Silent killer diseases.ppt

SILENT KILLER DISEASES Hypertension Amyloidosis Sleep Apnea By IFFAT FATIMA (08)

SILENT KILLER DISEASES Many diseases are silent killers in that they are silent (no symptoms or only vague symptoms) killer that they are deadly. There are a number of diseases that are known as "silent killers" because they gradually consume you without causing any serious symptoms in the early stages.

Facts of silent killers

Heart disease, hypertension and diabetes are major silent killer diseases

amyloidosis, Renal cell cancer , pancrenatic cancer, Hepatitis B or C infectio

Cancer as group Mesothelioma Heart disease Obstructive Sleep apnea

'Silent killer disease' are diseases that produces minimum or no symptoms and are capable of causing death if not treated.

SYSTEMIC HYPERTENSION Definitions of hypertension: Elevated arterial blood pressure is a major cause of premature vascular disease leading to cerebrovascular events, ischaemic heart disease and peripheral vascular disease.

Hypertension - Introduction 

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Silent Killer – painless complications It is the leading risk factor –MI, HF, CRF Stroke Responsible for the majority of office visits, Number one reason for drug prescription. 25% of population Complications bring to diagnosis but late…

Regulation of BP: BP = Cardiac Output x Peripheral Resistance  Endocrine Factors – Renin, Angiotensin, ANP, ADH, Aldosterone.

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Neural Factors – Sympathetic & Parasympathetic

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Blood Volume – Sodium, Mineralocorticoids, ANP

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Cardiac Factors – Heart rate & Contractility.

Control of Blood Pressure:

Blood Volume Na+, Aldosterone

BP Cardiac Factors Rate & Contract..

Vasoconstrictors Angiotensin II Catecholamines

Cardiac Output

Humoral Factors Vasodilators Pg & Kinins

Peripheral Resistance

Neural Factors Adrenergic – Cons ß Adrenergic - Dil

Local Factors pH, Hypoxia

Etiology 1- Essential: In more than 95% of cases, an underlying cause cannot be found. Proposed mechanisms include:  Excess renal sodium retention  Over activity of sympathetic nervous system  Exess of Renin angiotensin  Hyperinsulinemia  Alterations in vascular endothelium

Factors contributing to the development of Essential hypertension •Genetic Factors: hypertension is more common in some families and in some ethnic groups like African Americans •Environmental factors include obesity, alcohol, lack of exercise and excess salt intake

2- Secondary hypertension 

Renal: These account for over 80% of the cases of secondary hypertension. The common causes are diabetic nephropathy, chronic glomerulonephritis, adult polycystic disease, chronic tubulointerstitial nephritis.

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Endocrinal: These include Conn's syndrome, adrenal hyperplasia, acromegaly, Cushing's syndrome.

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Drugs and toxins Pregnancy-induced hypertension Vascular: coarctation of aorta, vasculitis

Complications 

Cerebrovascular disease and coronary artery disease are the most common causes of death, although hypertensive patients are also prone to renal failure and peripheral vascular disease.

HYPERTENSION Classification of blood pressure levels: (according to the British Hypertension Society) Category Systolic blood pressure pressure Optimal < 120 Normal < 130 High normal 130-139 Hypertension Grade I (mild) Grade 2 (moderate) Grade 3 (severe)

140-159 160-179 ≥180

Isolated systolic hypertension Grade 1 140-149 Grade 2 ≥160

Diastolic blood < 80 < 85 85-89 90-99 100-109 ≥110 < 90 < 90

HISTORY 

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The patient with mild hypertension is usually asymptomatic. Attacks of sweating, headaches and palpitations may point towards the diagnosis of phaeochromocytoma. Higher levels of blood pressure may be associated with headaches, epistaxis or nocturia. Breathlessness may be present owing to left ventricular hypertrophy or cardiac failure. Malignant hypertension may present with severe headaches, visual disturbances, fits, transient loss of consciousness or symptoms of heart failure.

Hypertensive Retinopathy: Grade I – Thickening of arterioles.  Grade II – Focal Arteriolar spasms. Vein constriction.  Grade III – Hemorrhages (Flame shape), dot-blot and Cotton wool and hard waxy exudates.  Grade IV - Papilloedema 

INVESTIGATIONS Routine investigation of the hypertensive patient should include:  ECG  Urine stix test for protein and blood  Fasting blood for lipids (total and highdensity lipoprotein cholesterol) and glucose  Serum urea, creatinine and electrolytes.

Investigation of selected cases Chest X-ray  Ambulatory BP recording  Echocardiogram  Renal ultrasound  Renal angiography  Urinary catecholamines  Urinary cortisol and dexamethasone suppression test  Plasma renin activity and aldosterone 

Non-pharmcological treatment 

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Weight reduction - BMI should be < 25 kg/m2 Low-fat and saturated fat diet Low-sodium diet - < 6 g sodium chloride per day Limited alcohol consumption - ≤ 21 units/week for men and ≤ 14 units/week for women Dynamic exercise - at least 30 minutes' brisk walk per day Increased fruit and vegetable consumption Reduce cardiovascular risk by stopping smoking and increasing oily fish consumption.

Amyloidosis 

Amyloidosis is a group of diseases that result from the abnormal deposition of a particular protein, called amyloid, in various tissues of the body.

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Amyloid protein can be deposited in a localized area and may not be harmful or only affect a single tissue of the body.

– Localized amyloidosis – Systemic amyloidosis

Pathogenesis native cell creates a protein which regress into the protein fragments

fragments or actual proteins could missfold along the way and make a bad protein

Proteolysis, which is a mechanism for protein digestion, to come and digest the miss-folded fragments and proteins

Oligomers and amyloid fibrils can go and cause cell toxicity and organ disfunction

When the fragments do not dissolve they get spit out of Proteolysis and they aggregate to form Oligomers