Cardiomyopathy

D E FI N I T ION

 Primary disease of the myocardium. Cardiomyopathy may be dilated, hypertrophic

or restrictive.

AETIOLOGY 

The majority are idiopathic.

Dilated:

 Post-viral myocarditis, alcohol, drugs (e.g. doxorubicin, cocaine), familial (25% of

idiopathic cases, usually autosomal dominant), thyrotoxicosis, haemochromatosis,

peripartum.

Hypertrophic:

 Up to 50% of cases are genetic (autosomal dominant) with mutations in

b-myosin, troponin T or a-tropomyosin (components of the contractile apparatus).

Restrictive:

 Amyloidosis, sarcoidosis, haemochromatosis.

EPIDEMIOLOGY 

Prevalence of dilated cardiomyopathy and hypertrophic cardiomyopathy

is 0.05–0.20%. Restrictive cardiomyopathy is rare.

HISTORY

Dilated:

 Symptoms of heart failure, arrhythmias, thromboembolism, family history of sudden

death.

Hypertrophic:

 Usually none. Syncope, angina, arrhythmias, family history of sudden death.

Restrictive:

 Dyspnoea, fatigue, arrhythmias, ankle or abdominal swelling.

Enquire about family history of sudden death.

EXAMINATION

Dilated:

 " JVP, displaced apex beat, functional mitral and tricuspid regurgitations, third heart

sound.

Hypertrophic:

 Jerky carotid pulse, double apex beat, ejection systolic murmur.

Restrictive:

 " JVP (Kussmaul’s sign: further " on inspiration), palpable apex beat, third heart

sound, ascites, ankle oedema, hepatomegaly.

INVESTIGATIONS

CXR: 

May show cardiomegaly, and signs of heart failure.

ECG:

All types: 

Non-specific ST changes, conduction defects, arrhythmias

Hypertrophic: 

Left-axis deviation, signs of left ventricular hypertrophy (see Aortic stenosis), Q

waves in inferior and lateral leads.

Restrictive: 

Low voltage complexes.

Echocardiography:

Dilated:

 Dilated ventricles with ‘global’ hypokinesia.

Hypertrophic: 

Ventricular hypertrophy (disproportionate septal involvement)

Restrictive: 

Non-dilated non-hypertrophied ventricles. Atrial enlargement, preserved systolic

function, diastolic dysfunction, granular or ‘sparkling’ appearance of myocardium in

amyloidosis.

Cardiac catheterization: 

May be necessary for measurement of pressures.

Endomyocardial biopsy: 

May be helpful in restrictive cardiomyopathy.

Pedigree or genetic analysis: Rarely necessary.

MANAGEMENT

Dilated:

 Treat heart failure and arrhythmias. Consider implantable cardiac defibrillators (ICD)

for recurrent VTs.

Hypertrophic: 

Treat arrhythmias with drugs, ICD for survivors of sudden death, reduce

outflow tract gradients, pacemaker, surgery (e.g. septal myomectomy, septal ablation

with ethanol). Screen family members with ECG or echocardiography.

Restrictive: 

No specific treatment. Manage the underlying cause.

Cardiac transplantation:

 May be considered in end-stage heart failure in all cardiomyopathy

types.

Cardiomyopathy (continued)

COMPLICATIONS

 Heart failure, arrhythmias (atrial and ventricular).

Dilated and hypertrophic cardiomyopathy:

 Sudden death and embolism.

Hypertrophic: 

Infective endocarditis.

PROGNOSIS

Dilated: 

Depends on the aetiology, New York Heart Association functional class and ejection

fraction.

Hypertrophic:

 Ventricular tachyarrhythmias are the major cause of sudden death.

Restrictive:

 Poor prognosis, many die within the first year after diagnosis.

0 تعليق

PH.Jafar Jassim 3/08/2021 01:15:00 ص

تابع القراءه

Aortic dissection

DEFINITION

 A condition where a tear in the aortic intima allows blood to surge into the aortic wall, causing a split between the inner and outer tunica media, and creating a false lumen.

AETIOLOGY 

Degenerative changes in the smooth muscle of the aortic media are the predisposing event. Common causes and predisposing factors are:

• hypertension;
• aortic atherosclerosis;
• connective tissue disease (e.g. SLE, Marfan’s, Ehlers–Danlos);
• congenital cardiac abnormalities (e.g. aortic coarctation);
• aortitis (e.g. Takayasu’s aortitis, tertiary syphilis);
• iatrogenic (e.g. during angiography or angioplasty);
• trauma;
• crack cocaine.

Stanford classification divides dissection into

•  type A with ascending aorta tear (most common);
•  type B with descending aorta tear distal to the left subclavian artery.

Expansion of the false aneurysm may obstruct the subclavian, carotid, coeliac and renal

arteries.

EPIDEMIOLOGY

 Most common in < between 40 and 60 years.

HISTORY

 Sudden central ‘tearing’ pain, may radiate to the back (may mimic an MI).Aortic dissection can lead to occlusion of the aorta and its branches:

Carotid obstruction: Hemiparesis, dysphasia, blackout.

Coronary artery obstruction: Chest pain (angina or MI).

Subclavian obstruction: Ataxia, loss of consciousness.

Anterior spinal artery: Paraplegia.

Coeliac obstruction: Severe abdominal pain (ischaemic bowel).

Renal artery obstruction: Anuria, renal failure.

EXAMINATION 

Murmur on the back below left scapula, descending to abdomen.

Blood pressure (BP):

 Hypertension (BP discrepancy between arms of >20 mmHg), wide pulse pressure. If hypotensive may signify tamponade, check for pulsus paradoxus.

Aortic insufficiency: 

Collapsing pulse, early diastolic murmur over aortic area.Unequal arm pulses.

There may be a palpable abdominal mass.

INVESTIGATIONS

Bloods: FBC, cross-match 10 units of blood, U&E (renal function), clotting.

CXR: Widened mediastinum, localized bulge in the aortic arch.

ECG: Often normal. Signs of left ventricular hypertrophy or inferior MI if dissection compromises the ostia of the right coronary artery.

CT-thorax: False lumen of dissection can be visualized.

Echocardiography: Transoesophageal is highly specific.

Cardiac catheterization and aortography.

MANAGEMENT

Acute: If suspected, CT-thorax should be performed urgently concurrent to resuscitation.

Resuscitate and restore blood volume with blood products. Monitor pulse and BP in both arms, central venous pressure monitoring, urinary catheter. Best managed in ITU setting.

 

Type A dissection: 

Treated surgically. Emergency surgery because of the risk of cardiac tamponade. Affected aorta is replaced by a tube graft. Aortic valve may also be replaced. 

Type B dissection:

 Can be treated medically, surgically or by endovascular stenting. Control BP and prevent further dissection with IV nitroprusside and/or IV labetalol (use calcium channel blocker if b-blocker contraindicated). Surgical repair may be appropriate for patients with intractable or recurrent pain, aortic expansion, end-organ ischemia or progression of dissection, and has similar outcome rates. Endovascular repair is a newer technique using endovascular stents and is available in some centres, although evidence of benefit is still lacking (ADSORB trial results pending). 

COMPLICATIONS

 Aortic rupture, cardiac tamponade, pulmonary oedema, MI, syncope, cerebrovascular, renal, mesenteric or spinal ischaemia. 

PROGNOSIS 

Untreated mortality: 30% at 24 h, 75% at 2 weeks. 

Operative mortality of 5–10%. A further 10% have neurological sequelae. 

Prognosis for type B better than type A.

0 تعليق

PH.Jafar Jassim 1/31/2021 12:04:00 ص

تابع القراءه

Tricuspid regurgitation 

DEFINITION 

Tricuspid regurgitation is backflow of blood from the right ventricle to the right atrium during systole.

AETIOLOGY 

Congenital: 

Ebstein anomaly (malpositioned tricuspid valve), cleft valve in ostium primum defect. 

Functional: 

Consequence of right ventricular dilation (e.g. in pulmonary hypertension), valve prolapse. 

Rheumatic heart disease: 

Associated with other valvular disease. 

Infective endocarditis: 

Common in IV drug users. Usually staphylococcal. 

Other:

 Carcinoid syndrome, trauma, cirrhosis (long-standing), iatrogenic (e.g. radiotherapy to the thorax). 

EPIDEMIOLOGY

 The epidemiology differs with various causes. Infective endocarditis probably most common cause. 

HISTORY

 Fatigue, breathlessness, palpitations, headaches, nausea, anorexia, epigastric pain made worse by exercise, jaundice, lower limb swelling. 

EXAMINATION 

Pulse: 

May be irregularly irregular due to AF (may occur with right atrial enlargement). 

Inspection: 

" JVP with giant v waves which may oscillate the earlobe. This is caused by transmission of right ventricular pressure to the great veins. There may be giant a wave, if the patient is in sinus rhythm. 

Palpation:

 Parasternal heave. 

Auscultation: 

Pansystolic murmur heard best at the lower left sternal edge, louder on inspiration (Carvallo sign). Loud P2 component of second heart sound. 

Chest:

 Pleural effusion. Causes of pulmonary hypertension (e.g. emphysema). 

Abdomen: 

Palpable liver (tender, smooth, pulsatile), ascites. 

Legs:

 Pitting oedema. 

INVESTIGATIONS 

Blood:

 FBC, LFT, cardiac enzymes, blood cultures. 

ECG: 

Tall P wave (right atrial hypertrophy) if in sinus rhythm. Changes indicative of other cardiac disease. 

CXR:

 Right-sided enlargement of cardiac shadow. 

Echocardiography: 

Extent of regurgitation estimated by colour flow Doppler. May be able to detect tricuspid valve abnormality (e.g. prolapse), right ventricular dilation. 

Right heart catheterization:

 Rarely necessary but may be considered to assess pulmonary 

artery pressure. 

MANAGEMENT 

Medical: 

Treat the underlying condition, e.g. infective endocarditis or functional regurgitation caused by pulmonary hypertension. Diuretics may be given for fluid retention. 

Surgery: 

Annuloplasty, plication or, rarely, replacement. Repair of the valve only in very severe tricuspid regurgitation, when the required doses of diuretics are large enough to cause metabolic consequences. Surgical removal of the valve may be required to eradicate 

the source of infection in IV drug users with infective endocarditis. 

COMPLICATIONS 

Heart failure, hepatic fibrosis. 

PROGNOSIS

 Prognosis varies depending on the underlying cause.

0 تعليق

PH.Jafar Jassim 1/30/2021 11:46:00 م

تابع القراءه

Pulmonary hypertension 

DEFINITION 

A consistently increased pulmonary arterial pressure (>20 mmHg) under resting conditions. 

AETIOLOGY 

Primary:

 Idiopathic. 

Secondary: 

Left heart disease (mitral valve disease, left ventricular failure, left atrial myxoma/ thrombosis), chronic lung disease (COPD), recurrent pulmonary emboli, " pulmonary blood flow (ASD, VSD, patent ductus arteriosus), connective tissue disease (e.g. SLE, systemic sclerosis), drugs (e.g. amiodarone). 

EPIDEMIOLOGY

 Primary pulmonary hypertension is usually seen in young females. 

HISTORY Dyspnoea (on exertion), chest pain, syncope, tiredness. 

Symptoms of the underlying cause (e.g. chronic cough). 

EXAMINATION 

Elevated JVP (Prominent a wave in the JVP waveform). 

Palpation:

 Left parasternal heave (right ventricular hypertrophy). 

Auscultation: 

Loud pulmonary component of S2 (S3/S4 may be heard), an early diastolic murmur (Graham–Steell murmur) caused by pulmonary regurgitation may be present, if tricuspid regurgitation develops (large cv wave and pansystolic murmur). 

Signs of the underlying condition, or right heart failure in severe cases. 

INVESTIGATIONS 

CXR: 

Cardiomegaly (right ventricular enlargement, right atrial dilation), prominent main pulmonary arteries (which taper rapidly), signs of the cause (e.g. COPD, calcified mitral valves). 

ECG:

 Right ventricular hypertrophy (right-axis deviation, prominent R wave in V1, T inversion in V1, V2), right atrial enlargement (peaked P wave in II, called ‘P pulmonale’); limb leads exhibit low voltage (R < 5 mm) in COPD. 

Echocardiography: 

To visualize right ventricular hypertrophy or dilation and possible 

underlying cause. 

Lung function tests: 

To assess for chronic lung disease. 

VQ scan: 

To assess for pulmonary embolism. 

Cardiac catheterization: 

To assess severity, right heart pressures and response to vasodilators. 

High resolution

 CT-thorax: 

Images pulmonary arteries and to diagnose lung disease. 

Lung biopsy: 

Assesses structural lung changes. 

MANAGEMENT 

Medical: 

Treat secondary cause. For primary pulmonary hypertension, consider: 

• . anticoagulation (warfarin); 
• .calcium channel antagonists (e.g. verapamil, nifedipine); 
• . prostacycline analogues (e.g. iloprost); 
• . endothelial receptor antagonist (bosentan) blocks vasoconstriction, but teratogenic, so only indicated in NYHA III or IV patients; 
• . phosphodiesterase inhibitor (e.g. sildenafil) promotes pulmonary smooth muscle relax￾ation reducing pulmonary hypertension. 

Surgical: 

Heart and lung transplantation may be an option for younger patients. 

COMPLICATIONS 

Right heart failure, arrhythmias (AF, VT, VF), sudden death. 

PROGNOSIS 

Chronic and incurable with unpredictable survival rate. Length of survival has improved to up to 15–20 years.

0 تعليق

PH.Jafar Jassim 1/30/2021 11:43:00 م

تابع القراءه

Pericarditis 

DEFINITION 

Inflammation of the pericardium, may be acute, subacute or chronic. 

AETIOLOGY 

• . Idiopathic; 
• . infective (commonly, coxsackie B, echovirus, mumps virus, streptococci, fungi, staphy￾lococci, TB); 
• . connective tissue disease (e.g. sarcoid, SLE, scleroderma); 
• . post-myocardial infarction (24–72 h) in up to 20% of patients; 
• . Dresslers syndrome (weeks to months after acute MI); 
• . malignancy (lung, breast, lymphoma, leukaemia, melanoma); 
• . mtabolic (myxoedema, uraemia); 
• . radiotherapy; 
• . thoracic surgery; 
• . drugs (e.g. hydralazine, isoniazid). 

EPIDEMIOLOGY 

Uncommon. The clinical incidence is <1 in 100 hospital admissions. More common in males. 

HISTORY 

Chest pain:

 Sharp and central, which may radiate to neck or shoulders. Aggravated by coughing, deep inspiration and lying flat. Relieved by sitting forward. 

Dyspnoea, nausea. 

EXAMINATION 

Fever, pericardial friction rub (best heard lower left sternal edge, with patient leaning forward in expiration), heart sounds may be faint in the presence of an effusion. 

Cardiac tamponade:

 " JVP, # BP and muffled heart sounds (Beck s triad). Tachycardia, pulsus paradoxus (reduced systolic BP by >10 mmHg on inspiration). 

Constrictive pericarditis (chronic): 

" JVP with inspiration (Kussmauls sign), pulsus para￾doxus, hepatomegaly, ascites, oedema, pericardial knock (rapid ventricular filling), AF. 

INVESTIGATIONS 

ECG: 

Widespread ST elevation that is saddle-shaped. 

Echocardiogram:

 For assessment of pericardial effusion and cardiac function. 

Blood:

 FBC, U&E, ESR, CRP, cardiac enzymes (usually normal). Where appropriate: blood cultures, ASO titres, ANA, rheumatoid factor, TFT, Mantoux test, viral serology. 

CXR: 

Usually normal (globular heart shadow if >250 mL effusion). Pericardial calcification can be seen in constrictive pericarditis (best seen on lateral CXR or CT). 

MANAGEMENT 

Acute: 

Cardiac tamponade treated by emergency pericardiocentesis. 

Medical: 

Treat the underlying cause, NSAIDs for relief of pain and fever. 

Recurrent:

 Low-dose steroids, immunosuppressants or colchicine. 

Surgical:

 Surgical excision of the pericardium (pericardiectomy) in constrictive pericarditis. 

COMPLICATIONS 

Pericardial effusion, cardiac tamponade, cardiac arrythmias. 

PROGNOSIS

 Depends on underlying cause. Good prognosis in viral cases (recovery within 2 weeks), poor in malignant pericarditis. Pericarditis may be recurrent (particularly in those 

caused by thoracic surgery).

0 تعليق

PH.Jafar Jassim 1/30/2021 11:40:00 م

تابع القراءه

Myocarditis 

DEFINITION 

Acute inflammation and necrosis of cardiac muscle (myocardium). 

AETIOLOGY 

Usually unknown (idiopathic). 

Infection: 

Viruses: e.g. Coxsackie B, echovirus, EBV, CMV, adenovirus, influenza. 

Bacterial: e.g. post-streptococcal, tuberculosis, diphtheria, Lyme disease. 

Fungal: e.g. candidiasis. 

Protozoal: e.g. trypanosomiasis (Chagas disease). 

Helminths: e.g. trichinosis. 

Non-infective: 

Systemic disorders (e.g. SLE, sarcoidosis, polymyositis), hypersensitivity myocarditis (e.g. sulphonamides). 

Drugs:

 Chemotherapy agents (e.g. doxorubicin, streptomycin) 

Others: 

Cocaine abuse, heavy metals, radiation. 

EPIDEMIOLOGY 

True incidence is unknown, as many cases are not detected at the time of acute illness. Coxsackie B virus is a common cause in Europe and the USA. Chagas disease is a common cause in South America. 

HISTORY 

Prodromal ‘flu-like’ illness, fever, malaise, fatigue, lethargy. 

Breathlessness (pericardial effusion/myocardial dysfunction). 

Palpitations. 

Sharp chest pain (suggesting associated pericarditis). 

EXAMINATION

 Signs of concurrent pericarditis or complications: heart failure, 

arrhythmia. 

INVESTIGATIONS 

Blood:

 FBC (" WCC in infective causes), U&E, " ESR or CRP, cardiac enzymes (may be "). To identify the cause (viral or bacterial serology, antistreptolysin O titre, ANA, serum ACE, TFT). 

ECG: 

Non-specific T wave and ST changes, widespread saddle-shaped ST elevation in pericarditis. 

CXR:

 May be normal or show cardiomegaly with or without pulmonary oedema. 

Pericardial fluid drainage: 

Measure glucose, protein, cytology, culture and sensitivity. 

Echocardiography: 

Assesses systolic/diastolic function, wall motion abnormalities, pericardial effusion. 

Myocardial biopsy:

 Rarely required (result does not influence management). 

MANAGEMENT 

Supportive:

 Bed rest, treatment of complications (heart failure, arrhythmias), pericardial drainage for compromising pericardial effusion. 

Steroids and immunosuppressants have been used in severe cases but are of unproven benefit. 

Surgical: 

Cardiac transplantation for severe cases. 

COMPLICATIONS 

Severe cases can lead to chronic inflammation, cardiac failure. Resolution of inflammation with different degrees of residual dilated cardiomyopathy, arrhythmias and death. 

PROGNOSIS 

Usually mild and self-limiting. Recovery is variable in patients with severe acute myocarditis.

0 تعليق

PH.Jafar Jassim 1/30/2021 11:38:00 م

تابع القراءه

 Mitral stenosis

DEFINITION

 Mitral valve narrowing causing obstruction to blood flow from the left atrium to the ventricle.

AETIOLOGY

 Most common cause is rheumatic heart disease (90%).

Rarer causes are congenital mitral stenosis, SLE, rheumatoid arthritis, endocarditis and atrial myxoma (rare cardiac tumour).

EPIDEMIOLOGY 

Incidence is declining in industrialized countries because of declining incidence of rheumatic fever.

HISTORY

 May be asymptomatic.

Presents with fatigue, shortness of breath on exertion or lying down (orthopnoea). Palpitations (related to AF).

Rare symptoms: Cough, haemoptysis, hoarseness caused by compression of the left laryngeal nerve by an enlarged left atrium.

EXAMINATION

 May have peripheral or facial cyanosis (malar flush).

Pulse: 

May be ‘thready’ or irregularly irregular (AF).

Palpation: 

Apex beat is undisplaced and tapping. Parasternal heave (right ventricular hypertrophy and pulmonary hypertension)

Auscultation:

 Loud first heart sound with opening snap.

Mid-diastolic murmur (presystolic accentuation if in sinus rhythm).

Evidence of pulmonary oedema on lung auscultation (if decompensated).

INVESTIGATIONS

ECG: 

May be normal, broad bifid p wave (p mitrale) caused by left atrial hypertrophy, AF or evidence of right ventricular hypertrophy in cases of severe pulmonary hypertension.

CXR:

 Left atrial enlargement, cardiac enlargement, pulmonary congestion; mitral valve may be calcified in rheumatic cases.

Echocardiography: 

To assess functional and structural impairments. Transoesophageal

gives better valve visualization.

Cardiac catheterization: 

Measures severity of heart failure.

MANAGEMENT

Medical: 

Anticoagulation for AF. Treat dyspnoea and heart failure with diuretics. Antibiotic cover for dental/invasive procedures. Cardioversion of AF may be considered.

Surgical:

 Mitral valvuloplasty, valvotomy or replacement if severe.

COMPLICATIONS 

AF and systemic embolism, pulmonary oedema, pulmonary hypertension and right heart failure, infective endocarditis.

PROGNOSIS

 Significantly worse if pulmonary hypertension or right heart failure develops.

0 تعليق

PH.Jafar Jassim 1/30/2021 11:34:00 م

تابع القراءه

 Hypertension 

DEFINITION 

Defined as systolic BP >140 mmHg and/or diastolic BP >85 mmHg measured on three separate occasions. Malignant hypertension is defined as BP  200/ 130 mmHg. 

AETIOLOGY 

Primary: 

. Essential or idiopathic hypertension (Commonest, >90% of cases). 

Secondary: 

• . Renal: Renal artery stenosis, chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney disease, chronic renal failure. 
• . Endocrine: Diabetes mellitus, hyperthyroidism, Cushings syndrome, Conns syndrome, hyperparathyroidism, phaeochromocytoma, congenital adrenal hyperplasia, acromegaly. 
• . Cardiovascular: Aortic coarctation, " intravascular volume. 
• . Drugs: Sympathomimetics, corticosteroids, oral contraceptive pill. 
• . Pregnancy: Pre-eclampsia. 

EPIDEMIOLOGY 

Very common. 10–20% of adults in the Western world. 

HISTORY 

Often asymptomatic. 

Symptoms of complications (see Complications). 

Symptoms of the cause. 

Accelerated or malignant hypertension: Scotomas (visual field loss), blurred vision, headache, seizures, nausea, vomiting, acute heart failure. 

EXAMINATION

 Measure on two to three different occasions before diagnosing hypertension and record lowest reading. 

There may be loud second heart sound, fourth heart sound. 

Examine for causes, e.g. radiofemoral delay (aortic coarctation), renal artery bruit (renal artery stenosis). Examine for end-organ damage, e.g. fundoscopy for retinopathy. 

Keith–Wagner classification of retinopathy: 

(I) ‘silver wiring’; 

(II) as above, plus arteriovenous nipping; 

(III) as above, plus flame haemorrhages and cotton wool exudates; 

(IV) as above, plus papilloedema. 

PATHOLOGY/PATHOGENESIS 

Fibrotic intimal thickening of the arteries, reduplication 

of elastic lamina and smooth muscle hypertrophy. Arteriolar wall layers replaced by pink hyaline material with luminal narrowing (hyaline arteriosclerosis). 

INVESTIGATIONS 

Blood: 

U&E, glucose, lipids. 

Urine dipstick: 

Blood and protein. 

ECG:

 May show signs of left ventricular hypertrophy (deep S wave in V1–2, tall R wave in V5–6, inverted T waves in I, aVL, V5–6, left-axis deviation) or ischaemia. 

Ambulatory BP monitoring (BP measured throughout the day): 

Excludes ‘white coat’ hypertension, allows monitoring of treatment response, assesses preservation of nocturnal dip. 

Others:

 Especially in patients <35 years or other suspected secondary cases (see relevant topics). 

MANAGEMENT 

Assessment and modification of other cardiovascular risk factors. 

Conservative: 

Stop smoking, ↓alcohol ,lose weight,  reduce dietary Na + .

Investigate for secondary causes: 

Worthwhile in young patients, malignant hypertension or poor response to treatment. 

Medical  : 

Treatment recommended for systolic BP   160 mmHg and/or diastolic BP   100 mmHg, or if evidence of end-organ damage. Other hypertension patients may still require treatment depending on other cardiac risk factors. Multiple drug therapies often necessary. 

. Thiazide diuretics (e.g. bendrofluamethiazide): Recommended first line, especially in >55- year-olds or black patients. 

. ACE inhibitors (e.g. ramipril) or angiotensin-II antagonist (e.g. losartan): First line in <55- year-olds, diabetic patients, heart failure or left ventricular dysfunction. 

. Ca2 þ channel antagonists (e.g. amlodipine): Recommended first line, especially in >60- year-olds or black patients. 

. b-Blockers (e.g. atenolol): Not preferred initial therapy, but may be considered in younger patients. Avoid combining with thiazide diuretic to reduce patient risk of developing diabetes. May increase risk of heart failure. 

. a-Blockers (e.g. doxazosin): Fourth-line agent. May be useful for patients with prostatism. 

Target BP: 

• .  140/85 mmHg (non-diabetic); 
• . 130/80 mmHg (diabetes without proteinuria); 
• .  125/75 mmHg (diabetes with proteinuria). 

Severe hypertension (diastolic BP > 140 mmHg): 

Atenolol or nifedipine. 

Acute malignant hypertension:

 IV b-blocker, labetolol or hydralazine sodium nitroprusside. Avoid very rapid lowering which can cause cerebral infarction. 

COMPLICATIONS

 Heart failure, coronary artery disease and MI, CVA, peripheral vascular disease, emboli, retinopathy, renal failure, hypertensive encephalopathy, posterior reversible encephalopathy syndrome (PRES), malignant hypertension. 

PROGNOSIS 

Good, if BP controlled. Uncontrolled hypertension linked with increased mortality (6 stroke risk and 3 cardiac death risk). Treatment reduces incidence of renal damage, stroke and heart failure.

0 تعليق

PH.Jafar Jassim 12/24/2020 01:08:00 ص

تابع القراءه

يجب أن يتمتع بالثقافة الطبية حتى وإن لم يكن يكن طبيباً  ، والتي تعتبر الثقافة والمعرفة تعتبر عصباً لحياة الإنسان ، وصحة المجتمع الذي يعيش فيه ، وفي هذا المقال سوف تتذكر مجموعة معلومات عامة تختص في مجال الطب.

 من أهمّ الغدد في جسم الإنسان: الغدة الجنبدرقية ، والنخامية ، والدرقية ، والجنسية ، والمعدة ، والكظرية ، والعرقية ، والبنكرياس ، 

واللعابية. 

ينقل القمل للإنسان مرض اسمه التيفوس. 

الغدد الليمفاوية تعمل على تصفية الدم وتطهيره. يطلق عملية غسيل الكلى. 

يعدّ الكبد العضو الوحيد في جسم الإنسان الذي يعود للنمو بعد اقتطاع جزء منه. 

في العام 1989 م تمتت عملية زراعة الكبد في شيكاغو الأمريكية. 

مرض انفصام الشخصية اسمه مرض الشيزوفرينيا. فصيلة الدم

 o + تسمّى باسم فصيلة الدم الكريمة. 

تعرف الذبحة الصدرية بأنّها عبارة عن ألم حاد وقصير الوقت يحدث في الصدر وذلك بسبب إصابة الشريان التاجي. 

فيتامين الوحيد الذي يكسبه الجسم من أشعة الشمس هو فيتامين د. 

يبلغ وزن مخضر الإنسان البالغ من 3 إلى 2 كغم. 

الغدة التي تصبّ جميع محتوياتها بشكل مباشر في الدم هي الغدد الصماء. 

يؤدي نقص فيتامين أ للإصابة بمرض العشى الليليّ. 

من أعراض مرض البلاجرا: الغثيان ، والاكتئاب ، والصداع ، والإسهال ، والتهاب الجلد. 

يعتبر الطبيب العربي مجدي يعقوب من أشهر جراحي القلب على مستوى العالم ، وفردريك بانتينج مكتشف الإنسولين ، والطبيب العربي ابن زهر مكتشف جرثومة الجرب ، وسالك مكتشف مصل شلل الأطفال. يقصد بمرض السرطان الانقسام غير العادي لخلايا الجسم دون توقّف. 

وظيفة كريات الدم البيضاء هي الدفاع عن الجسم ضد الأمراض والجراثيم. 

تقع الغدة الدرقية في الرقبة. 

مادة الميلانين هي المسؤولة عن تلوين جسم الإنسان. 

تعدّ العضلات أثقل من العظام. 

يبلغ عدد فقرات العمود الفقري ثلاثاً وثلاثين فقرة. 

يعتبر مخ ّالمرأة أقل وزناً من مخّ الرجل. يبلغ عدد عظام الجمجمة اثنتين وعشرين عظمة. 

يبلغ حجم الهواء الذي يستنشقه الإنسان في كل عام خمسة ملايين لتر.

يبلغ عدد ضربات قلب الحوت ضربة واحدة في الدقيقة الواحدة. 

يبلغ عدد خلايا الجسم في الإنسان ستين ترليون خلية. 

يبلغ عدد الخلايا العصبية الذي يملكها الإنسان ثمانية وعشرين بليون خلية. 

المسؤول عن التذوق هي الحليمات الذوقية في اللسان. 

تعتبر عضلة الفخذ أكبر عضلة في الجسم ، وعضلة الركاب في الأذن الوسطى أصغر عضلة ، وعضلة الفكين أقوى عضلة. 

ضم المعدة تتكون من المخاط ، ولو لم تكن كذلك له ضمت نفسها .

1 تعليق

PH.Jafar Jassim 7/29/2020 12:19:00 ص

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