Pharmacology: Renal agents
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| Heart Rate x Stroke Volume = | Cardiac Output!
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| Increase preload? | Stroke Volume increases
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| Increase afterload? | Stroke volume decreases
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| Increase contractility? | Stroke volume increases
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| Cardiac output x afterload= | Blood Pressure
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| Intravascular fluid baseline? Interstitial fluid baseline? Intracellular fluid baseline? What and how much does the intravascular fluid also contain? What 4 systems excrete fluid? | Intravascular: 3 liters PLUS 2 liters of RBCs. Interstitial: 9 liters. Intracellular: 30 liters. 4 systems: Kidneys, GI, Lungs, Skin
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| How much fluid is lost insensibly a day? What systems are insensible? | about 800 mL; Respiratory tract and skin.
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| Osmotic pressure main component? How do we keep this gradient high? | Potassium. We excrete sodium for maintenance of potassium gradient.
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| What happens to cell with high osmolality outside cell? | shrinkage
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| What happens to cell with low osmolality outside cell? | Swelling and possible rupture.
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| Where is ADH secreted from? Where does it act upon? What does it do? | Posterior pituitary; Acts upon DISTAL TUBULE and collecting duct. ADH saves water by concentrating urine, and is in response to volume depletion and increase osmolality.
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| What happens with fever to insensible losses? | Increase 100mL/day per degree. Ex (normal is 37) 39 degrees, we'd be losing 200mL extra per day so total insensible losses would be 1000mL.
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| What is the best method of fluid intake? | BY MOUTH!
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| What fluid would you give if you suspected acidosis? | Ringer's lactate, lactate metabolized generates bicarb
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| Benefit of giving 5% dextrose. Adverse? | dextrose will be metabolized quickly (giving energy as it does), leaving free water to go out into the body restoring isomolarity. Primarily used to maintain water balance in patients who are not able to take anything by mouth. Can cause hyponatremia
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| T/F: Synthetic colloids still used heavily | False, rarely used b/c we can give hypertonic Na solution to draw water out of interstitial fluids. Still used some in those refusing blood transfusion. They do increase O2 carrying capactiy.
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| Isotonic fluid: what it does, risks, example | Fluids remain intravascularly briefly and expand volume...good for hypotensive or hypovolemic. Risk of overloading exists. Ex: .9% saline
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| Hypotonic fluid: what it does, example | lower osmolarity than serum; fluids dilute intravascular fluid decreasing osmolarity. Water moves from vascular compartment to interstitial compartment and eventually into cells. Helpful when cells are dehydrated for dialysis etc. Ex: .45% saline.
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| Hypertonic fluid: what it does, example | Higher osmlarity than serum; fluid moves from intracellular and interstitial compartments into intravascular compartment. Stabilizes BP, increases urine output, correcting hypotinc hyponatremia, decreases edema. Ex: 3% saline
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| T/F: 3mL of isotonic crystalloid solution needed to replace 1mL of patient blood | True
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| Advantages/disadvantages of crystalloids | A: inexpensive, long shelf life, readily useable, variety of formulations. D: 2-3x volume of crystalloid to cause same intravascular expansion as single volume of colloid.
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| Dextrose saline | primarily used to replace water losses post-operatively, limited indication other than that. Doesn't cause water or salt overload.
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| T/F: Colloids readily cross the BBB. | False, initially, they stay almost entirely in intravascular space for a prolonged period of time compared to crystalloids
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| Advantages/disadvantages of colloids | A: don't cross BBB and stay in intravascular fluid a long time and are important in capillary fluid dynamics because they exert a long term osmotic force and draw fluid intravascularly. D: $$$, some adverse, platelet dysfn, can cause dramatic fluid shift
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| Signs of intravascular volume contraction (3) | Decrease JVP, postural hypotension, postural tachycardia
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| Solution of choice for hypovolemia (IV)? In general? | Normal saline (.9% NaCl); in general: by-mouth drinking.
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| 6 Rules of Fluid Replacement | 1) replace blood w/ blood 2) replace plasma w/colloid (preferably albumin) 3) Crystalloid when blood loss not pronounced. 4) Severe hemorrhage: blood, hypertonic saline, colloid. 5) Replace ECF w/saline 6) Rehydrate tissue w/dextrose water.
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| Generally effects of Dextrose, Normal Saline, and Colloids on compartments of fluid. | Dextrose will make blood hypotonic, and will expand to other compartments. Isotonic saline will move a little to interstitial and interstitial will draw from intracellular as well. Colloid (hypertonic) will draw fluid from intracellular and interstitial.
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| 4 Steps to IV Therapy | 1) Assess volume status 2) Determine Access 3) Select Fluid 4) Determine Rate
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| Calculate Free-water deficit | ((140/Na) -1) x TBW ; Administer deficit over 48-72 hrs unless deficit is small and can be administered in a shorter time.
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| Example of calculating Free-water deficit (Just look at the back of this slide for further understanding. NO NEED TO TRY TO READ MY MIND) | Serum Sodium = 145;
Weight 100 kg;
100Kg x 0.60 = 60L â Total Body Water;
Water Deficit = 60L x ((140/145) - 1);
Water Deficit = 60L x 0.035 â 2.1 L ;
(175cc/hour over 12 hours OR 44 cc/hour over 48 hours)
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| If a child has these, they are in shock until proven otherwise. (2) | Cool feet and thready pulses
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| T/F: In children, hypotension from blood loss occurs late in the progression of shock and is a sign of imminent cardiovascular collapse and death. How do you treat this? | TRUE, EMERGENCY; Give 20cc/kg of Ringer's Lactate or Normal Saline. If no response, give again
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| How much of cardiac output do kidneys receive? | 20%
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| Driving force in nephrons for exchange of water and salt? | how much sodium is around tubules (in the medulla), not how much sodium is in urine.
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| T/F: We want to target AT2 receptor with our medications? | False, we want to target AT1 receptor. This receptor is MUCH more strongly stiumulated by Angiotensin II
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| T/F: Aldosterone is the strongest mineralcorticoid we have for medication. | TRICKY TRICKY: actually false. Aldosterone is too strong to be used as a medication. Fluracortisole is actually the strongest derivative of aldosterone, and it is 1000x weaker than aldosterone.
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| Known benefits of ACEI (5) | 1) lowers HTN where thiazides and BB CONTRA 2) lowers HTN in HF 3) can limit size of MI 4) good in diabetic nephropathy 5) slows down, but does not stop or reverse renal failure
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| ACEI: Adverse and CONTRAs (5) | 1) First dose HypoTN 2) Constant dry cough 3) Urticaria/angioneurotic edema 4) Functional renal failure (goes down in ALL patients some) 5) Known teratogen: CONTRA in pregnancy. 5) Hyperkalemia as a result of reduced aldosterone secretion
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| Potassium-sparing diuretics (those not secreting urine with fluid): Which they are and precautions | Spironolactone, Trianguline, Amiloride. Avoid with ACEI (can lead to hyperkalemia.) Issues with painful gynecomastia.
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| ARBs: what do they do, CONTRAs/Adverse? | block angiotensin II at the AT1 receptor (not AT2 at all) with generally less adverse than ACEI; still avoid in pregnant patients.
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| Hyperkalemia: Sx, Psuedohyperkalemia | Sx: tall T waves, PR prolongation, QRS prolongation, VFib. potassium moves out of cells before venipuncture due to fist clenching or hemolysis of blood cells/misshandling [shaking] samples is another example (fractures RBCs, K into serum)
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| What serum potassium level is considered an emergency? | >7 meq/L
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| Fastest method of treating hyperkalemia (come on guys, this was on clin med exam!) How do you manage it after that? | Calcium gluconate, followed by Kayexalate (sodium polystryene) (these exchange sodium for potassium 1-3 respectively, then excrete) by enema (potentially better than oral it tastes so bad).
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| T/F: Small change in creatinine means a huge change in GFR | True
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| What does Cimetidine and Tirmethoprim do to serum creatinine? How? What do cefoxitin and flucytosine do? | Raise creatinine by blocking renal tubular secretions of creatinine (so it is retained). Cefoxitin interfere with laboratory creatinine assay
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| Pre-renal issues: Central problem? What are some meds that cause it? | Vasoconstriction is central problem (we need to keep patients hydrated). Amphotericin, noradrenaline, immunosuppresives, contrast agents reduce renal blood flow.
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| Intrarenal issues: Cause? Examples of meds that cause it. | some meds can cause localized allergic rxns affecting glomerulus (penicillins, sulfas, cephalosporins, cipro, PPIs). These can lead to ATN.
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| Post-Renal issues: what causes it? | usually caused by mechanical obstruction, drugs like ACYCLOVIR (he emphasized like 8 times) or Septra that precipitate in kidney.
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| Drug-Induced Crystalluria: What is it? What does it do? What drugs cause it? Prevention? | insoluble drugs in urine crystalize in distule tubule elevating risk for hypovolemia, high concentrations of drug, slow elimination. Often due to ACYCLOVIR and SULFONAMIDES. Prevention is key: HYDRATE and ensure diuresis.
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| Osmotic nephrosis: General, Cause, Effect | fairly uncommon; caused by high doses of mannitol, immunoglobulins, dextrans, starches. Direct effect on glomerular filtration or uptake of molecules by pinocytosis in proximal tubule.
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| Nephrotic syndrome: drugs that can cause it, what happens? | Drugs: NSAIDs, penicillamine, gold. Damages glomerulus and alters ability to prevent protein from being filtered. Tx: Ceasing drug.
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| Angioneurotic edema: Cause | associated with elevated bradykinin, and as bradykinins are metabolized by ACE, ACEI (not ARB) may have a causative role.
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| NSAIDs: What do they do and what are they? | almost all reversible inhibitors cyclooxygenase (key enzyme in formation of prostaglandins). 1) RBF partially regulated by prostaglandins. 2)INHIBIT PROSTAGLANDIN FORMATION, REDUCING BLOOD FLOW. 3) Implicated in interstitial nephritis and papillary damag
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| How do NSAIDs effect renal disease? | long term NSAID use can cause chronic renal insufficiency (6+ pills/day for 3 years increases risk.
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| Analgesic Nephropathy: what does it do? Results? | damage to 1 or both kidneys due to over-exposure of medications, esp OTC pain meds. Results: decreased blood flow to kidney, rapid consumption of antioxidants -> oxidative damage -> CRF
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| 6 indications for using diuretics | 1) HF (acute or chronic) 2) pulmonary edema 3) HTN 4) nephrotic syndrome 5) hypercalcemia 6) hypercalciuria
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| Loop Diuretics: CONTRA, how it works, what it treats | CONTRA in persons w/sulfa allergies. Acton on Na-K-Cl cotransporter in thick ascending limb of loop of Henle inhibiting reabsorption. Draws water into tubule. Treats edema, HTN, hypercalemia.
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| Furosemide What is it, Adverse | loop diuretic; highly protein bound. Adverse: rebound effects after single dose, hypokalemia, volume depletion, Ototoxicity (tinnitus). Strong dose -> hypotension -> AKI
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| Thiazide Diuretics: Examples, site of action, what does it do? Indications; Adverse | Hydrochlorothiazide, Bendrofluazide, etc. Site of action distal convoluted tubule. Blocks electroneutral Na/Cl exchanger (NCCT). Higher doses required in low GFR. I: antihypertensive esp w/ACEI, synergistic w/ loops. A: metabolic side effects
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| Mannitol: Use | sugar alcohol used to promote diuresis or prevent oliguric phase of ARF.
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| Dopamine: Use | naturally occuring catecholamine indicated for correction of hemodynamic imbalances present in shock or renal failure.
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| Which ABX -> ATN and what do they do or cause? | Aminoglycoside: Strepto, tobra, genti; increased dose -> toxicity, accumulate in proximal tubule, ototoxic, nephrotoxic. Amphotericin B: constriction of afferent arterioles, where toxicity occurs w/accumulation.
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| Lithium Toxicity | Tx: bipolar. Renal dysfn is primarily polyuria due to impaired concentrating ability. Also, CNS and CVS Sx. Tx: Supportive. Usually, toxicity occurs as result of inadequate fluid intake.
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| RCIN: Definition and Top 2 Risk Factors, Onset, Duration | RadioContrast Induced Nephropathy; defined as either greater than 25% creatinine or absolute increase in serum creatinine of 0.5 mg/dL. Top 2 risk factors: 1) Underlying CKD 2) Dehydration; Onset: 2 days, Duration: 7 days.
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| RCIN: Mechanism | 1) acute vasoconstriction induced by adenosine and endothelin. 2) oxidative stress on tubular cells 3) renal tubular cell toxicity from contrast accumulation in tubular cells
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| RCIN: Prophylaxis | 1) Use only when necessary 2) HYDRATION w/normal saline 3) low/iso-osmolar contrast 4) minimize contrast volume 5) N-acetylcysteine (scavenges free radicals)
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| What is the gold standard of GFR measurement? What method is typical? | Inulin lothalamate (untouched by kidneys and cleared through glomerulus function, giving precise clearance rate. We usually don't use this as eGFR is ALMOST as precise. (GFR (mL/min/1.73 m2) = 175 × (Crs)-1.154 × (Age)-0.203)
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| T/F: Creatinine levels give us a rough estimate of the GFR | True. Put in the eGFR equation, estimation becomes much more precise.
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| Chronic Kidney Disease: Risk Factors (a few top ones) | 1) DM, 2) HTN, CVD, Obesity, Metabolic syndrome, NSAIDs
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| Chronic Kidney Disease Staging | Stage 0: At risk patients Stage 1: Kidney damage w/ normal GFR Stage 2: GFR 60-89 Stage 3: GFR 30-59 Stage 4: GFR 15-29 Stage 5: GFR <15 or dialysis
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| What happens when there is low calcitriol? | Decreased Ca absorption from GI tract, increasing phosphate levels, lowering ionized calcium levels, thus calcium will be scavenged from bones. Low calcium levels stimulate parathyroid hormone secretion replacing calcified bone tissue with fibrous tissue.
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| Cincalcet | reduces parathyroid hyperplasia, increases parathyroid's Ca-sensing receptors decreasing hormone release (makes it think it is sensing more Ca than it actually is), helps us not scavenge Ca from bones
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| Metformin: When to stop it, Adverse | should stop if they become dehydrated (like surgery) as they will get N/V and we don't want to exacerbate volume depletion.
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| Metformin Induced Lactic Acidosis | largely eliminated in the kidneys, increases production/decreases clearance of lactate. Impairs ability of liver to remove lactate as blood pH falls. Take patients off metformin if they are in stage 3/4 of CRF.
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| Name two hypoglycemics | Sulfonylureas and Insulin
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| T/F: Statins are still effective even in renal failure | True
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| What does Ezetimibe do? | reduces cholesterol absorption at small intestine cellular brush border, but doesn't substantially reduce absorption of triglycerides.
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| What do you give for anemia? What do you want what levels to be at? Anything else you give? | Give EPO when hemoglobin levels drop below 9...want them at 11 or 12 g/dL. Levels of 13 and higher associated w/ stroke, MI, death from sludging. You also want to give iron with EPO to facilitate its absorption.
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| Iron | always given with EPO, oral sufficient but IV preferred (especially if on PPI). If taking orally, drink citirus juices. Only 25% is absorbed, leaving 75% in the GI darkening stools.
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| Phosphate | Dietary restriction sufficient for CKD. In later stages, phosphate binders like Ca salts or non-Ca phosphate binders may be necessary. Aluminum compounds are the best, but have some toxicity so are reserved for hyperphosphatemia.
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| Sevalamer | binds phosphate w/in intestinal lumen limiting absorption and decreasing serum phosphate w/o decreasing Ca. Can also bind to Vitamin D, E, A so administer at different times than those. Adverse: pruritis, vomiting, pharyngitis, limb/joint pain
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| T/F: Thiazides are preferential for diuresis at low GFRs | False, Loops are the best and work at GFRs as low as 5 mL/min
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| T/F: When left ventricular function depressed, spiralactone should be avoided. | True, use ACEI and BBs
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| Drug elimination by filtration controlled by these 3 things: | 1) GFR 2) plasma concentration of unbound drug 3) Extent of passive reabsorption of drug following filtration
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| Filtration has limited effect eliminating drugs that: (2) | 1) highly protein bound such as NSAIDs, penicillins, diuretics. 2) large molecular size or negative charges.
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| T/F: Active secretion results in the net transfer of the drug from the peritubular capillaries into the tubule lumen | True
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| Renal insufficiency can markedly alter pharmacokinetics for DOSING in the following ways (5) | 1) Absorption (PPIs)
2) Oral bioavailability
3) Volume of distribution (usually reduced [more impact on meds we use])
4) Drug binding to plasma proteins (recall this keeps drugs inactive)
5) Rates of metabolism and excretion (will it last too long?)
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| 4 ways renal failure complications affect drug absorption | 1) V/D in CKD 2) Hyperphosphatemia due to impaired excretion 3) Gastric pH increases in CKD 4) Bioavailability impacted as it is dependent on absorption.
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| T/F: With renal injury, drug metabolism may be decreased and levels of active drug increased, or levels of active metabolites decreased | True
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| Reasons to adjust doses in renal disease | since kidney is a major site of inactivation of drug, we don't have to give as much and what we give will last longer. This applies mainly to peptides like insulin, glucagon, parathyroid hormone and imipenem.
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| A decrease in protein binding from 99 to 95% results in how much of a rise in unbound or active drug concentration? | 4x
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| 3 ways to adjust the dose | 1) Extend the dosing interval 2) Reduce the maintenance dose 3) Administer a loading dose to achieve therapeutic levels quickly.
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| 4 specific medication considerations | 1) Dilantin: dose needs to be reduced 2) Digoxin: toxicity 3) Insulin: reduce dose 4) Acetaminophen (between this and NSAIDs, limited options...use small dose narcotics like morphine and codeine.
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