Chronic Renal Failure

Front 1

describe the stages of crf

Back 1

1- >90
2- 60-89
3-30-59
4-15-29
5- <15

Front 2

classification for etiology of crf

Back 2

- originated in the kidney
- caused by systemic disease
- caused by nephrotoxins

Front 3

staging of crf

Back 3

Stage 1 : Normal (GFR≥90)

Stage 2 : Generally asymptomatic: Loss of Renal Reserve: Up to 50% of Nephron Loss (90>GFR≥60):

Stage 3 : Up to 75% of Loss of Nephron, Generally asymptomatic, nocturia, hypertension, anemia (60>GFR≥30)

Stage 4 : nocturia, fatigue, cold intolerance, abnormal taste, anorexia, electrolyte disturbance: 5% to 25% of Renal Reserve (30>GFR≥15).
Stage 5 : malaise, lack of energy, pruritus, N& V, leg clamps, myoclonus, asterixis, seizures, clouded metal status, uremia, >90% loss of nephron (GFR<15).
Dialysis or Transplantation requires for survival.

Front 4

what are the initial pathogenic insults

Back 4

Vascular Sclerosis:
Diabetes: Glycosylation of glomerular structure and proteins, hyperfiltration and glomerular hypertension
Hypertensive nephrosclerosis
Atheroembolic disease
Others: Mostly immune-mediated injuries

Front 5

what are the Immunologic Mechanisms of Glomerular Injury

Back 5

1-Circulating immune complexes

2-In situ antigen-antibody interaction
Intrinsic glomerular antigen, e.g.., GBM antigens
Exogenous planted antigen

Front 6

what are the desired outcomes for the treatment of CRF

Back 6

Stage 1-Stage 3: Control and manage Susceptibility factors & Initiation factors and Slow progression of disease
GFR≥30 ml/min: stabilizing renal function

Stage 4-5 (GFR<30 ml/min): prevention of complications, extend the life and improve quality of life.

Front 7

Name potentially reverisible factors in crf?- 7

Back 7

COIN VHH
1)CHF
2) Obstruction
3) Infection,
4) Nephrotoxic agents,
5) Volume depletion
6) Hypertension,
7) Hyperuricemia (>15-20 mg/dl)

Front 8

What are the therapeutic intervention to slow the progression of CRF
- shadio

Back 8

1) Dietary Protein Restriction
2) Intensive Insulin Therapy ( for diabetes)
3) Optimizing hypertension control
4) ACEI (and ARB) therapy
5) Hyperlipidemia Treatment
6) Smoking cessation
7) Anemia treatment

Front 9

ace inhibitor effects

Back 9

1) renal protective effects
2) benefitical to diabetic and non diabetic patients
3) reduce intraglomerular presure as well as systemic pressure
4) reduce proteinuria
5) reduce rate of progress of renal failure

Front 10

what treatment is betetter in reducingg proteinuria: beta blockers, vasodiators, acei, or arbs

Back 10

acei and arbs

Front 11

captopril

Back 11

capoten (B)
acei

Front 12

lisinopril

Back 12

zestril, prinvil (B)
acei

Front 13

ramipril

Back 13

altace-B
acei

Front 14

benazepril

Back 14

lotensin-b
acei

Front 15

fosinopril

Back 15

monopril-b
acei

Front 16

trandolapril

Back 16

mavik-b
acei

Front 17

give some examples or arb

Back 17

irbesartan
losartan

Front 18

what are the management of complications for stage 4 and stage 5

Back 18

Fluid and Electrolyte Abnormalities

Treatment of Anemia

Secondary Hyperparathyroidism and Renal Osteodystrophy

Treatment of Cardiovascular
Disease in CKD

Other complications

Front 19

what are the implications of renal failure toxin buildup

Back 19

1) electrolyte accumulation
2) acid/base imbalance
3) azotemia
4) drug accumulation

Front 20

what the implicatins of rf of chronic hormonal depletion

Back 20

1) chronic anemia
2) reduced activation of Vid D

Front 21

pulmonary complications: problems and symptoms

Back 21

Problem:
Pulmonary edema
Poor gas exchange

Symptoms:
Shortness of breath
Rales / rhonchi
Sputum production
Cyanotic appearance

Front 22

cardio complications: problems and symtoms

Back 22

Problem:
Left ventricular failure / hypertrophy
Arrhythmias
Hypertension
Uremic pericarditis

Symptoms
Weight gain
Edema
Tired
Jugular venous distension
Chest pain
Dizziness

Front 23

neurocomplications: problems and symtpoms

Back 23

Problem:
Uremic waste accumulation
Altered electrolyte concentrations

Symptoms:
1) Uremic neuropathy
-Restless leg syndrome
-Leg cramps

2)Uremic encephalopathy
-Confusion
-Altered sleep pattern

Front 24

gastrointestinal complications: problem and symtoms

Back 24

Problem:
-Uremic toxin buildup
-Poor perfusion of GI tract

Symptoms:
-Anorexia, hiccups
-Metallic taste
-Nausea, vomiting
-Abdominal distention
-Ascites
-Gastric and colon ulcers

Front 25

hematological complications: problems and symptoms

Back 25

problems: anemia, uremic bleeding

symptoms:
anemia: normochrnomic, normocytic appearance of cells, tired, lack of energy

bleeding: abnormal onset , like when brushing teeth, slow clotting with injury

Front 26

dermatologic complications: problem and symmptoms

Back 26

problem
- poor perfusion of skin
-poor diet/ nut diff

symp
- pitting edema
-dry, flaking skin
- generalized uremic pruritis

Front 27

musculoskeltal complicatons: problems and symptoms

Back 27

problems:
- altered electrolyte elimnation
-altered electrolyte absorption- esp ca

symp
- renal osteodystrophy
- calcification of bv

Front 28

immunolgoical complications: P &S

Back 28

p:
- poor diet
- uremic induced dysfunction of immune cells
- poor protein utilizatin

s
-increase rate of infection
- lymphopenia
-impaired cell mediated immunity
- poor response to vaccines

Front 29

fluid accumulation shows to 2 symp what are they

Back 29

-peripheral edema
- pulmonary edema

Front 30

periperal edema shows what charac

Back 30

- swelling of tissue
- swelling of jonts

Front 31

pul edema shows what chrac

Back 31

-sac accumulation: rales, decreased gas exchange

- tissue fluid accumulation (lung tissue swells), shortness of breath b/c of work of moving swollen tissue

Front 32

charac of congestive heart failure and hypertension

Back 32

Congestive Heart Failure
-Increased pre-load (amount of fluid returning to heart)
-Overextension of left ventricle beyond point of maximal stretch
-Worsened by inflammation of pericardial sac due to uremia (uremic pericarditis)

Hypertension BP=(heart rate) x (stroke volume) x (resistance)
-Increased cardiac output from additional fluid
-Systemic vasoconstriction by autoregulation to increase glomerular filtration

Front 33

osmotic diuretics and carbonic anhydrase inhibitors work on which part of the kidney

Back 33

proximal tubule

Front 34

thiazide diuretics works on which site of the kidney

Back 34

distal tubule

Front 35

loop diuretics affect which part of the kidney

Back 35

loop

Front 36

K sparring diuretics work on which part of the kidney

Back 36

- collecting duct

Front 37

moa of loop diuretics

Back 37

-Paralyze Na / Cl pump in ascending Loop of Henle
-Significantly decreases counter current effect
-Sodium passes by loop to enter the distal tubule and collecting duct
-Sodium absorption mechanism in distal tubule and collecting duct can not handle extra sodium
-Sodium passes through to urine

Front 38

name loop diuretics agents

Back 38

- furosemide (lasix)
- bumetanide (bumex)
- torsemide (dermadex)
- ethacrynic acid (edecrin)

Front 39

when should you give furosemide oral of iv

Back 39

iv furosemide is diff from oral, iv reduces preload immediately, if u have pul edema give furosemide iv, reduce pul edema quickly

Front 40

generally compare furosemide, bumetanide and toresemide, edecrin

Back 40

bumex is 40x as strong as fur, fur is more commonly used, tosemide is newer, edecrin is used if you have a sulfa allergy

Front 41

compare the elimination of furosemide, butetanide and torsemide

Back 41

-furosemide only renal
-b&t= renal and hepatic

Front 42

is the half life for furosemide long for short

Back 42

short half life is short 6-8 hrs

Front 43

when do you used loop diuretic agents for

Back 43

- use to control fluid
- use in hypertension if can not use thiazide diuretics

Front 44

loop diuretics se

Back 44

-ototoxicity
- sulfa allergy
- electrolyte depletion

Front 45

how do you get ototoxciity when you use loop diuretics-

Back 45

- give large doses of loo
- when inject loop to quickly
- ethacrynic acid is the worst

Front 46

loop d cause what kind of electrolyte imbalances - 5

Back 46

- hypokalemia
-hypocalcemia
-hypomag
-hyperglycemia
-hyperuricemia

Front 47

which is the stronger diuretic loop or thiazide

Back 47

loop

Front 48

moa of thiazide d

Back 48

-Inhibits chloride / sodium transporter in distal tubule and collecting duct

-Sodium passes with urine to bladder
Ineffective if CrCl < 30 ml/min

Front 49

4 thiazide diuretic agents

Back 49

1) hctz (hydrodiuril)
2) chlorthiazide (diuril)
3) metolazone (zaroxolyn)
4) chlorthalidone (hygroton)
5) indapamide (lozol)

Front 50

hctz- gen

Back 50

hydrodiuril- b
thiazide

Front 51

chlorothaizide-gen

Back 51

b- diuril
thiazide

Front 52

metolazone- gen

Back 52

zaroxolyn- bran
thiazide

Front 53

chlorthalidone- gen

Back 53

b- hygroton

Front 54

indapmide- gen

Back 54

b- lozol

Front 55

use of thiazide diuretics

Back 55

1) use for fluid control
2) use if hypertension cannot use loop
3)can be used in combo w/ loop
to enhance response

Front 56

se of thaizide agents

Back 56

-cannot be used w/ pat who have sulfa allergy
- causes electrolyte depletions

Front 57

what electrolyte imbalances do thaizide d cause

Back 57

Hypokalemia
Hypomagnesaemia
Hypercalcemia
Hyperglycemia
Hyperuricemia

Front 58

moa of K sparring diuretics

Back 58

-Decreases activity of the Na / K pump
-Blocks the aldosterone effect (Spironolactone, Eplerenone)
-Inhibition of Na / K pump ATPase activity (Amiloride, Triamterene)
-Less sodium reabsorbed from lumen
-Passes into urine for net loss of sodium
-Water follows sodium
-Less potassium secreted into lumen of tubule

Front 59

K sparing d agents -4

Back 59

-spiranalactone (aldactone)
- amiloride (midamor)
- triamterene (dyrenium)
- eplerenone (inspra)

Front 60

spironolactone- gen

Back 60

aldactone- b
k sparrring d

Front 61

amiloride- gen

Back 61

midamor-b
k sparing d

Front 62

trimaterene-gen

Back 62

dyrenium- b
k sparing d

Front 63

eplerenone- gen

Back 63

inspra- b
k sparing d

Front 64

uses of K sparing d- 2

Back 64

1) block K loss when used in combo w/ thiazide or loop d
2) threat hyper aldosteronism (spironaolactone) in chf or cirrhosis of liver

Front 65

se of K sparing diuretics

Back 65

1) hyperkalemia
2) gynecomastia (spironolactone)

Front 66

give 3 diuretic combo

Back 66

Amiloride / Hydrochlorothiazide (Moduretic®)
Spironolactone / Hydrochlorothiazide (Aldactazide®)
Triamterene / Hydrochlorothiazide (Maxzide®)

Front 67

what treatment if you give if

1) crcl >30
2) crcl< 30
3) hypokalemia
4) sulfa allergy
5) fluid extraction from tissue

Back 67

1) crcl >30 - thiazide
2) crcl< 30 - loop or loop + thiazide
3) hypokalemia- K sparing
4) sulfa allergy- injectable ethacrynic acid, oral: K sparing d
5) fluid extraction from tissue- mannitol

Front 68

renal osteodystrophy in crf explained

Back 68

Major problem in crf: renal osteodystrophy

- p excreted by the kidney, p retention, get hyperphosphate
-ca and p bind together, serum ca levels going down, soft tissue precipitation,
-cause hypocalcemia

- dec production of vit D
- vit D is actated by the kidney, 1,25- calceferol, most active form of vit d, 100x more active than reg vit d, dec vit d levels
- vit D enhances ca absorption,
-

Get hypocalcemia
Hyporcalcemia, stimulate pth,
-pth main fxn maintain
-ca levels going down, produce more pth, mobilize the ca levels from the bone, the bone is the main reserve for ca in the body,
-dec renal tubule reabsor

-pth will normal ca and p levels
-if you don’t take ca or vit d, bone lose ca, b/c its mobilize to the serum,
-

-renal osteodtropy= soft bone diseae bc of loss of ca
- crf , cause metabolic acidosis, h + ions accumlate, develop metabolic acidosis
- pat receive aluminum, very slow excretion, accumulate in the bone,
-al comes from? Antacids, tap water,
- al not excreted in crf , will accumlate in the bone

1st step pat lose kidney fxn, reduced p excretion, hyperphos, reduce ca, vit d production is red, bone lose ca ???
Hypocalcemia, hyperphosphatemia, high pth
After awhile kidney does not respond to pth after awhile,

Role of acidosis
- shift ca, if severe enough, cause hypercalemia

Front 69

symptoms of hyperphosphatemia

Back 69

- cardio: arrhythmias, hypotension

- neurological: seizures, ca/p precipitation in soft tissue

Front 70

etiology of hyperPhosphatemia

Back 70

1) dec excretion: dec gfr (b/c of renal failure), inc renal tubular reabsorption (hypoparthyrodism)
2) inc inake
3) drugs: bisphosphonates, phosphorus containing enemas
4) release of intracell phosphorus to serum: rhabdomyosysis, diabetic ketoacidosis

Front 71

how do you treat hyperphosphatemia

Back 71

- limit P intake
-phosphate binders
- dialysis

Front 72

which of the phosphate binders needs an rx

Back 72

ca acetate (phos-lo)

Front 73

name phosphate binders ca products -3

describe the ca levels in each

Back 73

1) ca acetate (phos-lo)
2) ca carbonate (tums, oscal, etc)
3) calcium citrate (citracal)

40% ca carbonate < 25%-calcium acetate < 21%- calcium citrate

Front 74

moa of phosphate binders ca products

Back 74

ca bind to P from the food, insoluble complex formation and remove through stool, make sure pat take w/ meal

Front 75

phosphate binders ca prodcuts ae and comments on therapy

Back 75

-Adverse events: constipation, headache, hypercalcemia

-Calcium preferred phosphate binder due to safety and additional need for calcium supplementation
-All calcium products are interchangeable therapeutically
Go for the cheapest
-PhosLo requires prescription

Front 76

egs of phosphate binders aluminum products

Back 76

- aluminum carbonate
- alumin hydroxide

Front 77

ae of phosphate binder aluminum products

Back 77

- effect but long term complication make less preferable
- encephalopathy w/ long term use
-bone disease
- constipation

Front 78

egs of phosphage binders mg products
overall effectivness as a therapy

Back 78

- mg carbonate
-mg hydroxide

overall: mg products are inexpensive and effective, pooly tolerated due to diarrhea, can cause hypermg

Front 79

other phosphate binder products that do not use ca, al or mg products

Back 79

- sevelamer (renagel)
- lanthanum carbonte (fosrenol)

Front 80

sevelamer-gen

Back 80

b- renagel

Front 81

lanthanum carbonate- gen

Back 81

fosrenol
phosphate binder

Front 82

sevelemar moa and ae

Back 82

moa:
-polymer with positevely charged ions, binds to phosphate in GI tract,

ae: gi related, thrombosis, hyper/hyptension, cough

Front 83

lanthanum carbonate (fosrenol) ae

Back 83

- gi related

Front 84

etiology of hypocalcemia

Back 84

1) vit d deficiency: crf, lack of sunlight, lack in diet

2) dec intake: bc of rickets

3) gi disease: pancreatitis, small bowl disease, gi surgery

4) drugs: phenobarbital, phenytoin

5) hypoparathyroidism - hungry bone syndrome

6) mg def: amphotericin b, cyclosporine, furosemide, foscarnet, cisplatin

7) hyperphsophatemia

8) other drugs: loop d, calcitonin, bisphosphonates

Front 85

symptoms associated w/ hypocacemia

Back 85

-neuro
- cardiac
- neuromuscular- tetany

Front 86

describe the seveiryt of hypcacemia and if treatment is necessary

Back 86

Mild (> 7.5 mg/dL)
Asymptomatic and requires no treatment

Moderate (6.5 – 7.5 mg/dL)
Requires treatment (oral or intravenous)

Severe (< 6.5 mg/dL)
Symptoms including tetany, seizures, arrhythmias
Urgent IV treatment

Front 87

criteria of iv treatment of hypocalemia

Back 87

- moderate to severe
-symptomatic

Front 88

iv treatment for hypcalemia

how much ca is in each

Back 88

- ca gluconate 10%, 90mg ca
- cacl2 10%,272 mg ca

Front 89

special things you need to know about giving iv ca

Back 89

Do NOT mix Ca++ with bicarbonate, sulfates, carbonates, or phosphate-containing solutions due to potential precipitation

Do NOT administer IM or SC due to potential for extravasation leading to local necrosis and/or abscess formation

Front 90

oral treamtents for hypocalcemia

Back 90

- for mild to moderate hypcalcemia
-calcium carbonate (titralac, tums, oscal)

- glubionate, gluconate, lactate)
- more expensive
- less elemental ca/gm of salt than carbonate

Front 91

give active d products

Back 91

1) calcitriol (1,25 dihydroxycholecalciferol)
- Rocaltrol
-Calcijex

2) paricacitol
-Zemplar

3) doxercaciferol
- hectorol

Front 92

hctz and ca, what is its effect

Back 92

- hctz helps to promote ca in resbsorption in the kidneys

Front 93

when do you get 2ndary hyperpathyrodism

Back 93

later stage kidney failure
-kidney becomes resistant to pth stimulation
- parathyroid gland develops hyerplasiam
- pth is uremictoxin

Front 94

hyperparathyroid treaments
mild -moderate:
severe hyper:

Back 94

mild-moderate: drug therapy
severe: prathyroidectomy

Front 95

what are calcimimetics

Back 95

- cincalcet hydrochloride (sensipar)

Front 96

indication of sensipar

Back 96

2ndary hyperparathyroidsim in dialysis patients

Front 97

moa of sensipar

Back 97

- act on ca sensing receptor at the pth gland to mimic the inoized ca
- inc the sensitivity of the ca sensing receptor ca, reducing pth level

Front 98

cinacalcet

Back 98

use to treat 2ndary hyperparathyroidism
- reduce pth level and caxp
- expensive drug
- contraindicated and se: hypcalcemia and n &v