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109 Cards in this Set
- Front
- Back
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What is CKD? Define
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Chronic Kidney Disease
Term advocated to encompass all stages of CRF and ESRD Defined as a structural or functional damage to the kidneys for at least 3 months |
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Define structural CKD
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blood/protein in urine
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Define functional CKD
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reduction in GFR
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ACEi what do they ?
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reduce glomerular capillary pressure by vasodilation of the efferent arteriole
they also reduce risk of progression from micro to macro albuminuria additionally they are the strongest data in pts with type one DM |
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Name an ACEi drug
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- pril
captropril enalapril benazepril |
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adverse effects of ACEi
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increase potassium, incresae Scr, cough, angioedema
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ARBs do what?
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selective inhibition of Ag II at the AT1 receptor
presumed more complete attenuation of the Ag II action becasue non-ace pathways can generate AgII |
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What types of pharmacotherapy can you use for HTN/proteinuria ?
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ACEi
ARB CCB Diuretics B-Blockers Combination |
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Who does an ARB work the best for?
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type II DM
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name an ARB
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Lostartan
Irbesartan Valsartan |
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What adverse effects are found in the ARBs
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increase K, increase scr, with much less cough and angioedema then the cough
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CCB do what?
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reduce Glomerular pressure and reduce proteinuria
may prevent mesangial expansion and renal scarring |
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what are CCB used for? mainstay or add on
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add on therapy
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Diuretics do not lower what?
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do not lower urine protein excretion
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Beta blockers do not lower what?
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do not decrease urine protein excretion
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both diuretics and beta blockers are used as mainstay or add on therapy?
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add on therapy
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acei and arb combination therapy does what to angiotensin II?
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decreaseing angiotensin II to a greater extent than either agent alone
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acei and arb combination therapy does what urinary albumin?
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decreases it by 25-45% in type 1 and type 2 diabetics compared to monotherapy with acei or arb
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why would u add an aldosterone receptor antagonist added to ACEi or ARB
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Plasma aldosterone levels increase in patients with CKD and may contribute to renal injury, whereas blockade of RAA does not necessarily result in a constant decrease in plasma aldosterone levels
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examples of aldosterone receptor antagonist added to ACEi or ARB are?
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Inspra ( eplerenone ) = aldosterone receptor antagonist
Aldactone ( spironolactone ) = aldosterone receptor antogonist |
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what must you follow in the aldosterone receptor antagonist durgs when they are added to and ACEi or ARB
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K levels
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What is the strongest predictor for developing ESRD and CV morbidity and mortality
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Microalbuminuria
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What does ACEi and ARBs lower independent of antihypertensive effect?
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urinary protein excretion
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Major complications with CKD include? (4)
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Anemia
Secondary hyperparathyroidism Hyperkalemia Metabolic acidosis |
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why do those who have CKD experience anemia?
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decrease production in erythropoietin
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decribe anemia of CKD
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normocytic, normochromic
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to diagnose anemia of CKD you will see what in the labs
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decrease Hgb/Hct
decrease Reticulocyte count Symptoms of hypoxia |
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there are 3 ways to treat anemia of CKD name them
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Erythropoietin
Iron supplementation (IV therapy) Iron maintenance (oral therapy) |
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what are the 3 erythropoetin therapy choices?
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Epoetin or Procrit ( epoetin alpha )
Aranesp ( darbepoetin ) This is a Novel erythropoiesis stimulating protein (NESP) with a longer half-life |
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what is the mechanism of action for erythropoetin therapy
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1. Stimulates proliferation and differentiation of RBC precursors
2. Increases Hgb synthesis 3. Hastens release of reticulocytes from bone marrow |
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what are the adverse effects of erythropoetin?
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HTN and increased risk of thrombotic events
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there are cases of anemia of CKD where epo therapy is not working. why isn't it working?
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iron deficiency
infection/inflammation chronic blood loss folate/B12 deficiency Hemolysis |
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What is the goal for iron supplementation therapy?
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to prevent iron deficiency and maintain adequate iron stores
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what is a supplemental therapy to erythropoetin for anemia of CKD
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iron to promote adequate response to erthropoetin
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How do you diagnosis Fe deficiency anemia
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decreae MCV <80
decrease serum Fe increase TIBC |
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Diagnosis of IDA
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TSAT= Serum Fe/ TIBC x 100
TSAT= % iron immediately available for erythropoiesis Serum ferritin <100ng/ml |
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IV iron products: 3
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Iron dextran: InFeD, Dexferrum
Requires a 25mg IV test dose before first dose because of possible anaphylactoid reactions Sodium ferric gluconate complex: Ferrlecit ADE: hypotension (infusion related) Iron sucrose product: Venofer ADE: hypotension (infusion related) |
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what do you monitor with IV iron products? and when
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TSAT and ferritin in 1 month
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what CKD/ESRD pts do not need an oral iron therapy
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Those with a TSAT>50%
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names the oral iron therapy
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Ferrous sulfate
Ferrous gluconate Ferrous fumarate-Chromagen |
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which should you correct first in CKD pts, iron or erythropoietin?
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In patients with anemia of CKD, ALWAYS correct iron deficiency prior to or in conjunction with erythropoietin therapy
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when is an IV iron required
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whent he TSAT<20%
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pathophysiology of secondary hyperparathyroidism is?
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Initiating event is a decrease in Phos elimination by the diseased kidney, and a decrease in the active form of vitamin D production
increase serum Phos levels leads to decrease calcium levels The body’s response to hypocalcemia and decrease active vitamin D production is to stimulate PTH production |
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Complications of SHPT(secondary hyperparathyroid)
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Skeletal and soft tissue calcification
Cardiac Non-cardiac |
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Other complications of SHPT include bone problems.. elaporate
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Renal osteodystrophy = disorders of calcium, phosphorus and bone, in chronic renal disease.
Osteitis fibrosa cystica = most common osteodystrophy . Hyperphosphatemia of CKD -> hypocalcemia -> ↑ PTH -> cystic bone lesions with bone pain and/or pathologic fractures Osteomalacia = CKD -> ↓ active Vit . D -> ↓ G.I. Tract absorption of Ca & phosphorus -> ↓bone mineralization -> bone pain and/or pathologic fractures. |
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A non-pharmacologic way to improve SHPT is
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Restrict dietary phosphorus intake
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Pharmacological ways to improve SHPT is to give them?
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Phosphate binders
Correct hyperphosphatemia Vitamin D therapy/ calcimimetics decreases PTH secretion |
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What do phosphate binders do?
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Binds both exogenous phosphorus from gut and endogenous phosphorus from recirculation. This complex is subsequently eliminate in the feces.
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How must you take a phosphate binder to optimize their binding effect?
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WIith MEALS!
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Phosporus is NOT removed by Dialysis true or false
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false it is minimally removed by dialysis
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name the 4 major categories of phosphate binders
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Calcium containing products
Aluminum containing products Nonabsorbable polymer Other |
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Calcium containing products: name them and there s/e
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Calcium carbonate
Calcium acetate, Constipation, hypercalcemia, |
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Aluminum containing products name them and there s/e
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Amphojel, Alu-tab
Prevents hypercalcemia Aluminum toxicity, encephalopathy |
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ther are two medications used as phosphate binders wthich are not an aluminum containing product or a calcium containing product ?
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RenaGel
Does not contain calcium, aluminum or magnesium Risk of hypercalcemia is reduced Lanthanum Newest agent Chewable, low absorbability, phosphate binding similar to aluminum, more effective than calcium salts N/V, increase pill burden, $$$$ issues |
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How does Vitamin D therapy work?
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Inhibit PTH secretion; promotes GI absorption of calcium
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name the vitamin D therapy agents and their adverse effects
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Calcitriol (Rocaltrol )
Paricalcitol (Zemplar ) hypercalcemia |
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in summary what should one control with a SPHT pt
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Control of hyperphosphatemia with phosphate binders
Supplementation with Vit D analogs and/ or calcimimetics |
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why does hyperkalemia occur
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Redistribution of K+ into extracellular fluid during metabolic acidosis ( as H+ goes into cells, K+ comes out into plasma )
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how do u treat hyperkalemia
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Treatment depends on serum K+ level as well as presence or absence of EKG changes
Therapy usually initiated when K > 5.5mEq/L |
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how does insulin effected K+?
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Shifts extracellular K+ back into cell
Insulin stimulates K+ uptake by skeletal muscle and hepatic cells while glucose is given to avoid hypoglycemia Therefore give insulin IV + IV glucose (dextrose) |
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Sodium polystyrene + sorbitol (Kayexalate) is used to treat what? and how does it work?
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Less rapid effect than insulin in
Hyperkalemia shifting K+ back into the cells Exchanges sodium for K+ in the GI tract Maintenance therapy, as needed |
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other pharm that is mentioned with hyperkalemia (3) are but not mainstay?
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Calcium gluconate i.v.
No direct effect on K+ levels; protects myocardium Sodium bicarbonate Corrects acidosis 50 mEq IV Dialysis |
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What is the mechanism of action of insulin in reversing hyperkalemia?
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a. Protects the myocardium in the presence of EKG changes
b. Stimulates potassium uptake by skeletal muscle cells c. Stimulates sodium uptake in the gastrointestinal tract d. It does not directly reverse hyperkalemia but has an indirect effect on potassium levels |
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What is the main stay treatment for metabolic acidosis?
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Bicarbonate replacement therapy:
Sodium bicarbonate tablets 650mg (7.7 mEq of bicarbonate) Bicitra (sodium citrate and citric acid) 1ml= 1mEq of bicarbonate |
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What happens if acidosis is not corrected in a timely fashion?
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Buffering excess H+ ions may be accomplished by the release of calcium and phosphorus from bone thereby worsening bone disease
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What vitamins are water soluble and removed by hemodialysis?
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Vit C
B complex Folic Acid |
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What vit are not dialyzable and can accumulate in dialysis pts?
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A, D, E, K
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wHAT IS COMMONLY USED AS VITAMIN PREPARATIONS?
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Nephrocaps
Renal multivitamin Formula |
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Why do many patients with CKD often experience suboptimal care?
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Many patients with CKD go undetected
Care is fragmented among many health care practitioners There is an under-utilization of interventions to prevent progression of kidney disease |
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What is the goal of overall therapy in CKD pts?
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Goal of therapy is to stabilize renal function, and prevent or delay the need for dialysis
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What is the major intracellular cation? and its normal?
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K+ 3.5-5
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Potassium effects what activity?
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neuromuscular - cardiac conduction
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Hypokalemia is defined as
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(K+) < 3.5 mEq/L
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what is the most common electrolyte abnormality?
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hypo K
Usually well tolerated but can be life-threatening in severe cases |
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What is the etiology of hypo K? fyi there are a lot
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1. Drug therapy
2. Renal potassium wasting 3. Metabolic alkalosis ( which causes K+ to move into cells ) 4. GI losses (diarrhea/vomiting) 5. Inadequate intake 6. Magnesium depletion Reduces intracellular potassium concentrations Promotes renal potassium wasting |
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How do those with hypo K present?
Mild vs. severe presentation |
Mild (K+ 3-3.5mEq/L): N/V, weakness, constipation, myalgia, fatigue
Severe (K+ < 2.5mEq/L): muscle necrosis, paralysis, respiratory dysfunction. Cardiac arrhythmias: EKG changes: ST depression, t-wave inversion, u-wave elevation, wide QRS, heart block |
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Treatment of Hypokalemia
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Correct any underlying acid-base disorder
Encourage increase in potassium rich diets (potatos, beans, bananas, tomato paste,cantaloupe ) 3-3.5mEq/L: debatable to start therapy except in patients with underlying cardiac disorder < 3mEq/L: always treated to reach goal 4mEq/L Oral therapy preferred… much safer |
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what is the general rule for the treatment of hypokalemia?
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For every 0.1 mEq/L fall in potassium from 3.5mEq/L there is a corresponding 10 mEq deficit
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Should one give potassium in the IV form?
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only in severe cases, or NPO
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in what formulation should potassium be given?
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Potassium should be mixed in 0.9% NSS or 0.45% NaCl, NOT dextrose, because the dextrose increases insulin release, which drives K+ into cells, exacerbating the plasma hypokalemia.
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it is a good idea to monitor what during infusion of potassium?
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ECG
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What does magnesium do?
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Acts as a cofactor in many enzyme systems (ATP production)- role in neuromuscular function
Plays a significant role in renal reabsorption of K+ |
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what organ regulates the mg balance? normal?
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Kidney 1.5-2.4mg/dl
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hypomagnesaemia associated with WHAT disorders?
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GI tract:
malnutrition, alcoholism, malabsorption, diarrhea Kidney: Increased renal excretion: hypercalcemia, osmotic diuresis Drugs: Aminoglycosides, diuretics, digitalis & others |
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how will someone with hypo MG present?
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Neuromuscular: facial twitch, tremors, ataxia, tetany, seizures
Cardiac: atrial and ventricular arrhythmias, torsades de pointes Hypokalemia Hypocalcemia |
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how do u treat hypo MG ?
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1. Correct underlying cause
2. Supplement magnesium: oral, IV, IM 3. Asymptomatic (> 1 mEq/l): oral Milk of magnesia Magnesium gluconate Diarrhea is dose limiting adverse effect 4. Severe<1 mg/dl should be given I.V. |
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Hyper MG etiology?
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1. Renal insufficiency
2. Excessive intake (cathartics- Magnesium citrate) 3. Iatrogenic: MgSo4 given for eclampsia or severe pre-eclampsia 4. Hypothyroidism |
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presentation of hyper MG? mild vs. severe presentation?
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Mild usually asymptomatic
Moderate: N/V, loss of reflexes, hypotension, bradycardia, ECG changes (increase PR and QRS) Severe: Paralysis, coma, respiratory depression, AV block, cardiac arrest |
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Hyper MG Treatment
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1. Correct underlying cause
2. Intravenous calcium 3. Loop diuretic: Furosemide 4. Hemodialysis |
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Phosphorus is found where?
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Normal range 2.5-4.5 mg/dl
Majority in bones and soft tissues |
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what purpose does phosphorus have in the body?
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1.Phospholipids serve as critical elements in the structure of cell membrane
2.Phosphorus is the source high-energy bonds in the form of adenosine triphosphate (ATP) |
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Hypo P etiology? 3 ways
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1. Decreased intake: malnutrition, alcohol abuse
2. Decreased absorption: Vitamin D deficiency, hypoparathyroid, steroids, phosphate binders 3. Increased elimination: osmotic diuretics |
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presentation of Hypo P is ?
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Usually asymptomatic (1.5-2.5 mg/dl)
Cardiac: arrhythmias Muscular: myalgia, rhabdomyolysis Hematologic, Pulmonary and Neurologic: (lynch deleted what happens just that stuff happens in these three) |
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tx for hypophosphatemia
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Mild to moderate: asymptomatic given orally
Moderate to severe: given IV Parenteral phosphate: Na+ and K+ salts |
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Calcium is used in the body for?
3 major and 3 minor |
1. Calcium is vital for the functioning of cell membranes
2. Propagation of neuromuscular activity 3. Regulation of endocrine and exocrine function 1. Bone metabolism 2. Muscle contraction 3. Cardiac function |
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what are disorders of calcium related to?
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extracellular calcium concentrations
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what contains more than 99% of total body stores of calcium
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skeletal bone
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about 46% of ECF calcium is primarily bound to...
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plasma proteins (albumin)
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what is the active form of CA
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unbound or ionized
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what does extracellular calcium include?
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bound and unbound calcium
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hypo Ca causes of it?
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1. Post-op hypoparathyroidism
2. Renal insufficiency 3. Vitamin D deficiency -> check Vit D level 4. Magnesium deficiency Drugs ( loops, calcitonin, bisphosphonates,) ( Remember: thiazides ↓renal calcium excretion & can therefore be used to treat osteoporosis, whereas loop diuretics ↑ calcium excretion & can be used to treat hypercalcemia.Calcitonin & the bisphosphonates are used for osteoporosis.) |
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hypo CA manifestations:
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Neuromuscular: paresthesias
muscle cramps hypocalcemictetany** CV: ↓ myocardial contractility bradycardia hypotension |
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what is the PE test for hypo CA
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Chvostek sign
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What levels are measure in a BMP
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Na
K Ca Cl HCO3 Glucose BUN Creatine |
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what is a CMP?
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BMP plus phosphorus
Albumin and total protein Bilirubin ALT,AST, Alk phos |
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Tx for Hypo CA
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1. Asymptomatic associated with hypoalbuminemia
Oral therapy: Citracal + D ( elemental calcium) 2. Severe or symptomatic: I.V. calcium chloride or calcium gluconate Both: Monitoring every 4-6 hours and reassess |
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Hyper CA causes?
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Cancer
Primary hyperparathyroidism Thiazide diuretics, others |
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Hyper CA presentation
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< 13 mg/dl usually asymptomatic
> 13 mg/dl Acute: anorexia, N/V, constipation, polyuria, Chronic: metastatic calcification, nephrolithiasis > 15mg/dl = Hypercalcemia crisis Can lead to renal failure, coma, ventricular arrhythmias and death |
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Tx: hypercalcemia (7) what to do for crisis, if they have PTH, cancer, general, acute or chronic txs
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Hypercalcemia crisis requires dialysis
Surgery in PTH disorders Reduction of tumor load Volume expansion Calcitonin: inhibiting bone resorption and decreases renal reabsorption Loop diuretics Furosemide Ethacrynic acid Bisphosphonates: potent inhibitors of bone resorption Aredia ( pamidronate IV Others Limited role in acute treatment |
