3a chapter 5 lesson 2

A solution is composed of a solute dissolved in a solvent. In the sugar water described in Figure 5-1, the solute was sugar and the solvent was water, and the solute molecules diffused through the solvent. It is also possible for solvent molecules to diffuse. In the case of cells, the solutes are organic and inorganic compounds, and the solvent is water. The process by which water molecules diffuse across a cell membrane from an area of higher concentration to an area of lower concentration is called osmosis (ahs-MOH-sis). Because water is moving from a higher to lower concentration, osmosis does not require cells to expend energy. Therefore, osmosis is the passive transport of water. Direction of Osmosis The net direction of osmosis depends on the relative concentra- tion of solutes on the two sides of the membrane. Examine Table 5-1. When the concentration of solute molecules outside the cell is lower than the concentration in the cytosol, the solution outside is hypotonic to the cytosol. In this situation, water diffuses into the cell until equilibrium is established. When the concentration of solute molecules outside the cell is higher than the concentration in the cytosol, the solution outside is hypertonic to the cytosol. In this situation, water diffuses out of the cell until equilibrium is established. Observing Diffusion Materials 600 mL beaker, 25 cm dialysis tubing, funnel, 15 mL starch solution (10 percent), 20 drops Lugol’s solution, 300 mL water, 100 mL graduated cylinder, 20 cm piece of string (2) Procedure 1. Put on your disposable gloves, lab apron, and safety goggles. 2. Pour 300 mL of water in the 600 mL beaker. 3. Add 20 drops of Lugol’s solution to the water. CAUTION: Lugol’s solution is a poison and eye and skin irritant. 4. Open the dialysis tubing, and tie one end tightly with a piece of string. 5. Using the funnel, pour 15 mL of 10 percent starch solution into the dialysis tubing. 6. Tie the other end of the dialysis tubing tightly with the second piece of string, forming a sealed bag around the starch solution. 7. Place the bag into the solution in the beaker, and observe the setup for a color change. Analysis What happened to the color in the bag? What happened to the color of the water around the bag? Explain your observations. Quick Lab www.scilinks.org Topic: Osmosis Keyword: HM61090 mb06se_homs01.qxd 11/27/07 8:52 AM Page 98 HOMEOSTASIS AND CELL TRANSPORT 99 When the concentrations of solutes outside and inside the cell are equal, the outside solution is said to be isotonic to the cytosol. Under these conditions, water diffuses into and out of the cell at equal rates, so there is no net movement of water. Notice that the prefixes hypo-, hyper-, and iso- refer to the relative solute concentrations of two solutions. Thus, if the solution outside the cell is hypotonic to the cytosol, then the cytosol must be hyper- tonic to that solution. Conversely, if the solution outside is hypertonic to the cytosol, then the cytosol must be hypotonic to the solution. Water tends to diffuse from hypo- tonic solutions to hypertonic solutions. How Cells Deal with Osmosis Cells that are exposed to an isotonic external environment usually have no difficulty keeping the movement of water across the cell membrane in balance. This is the case with the cells of ver- tebrate animals on land and of most other organ- isms living in the sea. In contrast, many cells function in a hypotonic environment. Such is the case for unicellular freshwater organisms. Water constantly diffuses into these organisms. Because they require a relatively lower concentration of water in the cytosol to function normally, unicel- lular organisms must rid themselves of the excess water that enters by osmosis. Some of them, such as the paramecia shown in Figure 5-2, do this with contractile vacuoles (kon-TRAK-til VAK-y ̄ ̄o ̄ ̄o-OL), which are organelles that remove water. Contractile vacuoles collect the excess water and then contract, pumping the water out of the cell. Unlike diffusion and osmosis, this pumping action is not a form of passive trans- port because it requires the cell to expend energy. Copyright © by Holt, Rinehart and Winston. All rights reserved. (a) (b) Vacuole filling with water Vacuole contracting TABLE 5-1 Direction of Osmosis Condition External solution is hypotonic to cytosol External solution is hypertonic to cytosol External solution is isotonic to cytosol Net movement of water into the cell out of the cell none H2O H2O H2O H2O H2O H2O The paramecia shown below live in fresh water, which is hypotonic to their cytosol. (a) Contractile vacuoles collect excess water that moves by osmosis into the cytosol. (b) The vacuoles then contract, returning the water to the outside of the cell. (LM 315) FIGURE 5-2 100 CHAPTER 5 (a) HYPOTONIC Cell walls (b) HYPERTONIC (a) ISOTONIC (b) HYPOTONIC (c) HYPERTONIC Other cells, including many of those in multicellular organisms, respond to hypotonic environments by pumping solutes out of the cytosol. This lowers the solute concentration in the cytosol, bring- ing it closer to the solute concentration in the environment. As a result, water molecules are less likely to diffuse into the cell. Most plant cells, like animal cells, live in a hypotonic environ- ment. In fact, the cells that make up plant roots may be surrounded by water. This water moves into plant cells by osmosis. These cells swell as they fill with water until the cell membrane is pressed against the inside of the cell wall, as Figure 5-3a shows. The cell wall is strong enough to resist the pressure exerted by the water inside the expanding cell. The pressure that water molecules exert against the cell wall is called turgor pressure (TER-GOR PRESH-er). In a hypertonic environment, water leaves the cells through osmosis. As shown in Figure 5-3b, the cells shrink away from the cell walls, and turgor pressure is lost. This condition is called plasmolysis (plaz-MAHL-uh-sis), and is the reason that plants wilt if they don’t receive enough water. Some cells cannot compensate for changes in the solute con-

Chapter 22 Antihypertensive Drugs Hypertension Defined (JNC-8) Pharmacology Overview 7 main categories of drugs to treat HTN Adrenergic drugs (old friend) Angiotensin-converting enzyme (ACE) inhibitors Angiotensin II receptor blockers (ARBs) Calcium channel blockers (CCBs) Diuretics Vasodilators Direct renin inhibitors A. Adrenergic Drugs: 5 Subcategories and where they act A1. Adrenergic neuron blockers (central and peripheral)- we won’t talk about this A2. Alpha1 receptor blockers (peripheral) A3. Alpha2 receptor agonists (central) A4. Beta receptor blockers (peripheral) A5. Combined α and β receptor blockers (peripheral) A2. Peripherally Acting Adrenergic DrugAlpha1 Blockers (we’ve met these) Doxazosin, prazosin, alfuzosin Block alpha1-receptors which causes BP to decrease Reduces peripheral vascular resistance and BP by dilating both arterial and venous blood vessels Main Use: benign prostatic hyperplasia (BPH) Alpha1 Blockers REMEMBER Tamsulosin (Flomax)* is an α1 blocker BUT *Tamsulosin is not used to control BP, just for BPH. A3. Centrally Acting Adrenergic DrugsAlpha 2 agonist Clonidine and methyldopa 1- Stimulate alpha2-adrenergic receptors. in the brain Decreases sympathetic outflow from the CNS which decreases NE production 2. Stimulate alpha2-adrenergic receptors in kidneys remember alpha 2 opposes alpha 1 Dilates peripheral blood vessels → lowers peripheral resistance → Results in decreased BP So ….Clonidine (Catapres) Used primarily for its ability to decrease blood pressure in an urgent setting Also use in opioid withdrawal as previously discussed Oral (multiple times a day), and topical patch formulations Do not stop abruptly as it may lead to rebound hypertension In reality, Clonidine and methyldopa Not prescribed as first-line home antiHTN drugs High incidence of unwanted adverse effects: orthostatic hypotension, fatigue, and dizziness MIGHT be uses as adjunct drugs after other drugs have failed, in conjunction with other antiHTN such as diuretics A4. Adrenergic Drugs Selective Beta 1 Blockers Metoprolol, Atenolol Reduction of HR through β1 receptor blockade (remember adrenergic blocking of this receptor???) HR results in BP Cause reduced secretion of renin = BP A4. Adrenergic Drugs Selective Beta1 Blockers Nebivolol (Bystolic) Uses: hypertension and HF Action: blocks β1 receptors and produces vasodilatation, which results in a decrease in SVR High doses loses selectivity and blocks both β1 and β2 Less sexual dysfunction All BB- Do not stop abruptly; must be tapered over 1 to 2 weeks A4. Adrenergic Drugs NONSelective Beta Blockers Propranolol Acts equally on β1 and β2 Other uses include situational anxiety associated with public speaking, test taking As mentioned on previous slide, nebivolol at high doses becomes beta nonselective A5. Dual-Action Adrenergic Drugs α1 and β Receptor Blockers Dual antihypertensive effects of reduction in heart rate (beta1 receptor blockade) and vasodilation (alpha1 receptor blockade) Examples are carvedilol (common) and labetalol (not as common) A5. Dual-Action Adrenergic Drugs α1 and β Receptor Blockers Carvedilol (Coreg) Widely used drug that is well tolerated Uses: HTN, mild to moderate HF in conjunction with digoxin, diuretics, and ACE inhibitors Contraindications: severe bradycardia or unstable HF, bronchospastic conditions such as asthma, and various cardiac conduction problems Adrenergic Drugs Indications - HTN But also for Glaucoma (topical) BPH: doxazosin, prazosin, and terazosin (2 for 1) Management of severe HF when used with cardiac glycosides and diuretics Contraindications Acute HF- have to stabilize first MOAIs- yeah doesn’t everything interact with MAOIs? Peptic ulcers Severe liver/kidney disease Asthma (with beta blockers) Adrenergic Drugs: Adverse Effects Orthostatic hypotension 1st-dose syncope Rebound hypertension with abrupt discontinuation Most common: Dry mouth, drowsiness, constipation, sedation Interactions- always check for specific drug interactions Can cause additive CNS depression with alcohol, benzodiazepines, opioids Question #1 When administering an alpha-adrenergic drug for hypertension, it is most important for the nurse to assess the patient for the development of what response? Hypotension Hyperkalemia Oliguria Respiratory distress Answer A Hypotension This is a key point in patient education These drugs have strong vasodilating properties and may cause severe hypotension, especially at the beginning of therapy. B. Angiotensin-Converting Enzyme Inhibitorsaka ACE Inhibitors or ACEi Large group of safe and effective drugs Currently are 10 ACEi Often used as first-line drugs for HF and hypertension May be combined with a thiazide diuretic, loop diuretic, or Calcium Channel Blocker (CCB) You need to understand the basics ACE Inhibitors: Review RAAS ACE converts angiotensin I, formed through the action of renin, to angiotensin II Angiotensin 2 is a potent vasoconstrictor and also induces aldosterone secretion by the adrenal glands Aldosterone stimulates sodium resorption (H20 follows Na Both act to raise BP which causes kidneys to reduce renin production ACEi= Great drug to treat HTN BUT contraindicated in pregnancy (2nd,3rd trimester due to fetal renal damage) and breastfeeding first few weeks after birth B. ACE Inhibitors - PRIL Lisinopril (Prinivil) super common, often the 1st drug Enalapril (Vasotec) also common Captopril (Capoten) great if liver disease present Benazepril (Lotensin) Fosinopril (Monopril) Perindopril (Aceon) Quinapril (Accupril) Ramipril (Altace) Trandolapril (Mavik) Primary Effects of the ACE Inhibitors Prevent Na (and H2O) resorption by inhibiting aldosterone secretion (volume reduction) (GO BACK TO RAAS DIAGRAM) blood volume decreases work of the heart preload, or the left ventricular end-diastolic volume which is important in HF ACE SUMMARY OF ACTIVITY 1) Prevent vasoconstriction caused by angiotensin 2 (2) Prevent aldosterone secretion  less sodium and water resorption Cardioprotective Effects of ACEi They slow progression of left ventricular hypertrophy (ventricular remodeling) after MI so considered cardioprotective ACE inhibitors have been shown to decrease morbidity and mortality in patients with HF Renal Protective Effects of ACEi ACE inhibitors: reduce glomerular filtration pressure by volume reduction Cardiovascular drug of choice for patients with diabetes since it helps protect kidneys by reducing pressure. Sometimes used low dose for kidney protection with DM without HTN B. ACEi Enalapril (Vasotec) Only ACEi available in both oral and IV Enalapril IV does not require cardiac monitoring Oral enalapril: prodrug (metabolized in liver) Improves patient’s chances of survival after an MI Reduces the incidence of HF B. ACEi Captopril (Capoten) Uses: prevention of ventricular remodeling after MI; reduce the risk of HF after MI Shortest half-life Must be administered multiple times throughout the day so this limits its use Not a prodrug so good for patient with liver disease Question #2 A patient with diabetes has a new prescription for the ACE inhibitor lisinopril. She questions this order because her provider has never told her that she has hypertension. What is the best explanation for this order? The doctor knows best The patient is confused This medication has cardioprotective properties This medication has a protective effect on the kidneys for patients with diabetes Answer D ACE inhibitors have been shown to have a protective effect on the kidneys because they reduce glomerular filtration pressure. This property makes them the cardiovascular drug of choice for patients with diabetes. Question #3 A patient with a history of pancreatitis and cirrhosis is also being treated for hypertension. Which drug will most likely be ordered for this patient? Clonidine Prazosin Diltiazem Captopril Answer D Captopril Captopril is not a prodrug; therefore, it does not need to be metabolized by the liver to be effective. This is an advantage in patients with liver disease. ACE Inhibitors: Adverse Effects *Dry, nonproductive cough, which reverses when therapy is stopped. This is a class effect Dizziness- Note: First-dose hypotensive effect may occur Headache & Fatigue Possible hyperkalemia ** Angioedema: rare but potentially fatal Not safe in pregnancy-are contraindicated during the second and third trimesters of pregnancy because of increased risk of fetal renal damage C. Angiotensin II Receptor Blockers(ARB) Considered an alternative to ACEi Less likely to cause a dry cough and hyper K+ that is common with ACE inhibitors Angiotensin II Receptor Blockers: Mechanism of Action Go back to RAAS diagram! ARBs affect primarily 2 places 1. Vascular smooth muscle - blocks vasoconstriction 2. Adrenal gland -Selectively blocks the binding of Ang 2 to certain Ang 2 receptors inhibiting secretion of aldosterone Lowers volume retention and BP Angiotensin II Receptor Blockers -ARTAN Losartan (Cozaar)- very common Eprosartan (Teveten) Valsartan (Diovan) Irbesartan (Avapro) Candesartan (Atacand) Olmesartan (Benicar) Telmisartan (Micardis) Azilsartan (Edarbi) C. ARB Losartan (Cozaar) Beneficial in patients with HTN and HF Used with caution in patients with kidney or liver dysfunction and in patients with renal artery stenosis ***Not safe for breastfeeding women and should not be used in pregnancy (Cat C 1st trimester, Cat D 2nd-3rd trimester), potential fetal toxicity Appear to be equally effective for the treatment of hypertension and well tolerated ARBs less likely to cause cough and hyperK+ but can still happen Evidence that ARBs are associated with lower mortality after MI than ACE inhibitors Never take ACEi and ARBs at the same time* 5. Calcium Channel Blockers (CCB) Primary use: HTN, angina, some dysrhythmias Cause smooth muscle relaxation by blocking the binding of calcium to its receptors, preventing muscle contraction Results in: Relaxed blood vessels to the heart Decreased peripheral smooth muscle tone Decreased SVResistance Decreased BP E. Diuretics First-line antiHTN in JNC 8 guidelines Decreases fluid volume The results from diuresis: preload, Peripheral resistance Overall effect  Decreased workload of the heart and decreased BP Thiazide diuretics are the most commonly used diuretics for HTN Ie hydrochlorothiazide (HCTZ), chlorthalidone We will discuss diuretics further in the chapter on diuretics F. Vasodilators Directly relax arterial or venous smooth muscle (or both) Results in: Decreased SVR Decreased afterload Peripheral vasodilation Indicated for treatment of HTN May be used in combination with other drugs F. Vasodilators Hydralazine (Apresoline) Orally: routine cases of essential hypertension Injectable: hypertensive emergencies BiDil: specifically indicated as an adjunct for treatment of HF in African-American patients F. Vasodilators Sodium Nitroprusside (Nitropress) *Sodium nitroprusside and IV diazoxide are reserved for the management of hypertensive emergencies. Contraindications: severe HF, known inadequate cerebral perfusion (especially during neurosurgical procedures) F. Vasodilators Adverse Effects Hydralazine: dizziness, headache, tachycardia, edema, dyspnea, N/V/D, vitamin B6 deficiency, rash Sodium nitroprusside: hypotension, bradycardia, decreased platelet aggregation, rash G. Direct Renin Inhibitors Aliskirin (Tekturna) Blocks the RAS pathway at the point of activation. Inhibiting renin production prevents the downstream production of Ang II (potent vasoconstrictor) Adverse effects: N/V, severe hypotension, hyponatremia, hyperkalemia… Contraindicated in patients with DM taking ACEi or ARB Miscellaneous Antihypertensives Eplerenone (Inspra) Newer class of drugs called selective aldosterone blockers (remember RAAS?) Reduces BP by blocking the actions of aldosterone at its corresponding receptors in the kidney, heart, blood vessels, and brain Indications: routine treatment of hypertension and for post-MI HF Contraindicated if serum potassium levels are high (above 5.6 mEq/L) A Special Form of HTNTreatment of Pulmonary Hypertension Sildenafil and Tadalafil Commonly used for erectile dysfunction Used for pulmonary hypertension but with different trade names Sildenafil: Revatio* (Viagra for ED) Tadalafil: Adcirca* (Cialis for ED)

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