Respiratory/renal Test 4 Set2

Front 1

Intact Nephron Hypothesis of CKD (4)

Back 1

1)progressive kidney disease results from injury and loss of fxning nephrons resulting in a decline in kidney fxn over time
2)as nephrons die the remaining ones undergo adaptive changes by increasing single nephron GFR (resulting in incr glomerular pressure)
3)Incr glomerular pressure and plasma flow leads to structural damage (glomerulosclerosis)
4)progressive and continuous cycle of nephron destruction until ESRD results

Front 2

Glomerulosclerosis (2)

Back 2

1)hypertrophy
2)and irreversible loss of nephron fxn

Front 3

Progression of CKD is assessed by....

Back 3

GFR/CrCL

Front 4

SUSCEPTIBILITY (incr risk for development of CKD) risk factors (6)

Back 4

1)low income/education
2)black/asian/native american
3)advanced age
4)family history
5)dyslipidemia
6)reduced kidney mass/low birth weight

Front 5

INITIATION (directly initiates kidney disease) risk factors (5)

Back 5

1)DM
2)HTN
3)autoimmune disease
4)polycystic kidney disease
5)drug toxicity

Front 6

PROGRESSION (cause worsening kidney fxn and faster decline) risk factors (4)

Back 6

1)poor glycemic control in DM
2)elevated BP
3)high levels of proteinuria
4)smoking

Front 7

Assessment of Kidney Fxn (4)

Back 7

1)GFR/CrCL/CG
2)urine albumin (proteinuria is the key marker for structural kidney damage even w/ normal GFR)
3)albumin is used as most reliable marker of urine protein excretion
4)microalbuminuria is primary screening test for kidney damage

Front 8

Normal Albuminuria (3)

Back 8

a)spot urine collection less than 30 (mg albumin:gram creatinine ratio)
b)24hr urine collection less than 30mg/24hr
c)timed collection less than 20mcg/min

Front 9

Microalbuminuria (3)

Back 9

a)spot urine collection 30-300 (mg albumin:gram creatinine ratio)
b)24hr urine collection 30-300mg/24hr
c)timed collection 20-200mcg/min

Front 10

Macroalbuminuria OR Clinical albuminuria (3)

Back 10

a)spot urine collection more than 300 (mg albumin:gram creatinine ratio)
b)24hr urine collection more than 300mg/24hr
c)timed collection more than 200mcg/min

Front 11

Urine Albumin
a)how to collect
b)conditions that falsely elevate (5)
c)normal urine Cr excretion
d)protein excretion in severe nephropathy...

Back 11

a)atleast 2 specimens collected in 3month period should be abnormal before considering dx due to variability in urinary albumin excretion

b1)exercise within 24h
b2)infexn/fever
b3)pregnancy
b4)hematuria
b5)CHF

c)1-2g/day
d)3-3.5g/day

Front 12

Stage 1 CKD
a)GFR
b)desc

Back 12

1)GFR over 90
2)kidney damage with normal or incr GFR

Front 13

Stage 2 CKD
a)GFR
b)desc
c)symptoms

Back 13

a)60-89
b)kidney damage w/ mild GFR decr (adaptive changes compensate for decr fxnal mass)
c)asymptomatic

Front 14

Stage 3 CKD
a)GFR
b)desc
c)symptoms (3)

Back 14

a)30-59
b)moderate GFR decr (underlyin process may be reversed)

c1)nocturia
c2)HTN
c3)mild anemia

Front 15

Stage 4 CKD
a)GFR
b)desc
c)symptoms (4)

Back 15

a)15-29
b)severe GFR decr (irreversible decr in kidney fxn)

c1)nocturia
c2)worsening anemia
c3)metabolic acidosis
c4)incr K,P--decr Ca

Front 16

Stage 5 CKD
a)GFR
b)desc
c)symptoms (5)

Back 16

a)less than 15
b)ESRD (dialysis/transplant dependent to relieve s/sx)

c1)pruritis
c2)little/no urine
c3)worsening electrolyte imbalance
c4)bone pain/fractures
c5)intractable n/v

Front 17

Uremia?

Back 17

COVERS STAGE 4/5; s/x of stage 4/5 due to toxins building in blood

Front 18

When to screen in CKD (3)

Back 18

1)Catch it before stage 4
2)screen if person has risk factors b/c if you catch it in stages 1-3 you can slow damage
3)stages 4/5 it is hard to slow progression

Front 19

____ causes most ESRD (2)

Back 19

1)DM
2)HTN

Front 20

Mortality and ESRD (5)

Back 20

1)adverse outcomes of CKD include loss of kidney fxn, kidney failure AND
2)cardiovascular disease

1)leading causeS of death in ESRD is CV related events (MI)
2)infection
3)cerebrovascular disease

Front 21

Interventions to delay progression of CKD (5)

Back 21

1)optimize glycemic control in DM 1/2 (goal is A1c under 7%)
2)Goal BP is <130/80 (first line agents w/ proteinuria is ACEI/ARB)
3)optimize lipid levels (LDL under 100)
4)smoking cessation
5)restrict protein to less than 0.6g/kg/day

Front 22

CKD Complications (8 of many)

Back 22

1)anemia
2)CV disease
3)metabolic bone disease
4)malnutrition, vitamin deficiencies, anorexia
5)F&E disorders (na/K/water)
6)metabolic acidosis
7)uremia
8)pruritis

Front 23

HTN in CKD
a)importance (3)
b)goals of therapy (3)

Back 23

a1)75% of pts w/ CKD have HTN
a2)risk factor for kidney disease
a3)risk factor for CV disease

b1)BP below 130/80
b2)slow progression of kidney disease
b3)reduce risk of CV disease

Front 24

HTN in CKD tx (5)

Back 24

1)lifestyle mod (Na <2.4g/day)
2)consider pharmacologic therapy in all CKD pts to slow progression of CKD
3)follow JNC7 guidelines for HTN management
4)most CKD pts will require multiple agents to reach goals
5)maximize dose of one agent before adding another

Front 25

Pharmacologic therapy of HTN in CKD (5)

Back 25

1)preferred agent is ACEI/ARB (slow progression of CKD/decr proteinuria)
2)diuretic is 2nd line (CrCL over 30 use thiazide; under 30 use loop)
3)consider compelling indications when choosing additional agents
4)non-DHP CCB's decr proteinuria BUT may raise levels of transplant meds
5)K+ sparing diuretics/aldosterone antagonists incr risk of hyperkalemia in stage 4/5

Front 26

Anemia of CKD (def's)
a)heme
b)erythrocyte
c)hemoglobin
d)erythropoietin
e)erythropoiesis

Back 26

a)oxygen carrying iron complex found in hemoglobin
b)mature RBC
c)red respiratory protein of erythrocytes, transports oxygen from lungs to tissues
d)regulatory hormone responsible for stimulating erythropoiesis and for protecting erythroid precursor cells
e)differentiation of stem cells into erythrocytes

Front 27

____ are necessary for optimal erythropoiesis to occur (2)

Back 27

1)erythropoietin
2)adequate supply of iron

Front 28

Erythropoiesis feedback loop (6)

Back 28

1)hypoxia due to decr RBC count; OR decr availibility of O2 to blood; OR incr tissue demands for O2
2)=reduced O2 levels in blood
3)kidney releases erythropoietin
4)erythropoietin stimulates red bone marrow
5)enhanced erythropoiesis = more RBCs
6)incr O2 carrying ability of blood

Front 29

Iron Overview
a)adult total body iron content
b)diet consists of...
c)transported via...
d)HIGHLY CONSERVED (3)

Back 29

a)3.4g
b)10-20mg iron but only absorb 1-2mg (10%)
c)TRANSFERRIN (75% to bone marrow for Hgb; 10-20% stored in ferritin within RES)

d1)normal iron loss/day: 1-2mg/day
d2)no physiologic excretion
d3)recycled and replaced in balance

Front 30

Pathophysiology of Anemia of CKD (3)

Back 30

1)DUE TO IMPAIRED ERYTHROPOIESIS
2)endogenous erythropoietin production decr w/ impaired kidney fxn (= decr Hgb/RBC= anemia)
3)low iron stores in CKD (10% of normal)

Front 31

Low iron stores in CKD pts due to.... (4)

Back 31

1)decr iron uptake
2)low protein diet
3)phosphate binder therapy (binds iron supplements)
4)worse in dialysis pts

Front 32

RBC indices (in decr iron CKD) (3)

Back 32

1)typically hypoproliferative pattern (normolytic--normal shape; normochromic--normal color)
2)Microcytic (hypochromic pattern seen w/ iron decr)
3)Macrocytic (seen w/ folic acid &/or B12 decr)

Front 33

Clinical manifestations of CKD iron deficiency (4)

Back 33

1)pallor
2)decr cognition
3)LVH
4)CHF

Front 34

Evaluation of iron deficiency in CKD (4 and last one w/ 5)

Back 34

1)monitor Hgb levels
2)eval of anemia (Hgb less than 13.5 for males; 12 for females)
3)non-renal causes should be excluded

4a)labs: RBC indices
4b)absolute reticulocyte count
4c)iron profile
4d)WBC count
4e)platelet count

Front 35

Assessment of Iron Status**** (2 w/ the first having 3)

Back 35

1)TSAT 20-50%
a)measure of iron immediately available for erythropoiesis
b)indicates the saturation of transferrin w/ iron
c)total iron binding capacity (TIBC)--total capacity of transferrin to bind iron

2)serum ferritin 100-800 (measure of iron storage)

Front 36

Types of iron deficiencies (2)

Back 36

1)ABSOLUTE--Tsat less than 20, serum ferritin under 100 (IV IRON NEEDED)

2)Fxnal-- Tsat under 20; normal/elevated serum ferritin (GIVE IRON SUPPLEMENT)

Front 37

Oral Iron Replacement
a)clinical considerations (2)
b)ADR's (2)
c)how much to admin

Back 37

a1)may be used in pt W/O IV access who does NOT have absolute iron deficiency
a2)poor F--admin on empty stomach

b1)n/v--take w/ food/snack or switch to another salt form
b2)consipation/dark stool

c)need 200mg ELEMENTAL iron per day in divided doses

Front 38

Oral Iron Salts (5)

Back 38

1)ferrous sulfate
2)ferrous gluconate
3)ferrous fumarate
4)polysaccharide iron
5)heme iron polypeptide

Front 39

Ferrous Sulfate
a)common brand names (2)
b)units/day for 200mg elemental iron

Back 39

a1)Slow FE
a2)Fer-In-Sol

b)3tablets in divided doses

Front 40

Ferrous Gluconate
a)common brand names
b)units/day for 200mg elemental iron

Back 40

a)Feratab
b)5 tablets in divided doses

Front 41

Ferrous Fumarate
a)common brand names (2)
b)units/day for 200mg elemental iron

Back 41

a1)femiron
a2)feostat

b)3capsules in divided doses

Front 42

Polysaccharide iron
a)common brand names (2)
b)units/day for 200mg elemental iron

Back 42

a1)niferex
a2)nu-iron

b)2capsules in divided doses

Front 43

Heme iron polysaccharide
a)common brand names (2)
b)units/day for 200mg elemental iron

Back 43

a1)proferrin-ES
a2)proferrin-forte

b)17tablets in divided doses

Front 44

IV iron
a)clinical considerations (2)
b)common dosing (4)
c)ADR (4)

Back 44

a1)used when pt has IV access and ALWAYS when pt has absolute iron deficiency
a2)preps are large MW of iron and sugar

b1)admin 1000mg in divided doses
b2)only small doses by IV push
b3)larger doses over prolonged dosing interval
b4)do infusion over 1-2h or divided dosing over 8-10h AND maintenance doses weekly

c1)analphylaxis (TO IRON DEXTRAN)
c2)hypotension
c3)dizzy/HA
c4)arthralgia/back pain

Front 45

Test doses of IV iron? (2)

Back 45

a)recommended w/ iron dextran formulation to reduce risk
b)25mg slow IV push over 30s then observe pt over 1h

Front 46

Tx goals of IV iron (3)

Back 46

a)Tsat 20-50
b)ferritin 100-800
c)monitor iron monthly for 3months then once every 3months if Hgb stable

Front 47

Iron overload (4)

Back 47

a)deposits of excess iron may affect organ systems
b)may lead to cardiac, hepatic and pancreatic dysfxn
c)maintain serum ferritin and Tsat below upper threshold
d)dc iron if upper threshold or if symptomatic use deferoxamine (Desferal)

Front 48

IV iron preparations (3)

Back 48

1)iron dextran
2)ferric gluconate
3)iron sucrose

Front 49

Iron dextran
a)brand names (2)
b)test dose?
c)absolute iron deficiency dose
d)maintenance dose
e)considerations (2)

Back 49

a)InFeD, DexFerrum
b)YES (500mg in 250mL IV over 1h)
c)100mg IV x 10doses
d)50mg IV weekly

e1)must be processed by RES before stored and available for heme synthesis
e2)higher incidence of ADR's

Front 50

Ferric Gluconate
a)brand names
b)test dose?
c)absolute iron deficiency dose
d)maintenance dose
e)considerations (2)

Back 50

a)Ferriecit
b)NO
c)125mg IV x 8doses
d)62.5mg IV weekly

e1)hypersensitivity cross rxns w/ iron dextran possible
e2)preferred over iron dextran due to safety

Front 51

Iron Sucrose
a)brand names
b)test dose?
c)absolute iron deficiency dose
d)maintenance dose
e)considerations (2)

Back 51

a)Venofer
b)NO
c)100mg IV x 10doses
d)50mg IV weekly

e1)rare anaphylaxis rxns
e2)preferred over iron dextran due to safety

Front 52

Erythrocyte Stimulating Agents (ESA)
a)MOA
b)ADR's (4)

Back 52

a)stimulates erythropoiese by the same mechanism as endogenous erythropoeitin

b1)HTN
b2)HA/arthralgia/bone pain
b3)seizures
b4)thrombotic events (MI, CVA, TIA, PE) but RARE

Front 53

ESA black box warning (2)

Back 53

1)use lowest dose that will gradually increase the Hgb [] to the lowest level sufficient to avoid the need for RBC transfusion
2)ESAs incr risk for death and for serious CV events when admin to a target Hgb over 12

Front 54

Before starting ESA treatment... (3)

Back 54

1)other causes of anemia should be excluded (decr erythropoietin is only cause ESA treats)
2)HTN should be corrected (resistance to tx is caused by low iron)
3)eval iron status (Tsat over 20 and Ferritin over 100)

Front 55

Principles of therapy and monitoring of ESAs (4 and last one w/ 3)

Back 55

1)repletion and maintenance of iron balance for maximizing response
2)effect of therapy is dependent on dose/duration
3)reliance on Hct is NOT optimal for assessing response to ESA (use Hgb)

4)Hgb monitoring
a)monitor 2x/wk for 2-6wks @ initiation and after dose adjustments until stabilized
b)Hgb levels NOT over 12
c)Hgb levels NOT rise over 1 per 2wk time period

Front 56

Epoetin Alfa
a)brand names (2)
b)storage
c)half-life
d)starting dose

Back 56

a1)epogen
a2)procrit

b)refrigerate (36-46F)
c)4-13h IV, 27h SC
d)50-100U/kg 3x/wk IV or SC

Front 57

Darbepoetin Alfa
a)brand names
b)storage
c)half-life
d)starting dose

Back 57

a)Aranesp
b)refrigerate (36-46F)
c)21h IV, 49h SC
d)0.45mcg/kg 1x/wk IV or SC

Front 58

When to reduce ESA dose by 25% (2)

Back 58

1)Hgb approaches 12
2)Hgb incr greater than 1 in any 2wk period

Front 59

Incr ESA dose when? (2)

Back 59

1)Hgb does NOT incr by 2 after 8wks of therapy AND
2)Hgb remains at a level insufficient to avoid RBC transfusion

Front 60

Maintenance dose of ESA (2)

Back 60

1)individually titrate to achieve and maintain lowest Hgb sufficient to avoid need for RBC transfusion
2)NOT TO EXCEED 12

Front 61

Epoetin/Darbepoetin conversion (2)

ESA resistance? (3)

Back 61

1)if epoetin is given 2-3x weekly give darbepoetin 1x/wk
2)if epoetin is given weekly give darbepoetin every 2wks


1)if pt fails to respond or response decr, eval for causes of resistance
2)PRIMARY- iron deficiency
3)SECONDARY- infexn, inflammation, malnutrition, Al toxicity

Front 62

Pharmacodynamic effect of epoetin or darbepoetin on Hct? (3)

Back 62

1)average half-life of RBC is 64d
2)10d after therapy is when you see first signs of incr in RBCs
3)new steady state of RBCs after 64d (b/c its their half-life0

Front 63

Normal physiology of kidney and metabolic acidosis (2 w/ 2 each)

Back 63

1)enough H+ ion will be generated to:
a)reabsorb filtered bicarb
b)excrete 1mg/kg H+ per day to maintain A/B balance

2)urine is buffered to facilitate acid secretion
a)ammonia production in kidney
b)filtered phosphates excreted

Front 64

Pathophysiology of metabolic acidosis of CKD (3)

Back 64

1)renal ammonia generation and filtration of phosphate is DECR due to decr renal mass
2)results in decr urinary buffering capacity and continuous positive H+ balance
3)results in metabolic acidosis

Front 65

Consequence of metabolic acidosis (acidemia) (3)

Back 65

1)fatigue/poor exercise tolerance
2)incr hyperkalemia
3)decr albumin synthesis

Front 66

Tx GOALS of metabolic acidosis in CKD (4)

Back 66

1)goal is to get bicarb to 22 while avoiding metabolic alkalosis
2)maintain normal serum potassium (as acidosis corrects, serum K+ may decr0
3)maintain fluid balance (monitor for fluid retention due to Na content of supplements)
4)improve pt symptoms (fatigue/exercise intolerance)

Front 67

Alkalinizing Agents (4)

Back 67

1)Sodium citrate and citric acid
2)Tricitrate (potassium citrate, sodium citrate, citric acid)
3)Potassium bicarb, potassium citrate
4)sodium bicard tablets

Front 68

Sodium citrate/citric acid
a)brand names (2)
b)how it works
c)dosing

Back 68

a)Bictira oral solution, Bicitra-LC oral solution
b)citrate is rapidly metabolized to bicarb
c)1mL solution = 1mEq bicarb equivalent

Front 69

Tricitrate (potassium citrate, sodium citrate, citric acid)
a)brand names (3)
b)how it works
c)dosing (3)

Back 69

a)Polycitra, Polycitra-LC, Polycitra-K
b)citrate rapidly metabolized to bicarb

c)1mL = 2mEq bicarb equivalent
a)polycitra/LC: 1mEq K and 1mEq Na per 1mL
b)polycitra-K: 2mEq K+ per 1mL

Front 70

Potassium bicarb, potassium citrate
a)brand names (2)
b)how it works
c)dosing? (2)

Back 70

a)K-lyte, K-lyte DS TABLETS
b)effervescent tablet that disolves in water

c)K-lyte TABLET has 25mEq bicarb equivalent
c)K-lyte DS TABLET has 50mEq bicarb equivalent

Front 71

Sodium bicarb tablets
a)dosing

Back 71

650mg = 7.7mEq bicarb equivalents

Front 72

Alkalinizing agents
a)ADR's (3)
b)drug interactions

Back 72

a1)n/v/d
a2)metabolic alkalosis
a3)ab cramps/bloating

b)urinary alkalinization causes effect on drug elimination

Front 73

Alkalinizing Agents counseling (4)

Back 73

1)admin all products (tabs or liquids) after meals
2)crystals/effervescent tablets dissolve in chilled water prior to admin
3)refrigerate liquid solutions and dilute 1:1 with chilled water to make more palatable
4)avoid citrate products w/ Al-containing antacids (enhances Al-related toxicities)

Front 74

Average values of
a)water
b)Na
c)glucose
d)urea
amount filtered per day, amount excreted, % reabsorbed WITH NORMAL KIDNEY FXN

Back 74

a)180L/day filtered, 1.8L excreted, 99% reabsorbed

b)630g/day filtered, 3.2g excreted, 99.5% reabsorbed

c)180g/day filtered, 0g excreted, 100% reabsorbed

d)56g/day filtered, 28g excreted, 50% reabsorbed

Front 75

With normal kidney fxn:
a)FEna
b)usual sodium intake
c)water balance (reabsorption vs. excretion) is maintained by...
d)urine is concentrated/diluted b/w...

Back 75

a)1-3%
b)120-150mEq per day
c)ADH which is synthesized in response to extracellular volume and serum osmolality
d)50-1200 to maintain fluid balance

Front 76

In stage 4/5 CKD loss of kidney fxn results in...(regards to Na/water balance in CKD) (6)

Back 76

1)decr GFR enough that Na/water retention occurs causing an incr in intravascular volume
2)this elevates left atrial pressue resulting in secretion of ANP causing a diuretic effect
3)incr in FEna up to 20% can occur
4)with incomplete compensatino a slightly volume overloaded state occurs
5)urine osmolaltiy becomes fixed similar to plasma (300) b/c loss of ability to concentrate urine
6)unable to effectively adapt to abrupt changes in diet Na/water

Front 77

Clinical management of Na/water in CKD (3)

Back 77

1)avoid adding salt to diet
2)avoid large changes in diet Na/water
3)diuretic therapy may be needed to control edema/BP

Front 78

Loop diuretic and management of diuretic resistance (in CKD) (2)

Back 78

1)decr filtration in CKD results in decr delivery of diuretic to the site of action
2)so larger doses of diuretic may be reqd in pts w/ CKD than pts w/o

Front 79

3 steps in loop diuretic use and management of diuretic resistance

Back 79

1)find the effective diuretic dose
2)maximize Na excretion
3)consider distal tubule hypertrophy (DTH)

Front 80

Find the effective diuretic dose
a)principle (2)
b)management (4)

Back 80

a1)decr GFR = decr diuretic [] so incr dose
a2)ceiling dose is single dose above which diuresis is NOT incr and there is an incr is ADR's

b1)admin usual dose of loop diuretic
b2)eval diuresis by measured urine output over time
b3)adequate UO = effective diuretic dose (>1mL/kg/hr)
b4)inadequate UO = double diuretic dose and readmin (keep doubling til diuresis achieved or ceiling dose reached)

Front 81

Maximize Na excretion
a)principle
b)management

Back 81

a)w/ severe kidney dysfxn overall Na excretion is small due to few fxning nephrons

b)admin effective diuretic dose (or ceiling dose) as frequently as needed to achieve goal diuresis

Front 82

Maximize Na excretion
a)principle
b)management

Back 82

a)w/ severe kidney dysfxn overall Na excretion is small due to few fxning nephrons

b)admin effective diuretic dose (or ceiling dose) as frequently as needed to achieve goal diuresis

Front 83

Consider distal tubule hypertrophy (DTH)
a)principle (3)
b)management (3)

Back 83

a1)chronic mobilization of Na from the ascending LoH past the distal tubule results distal cellular hypertrophy
a2)AND a greater capacity for Na reabsorption in the distal portion of the nephron (= DECR DIURETIC RESPONSE)
a3)REFERS TO DIURETIC RESISTANCE that may occur w/ chronic/long-term loop diuretic use

b1)acute--admin HCTZ 25-50mg OR metalazone 2.5-5mg po
b2)in 60min follow with effective/ceiling dose of IV loop
b3)freq. monitoring of F&E is critical

Front 84

Monitoring parameters for diuretic therapy
a)subjective (2)
b)objective (3)
c)physical exam (3)
d)lab (2)

Back 84

a)SOB, DOE

b)urine I/O, body wt (want less than 1kg loss/day), BP

c1)signs of volume overload: rales
c2)JVD
c3)peripheral edema

d1)chem7 for renal fxn/electrolytes
d2)Mg/Ca if indicated

Front 85

Pathophysiology of K balance in CKD (4/5) (2)

Back 85

1)K+ excretion maintain by incr in distal tubular secretion (FEk = 125% normal is 25%)
2)until ESRD develops then excretion of K thru feces maintains balance

Front 86

Clinical considerations in CKD of K+ balance (2)

Back 86

1)poor tolerance of excess K+ supplementation (but diet restriction not necessary til ESRD)
2)K+ sparing diuretics, non-selective BB, ACEI/ARB can lead to exacerbation of K+ imbalance

Front 87

Management of K+ balance in CKD (2 and latter has 2)

Back 87

1)consistent diet intake of K+ (50-80mEq/kg of IBW)
2)prevent constipation by:
a)incr diet fiber thru food or bulk-forming laxatives (Metamucil or Fibercon) w/ adequate fluid intake
b)regular use of stool softener: docusate Na 100mg bid OR docusate Ca 240mg qd

Front 88

Vitamin admin in CKD (3 and the last has 6)

Back 88

1)A,K,E supplements not recommended
2)D supplements individualized

3)B1,2,6,12
a)C
b)biotin
c)pantothenic acid
d)niacinamide
e)folic acid
WATER SOLUBLES (OFTEN DEFICIENT)

Front 89

Routes to renal osteodystrophy (2 main ones)

Back 89

1)hypocalcemia leads to INCR PTH
2)impaired bone mineralization

Front 90

Routes to hypocalcemia (2 w/ 3 each)

Back 90

1)nephron loss leads
a)impaired phosphate excretion so phosphate retention leading to...
b)hypocalemia

2)nephron loss
a)decr 1,25 (OH) vitamin D
b)decr intestinal Ca absorption
c)hypocalcemia

Front 91

Other consequences of nephron loss and Renal Osteodystrophy (2 w/ 3,2)

Back 91

1)impaired phosphate excretion leads to incr phosphate levels
2)leads to incr CPP (calcium phosphate product/complex)
3)leads to soft tissue metastatic calcification

1)decr 1,25 (OH) vitamin D leads to impaired bone mineralization
2)leads to osteomalacia leading to renal osteodystrophy directly

Front 92

Consequences of hypocalcemia in Renal Osteodystrophy (5)

Back 92

1)INCREASED PTH WHICH LEADS TO:
a)incr renal Ca reabsorption
b)decr renal tubular reabsorption of phosphate
c)incr demineralization
d)this leads to osteitis fibrosa cystica
e)which directly leads to renal osteodystrophy

Front 93

2 other mechanisms of renal osteodystrophy

Back 93

1)metabolic acidosis
2)aluminum overload

Front 94

Laboratory markers of Renal Osteodystrophy (4)

Back 94

1)phosphorus: hyperphosphatemia directly/indirectly lowers serum calcium

2)calcium: hypocalcemia stimulates PTH production

3)PTH: hyperparathyroidism is a marker of Ca and phosphate bone resorption

4)Alkaline phosphate: though non-specific, elevation may inidicate ongoing bone resorption

Front 95

Skeletal complications of renal osteodystrophy (3 w/ 2each)

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1)OSTEITIS FIBROSA CYSTICA
a)due to high bone turnover
b)generally associated w/ high circulating levels of PTH

2)OSTEOMALACIA
a)due to low turnover of bone
b)generally associated w/ low vitamin D activity

3)ADYNAMIC BONE DISEASE (FROZEN BONES)
a)a low turnover bone disease
b)high Ca-containing phosphate binders and high vit D use leading to OVER SUPPRESSION OF SERUM PTH

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Other complications of Renal osteodystrophy (5)

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1)incr vascular calcification
2)CV disease
3)death in hemodialysis pts
4)secondary hyperparathyroidism w/ PTH over 495 = incr morbiditiy/mortality (including sudden death)
5)risk of death 34% higher w/ Ca-P product of over 72 vs. under 52

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Management of high phosphorus in Renal Osteodystrophy includes... (2)

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1)diet P restriction (0.6-0.8g/kg/day) of protein and limit intake of foods w/ phosphate additives
2)Phosphorus binders (limit GI absorption of phosphorus)