Cholesterol level

CHOLESTEROL

Your liver produces approximately 1,000 milligrams of cholesterol each day. This waxy substance helps your body produce hormones and vitamins and assists in the digestion of fats. You add cholesterol to your system by eating it in the form of animal fats such as egg yolks, milk, meat and cheese. Too much cholesterol from animal sources puts you at risk of serious health problems such as heart attack and stroke, according to the American Heart Association. When your doctor tests your total cholesterol, HDL and LDL, and triglyceride levels, the results are expressed as milligrams per deciliter, commonly written as mg/dL.

Total Cholesterol Level	Category
Less than 200 mg/dL	Desirable
200-239 mg/dL	Borderline High
240 mg/dL and above	High

HDL

High-density lipoproteins, or HDLs, bind with cholesterol to move it out of the blood and into the liver. The cholesterol is then processed by the liver and removed from the body. The American Heart Association says you should have an HDL level of 50 mg/dL or higher if you are an adult male and 60 mg/dL or higher if you are an adult female. If your HDL numbers are below these levels, the cholesterol in your bloodstream will be trapped and could lead to narrowed and clogged arteries.

LDL

Low-density lipoproteins, or LDLs, bind to cholesterol and deliver it to the arteries. If your LDL levels are too high, cholesterol becomes wedged in the artery walls and turns into plaque. This plaque can increase until the artery is blocked or can break free as a clot. When a clot moves toward the heart or brain, you can experience heart attack or stroke. Your LDL levels should be under 130 mg/dL, according to the American Heart Association.

TRIGLYCERIDES

Blood fats are called triglycerides. They are manufactured by the body when there is an excess of carbohydrates in the bloodstream. These fats float around in your blood, making it thick. Eventually, your blood cannot flow easily and arteries and veins can become thick and narrow. Your triglyceride levels should be under 150 mg/dL, according to the American Heart Association.

Cardiovascular diseases-Heart Failure-VI

• Heart is not able to maintain the cardiac output to meet the need of the body tissues or it can do it only at an elevated filling pressure or elevated force of contraction.
• Normal cardiac output depends on preload,afterload and Myocardial contractility.
• Increase in preload and afterload causes left ventricular hypertrophy.It also increases myocardial work.(Starling's law and law of laplace).
• First activation of Renin angiotensin system and sympathetic nervous system,try to compensate cardiac compensation by altering the afterload,preload and myocardial contractility but latter on they become counterproductive and reduce cardiac output by causing increase in peripheral resistance,which further stimulates renin angiotensin system.Angiotensin causes release of aldosterone  that leads to retention of salt and water that causes increase in preload.
• Signs & Symptoms-

1. Dyspnoea
2. Orthopnoea
3. Cheyne-stokes respiration
4. Vomitting
5. Perspiration
6. Nausea
7. Cough 
8. Tachycardia
9. Cold extremities
10. Low B.P
11. Right heart failure leads to Peripheral edema,ascites,Hepatomegaly
12. Left heart failure leads to Pulmonary edema

• Investigations-

1. ECG-St segment elevation with q wave deepening and t wave inversion.
2. X ray shows cardiomegaly
3. Rise in enzyme levels of CK,AST and LDH

• Drug regime-Oxygen therapy,Ace inhibitors/angiotensin antagonist,Diuretics(furosemide),salt restriction,Aspirin and clopodegrel,Beta blockers(only in after correction of heart failure)
• Initially cardiac glycosides were used like digitalis but they were found to be toxic and after the discovery of Ace inhibitors and high ceiling diuretics,the use of digitalis is avoided and mild to moderate cases of heart failure are treated by using Ace inhibitors and diuretics.

Cardiovascular diseases-Myocardial infarction-IV

Myocardial Infarction-

• Untreated angina leads to myocardial infacrtion.
• Many early deaths are due to ventricular fibrillation or cardiac arrest.
• C/f-Pain,Dyspnoea,Vomiting,Nausea,perspiration.
• Nausea and vomitting during the attack can be due to sympathetic stimulation.
• Tachycardia(due to sympathetic stimulation),Cold extremities,Hypotension.
• Investigations-

1. ECG- In initial hours there is ST segment elevation and latter followed by deepening of Q wave followed by T wave inversion.
2. Changes in plasma enzyme levels of Creatinine kinase(CK),Aspartate dehydrogenase(ADH),Lactic acid dehydrogenase.CK starts appearing into blood after 4-6 hrs of infarction and reaches its peak after 12 hours of infarction and Vanishes after 2-3 days of infarction.LDH start to appear after 12 hours of attack and reach its maximum after 2-3 days of attack.
3. X ray-cardiomegaly with pulmonary congestion
4. Echocardiography
5. Drug regime-Oxygen therapy,I.V Morphine(10mg),Streptokinase/Alteplase, Anti platelet drugs(aspirin and clopodigrel),Beta Blockers,TNG

Regular drug regime includes Aspirin/clopodigrel or combination,ACE inhibitors,Beta blockers.

Cardiovascular diseases-angina-III

Angina-

• Episodic chest pain resulting from transient myocardial ischemia.
• It occurs due to an imbalance between myocardial oxygen demand and supply.
• Atherosclerosis in the coronary arteries is the most common cause.
• Attacks get provoked by exercise,emotional disturbances,heavy meals.
• Pathology-Due to atherosclerotic plug in coronay arteries the blood supply to sub endocardial region gets affected and as the blood starts filling the ventricles the sub endocardial crunch develops during the diastole and pain is felt.
• All drugs administered reduces the cardiac workload.
• Signs and symptoms-Pain in chest radiating to the neck and left arm
• Stable angina-Attack happens Occasionally on exertion and get relieved by rest.
• Unstable angina-Attacks that become quite frequent or attacks which don't get resolved by rest.
• Prinzmetal's angina-Angina happening due to spasm in coronary vessels.Attacks happen during sleeping and even at rest.
• Angina can further lead to Myocardial infarction and Heart failure
• ECG changes-Angina shows ST segment depression and T wave inversion.
• Drug regime-Trinitrogylcerin,Aspirin,clopodegrel,Beta blockers,Calcium channel blockers.
• TNG,Aspirin,Beta blockers form the main stay of drug regime.
• TNG(0.5mg) placed under the tongue and is crushed by teeth will relieve anginal attack with in 2-3 min and effect will remain for 10-30 min.Sub lingual Aerosol sprays are also available that don't get detoriated.
• TNG detoriate on exposure so it should be replaced after  about 8 weeks of opening the bottle.It should produce headache(side effect) ,if it doesn't than it means that TNG has been detoriated and should be replaced.

CARDIOVASCULAR-HYPERTENSION-II

• There is no definite dividing line between normal and high blood pressure, arbitrary values have been established to define hypertension.
• According to JNC VII classification Normal B.P < 120/80 mm of Hg.
• Hypertension stage I-systolic B.P. 140-159 mm of Hg ; Diastolic B.P. 90-99 mm of Hg  Stage II-systolic B.P. > 160 mm of Hg ; Diastolic B.P.>100
• Those lying between 120/80 - 139/89 mm of Hg are in prehypertensive condition.
• Those with B.P 200/140 mm of Hg are called as malignant hypertensives.
• WHO has used 160/95 mm Hg as upper limit of normal.
• Normal B.P. value also depend on the age of patient. 

• Type of Hypertension-Primary and secondary
• Primary-Essential
• Secondary-Renal diseases;Cushing syndrome;Conn's syndrome;Phaeochromocytoma;Hyperparathyrodism;Myxodema(hypothyroidism)
• Precipitating factors for Essential hypertension-

1. Age
2. Sex(males>females)
3. Smoking
4. Alcoholism
5. Diabetes
6. Obesity
7. Anxiety
8. High table salt intake

• Drugs used-

1. ACE inhibitors
2. Angiotensin antagonist
3. Beta blockers
4. Diuretics
5. CCB

• Cardiovascular risk factors-Age>60 yr;Family history;Smoking;Alcoholic;Dyslipidemia(LDL high HDL low);Diabetes mellitus;Hypertension
• When risk is assessed as low or medium,first try to decrease B.p by using non pharmacological methods and keep monitoring the B.P. for 3 to 6 months.
• Drugs should be started when B.P continues to remain above 140/90 mm of Hg.
• Except for grade III B.P (180/110),start with drug mono therapy.
• Initiate therapy at low dose.Increase the dose gradually
• If response is not desirable than add a drug from another group.
• One ingredient of the drug should be thiazide.
• Diuretics,ACE inhibitors,CCB all increases plasma renin activity and beta blockers reduce plasma renin.
• ACE inhibitors are the most appropriate anti hypertensives to be used in patients with Diabetes,nephropathy,CHF,LVF.They are though contraindicated in bilateral renal artery stenosis,pregnancy and hyperkalemia.
• Beta blockers-They are mild anti hypertensives.Indicated in Angina or post MI cases,high renin cases  and pregnancy induced hypertension.They are avoided in CHF,LVF,Asthmatics,conduction defects,Diabetes.
• Calcium channel Blockers-They are to be used in cases of asthma,low renin hypertension,pregnancy induced hypertension.Should be avoided in cases of conduction defects,CHF,LVF,Post MI cases.
• Diuretics-They are to be used in low renin hypertension,Renal diseases,CHF,LVF,angina,post MI hypertension.To be avoided in pregnancy,hypokalemia(not with potassium sparing diuretics),Diabetes.
• Nifedipine decreases insulin release but this is not seen with other long acting DHP's so they can be safely used in diabetics.
• Potassium is must for insulin action.Diuretics for that reason should be avoided in diabetics but can be given with potassium sparing diuretics.
• Furosemide is a weaker anti hypetensive than thiazides.They are to be given only when there is a chronic renal failure,CHF or resistance to thiazide.
• Diuretics potentiate all other anti hypertensive action.They are synergistic to ACE inhibitors. 
• Alpha blockers(parazosin,terazosin) are found to be more effective in reducing B.P than Beta blockers.They are anticholinergic,and can be administered safely in diabetics.
• ACE+Diuretics/Angiotensin antagonist+Diuretics are mostly used drug regime used regularly.

CARDIOVASCULAR-I

• Various drugs used to in cardiovascular diseases are-

1. ACE inhibitors
2. Angiotensin antagonist
3. Diuretics
4. Beta Blockers
5. Calcium channel blockers
6. Cardiac Glycosides
7. Trinitroglycerine
8. Others

• Various cardiovascular diseases-

1. Hypertension
2. Angina (stable,unstable,prinzmetal's angina)
3. Infarction
4. Heart failure(CHF,LVF) 

• La place Law- Ventricular wall tension=Ventricular pressure*Ventricular radius
• Starling's Law-Force of contraction of muscle is directly proportionality to the length of fiber before the onset of contraction.
• Cardiac Output is directly proportional to H.R,Venous return,Force of contraction and is inversely proportional to T.P.R
• Whenever Volume overload increases(Increased blood volume) or T.P.R increases,hypertrophy and remodeling in heart and blood vessels occur.This leads to Ventricular Hypertrophy and thickening of ventricular walls.As this happens,according to La place rule,wall tension increases,leading to reduce heart functioning.
• ACE inhibitors- Reduces T.P.R;Reduces Heart rate;Increases Cardiac output;Increases renin level and decreased aldosterone and ADH secretion;Increased loss of sodium and water(due to better renal perfusion),left ventricular remodelling.Side effects-Cough (bradykinin release),Fetopathic,First Dose hypotension,Hyperkalemia.
• Angiotensin antagonist-More potent with less side effects than ACE inhibitors.
• Beta Blockers-Decreases heart rate;force of contraction and Cardiac output;T.P.R initially increases(Alpha mediated vasoconstriction) but latter on T.P.R decreases(Due to reduced C.O);Decreases renin release.Effective as mild anti hypertensive,angina pectoris and after correction of MI to increase the life expectancy and prognosis.Cardioselective drugs(Beta 1 blockers) are more useful for treating angina.
• Calcium Channel Blockers-Various CCB available are as-VERAPAMIL,DILTIAZEM,NIFEDIPINE

VERAMPIL-Dilate arterioles and block alpha blockers-reduce T.P.R;Reduces heart rate(by reducing SA node and AV node conduction);Reduces myocardial contractility;Cardiac output remains normal by reflex sympathetic stimulation;Increases coronary blood flow.Should not be given along with the Beta blockers.

NIFEDIPINE-Dilate arterioles-Reduces T.P.R;Much higher sympathetic stimulation;less SA and AV node conduction reduction;H.R,contractility and C.O. increases due to sympathetic stimulation;Increases coronary blood flow.

DILTIAZEM-Less potent vasodilator;SA AND AV node depression;Modest negative inotropic effect.

• Diuretics-Increases loss of water,Sodium and potassium loss-Reduces preload(decreased blood volume),C.O and T.P.R(by loss of sodium).They potentate action of other antihypertensive drugs.

Various types of diuretics are- FUROSEMIDE,THIAZIDES,ACETAZOLAMIDE,Potassium sparing diuretics-SPIRINOLACTONE
FUROSEMIDE-They are very potent diuretics and act on the ascending loop of henle.They also account for the loss of sodium,calcium,potassium,magnesium.High ceiling diuretics are given only in -Renal faliure/insufficiency,CHF,hypertensive emergency otherwise thiazides are used.
THIAZIDES-Act on PCT and DCT.Avoid absorption of sodium.
ACETAZOLAMIDE-Acts on PCT and DCT,avoid absorption of sodium bicarbonate.Weak Diuretic
Potassium sparing Diuretics-They inhibit aldosterone sensitive Na/K exchange in collecting tubules.
Furosemide and thiazides causes hypokalemia and alkalosis whereas spirinolactone can lead to hyperkalemia and acidosis.

• Cardiac Glycosides-Eg.Digitalis.There main action is to reduce the heart rate and increasing the force of contraction there by increasing the cardiac output,keeping the demand of oxygen same.Adrenaline do the same but it increases the demand of oxygen too.Now a days its not used due to its high toxicity.
• Trinitroglycerine-They are the drugs that causes vasodilatation in the peripheral vessels,decreases venous return and thereby reducing the preload,They also reduce the oxygen demand and the force of contarction;TNG also reduces afterload by reducing the T.P.R;They also causes redistribution of coronary blood,thereby increasing blood to ischaemic area of heart.

The dilator effect on large coronary vessels is the main action of TNG,which is used in treating angina and ischemia.

• Other drugs-

ASPIRIN,CLOPIDOGREL,DIPYRIDAMOLE- Anti platelet drugs
STREPTOKINASE,ALTEPLASE-For thrombolysis

MORPHINE-For Analgesia

DIAZEPAM-Sedatives

Hypothalmus and Pitutary Gland

The hypothalamus is a region of the brain that controls an immense number of bodily functions. It is located in the middle of the base of the brain, and encapsulates the ventral portion of the third ventricle.

The pituitary gland, also known as the hypophysis, is a roundish organ that lies immediately beneath the hypothalamus, resting in a depression of the base of the skull called the sella turcica ("Turkish saddle") Careful examination of the pituitary gland reveals that it composed of two distinctive parts: The anterior pituitary or adenohypophysis is a classical gland composed predominantly of cells that secrete protein hormones. The posterior pituitary or neurohypophysis is not a separate organ, but an extension of the hypothalamus. It is composed largely of the axons of hypothalamic neurons which extend downward as a large bundle behind the anterior pituitary. It also forms the so-called pituitary stalk, which appears to suspend the anterior gland from the hypothalamus.

 Secretion of hormones from the anterior pituitary is under strict control by hypothalamic hormones.A key to understanding the endocrine relationship between hypothalamus and anterior pituitary is to appreciate the vascular connections between these organs.