Exam 2 NUR521 Study Guide PDF

Exam 2 NUR521 Module Q Topic s Module 4: 15  Hemodynamics Cardio o Review the circulatory system and cardiac output regulation. vascular I  Diuretics...

Exam 2 NUR521 Module Q Topic s Module 4: 15  Hemodynamics Cardio o Review the circulatory system and cardiac output regulation. vascular I  Diuretics o Review the PPT slide that shows where each class of diuretics work in the kidney. Sites of Diuretic action  PCT: The PCT has a high resorptive capacity. A large fraction (about 65%) of filtered sodium and chloride is reabsorbed at the PCT. In addition, essentially all of the bicarbonate and potassium in the filtrate is reabsorbed here. Solutes and water are reabsorbed at equal rations, so this urine remains isotonic.  Loop of Henle: The descending limb of the loop of Henle is freely permeable to water. Hence, as tubular urine moves down the loop and passes through the hypertonic environment of the renal medulla, water is drawn from the loop into the interstitial space. This process decreases the volume of the tubular urine and causes the urine to become concentrated (tonicity increases to about 1200 mOsm/L).  Early segment of distal convoluted tubule: About 10% of filtered sodium and chloride is reabsorbed in the early segment of the distal convoluted tubule. Water follows passively.  Distal Nephron: The distal nephron is the site of two important processes. The first involves exchange of sodium for potassium and is under the influence of aldosterone. The second determines the final concentration of the urine and is regulated by antidiuretic hormone (ADH).  Sodium-Potassium Exchange: Aldosterone, the principal mineralocorticoid of the adrenal cortex, stimulates reabsorption of sodium from the distal nephron. At the same time aldosterone causes potassium to be secreted. Although not directly coupled, these two processes—sodium retention and potassium excretion—can be viewed as an exchange mechanism. Aldosterone promotes sodium– potassium exchange by stimulating cells of the distal nephron to synthesize more of the pumps responsible for sodium and potassium transport Compare and contrast the diuretics presented in the module.  How do they work? o Furosemide (LOOP diuretic) MOA: acts in the thick segment of the ascending limb of the loop of Henle, blocks reabsorption of Na and Cl, preventing reabsorption of water which = profound diuresis even when renal blood flow and GFR are low. If tx is insufficient with just Lasix, it can  be combined with a thiazide diuretic (no use in combining with any other loop diuretic). o Hydrochlorothiazide/Microzide (Thiazide diuretic) MOA: steroid derivative, promotes urine production by blocking reabsorption of Na and Cl in the early segment of the distal convoluted tubule  water retention in nephron and increased flow of urine o Spironolactone/ Aldactone (Aldosterone Antagonist, potassium-sparring diuretic): blocks the action of aldosterone in the distal nephron  retention of K and excretion of Na. Diuresis is scanty because most Na has already been reabsorbed before reaching the distal tubule. o Triamterene/ Dyrenium (non-aldosterone antagonist, potassium-sparring diuretic): disrupts Na-K exchange in the distal nephron by direct inhibition  decreased Na reabsorption and reduced K secretion  Na excretion is increased K is conserved. Minimal diuresis.  What is the indication of use? o Furosemide USE: when rapid or massive mobilization of fluid is required such as pulmonary edema associated with CHF, edema from heart, liver, or kidney that haven’t responded to other drugs, and/or HTN o Thiazide USE: HTN, edema in CHF, hepatic, or renal disease o Spironolactone USE: HTN, edema, CHF (blocking aldosterone creates protective effects), counteracts K-wasting diuretics, off-label: acne, hair loss, hirsutism, hormone therapy for transgender females. o Triamterene USE: HTN, edema, combo drug can augment Lasix and counteract K wasting effects  What factors should be considered when choosing which diuretic to prescribe a patient? Produce some example scenarios of when you would prescribe one versus the other. How does renal function come into play? o Furosemide: more loss of fluid and electrolytes than any other diuretic, K wasting, do not give if K is low, beer criteria use in caution in pts over 65 who are at higher risk for hyponatremia o Thiazide: MUST have an adequate kidney function to work (minimum 20-30mL/min), CI with digoxin, lithium, and other HTN meds.  BBW? o ALL diuretics can cause profound diuresis with fluid and electrolyte depletion o Loop & thiazide AE: hyponatremia, hypochloremia, dehydration, hypotension, hypokalemia, ototoxicity (loop), hyperglycemia, hyperuricemia, reduced HDL, increased LDL o Spironolactone BBW: shown to cause tumors in rats, avoid unnecessary use.  o Spironolactone AE: hyperkalemia (dysrhythmias), deep voice, impotence, menstrual irregularities, hirsutism o Triamterene BBW: hyperkalemia  How would you know if your patient was experiencing AE like ototoxicity, dehydration, hypo or hyperkalemia, and hypotension. What would be subjective and objective findings?  What important information would you teach your patient about each of these drugs? HTN  What is included in the workup for HTN? o EKG o Urinalysis o H&H o BMP: Electrolytes, Kidney function, and Glucose o Uric acid o Triglycerides and cholesterol  What lifestyle modifications should you discuss with your patient? o Sodium restricted diet o Restrict alcohol consumption o Aerobic exercise, Healthy body weight o Smoking cessation Know about the RAAS and how this affects fluid and blood pressure changes in the body.  RAAS: Decreased perfusion pressure in the afferent arteriole stimulates secretion of renin by juxtaglomerular cells  renin reacts with Angiotensin in liver to make Angiotensin I  Angiotensin I converts to Angiotensin II in the lungs  Angiotensin II causes vasoconstriction in the blood vessels  Angiotensin II becomes III in the adrenal cortex stimulating aldosterone release  Aldosterone increases Na and water reabsorption by kidney tubules which = increased blood volume & increased BP (slide 35)  Review HTN guidelines presented in PPT and module.  Drug of choice for pregnant women with mild pre-eclampsia: labetalol and methyldopa, MgSO4 used for seizures  In older adults, avoid central acting alpha agonists and peripheral alpha 1 antagonists, start low doses, risk of orthostatic hypotension is high   In African Americans, diuretics are 1st choice. CCBs and α/β blockers are also effective. HOWEVER, monotherapy with β blockers or ACEIs is less effective in African Americans than in Caucasians. BUT for example, if pt is black and has DM I and proteinuria, give ACEI  When BP cannot be adequately controlled with a single drug, one of several two-drug combinations are recommended: an ACEI plus a thiazide diuretic, an ACEI plus a CCB, or a β blocker plus a thiazide. Review what comorbid conditions influence a prescriber’s choice of antihypertensive medication.  HTN & CKD: ACE inhibitor + loop diuretic (avoid thiazide and potassium sparring drugs; ineffective), if intolerant to ACE, do ARB  HTN & DM: ACE inhibitors, ARBs, Ca Channel blockers (CCBs) are preferred o ACEIs & ARBs can slow progression of renal damage and reduce albuminuria  o B blockers can mask sings of hypoglycemia  o Thiazide & loop diuretics can cause hyperglycemia   ACEIs are great for comorbid conditions! RAAS Drugs  Know how these drugs work and how they affect the RAAS. o RAAS inhibitors; captopril and enalapril are safe for use in kids o 25% decrease in stroke in patients 55-80 using losartan vs. atenolol, 20% decrease in DM with candesartan vs placebo  Compare and contrast ACE-I and ARB. What are the differences in these drugs? What are the similarities? When would it be better to prescribe one or the other? o ACEI “Prils”: blocks the conversion of angiotensin I to II  vasodilation, decreased blood vol & cardiac remodeling, potassium retention and fetal injury can occur. ACEI also increase levels of bradykinin through the inhibition of Kinase II which also  vasodilation, COUGH, and rarely angioedema  How does a direct Renin inhibitor work? What patient teaching would be included with our prototype drug in this class? o Lisinopril (Privinil, Zesteril) – ACEI – 2.5-40 mg  MOA: lowers angiotensin II levels  dilation of blood vessels, decreased blood volume, reduce cardiac afterload, increase CO, venous dilation, suppresses aldosterone, reduces GFR   USE: LV dysfunction, HTN, nephropathy (DM & nonDM), HTN, CHF, acute MI, prevention of MI, stroke, and death r/t CV events (ramipril), diabetic retinopathy (enalapril)  CI: rental artery stenosis (can lead to renal failure) & pregnancy  PE: take with food, first dose hypotension (start with low dose, check BP at home if hypotension develops lay down), avoid K supplements, notify HCP for cough & facial swelling, avoid diuretics & lithium, NSAIDS can reduce effects of ACEIs  AE: first dose hypotension, hyperkalemia (due to inhibition of aldosterone & angiotensin II), cough (bradykinin accumulation), renal failure (in pts with renal problems), angioedema (serious but rare)  BBW: fetal injury o Losartan (Cozaar) – ARB –25-100 mg  MOA: blocks action of angiotensin II at receptor sites (similar to ACEI but blocks AII in a different way)  dilates arterioles & veins, decreases aldosterone which  increased renal excretion of Na & water  Use: HTN, CHF, diabetic nephropathy, MI, stroke prevention  Same CI as ACEI  Less AE than ACEIs; ARBs don’t cause hyperkalemia, no cough side effect,  PE: notify HCP for cough & facial swelling  BBW: fetal injury o Aliskiren (Tekturna) – direct renin inhibitor (DRI) – 150-300 mg  MOA: binds tightly with renin, inhibiting the cleavage of angiotensinogen to angiotensin I, influences the entire RAAS system  USE: HTN  BBW: fetal injury  AE: usually well tolerated, rare: cough, angioedema, hyperkalemia, diarrhea  Pt ed: high fat meals decrease absorption, interacts with grapefruit juice How does Inspra work? What is it used for? What factors should be considered by the provider when adding this drug to a current regimen.  Eplerenone (Inspra): Potassium sparring aldosterone antagonist (25 & 50 mg) o MOA: selective blockage of aldosterone receptors without blocking receptors for other steroid hormones; promotes retention of potassium & increased secretion of Na and water which   reduced blood volume and BP o USE: HTN & HF after tx with ACEI and BBs o AE: has less AE than spironolactone because it’s more selective, hyperkalemia o Current guidelines recommend adding an aldosterone antagonist to HF therapy but only in pts with symptoms despite tx with ACEIs and BBs o Pt ed: hyperkalemia – dizziness, confusion, abnormal HR, numbness, tingling o CI: K supplements, impaired renal fx, DM II with microalbuminuria CCB  MOA? Prevent calcium ions from entering cells. Biggest effect on heart, blood vessels, vascular smooth muscle (VSM).  prevents contraction  vasodilation. Similar effect on heart as Beta blockers; reduce hearts contractile force, reduce HR, suppress conduction through AV node  Use? Tx HTN, angina pectoris, cardiac arrythmias  CI? Hypotension, sick sinus syndrome, 2nd or 3rd degree HB, grapefruit juice, can intensify effects of beta blockers  AE: eczematous rash in older adults, dizziness, flushing, HA, edema of ankles & feet, worsening of HB  When would you pick one prototype over the other? o Non-dihydropyridine  Verapamil can be used in infants  Diltiazem (Cardizem)  Tx: Dysrhythmias (a. flutter, a. fib, SVT), angina, htn o Dihydropyridines  Nifedipine (Procardia) 10-20 mg IR and 30-60 mg ER  Unlike Verapamil & Cardizem, nifedipine produces very little blockade of calcium channels in the heart and so nifedipine cannot be used to treat dysrhythmias, does not cause cardiac suppression, and is less likely than verapamil to exacerbate preexisting cardiac disorders. Nifedipine also differs from verapamil in that it is more likely to cause reflex tachycardia.  Indirect Reflex Effects: By lowering blood pressure, nifedipine activates the baroreceptor reflex, thereby causing sympathetic stimulation of the heart. Because nifedipine lacks direct cardio suppressant actions, cardiac stimulation is unopposed; hence heart rate and contractile force increase. It is important to note that reflex effects occur primarily with the immediate-release (IR) formulation of  nifedipine, not with the slow-release (SR) formulation. This is because the baroreceptor reflex is turned on only by a rapid fall in blood pressure; a gradual decline will not activate the reflex.  With the IR formulation, blood levels of nifedipine rise quickly; hence blood pressure drops quickly and the reflex is turned on. Conversely, with the SR formulation, blood levels of nifedipine rise slowly, so blood pressure falls slowly and the reflex is blunted. So usually the SR/ER is prescribed and coupled with beta blockers to avoid this and decrease anginal pain!  Use: Long-term use reduces the rates of overt heart failure, coronary angiography, and coronary bypass surgery but not rates of stroke, myocardial infarction, or death. Also, because nifedipine causes minimal blockade of calcium channels in the heart, the drug is not likely to exacerbate AV block, heart failure, bradycardia, or sick sinus syndrome. Nifedipine is preferred to verapamil for patients with these disorders.  Pt education: Record anginal episodes, BP, AE Vasodilators  What would you teach your patient about the use of hydralazine? o MOA: dilates arterioles  decrease peripheral resistance & lowers arterial BP o Use: HTN crisis, HF (reduces afterload for a short time in CHF) o Can be used in infants 1 month o Was common in past, now it has been replaced by newer antiHTN meds o Requires combo with BB to prevent reflex tachycardia o CI: CAD  angina attacks o High risk for falls in older adults (polypharmacy & orthostatic hypotension) HF o Review patho and stages of HF (4 stages)  HF is ventricular dysfunction, reduced CO, insufficient tissue perfusion, fluid accumulation. Tx: diuretics, RAAS inhibitors, beta blockers, digoxin  Systolic HF (LV dysfunction) now known as HF w/ reduced EF (HFrEF) – LV can’t contract properly  heart cannot pump the blood out with enough force  Diastolic HF (HFpEF – preserved) – LV can’t relax, muscle is stiff  heart can’t fill properly   Left – if LV pumps inefficiently, blood backs up into the lungs – pulmonday edema (rales, wheezes, blood-tinged sputum, low O2, S3) & leads to…  Right – if RV pumps inefficiently, blood backs up into the venous system (back in body) – liver congestions, ascites, edema in legs  RHF occurs because of LHF o How does digoxin work? What do you need to know about dosing and administration? What is s/s  of toxicity? What is the antidote?  MOA: treats CHF & dysrhythmias; (+) Inotropic action, increase myocardial contraction force  increase CO, alter eclectic activity of the heart (neurohormonal), reduces s/s of HF but does not prolong life (2nd line agent),  AE/CI: digoxin-induced dysrhythmias, Narrow therapeutic window, hypokalemia (increases risk of dysrhythmia), many interactions, hold for HR 100 despite max statins o Describe lifestyle changes you would address with your patient.  Eat better, move more, stop smoking, healthy BMI, manage stress  Statins o What should you teach your patient about statins? o Who needs to take a statin?  Metabolic Syndrome o How do you diagnose metabolic syndrome (syndrome X) – a bunch of metabolic abdnormalities associated w/ high risk for AASCVD & DM II:  High TG levels >150-200 mg/dL (or undergoing drug therapy for high TGs)  Low HDL cholesterol 130/85  Waist circumference >35-40 inches  Angina Pectoris o What is CI for NTG? DO NOT USE with Sildenafil (Viagra) MOA for Anti-Anginal: o Nitroglycerin (Organic Nitrate) – acts directly on vascular smooth muscle (VSM) to promote vasodilation (mostly in veins), nitrate gets taken up by VSM & converted to Nitric oxide  In pts with Stable Angina, NTG does not increase blood flow to ischemic areas of the heart, pain relief results from effects of NTG on peripheral blood vessels  In Variant angina, NTG acts by relaxing/preventing spasm in coronary arteries, drug increases O2 supply, it does not reduce demand! (slide 34) o Ranolazine (Ranexa) – reduces Na & Ca in myocardial cells, used for 1st line tx for chronic angina, often combined w/ nitrates, BBs, CCBs  Anticoagulation and Antiplatelet Drugs o Use the compare and contrast chart to help you with these medications. o Why would you use one versus the other? Advantages? Disadvantages? o How do you monitor these drugs? o What are contraindications for these drugs? o What would you teach your patients?  Anemia o How do you assess for anemia? o How do you diagnose anemia?  Iron Deficiency – macrocytic anemia (vit C enhances absorption) o How do you treat iron deficiency?  Ferrous sulfate iron therapy (slide 57)  Vitamin B12 Deficiency o What are presenting s/s of vitamin B12 deficiency? Anemia & injury to the nervous system (neurologic damage may never resolve) o In most cases, vitamin B12 deficiency is the result of impaired absorption resulting from regional enteritis, celiac disease, antibodies against intrinsic factor, and bariatric surgery and can cause a megaloblastic and macrocytic anemia o Causes demyelination of neurons causing paresthesias and reduced DTRs, later leading to loss of memory, mood changes, hallucinations, and psychosis  Folic Acid Deficiency – same as B12 deficiency but isolated folic acid deficiency does not cause the  neurologic abnormalities that vit B12 deficiency does o When is folic acid used? Needed during pregnancy to prevent neural tube defects (400-800 ug/day) Module 6: 20 Diabetes: Endocrine  Define and differentiate the different types of diabetes.  Know the screening criteria for prediabetes and diabetes in adults, children, and adolescents. o If tests normal, repeat q 3 years or with change in risk  What are the diagnostic criteria for prediabetes? o FPG (plasma glucose) 100-125 mg/dL o A1C 5.7-6.4% o 2-h PG 140-199 mg/dL  What are the diagnostic criteria for diabetes? o FPG >126 o 2-h PG >200 or Random PG >200 o A1C >6.5  How often should a HgA1C be ordered to assess glycemic target?  o 2x a year in pts with stable glycemic control and are meeting tx goals o Quarterly (q 3 months) & prn in pts whose therapy recently changed or are not meeting goals  Explain the pharmacologic approach to obesity management for the treatment of T2DM.  Explain the pharmacologic approach to treating type 1 diabetes. o Mx daily injections of prandial & basal insulin or continuous subcutaneous insulin infusion o Use rapid acting insulin analogs to reduce hypoglycemia risk  Explain the pharmacologic approach to treating type 2 diabetes. o Guided by person-centered tx factors (comorbidities, tx goals, social determinants of health, lifestyle)  o An angiotensin-converting enzyme (ACE) inhibitor (e.g., lisinopril) or an angiotensin II receptor blocker (ARB; e.g., losartan) can reduce the risk for diabetic nephropathy, a long-term consequence of poor glycemic control. These same drugs are preferred agents for managing diabetic hypertension. o Metformin or combo therapy o Early intro of insulin should be considered if there is evidence of ongoing catabolism (weight loss), hyperglycemia s/s, or when A1C levels (>10%) or BG levels (>300) are high. o Glucagon-like peptide 1 receptor agonist is preferred to insulin when possible or at least combine o Re-eval q 3-6 months, beware of overbasalization (if dose > 0.5u/kg/day)  What is the A1C target goal for older adults? What are older adults at risk for and how should their management be personalized? o At risk for overtreatment & polypharmacy; tx goals should be de-intensified and simplified to reduce hypoglycemia risk o A1C goal is individualized. For pts with a hx of severe hypoglycemia & limited life expectancy target should be