Chronic Kidney Disease

Front 1

A progressive loss of renal function over months to years
(replacing normal kidney tissue with fibrotic tissue)

Back 1

Chronic Kidney Disease

Front 2

Chronic Kidney Disease

Back 2

presence of structural kidney damage and/or GFR <90mL/min for 3 months or more

Front 3

what is the proposed mechanism or chain of events in CKD

Back 3

1. Loss of nephron mass
2. Glomerular capillary HTN
3. Proteinuria

Front 4

three major risk factors for development of CKD

Back 4

1. Diabetes mellitus
2. HTN
3. Glomerulonephritis

Front 5

What is the most common risk factor of CKD

Back 5

Diabetes Mellitus

Front 6

accumulation of glycated products leads to loss of intraglomerular pressure, resulting in scarring of glomerular capillaries

Back 6

Diabetes mellitus(most common risk factor for CKD)

Front 7

higher BP in glomerular capillaries lead to damage to vessels, lose intraglomerular pressure, resulting in nephroschlerosis

Back 7

HTN(risk factor of CKD)

Front 8

Helpful in identifying CKD at risk- patients

Back 8

increased age, racial minority, low birth weight, genetics, hyperlipidemia

Front 9

These factors hasten the functional decline and increase risk of ESRD one damage has been done

Back 9

uncontrolled hyperglycemia and HTN, proteinuria, obesity, smoking, hyperlipidemia

Front 10

Amount of protein on dipstick or in 24hr collection that quantifies for proteinuria

Back 10

300mg/day

Front 11

Stage 3 CKD

Back 11

GFR = 30-59ml/min
(moderately decreased)

Front 12

Stage 2 CKD

Back 12

GFR = 60-89ml/min
(mildly reduced)

Front 13

Stage 4 CKD

Back 13

GFR = 15-29ml/min
(severely decreased)

Front 14

Stage 5 CKD

Back 14

GFR = <15ml/min (or on dialysis)
(ESRD or kidney failure)

Front 15

Do you use Cockrault Gault equation when patient is on dialysis?

Back 15

No. GFR is automatically <10ml/min

Front 16

common symptoms of CKD

Back 16

fatigue, cold intolerance, shortness of breath, palpitations, muscle cramps, depression

Front 17

Signs of CKD

Back 17

elevated BUN and SCr, electrolyte problems, HYPER(Mg, PO4, Ca), anemia, decreased OU, decreased Vit D, Acidosis, Edema

Front 18

how do ACEIs/ARBs help with CKD

Back 18

reduce blood pressure, lower proteinuria

Front 19

Goal Blood Pressure

Back 19

<130/80mmHg

Front 20

2 major adverse events when patient with CKD is taking ACEIs/ARBs

Back 20

acute worsening of renal function and hyperkalemia

Front 21

lisinopril(Zestril)
captopril(Capoten)
ramipril(Altace)
enalapril(Vasotec)

Back 21

Angiotensin Converting Enzyme Inhibitors (ACEIs)

Front 22

irbesartan(Avapro)
candesartan(Atacand)
losartan(Cozaar)
valsartan(Diovan)

Back 22

Angiotensin Receptor Blocker (ARB)

Front 23

Issues when Uremic Waste accumulates

Back 23

1. coronary artery disease
2. pericarditis
3. uremic bleeding
4.uremic encephalopathy
5. pruritis

Front 24

circulating toxins cause chronic inflammation. Inflammation increases risks of plaque rupture, clot formation, MI

Back 24

Coronary artery disease(uremic waste accumulation)

Front 25

inflammation of pericardial sac. If severe, restrict movement of heart, reducing stroke volume

Back 25

Pericarditis (uremic waste accumulation)

Front 26

clotting function impaired because toxins coat platelets.

Back 26

Uremic Bleeding (uremic waste accumulation)

Front 27

toxins in CNS interfere with neuronal activity, displace neurotransmitters

Back 27

Uremic Encephalopathy

Front 28

Toxin enter the skin

Back 28

Pruritis

Front 29

Signs and Symptoms of Uremic Waste Accumulation

Back 29

fatigue, weakness, shortness of breath, mental confusion, bleeding

increased BUN/SCr, EKG changes, bleeding on the brain

Front 30

how do you treat uremic waste accumulation

Back 30

remove the waste with dialysis or transplant

Front 31

Main issue with RAAS activation

Back 31

HTN

Front 32

Signs and Symptoms of RAAS activation (HTN)

Back 32

usually asymptomatic
blurred vision or confusion(HTN emergency)

BP > 130/80mmHG

Front 33

how many drugs are commonly used to treat HTN

Back 33

3-4 medications

Front 34

what is the treatment of HTN

Back 34

1. sodium restriction to 2-3g/day
2. ACEIs/ARBS (preferred)

Front 35

If blood pressure is greater than 130/80, what is the first step taken according to JNC-7

Back 35

Starting ACEI or ARB

Front 36

If ACEI or ARB doesnt lower blood pressure, according JNC-7 what is the step 2

Back 36

adding a diuretic

Front 37

According to JNC-7, if CrCl is greater than or equal to 30 use...

Back 37

thiazide diuretic

Front 38

According to JNC-7, if CrCl is less than 30 use...

Back 38

loop diuretic

Front 39

Left ventricular hypertrophy, pulmonary edema, and GI edema are associated with what?

Back 39

Fluid overload

Front 40

What is Left Ventricular Hypertrophy?

Back 40

harder for heart to circulate blood, pumps harder and begins to hypertrophy, enlarge heart requires more oxygen. early steps of heart failure

Front 41

fluid gets into lungs, enters alveoli, cannot perform gas exchange

Back 41

pulmonary edema

Front 42

absorption of nutrients and meds reduced because of edematous mucosa

Back 42

GI edema

Front 43

Signs and Symptoms of Fluid Overload

Back 43

weight gain, fatigue, shortness of breath, metallic taste

edema, changes in UO, foaming of urine, ab distension

Front 44

Can you use sodium and water restriction in the treatment of fluid overload?

Back 44

yes

Front 45

What are the four different types of diuretics?

Back 45

1. Thiazides
2. Loops
3. Carbonic Anhydrase Inhibitors
4. Potassium-Sparing

Front 46

are thiazide diuretics effective at CrCl <30ml/min

Back 46

No

Front 47

HCTZ, metolazone

Back 47

thiazides

Front 48

using dosing of furosemide which is a loop diuretic

Back 48

40-80mg PO/IV

Front 49

which diuretic can cause metabolic acidosis

Back 49

carbonic anhydrase inhibitors

Front 50

acetazolamide is what kind of diuretic

Back 50

carbonic anhydrase inhibitors

Front 51

spironolactone, eplerenone, triamterene, amiloride are what kind of diuretic? and can cause what?

Back 51

potassium-sparing ; hyperkalemia

Front 52

What are signs and symptoms of hyperkalemia

Back 52

dissiness, restless leg syndrome, cramps

EKG changes

Front 53

PTH and Calcium have what kind of relationship

Back 53

Inverse: as PTH increases, calcium decreases

Front 54

PTH and Phosphorous have what kind of relationship

Back 54

Direct: as PTH increases so does phosphorous

Front 55

signs and symptoms of bone metabolism disorder and hyperparathyroidism

Back 55

decrease range of motion, gritty sensation in eyes, redness, inflammation

increased HR and BP, bone pain, Increase PO4, increase Ca-PO4, decreased vit D

Front 56

stimulated PTH (increased excretion of PO4)
inactive Vit D (limited absorbed calcium)

Back 56

Bone metabolism disorder and hyperparathyroidism

Front 57

When you do you treat bone metabolism disorder and hyperparathyroidism

Back 57

PTH > 300pg/ml
Ca-PO4 product > 55

Front 58

Does the value Ca-PO4 product of <55 stay the same or change through Stage 3, 4, 5?

Back 58

Stays the same.

Front 59

Calcium Carbonate
(Tums)

Back 59

1st line calcium salt
binds dietary phosphate
inexpensive
ADR: constipation, hypercalcemia

Front 60

Calcium Acetate
(Phoslo)

Back 60

1st line calcium salt
binds dietary phosphate
ADR: constipation, hypercalcemia
Inexpensive

Front 61

Expensive 2nd line phosphate binders
Used when calcium salts are ineffective

Back 61

Sevelamer (Renvela/Renagel)
Lanthanum (Fosrenol)

Front 62

Last line phosphate binders
Acute use do to potential of accumulation

Back 62

Aluminum Hydroxide
Magnesium Hydroxide(Milk of Magnesia)

Front 63

When is a Vitamin D precursor recommended?

Back 63

serum vitamin D levels <30ng/ml

Front 64

Active Vitamin D products are used when?

Back 64

Stage 5 CKD

Front 65

vitamin D precursors

Back 65

ergocalciferol (Vitamin D2)
cholcalciferol (Vitamin D3)

Front 66

Active Vitamin D

Back 66

Calcitriol (Rocaltrol - Oral, Calcijex - IV)
Paricalcitol (Zemplar - Oral/IV)
Doxercalciferol (Hectorol - Oral/IV)

Front 67

What calcimimetic increases sensitivity of calcium-sensing receptor of parathyroid gland which then decreases PTH release

Back 67

Cinacalcet (Sensipar)

Front 68

The normal dosing for cinacalcet (Sensipar) is?

Back 68

30mg Po daily, increase by 30mg daily to a max of 180mg/day

Front 69

When do you not use Cinacalcet (Sensipar)

Back 69

if corrected Ca < 8.4mg/dL

Front 70

what happens in kidney failure because of a decrease in erythropoietin?

Back 70

Anemia

Front 71

What drugs are used to treat anemia in CKD

Back 71

Epoetin - synthetic erythropoietic agent
Iron supplement (TSTAT% must be 20%)

Front 72

patients with CKD are at a high risk for developing this major cause of mortality

Back 72

atherosclerotic cardiovascular disease

Front 73

Kidneys are unable to excrete Hydrogen and Anion Gap is present

Back 73

Metabolic Acidosis

Front 74

Treatment of Biocarb Oral Therapy of 650mg or bicarb in IV fluids

Back 74

Metabolic Acidosis

Front 75

When do you use renal replacement therapy in CKD

Back 75

CrCl ~10-15ml/min (earlier in diabetics), uncontrolled BP or heart failure, neurologic deficits

Front 76

When do you use renal replacement therapy in AKI

Back 76

A: acid-base abnormalities
E: electrolyte imbalances
I: intoxications (lithium, methanol, ethylene glycol
O: fluid Overload
U: Uremia

Front 77

What are the 2 leading causes of mortality in relation to renal replacement therapy?

Back 77

Cardiovascular events
Peritonitis

Front 78

3 types of renal replacement therapy (RRT)

Back 78

1. Hemodialysis (HD)
2. Peritoneal Dialysis (PD)
3. Kidney transplant

Front 79

Advantages: intermittent, technique failure rate low, closer monitoring, better efficacy
Disadvantages: multiple visits/week, hypotension, muscle cramps, high risk of infection

Back 79

Hemodialysis

Front 80

Advantages: more hemodynamically stable, better preservation of renal function, ambulatory, convenient route
Disadvantage: reduced appetite, risk of peritonitis, technique failure rate high, non-compliance, catheter malfunction

Back 80

Peritoneal Dialysis

Front 81

Blood is taken from the arterial system and pumped through a dialyzer

Back 81

Hemodialysis

Front 82

Arteriovenous fistula (AVF)

Back 82

surgical connection of artery to vein
1st choice
Permanent, 2 months to heal

Front 83

Arteriovenous Graft (AVG)

Back 83

surgical placement of plastic tube between artery and vein
2nd choice
heals 2-3 weeks, higher rates of infection and thrombosis

Front 84

Venous catheter

Back 84

temporary use waiting for AVF or AVG
Greater risk of thrombosis and infections

Front 85

3x/week for 4 hours
blood circulated 300-500mL/min

Back 85

In-center dialysis

Front 86

6days/week for 2-3 hours
training is required

Back 86

Home dialysis

Front 87

6 days/week for 6-8 hours
less adverse effects

Back 87

Nocturnal dialysis

Front 88

high efficiency and high flux membrane filters allow for shorter or longer dialysis times?

Back 88

Shorter times

Front 89

Goals of hemodialysis (HD)

Back 89

achieve dry weight
target post-dialysis weight
free of edema
removal of endogenous waste products

Front 90

Peritoneal dialysis

Back 90

peritoneum acts as dialyzer membrane

Front 91

is continuous ambulatory peritoneal dialysis or automated peritoneal dialysis more common?

Back 91

continuous ambulatory peritoneal dialysis (CAPD)

Front 92

CAPD

Back 92

dialysate instilled by gravity
1-3L exchanges during day every 4-6 hrs

Front 93

APD

Back 93

dialysate instilled by cycler machine
Overnight

Front 94

Most common complications of hemodialysis (HD)

Back 94

hypotension, muscle cramps, thrombosis at access site, infections

Front 95

alpha adrenergic agonist given before dialysis if hypotension occurs

Back 95

midodrine

Front 96

criteria for hypotension in hemodialysis

Back 96

drop of >30mmHg in systolic pressure
<90mmHg during a session

Front 97

two medications used to help with thrombosis of access site in HD

Back 97

alteplase and reteplase

Front 98

Gram + infections that are treated aggressively that occur in hemodialysis

Back 98

AV fistula infections

Front 99

What do you treat AV fistula infections with?

Back 99

Vancomycin and aminoglycoside(diabetes, HIV, etc)

Front 100

treated with antibiotic coverage for Gram +, Gram -, and enterococcus in HD

Back 100

AV graft infections

Front 101

what type of dialyzer reactions are common?

Back 101

anaphylactic, complement activation

Front 102

Common complications in peritoneal dialysis

Back 102

mechanical problems(kinking and catheter migration)
diabetes(glucose load)
Cardiovascular disease
peritonitis
exit site & tunnel infections

Front 103

sign of possible peritonitis

Back 103

cloudy effluent(dialysis bag) and abdominal pain

Front 104

If patient is on dialysis, is dosing based on CrCl or GFR? if no, what do you use? if yes, explain

Back 104

No. Use resources (bennetts and DI handbook)

Front 105

drug characteristics that determine removal by dialysis

Back 105

molecular weight
protein binding
volume of distribution

Front 106

What are the 6 steps to adjust drug dosages in patients with renal impairment

Back 106

1. obtain history, demographics
2. estimate CrCl (Cockcroft-Gault)
3. review medications
4. individualize treatment
5. monitor
6. revise as needed