Kidney of Ox, horse, Pig and Dog

Structure of kidney

The anatomy and physiology of the kidney

The excretory function of the kidney

12 Kenji SCIENCE8 Parts of a Kidney

Exercise 24-25 (Stomach worms of Equids & Pigs; Kidney Worms and Pinworms)

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)

1. Eat slowly, chew your food well. It takes twenty (20) minutes before your stomach sends a clear message to your brain that you're full. Take your time and savor the flavor of your meal. 2. Eat well When your body doesn't receive the required nutrients, your metabolism slows down. Metabolism is the rate at which you burn calories while resting. So, if you don't eat enough, fewer calories will be burnt and there will be less fat loss. You should eat small meals at regular intervals to keep your energy levels high. 3. Eat less red meat Red meats are high in saturated fat and should be avoided by people with high cholesterol. Chicken and fish are the best meats to consume. These meats can be baked, grilled or roasted. 4. Eat more fiber foods Add fiber to your diet, this adds bulk to your food and prevents constipation. Whole grain foods like oatmeal, bran, wheat germ and brown rice, fruits, especially with skins, prunes, etc, are all Seven (7) healthy eating habits for your guidelines: How you eat your food is as important as what you eat. So, the next time you sit down to eat, enjoy your meal by keeping these pointers in mind. Home Economics and Livelihood Education 7 Seibo College 157 good sources of fiber. Fiber helps in binding cholesterol, which results to less production of bad cholesterol. 5. Have calcium-rich foods Aside fro milk other sources of calcium and protein are red kidney beans, mustard greens, etc. Proteins can be found in meats, sprouts, soya, etc. 6. Eat foods that contain iron These include liver, fruits like watermelon, vegetables like spinach, beans, beets and broccoli, whole grains, dried fruits, especially prunes, sunflower seeds, etc. 7. Relish the flavors You may have heard some of these before. But the best good food habit, which we all seem to overlook, is to actually taste and enjoy the flavor of the food with your emotions instead of just your tongue. How can we prevent malnutrition? Following are the checklists of steps to prevent malnutrition.  Nutrition campaign on the importance of food nutrients.  Proper selection, preparation and serving of well-balanced meals.  Vegetable gardening in schools and at home.  Intensive program from the government especially for the less privileged members of the community.

The endoplasmic reticulum (EN-doh-PLAZ-mik ri-TIK-yuh-luhm), abbre- viated ER, is a system of membranous tubes and sacs, called cisternae (sis-TUHR-nee). The ER functions primarily as an intracellu- lar highway, a path along which molecules move from one part of the cell to another. The amount of ER inside a cell fluctuates, depending on the cell’s activity. There are two types of ER: rough and smooth. The two types of ER are thought to be continuous. Rough Endoplasmic Reticulum The rough endoplasmic reticulum is a system of interconnected, flattened sacs covered with ribosomes, as shown in Figure 4-15. The rough ER produces phospholipids and proteins. Certain types of proteins are made on the rough ER’s ribosomes. These proteins are later exported from the cell or inserted into one of the cell’s own membranes. For example, ribosomes on the rough ER make digestive enzymes, which accumulate inside the endoplasmic retic- ulum. Little sacs or vesicles then pinch off from the ends of the rough ER and store the digestive enzymes until they are released from the cell. Rough ER is most abundant in cells that produce large amounts of protein for export, such as cells in digestive glands and antibody-producing cells. Smooth Endoplasmic Reticulum The smooth ER lacks ribosomes and thus has a smooth appear- ance. Most cells contain very little smooth ER. Smooth ER builds lipids such as cholesterol. In the ovaries and testes, smooth ER produces the steroid hormones estrogen and testosterone. In skeletal and heart muscle cells, smooth ER releases calcium, which stimulates contraction. Smooth ER is also abundant in liver and kidney cells, where it helps detoxify drugs and poisons. Long-term abuse of alcohol and other drugs causes these cells to produce more smooth ER. Increased amounts of smooth ER in liver cells is one of the factors that can lead to drug tolerance. As Figure 4-15 shows, rough ER and smooth ER form an interconnected network. Copyright © by Holt, Rinehart and Winston. All rights reserved. reticulum from the Latin rete, meaning “net”; reticulum means “little net” Word Roots and Origins The endoplasmic reticulum (ER) serves as a site of synthesis for proteins, lipids, and other materials. The dark lines in the photo represent the membranes of the ER, and the narrow lighter areas between the dark lines show the channels and spaces (cisternae) inside the ER. FIGURE 4-15 Smooth ER Ribosomes Rough ER Cisternae 82 CHAPTER 4 GOLGI APPARATUS The Golgi apparatus, shown in Figure 4-16, is another system of flattened, membranous sacs. The sacs nearest the nucleus receive vesicles from the ER containing newly made proteins or lipids. Vesicles travel from one part of the Golgi apparatus to the next and transport substances as they go. The stacked membranes modify the vesicle contents as they move along. The proteins get “address labels” that direct them to various other parts of the cell. During this modification, the Golgi apparatus can add carbohydrate labels to proteins or alter new lipids in various ways. VESICLES Cells contain several types of vesicles, which perform various roles. Vesicles are small, spherically shaped sacs that are surrounded by a single membrane and that are classified by their contents. Vesicles often migrate to and merge with the plasma membrane. As they do, they release their contents to the outside of the cell. Lysosomes Lysosomes (LIE-suh-SOHMZ) are vesicles that bud from the Golgi appa- ratus and that contain digestive enzymes. These enzymes can break down large molecules, such as proteins, nucleic acids, car- bohydrates, and phospholipids. In the liver, lysosomes break down glycogen in order to release glucose into the bloodstream. Certain white blood cells use lysosomes to break down bacteria. Within a cell, lysosomes digest worn-out organelles in a process called autophagy (aw-TAHF-uh-jee). Lysosomes are also responsible for breaking down cells when it is time for the cells to die. The digestion of damaged or extra cells by the enzymes of their own lysosomes is called autolysis (aw-TAHL-uh-sis). Lysosomes play a very important role in maintaining an organism’s health by destroying cells that are no longer functioning properly. Copyright © by Holt, Rinehart and Winston. All rights reserved. The Golgi apparatus modifies many cellular products and prepares them for export. FIGURE 4-16 CELL STRUCTURE AND FUNCTION 83 Peroxisomes Peroxisomes are similar to lysosomes but contain different enzymes and are not produced by the Golgi apparatus. Peroxisomes are abundant in liver and kidney cells, where they neutralize free radicals (oxygen ions that can damage cells) and detoxify alcohol and other drugs. Peroxisomes are named for the hydrogen peroxide, H2O2, they produce when breaking down alco- hol and killing bacteria. Peroxisomes also break down fatty acids, which the mitochondria can then use as an energy source. Other Vesicles Specialized peroxisomes, called glyoxysomes, can be found in the seeds of some plants. They break down stored fats to provide energy for the developing plant embryo. Some cells engulf material by surrounding it with plasma membrane. The resulting pocket buds off to become a vesicle inside the cell. This vesicle is called an endosome. Lysosomes fuse with endosomes and digest the engulfed material. Food vacuoles are vesicles that store nutrients for a cell. Contractile vacuoles are vesicles that can contract and dispose of excess water inside a cell. Protein Synthesis One of the major functions of a cell is the production of protein. The path some proteins take from synthesis to export can be seen in Figure 4-17. In step , proteins are assembled by ribosomes on the rough ER. Then, in step , vesicles transport proteins to the Golgi apparatus. In step , the Golgi modifies proteins and pack- ages them in new vesicles. In step , vesicles release proteins that have destinations outside the cell. In step , vesicles containing enzymes remain inside the cell as lysosomes, peroxisomes, endo- somes, or other types of vesicles. 5 4 3 2 1 Copyright © by Holt, Rinehart and Winston. All rights reserved. Proteins are assembled by ribosomes on the rough ER. Vesicles carry proteins from the rough ER to the Golgi apparatus. Proteins are modified in the Golgi apparatus and enter new vesicles. Some vesicles release their proteins outside the cell. Other vesicles remain in the cell and become lysosomes and other vesicles. Nucleus

Related quizzes

Related quizzes