflammatory cells, and as a result causing proliferation of smooth muscle cells.

3.   Aggregation of the platelet causes formation of small thrombus.

4.   This causes mild inflammatory reaction which together with foam cells is incorporated into the atheromatous plaque.

 

Clinical effects on various organs

 

 

Clinical effect depends on the artery type, size.

Large arteries that get affected most often are the aorta, renal, mesenteric and carotids whereas medium arteries involve cerebral arteries and coronary arteries.

According to the symptoms atherosclerotic disease involves most often the following.

a)   Heart- Myocardial infarction, ischemic heart disease

b)   Brain- chronic ischemic brain damage, cerebral damage, cerebral infarction and stroke.

c)    Aorta- aneurysm, thrombosis and embolisation to other organs.

d)   Small intestine- ischemic bowel disease, infarction

e)   Lower extremities - intermittent claudication, gangrene. 

Diagnosis

 Atherosclerosis can be diagnosed by

MRI, CT scans and ultrasounds. 

Through blood tests we can also diagnose hdl levels(high density lipoprotein) which increases due to deposition of fats in blood vessels.

 

 

TREATMENT

 

1.  FIRSTLY, lifestyle changes should be done in order to prevent the conditions to appearance of atherosclerotic plaques in the vessels. Changes like food eating habits simultaneously with the habit of exercising regularly.

2.   SECONDLY, medication treatments like fibrinolytic drugs, anti atherosclerotic drugs and also symptomatic treatment of the risk factors happened to the patient like medication for the hypertension and other.

3.  THIRDLY AND LASTLY, surgical treatment is done if it is a severe case atherosclerotic plaque in the vessel which is blocking the way of blood cells and leading to embolisation in the organs.

 

                                               -  by Dr. Ravi Ranjan

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CHRONIC OBSTRUCTIVE PULMONARY DISEASE

Chronic obstructive pulmonary          disease (copd)

It is a combination of clinical signs of chronic obstructive bronchitis(inflammation of narrowing of bronchi) and emphysema(changes of lung tissue structure).COPD is irreversible disease increasing worldwide because of the increase in smoking in developing countries, the reduction in mortality due to infectious diseases and the widespread use of biomass fuels. Prevalence, incidence and mortality rates increase with age. Prevalence is higher in men, but total mortality is similar in both sexes.

ETIOLOGY

•       Cigarette smoking

•       Genetic factors (alpha1-antitrypsin deficiency)

•   Air pollution, airway infections

PATHOPHYSIOLOGY

*Inflammation –It generally occurs in our body due to foreign particle irritation after getting in contact with our epithelium, in this disease COPD inflammatory response is triggered by increase in activity of protease activity and decrease in anti protease activity which thus cause break down of elastin and connective tissue in our lungs and this causes problems in normal repair processes of tissues. In patients with COPD activated neutrophils and other inflammatory cells release proteases as a part of inflammatory process; protease activity exceeds anti protease activity and tissue destruction and mucous hyper secretion starts.

* Infection – Smoking and airflow obstruction may lead to impaired mucus clearance in lower airways, which predisposes to infection.

* Airflow limitation – due to mucus hyper secretion, mucus plugging, mucosal edema, bronchi spasm all these mechanism occur due to airway obstruction. As alveolar wall destroy due to loss of elastic recoil and lung hyperinflation.

CLINICAL SIGNS

- Productive cough

- Dyspnea

- Wheezing

- Lung hyperinflation

- Decreased heart and lung sounds

- Increased anteroposterior diameter of the thorax

- Cyanosis of skin and lips

DIAGNOSIS

+ Pulmonary function tests- that is forced expiratory volume test (FEV1), Forced vital capacity test (FVC).

+ Instrumental and laboratory tests-chest x-rays, CT scan.

+Adjunctive tests –alpha1-antitrypsin levels, ECG, CBC, Sputum analysis.

TREATMENT

·     Inhaled bronchodilators –these includes beta agonists like Fenoterol , salbutamol and anti cholinergic; tiotropium bromide is used over ipratropium as powder formulation , corticosteroids; fluticasone and beclamethasone are used

·     Supportive care(stopping smoking, oxygen therapy, pulmonary rehabilitation)

·     Metered dose inhalers (MTIs) or dry powder inhaler is preferred over nebulizer home treatment.

·     Theophylline, oxygen therapy, vaccinations and pulmonary rehabilitations are widely used.

·     Expectorants and mucosolvents lasolvan ,acetylcysteine are used in order to dissolve the drainage function of bronchi

·     Antibiotics are recommended for exacerbation in patients with purulent sputum. If the infectious organism is resistant, amoxicillin, fluoroquinolones, cephalosporin’s of 2^nd generation and extended spectrum macrolides are indicated.

  

                                                                                                             

                                                                                                             -by Dr. Ravi Ranjan

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SYSTEMIC LUPUS ERYTHEMATOUS

         SYSTEMIC LUPUS ERYTHEMATOUS

What is Systemic Lupus Erythematous?

 It is an autoimmune disorder characterized by inflammation of blood vessels and connective tissue resulting in multi system involvement .The clinical manifestations are variable and the course unpredictable. Childhood SLE is usually more severe and has a poorer prognosis than adult SLE. the hallmark of SLE is the presence of antinuclear antibodies. The female predominance characteristic of adult SLE usually not apparent in young children.

   What can be the causes of it?

(i)Genetic factors 
(ii)Environmental agents
(iii)Infectious agents
(iv)Ultraviolet rays
(v)Dietary factor
(vi)Effect of drug or chemical agents

 SLE is predominately a disease of women with frequency in 1in 700 among women between ages of 20-64 anf female to male ratio of 9:1,so age and gender is also a factor for systemic lupus erythematous.

What is diagnosis criteria for it?

  1  Positive immunoserology(antibodies to dsDNA/smith nuclear antigen) 

 2 Positive findings of  antiphospholipid antibodies(IgG/IgM anticardiolipin)   

 3 Lupus anticoagulants 

4  Positive antinuclear antibody test

5 Veneral disesase research laboratory test(VDRL)

What can be the symptoms of this disease? 

The symptoms of SLE is can be checked by physical examination of  the patient as a lot of signs of it can be identified through it, for example:

(i)The malar rash which is virtually pathognomic of SLE, may not be apparent initially.It involves the cheek, bridge of nose and lower eyelids but spares the nasolabial folds .

(ii)Discoid lesions are rare in childhood onset SLE.

(iii)Oral ulcerations may involve the buccal mucosa or palate and characteristically painless
(iv)Some children may have frontal alopecia.
(v)Arthritis is usually mild and always non erosive.
(vi)Renal involvement is a dreaded complication of SLE and one the commonest causes of mortality in children.

•  Neurological features may include psychosis ,seizures and chorea .There may be no correlation between the severity of clinical involvement and findings on neuroimaging .

• Hematologic abnormalities include a Coombs' positive hemolytic anemia,leukopenia,lymphopenia and thrombocytopenia . In addition there may be coagulation abnormalities due to secondary antiphospholipid antibody syndrome .Cardiac manifestations may include pericarditis,myocarditis or verrucous(Liebman-sacks) endocarditis.                                               

 Serological diagnostic values in diagnosis of this disease

+Almost all patients with SLE have demonstrable antinuclear antibodies.Presence of anti-double stranded DNA antibodies is highly specific of SLE.The titers of these antibodies usually correlate with disease activity .

+Anti-histone antibodies are characteristic of drug-induced lupus(e.g following phenytoin,isoniazid,hydralazine) but in such cases anti dsDNA antibodies are usually absent and serum complement level is not decreased.

+Anti-ro antibodies are believed to play a role in the development of congenital heart block characteristic of neonatal lupus syndromes.These heart blocks are permanent.Anti-Sm antibodies are a marker for CNS lupus.

 What shall be the treatment and therapies for such disease?

• Glucocorticoids and hydroxychloroquine form the main stay of therapy of lupus .

• Prednisolone is started in doses of 1-2 mg/kg/day and gradually tapered over several months ,according to disease activity.

• Arthritis usually responds to NSAID's.

• Life threatening complications (such as nephritis,myocarditis) may warrant use of intravenous pulses of methlyprednisolone(30mg/kg/day)for 3-5days 

• Rituximab, monoclonal antibody to CD20 has also been found to be effective in such situations .

• Use of monthly pulses of IV cyclophosphamide has considerably improved the long term outcomes

• Infections must be treated aggressively with appropriate antimicrobial s and the steroid dose hiked up during such episodes .

                                                         -BY DR. RAVI RANJAN

                                                        -BY DR. TANYA SHARMA 

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