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PHARMACOLOGY 2


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[Front]


maintain homeostasis depending on the continuous & controlled movement of blood thru capillaries Consists: Heart & Blood vessels (AVC)
[Back]


CVS – aka blood-vascular, circulatory system

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PHARMACOLOGY 2 - Marcador

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PHARMACOLOGY 2 - Detalles

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Blood Circulation IN ORDER
1 S / I vena cava 2 Right atrium 3 Tricuspid valve 4 Right ventricle 5 Pulmonary artery 6 Lungs 7 Left atrium 8 Mitral valve 9 Left ventricle 10 Aorta 11 Distribute to tissues
Impulse of the Heart (In order)
1 Sinoatrial Node 2 Atrio-ventricular Node 3 Atrio-ventricular Bundle 4 Ventricles
1 Chronotrophic effect 2 Volume of blood ejected by the heart per beat 3 Inotropic Effect
1 Tachycardia (fast heart rate) 2 Stroke volume 3 Increased force of contraction
Normal
Less than 120/80 mmHg
Elevated
120-129/80 and below
Stage I
130-139/80-89 mmHg
Stage II
Above 140 /90mmHg
Primary Prevention (Hypertension) First Line:
Thiazide diuretic, ACE Inhibitors or ARB or combo
Diabetes Mellitus First Line: Sequential Therapy:
First Line: ACE Inhibitors (Angiotensin-converting enzyme inhibitors) Sequential Therapy: Thiazide, CCB or Beta blocker
Chronic Kidney Disease First Line:
ACE Inhibitors (Angiotensin-converting enzyme inhibitors)
Coronary Artery Disease First Line: Sequential Therapy:
First Line: ACE Inhibitors (Angiotensin-converting enzyme inhibitors) or ARB or B-blockers Sequential Therapy: Thiazide (BP CONTROL) CCB or Beta blocker (ISCHEMIA CONTROL)
Prior Ischemic Stroke First Line:
ACE Inhibitors (Angiotensin-converting enzyme inhibitors) and Thiazide
Left Ventricular Dysfunction First Line: Sequential Therapy:
First Line: ACE Inhibitors (Angiotensin-converting enzyme inhibitors), Thiazide and B-blockers Sequential Therapy: 1 Aldosterone Antagonist (SEVERE HEART FAILURE) 2 Hydralazine & Isosorbide
Traditionally, the first choice for the initial treatment of chronic hypertension.
Thiazide-type diuretic or a ß-adrenergic receptor blocker
Principal function of Loop of Henle
The recovery of water and sodium chloride from urine.
Adverse effects of BB
1 Common effects: bradycardia, hypotension, and CNS side effects such as fatigue, lethargy, and insomnia βB may decrease libido and cause erectile dysfunction, which can severely reduce patient compliance. 2 Alterations in serum lipid patterns 3 Drug withdrawal: Abrupt withdrawal may induce ANGINA, MI, and even sudden death in patients with ischemic heart disease.
While on ACE Inhibitors, we should monitor __
1 Potassium Levels K supplements and K-sparing diuretics should be used with caution due to the risk of hyperkalemia. 2 Serum Creatinine Levels particularly in patients with underlying renal disease.
Are alternatives to the ACE inhibitors.
Losartan and irbesartan (ANGIOTENSIN II RECEPTOR BLOCKERS(ARBs))
Adverse effects of ARBs
1 Do no increase BRADYKININ Levels 2 May be used as first-line agents for HTN, esp in patients with a compelling indication of DM,HF, or CKD. 3 Similar effects as ACEIn, although the risks of cough and angioedema are significantly decreased.
Renin Inhibitor Side Effects
Diarrhea, cough, angioedema, Not for Pregnant (Fetal Toxicity)
Classes of CCB
1 Diphenylalkylamines: Verapamil 2 Benzothiazepines: Diltiazem 3 Dihydropyridines : Nifedipine (prototype), Amlo,felo,isra,nicar,nisol
Have been shown to reduce morbidity and mortality associated with heart failure.
Α-/β-ADRENOCEPTOR–BLOCKING AGENTS Drugs: Labetalol and carvedilol block α1, β1, and β2 receptors.
Hydralazine A/E
Include headache, tachycardia, nausea, sweating, arrhythmia, and precipitation of angina.A lupus-like syndrome can occur with high dosages, but it is reversible upon discontinuation of the drug.
HYPERTENSIVE EMERGENCY medications
CCB (nicardipine and clevidipine) nitric oxide vasodilators (nitroprusside and nitroglycerin), adrenergic receptor antagonists (phentolamine, esmolol, and labetalol), vasodilator hydralazine dopamine agonist fenoldopam.
__ therapy may lower BP more quickly with minimal adverse effects.
Combination therapy with separate agents or a fixed-dose combination pill
Vasoconstrictor compensatory mechanisms includes:
1) Stimulation of the sympathetic nervous system 2) Stimulation of the renin-angiotensin system
Cardiac Muscle Contraction (in order)
1 Rapid depolarization occurs when fast‐opening Na + channels in the sarcolemma open and allow an influx of Na + ions into the cardiac muscle cell. The Na + channels rapidly close. 2 A plateau phase occurs during which Ca 2+ enters the cytosol of the muscle cell. Ca 2+ enters from the sarcoplasmic reticulum (endoplasmic reticulum) within the cell and also from outside the cell through slow‐opening Ca 2+channels in the sarcolemma. the Ca 2+ channels open, K + channels, which normally leak small amounts of K + out of the cell, become more impermeable to K + leakage. 3 Repolarization occurs as K + channels open and K + diffuses out of the cell. At the same time, Ca 2+ channels close. These events restore the membrane to its original polarization, except that the positions of K + and Na + on each side of the sarcolemma are reversed. 4 A refractory period follows, during which concentration of K + and Na + are actively restored to their appropriate sides of the sarcolemma by Na +/K + pumps. The muscle cell cannot contract again until Na + and K + are restored to their resting potential states.