Exam 2 Kidneys, Diuretics, CKD, Dialysis, and AKI Flashcards
1
Q
What cells in the glomerulus aid in filtration?
A
The podocytes
2
Q
What cells in the glomerulus produce growth factors, matrix proteins, and contract?
A
Mesangial cells
3
Q
What is azotemia?
A
Condition characterized by elevated BUN and SCr, due to decreased GFR
4
Q
What is uremia?
A
Excess of urea and other nitrogenous waste in the blood – toxic! Many other metabolic/GI/CV/etc alterations involved in addition to renal of excretory function
5
Q
What is proteinuria?
A
The presence of protein (albumin) in urine
6
Q
What is hematuria?
A
The presence of blood in urine. If visible to naked eye, called gross hematuria.
7
Q
What does edema lead to?
A
Circulatory congestion
8
Q
True or false: CKD is classified with the RIFLE system which is based on the anatomical area of injury (prerenal/intrinsic/postrenal)
A
False – this system is used to classify acute kidney injury
9
Q
What disease is characterized by progressive loss of kidney function due to parenchymal fibrosis (change of structure with increased fibroblasts)?
A
Chronic kidney disease
10
Q
What three chronic conditions can be especially bad for the kidneys?
A
HTN, DM, and HLD
11
Q
What two options do patients with ESRD have?
A
Hemodialysis or transplant
12
Q
What must be present for dialysis to work?
A
A semipermeable membrane separating the blood and dialysate.
13
Q
What is the semipermeable membrane in peritoneal dialysis?
A
The peritoneal membrane (peritoneum) that lines the abdominal viscera.
14
Q
The stomach, liver, and kidneys can all be adversely affected by what class of drugs?
A
Analgesics and NSAIDS
15
Q
What is the general term for kidney inflammation?
A
Nephritis
16
Q
What body system has the greatest potential to harm the kidneys?
A
The immune system – immune pathogenesis, either antibody or cell mediated injury
17
Q
In what three ways can antibodies harm the kidneys?
A
- Immune complex deposition as antibodies stuck in filtration membrane
- Anti-glomerular basement membrane (GBM) antibodies
- Antibody against another part of the glomerulus
18
Q
Antibody and cell-mediated injury both lead to what end consequence?
A
Damage causes injury and detachment of epithelial cells in glomerulus, allowing protein leakage through GBM and filtration slits
19
Q
What is the difference between NephrOTIC syndrome and NephRITIC syndrome?
A
Both lead to protein leakage, but only nephritic syndrome has RBC leakage too. Therefore, nephritic syndrome is more serious.
20
Q
What is the general cause of primary glomerulonephritis?
A
Problems originating within the glomerulus.
21
Q
Nephrosis is…
A
any disease of the kidney leading to degeneration of renal tubular epithelium
22
Q
Nephritis is…
A
inflammation of the kidney.
23
Q
Is azotemia associated with nephrotic syndrome or nephritic syndrome?
A
Nephritic syndrome
24
Q
What is oliguria?
A
Low urine output
25
What are the two mechanisms for acute pyelonephritis?
Hematogenous (from blood) or ascending (due to bladder infection, vesicoureteral reflux, and internal reflux)
26
True or false: Cysts are precursors to tumors
False
27
What is the name of the autosomal dominant genetic cyst disease of the kidneys?
Adult Polycystic Kidney Disease (APKD)
| Eventually destroys structure of kidney and leads to intermittent gross hematuria
28
What is the name of the autosomal recessive genetic cyst disease of the kidneys?
Childhood Polycystic Kidney Disease
Serious symptoms usually present at birth
Infants may die from pulmonary or renal failure, if survive develop liver cirrhosis
29
Diuresis is...
an increase in urine volume
30
Natriuresis is...
an increase in renal sodium excretion
31
In addition to nephrotic syndrome and nephritic syndrome, what is the third important glomerular syndrome?
Chronic glomerulonephritis
| Usually associated with systemic chronic diseases like HTN, DM, SLE
32
Are kidney cysts always due to genetic mutations?
No, simple cysts seem to randomly happen and are more common
33
What cells in the nephron sense the rate of Na and Cl absorption, control GFR, and control renin release?
The cells in the macula densa
34
What portions of the nephron is the macula densa next to?
The distal convoluted tubule and the glomerulus (sense from DCT, signal to juxtaglomerular cells)
35
What cells are responsible for producing renin?
The juxtaglomerular cells
36
In which of the following is water more permeable? Thin limb of the loop of hence or thick limb of loop of henle
Water is more permeable in the thin limb.
37
What hormone controls calcium reabsorption?
Parathyroid hormone
38
Where in the nephron do loop diuretics act?
The thick ascending limb
39
Where in the nephron do osmotic diuretics act?
The thin descending limb
40
Where in the nephron do the thiazides act?
The distal convoluted tubule
41
Where in the nephron do potassium-sparing diuretics act?
The collecting duct
42
Where in the nephron do carbonic anhydrase inhibitors act?
The proximal tubule
43
What diuretic class acts on the distal convoluted tubule?
Thiazides
44
What diuretic class acts on the thick ascending limb?
Loop diuretics
45
What diuretic class acts on the proximal tubule?
Carbonic anhydrase inhibitors
46
What diuretic class acts on the collecting duct?
Potassium-sparing diuretics
47
What diuretic class acts on the thin descending limb?
Osmotic diuretics
48
What kind of diuretic is acetazolamide (Diamox)?
Carbonic anhydrase inhibitor
49
How do carbonic anhydrase inhibitors work?
They block carbonic anhydrase, which makes sodium and bicarbonate stay in the urine, so water stays with them.
50
Name four disadvantages of carbonic anhydrase inhibitors
1. The kidney accommodates relatively quickly
2. They are not as effective
3. They cause loss of bicarbonate, risk of acidosis
4. They destroy the proton gradient in the proximal tubule... less H+ secreted in exchange for sodium
51
In what situations would it be appropriate to use a CA inhibitor?
Metabolic alkalosis, altitude sickness (think respiratory alkalosis), glaucoma, and urinary alkalization to trap acidic drugs
52
What toxicities are associated with CA inhibitors (acetazolamide)?
Hyperchloremic metabolic acidosis, renal stones, potassium wasting, drowsiness/paresthesia
53
Under what stituations are CA inhibitors contraindicated?
Hepatic cirrhosis (CA inhibitor increases ammonium retention), sulfa allergies
54
What class of diuretics includes furosemide, bumetanide, torsemide, and ethacrynic acid?
Loop diuretics
55
What do loop diuretics block and how does this cause diuresis?
Loop diuretics block the NKCC transporter, which results in increased levels of Na, K, Cl, Mg, and Ca in the urine. Water follows.
56
What group on a CA inhibitor absolutely must be present for activity?
An unsubstituted sulfamoyl group (H2NO2S)
57
Substitution with an amine across from the sulfamoyl group has what effect on natriuretic activity? CA inhibitor activity?
Increases natriuretic activity but decreases CA inhibitor activity
58
Do Cl-, Br-, CF3-, and NO2- increase or decrease diuretic activity on a CA inhibitor?
Increase
59
The second sulfamoyl group on a CA inhibitor can be replaced with what kind of group to increase diuretic activity but decrease CA inhibitory activity?
An electrophilic group (aka carboxyl, etc.)
60
What is another name for loop diuretics?
High ceiling diuretics
61
What two chemical substituents must always be present on a loop diuretic?
A sulfamoyl and a carboxyl on 1 and 5 respectively
| A secondary amine must be in the 2 or 3 position
62
What is unique about ethacrynic acid?
It is a prodrug, becomes attached to either cysteine or glutathione in the body. Safe for those with sulfa allergies.
63
What toxicities are associated with loop diuretics?
Dehydration, hypokalemic metabolic alkalosis, ototoxicity, hyperuricemia (gout concern), hypomagnesemia
64
Furosemide and bumetanide should not be used in patients with...
sulfa allergies
65
Do loop diuretics act more rapidly or slowly?
Rapidly
66
List indications for loop diuretic therapy
Edema, acute hypercalcemia, hyperkalemia, acute renal failure, anion overdose
67
What transporter do thiazide diuretics target in the distal convoluted tubule?
The Na Cl symporter
68
What are chlorothiazide and and hydrochlorothiazide?
Thiazide diuretics
69
What is chlorthalidone (Hygroton)?
A thiazide-like diuretic
70
How do the thiazides affect Na, Cl, and Ca reabsorption?
The decrease sodium and chloride absorption, leaving them in the urine, and increase calcium reabsorption due to the presence of a Ca/Na antiporter
71
What are the clinical uses for thiazides?
HTN, CHF, kidney stones from idiopathic hypercalcuria, and nephrogenic diabetes insipidus
72
What toxicities are associated with the thiazides?
Hypokalemic metabolic alkalosis, hyperuricemia, impaired carbohydrate tolerance, hyperlipidemia, hyponatremia
73
What patients should absolutely not receive thiazides?
Patients with sulfa allergies
74
How do potassium-sparing diuretics function?
They block sodium reabsorption channels in the collecting duct
75
How do potassium-sparing diuretics spare potassium?
When they block sodium reabsorption, potassium is no longer excreted in exchange for sodium.
76
True or false: Potassium-sparing diuretics are highly effective at diuresis.
False. Often used in combination.
77
What are the clinical uses for amiloride (Midamor), a potassium-sparing diuretic?
CHR or hypertension in combination with a thiazide or loop diuretic.
78
What toxicities are associated with potassium sparing diuretics?
Hyperkalemia, hyperchloremic metabolic acidosis
79
Under what circumstances should amiloride not be given?
With potassium supplements or ACE inhibitors (which also retain potassium)
80
What are the clinical uses for triamtereme (Dyrenium)?
Edema associated with CHF, hepatic cirrhosis, nephrotic syndrome, or hyperaldosteronism
81
Under what circumstances should triamterene not be given?
Kidney stones, with potassium supplements, or with ace inhibitors
82
Where in the nephron do aldosterone antagonists act?
On nuclear receptors in the collecting duct cells
83
What is the net effect of aldosterone antagonists?
Decreased number of sodium channels, enhanced channel removal, inhibited transport of sodium to the blood
84
What additional action does spironolactone (Aldactone) have that eplerenone (Inspra) does not?
Inhibition of 5a-reductase, stopping metabolization of aldosterone to active metabolites
85
What are the clinical uses for spironolactone?
HTN or CHF in combination with other diuretics, mineralocorticoid excess, aldosteronism (primary or secondary resulting from CHR, cirrhosis, or nephrotic syndrome)
86
What toxicities are associated with spironolactone (Aldactone)?
Hyperkalemia, hyperchloremic metabolic acidosis, gynecomastia, impotence, BPH --> steroid!
87
Under what conditions should spironolactone not be used?
If chronic renal insufficiency or at the same time as potassium supplements, ACE inhibitors, or potassium sparing diuretics.
88
Which aldosterone antagonist is more selective--spironlactone or eplerenone?
Eplerenone (Inspra) -- selective to receptors in kidney, heart, bv, brain
89
What are the clinical uses for eplerenone?
HTN. Will reach full effect in 4 weeks.
90
What toxicities are associated with eplerenone?
Hyperkalemia, hypertriglyceridemia
91
Under what conditions should you not use eplerenone?
With potassium supplementation, potassium sparing diuretics, ACE inhibitors, or CYP 3A4 inhibitors, chronic renal insufficiency, diabetes with microalbuminuria
92
How does mannitol work?
This sugar is excreted but cannot be reabsorbed, so it increases the osmotic pressure of the urine which draws more water into the urine to be excreted. Limits water reabsorption in the proximal tubule and descending limb
93
What effect does mannitol have on urine electrolytes?
Little to none. Mannitol causes diuresis without naturesis.
94
How is mannitol used clinically?
To increase urine volume or to reduce intracranial or intraocular pressure
95
What toxicities are associated with mannitol?
Extracellular volume expansion (peripheral swelling due to mannitol other tissues), dehydration, hypernatremia
96
What is the name of the only ADH antagonist?
Demeclocycline (Declomycin)
97
How does demeclocycline function?
It inhibits the effects of ADH at the collecting duct, stopping insertion of H20 channels and therefore reducing water reabsorption
98
When should demeclocycline be used?
SIADH, elevated ADH
99
What toxicities are associated with demeclocycline?
Nephrogenic diabetes insipidus, renal failure
100
What is ESRD?
End stage renal disease--the point where the kidney function is so impaired that the patient must either get a transplant or go on dialysis
101
What are the three major causes of CKD?
Diabetes mellitus, hypertension, and glomerulonephritis
102
What equation estimates GFR and is used to stage CKD?
MDRD equation
103
What albumin range is considered moderately increased?`
30-300mg/g
104
What GFR stages are considered worrisome? What number is GFR under in these cases?
Stages 3a-5; Less than 60 mL/min/1.73m^2
105
What are the breaks for staging GFR?
90, 60, 45, 30, 15
106
What is the cockroft gault equation?
CrCl = (140-age)(IBW)/(SCr*72) x 0.85 if female
107
What weight should you use in the cocroft gault equation if the patient is obese (>130% IBW)?
Adjusted body weight (=0.3(actual-ideal)+ideal)
108
What five general complications can result from CKD?
Buildup of waste products in blood, fluid overload, metabolic acidosis, anemia, and mineral and bone disorder
109
Name four symptoms that can result from uremia
Uremic fetor, uremic frost, metallic taste, encephalopathy
110
Which cells hypertrophy in diuretic resistance?
DCT cells. Counteract by adding thiazides.
111
What class of diuretics should be avoided in CKD patients?
Potassium sparing diuretics
112
Which class of diuretics works better when CrCl <30mL/min -- thiazides or loops?
Loops
113
In CKD patients, does fluid restriction usually treat fluid overload sufficiently?
Trick question -- fluid restriction not generally necessary if sodium intake controlled although free water intake should be avoided.
114
In addition to sodium restriction, what other treatment can be used for fluid overloaded CKD patients?
Diuretics
115
Which diuretics are permissible for a patient with sulfa allergies?
Ethacrinic acid, potassium sparing diuretics, aldosterone antagonists, ADH antagonists, mannitol
116
What electrolyte dietary intake should be strictly restricted?
Potassium -- limit to 3 gm/day
117
What electrolyte imbalance are ESRD patients remarkably tolerant to?
Hyperkalemia -- aim for 4.5 - 5.5 pre-dialysis
118
What are the three major problems in mineral and bone disorder?
Hyperphosphatemia, hypocalcemia, and decreased vitamin D
119
What do the three major problems in mineral and bone disorder (CKD-MBD) lead to?
Increased serum intact PTH (iPTH)
120
True or false: Secondary hyperparathyroidism is largely asymptomatic until late stages, when it is not easy to treat
True
121
What is the mechanism of action for phosphate binders?
They bind dietary phosphate ingested with food (so must be taken with food) and allow them to be eliminated in the feces
122
What phosphate binder is cheaper -- calcium carbonate or calcium acetate?
Calcium carbonate (Tums)
123
What is the biggest disadvantage of calcium containing phosphate binders?
Possible absorption of calcium, which could cause more soft tissue calcification
124
Which calcium containing phosphate binder is better if cost is not an issue?
Calcium acetate -- binds twice as much phosphate, fewer hypercalcemic events
125
Of the non-calcium phosphate binders, which is the best as far as low ADEs and other beneficial effects?
Sevelamer carbonate (Renvela)
126
Which non-calcium containing phosphate binder has significant interactions with levothyroxine and other CKD drugs like paricalcitol and cinacalcet?
Sucroferric oxyhydroxide (Velphoro)
127
Which phosphate binders are strongly affected by pH?
Calcium containing binders are almost 0% effective at low pH (such as the stomach)
128
What two other positive effects does sevelamer carbonate have on the body?
It decreases LDL by 15-30% and decreases uric acid in the blood.
129
What side effect of iron containing phosphate binders should patients be aware of?
They may darken or discolor stool.
130
What non calcium containing phosphate binder has been almost entirely discontinued?
Amphojel (aluminum hydroxide) due to aluminum toxicity leading to anemia. Only for short term b/c cannot excrete aluminum.
131
Which iron containing binder actually increases TSAT and ferritin?
Auryxia (ferric citrate).
132
What foods are high in phosphorus?
Meat, dairy, beans, nuts, beer, pop
133
What should daily dietary phosphorus be limited to?
800-1000mg
134
Under what circumstances should phosphorus intake be limited?
If PTH > target range for stage 3, 4, or 5. OR
Phos >4.6mg/dL for stage 3 and 4
Phos >5.5mg/dL for stage 5
135
What is the active form of vitamin D?
Calcitriol
136
Where are the inactive forms of vitamin D converted?
Cholecalciferol (D3) and Ergocalciferol (D2) in the liver,
| 1,25-dihydroxyvitamin D in the kidney to active form
137
What are the two inactive forms of Vitamin D that we administer to patients?
Ergocalciferol (Calciferol) and Cholecalciferol
138
Which CKD patients should receive inactive vitamin D supplements?
Stage 3 and stage 4 or if iPTH is elevated but inactive vitamin D is normal or low.
139
Which CKD patients should receive active vitamin D supplements?
Stage 5 or if both inactive vitamin D and iPTH are elevated (not being converted)
140
What is the goal of vitamin D therapy in CKD patients?
To decrease the amount of iPTH by increasing the amount of vitamin D that the parathyroid gland senses.
141
What is the undesired effect of active vitamin D products?
Elevation of blood calcium
142
What is special about doxercalciferol (Hectorol)?
It is a pro-hormone that becomes activated in the liver at a more natural rate, maintaining more even serum concentrations.
143
Which two activated vitamin D supplements lead to a >30% reduction in iPTH and have a lower calcemic activity?
Paricalcitol (Zemplar) and doxercalciferol (Hectorol)
144
For what reasons would you choose paricalcitol over doxercalciferol?
Paricalcitol is approved for pediatric patients and has the most favorable ADE profile
145
What activated vitamin D compound has higher incidence of hyperphosphatemia even though it more closely resembles body vitamin D kinetics?
Doxercalciferol
146
For what reasons would you use calcitrol over doxercalciferol?
Calcitriol is cheaper and approved for pediatrics
147
What activated vitamin D compound carries the greatest risk of hypercalcemia?
Calcitriol
148
What is the name of the only calcimimetic drug?
Cinacalcet (Sensipar)
149
How does cinacalcet work?
It mimics the action of calcium by binding the receptor and inducing conformational change, sending a signal to decrease iPTH secretion
150
What notable drug does cinacalcet interact with?
Velphoro (sucroferric oxyhydroxide)
151
What is the disadvantage inherent in cinacalcet's mechanism of action?
When all calcium receptors are bound with cinacalcet, the body cannot sense or respond to a dangerous drop in blood calcium.
152
What is the advantage of giving inactive vitamin D over active vitamin D?
The kidney will convert inactive vitamin D as needed, rather than dumping the activated form into the system.
153
What four causes contribute to anemia in CKD patients?
Decreased erythropoietin, decreased RBC life from uremia, and vitamin/blood loss during dialysis
154
What type of anemia do CKD patients tend to have?
Iron deficiency (microcytic) anemia
155
What is a normal MCV?
80-96 um^3
156
What is a normal RDW (red cell distribution width)?
11.5 - 14.5%
157
What is the best assessment parameter for anemia?
Hemoglobin (Hb)
158
At what lab value for hemoglobin should we do further workup or diagnose anemia?
Males -- <12g/dL
159
How often should hemoglobin be monitored for anemia?
Annually in CKD 3, biannually in CKD 4-5ND, and q3mos in CKD 5D
If PMH anemia, monitor CKD 3-5ND q3mos and CKD 5D q month
160
What two general types of treatment are available for CKD patients with anemia?
Iron therapy and erythropoiesis stimulating agents
161
When should you supplement with iron?
If TSAT <500ng/mL
| Monitor these every 3 months
162
For which patients is oral iron appropriate for?
CKD stage 3-4 or peritoneal dialysis patients. NOT enough for hemodialysis patients
163
What is the recommended daily dose of elemental iron?
At least 200mg
164
What side effects are associated with oral iron?
Stomach upset
165
What counseling tips should you tell patients on oral iron supplements?
Take with orange juice, separate from food, separate from Ca++ by 2hours, avoid meds that increase stomach pH
166
What is different about heme iron vs elemental iron?
Heme iron is absorbed better and from a different site, so not subject to the 200mg daily iron rule.
167
What is heme iron available as?
Proferrin ES, proferrin Forte
168
IV iron supplementation is recommended for what patients?
CKD stage 5D
169
Which IV iron supplement interferes with MRI for up to 3 months?
Feraheme (ferumoxytol)
170
Which iron dextran brand should be avoided due to higher risk for anaphylaxis due to higher Mw iron?
Dexferrum
171
Which IV iron supplement requires a test dose before it is administered with hemodialysis?
Iron dextran (InFed/Dexferrum)
172
Which IV iron supplement is approved for non-CKD patients?
Iron sucrose (Venofer)
173
What side effects may be caused by IV iron products?
Flushing, dizziness, and hypotension
174
How often should ferritin and TSAT be monitored in IV iron + hemodialysis patients?
Every 1-3 months
175
What can oxidative stress due to free iron in the blood lead to?
Atherosclerosis, proteinuria, renal tubular damage
176
When is it appropriate to use an erythropoiesis stimulating agent?
After all other correctable causes of anemia have been addressed due to high price.
CKD 3-5ND -- if Hb <10g/dL, falling at rapid rate, needed to avoid transfusion
CKD 5D -- when Hb between 9 and 10 g/dL
177
Why should ESAs not be used to increase Hb above 11.5 g/dL?
Although this would improve QOL, it also increases incidence of CVAs (strokes).
178
What general hemoglobin range should be your goal with ESAs?
10 - 11 g/dL
179
How do erythropoiesis stimulating agents (ESAs) work?
They stimulate erythroid progenitor cells.
180
What are the two ESA drugs?
Recombinant human erythropoietin (Epogen, Procrit, EPO) and darbepoetin alfa (Aranesp)
181
Which ESA has a longer half life and may be given less frequently?
Darbepoetin alfa (Aranesp)
182
Which ESA is cheaper if given subcutaneously?
Epogen -- because SC dose is 2/3 IV dose if target reached
183
Which ESA is dosed in units? Which is dosed in mcg?
Units: Epogen
Mcg: Aranesp
184
What adverse effects are associated with ESAs?
Pure red cell aplasia (PRCA) where antibodies develop to erythropoietin, HTN (23% patients) leading to increased cardiac arrest, seizure, stroke, exacerbations of HF, HTN, and MI
185
How often should you monitor Hb during initiation of ESA therapy?
Weekly
186
How often can you adjust the ESA dose?
No more than every 4 weeks
187
What is the goal rate of increase in Hb?
1-2 g/dL increase per month
188
By what percentage should you increase/decrease the dose if Hb has not increased at a fast enough rate/if Hb approaches 11?
25%
189
What acid/base disorder are ESRD patients susceptible to? Why?
Metabolic acidosis because they cannot excrete H+ ions.
190
When is metabolic acidosis secondary to ESRD treated?
When bicarb <20mEq/L
191
How is metabolic acidosis secondary to ESRD treated?
Increased bicarbonate in dialysate, shohl's solution OR sodium bicarbonate tablets
192
What amount of protein should a CKD patient receive? How about an ESRD patient?
CKD (stage 3-5ND): 0.8 g/kg/day if GFR <30ml/min
| ESRD: 1.2 g/kg/day due to protein loss through dialysis
193
What types of vitamins need to be replaced in patients on dialysis?
Water soluble vitamins -- B and C (Nephrocaps, Nephron FA)
194
If a CKD patient is 60 yo?
60 yo: 30 - 35 kcal/kg/day
195
True or false: CrCl is an accurate measure of acute kidney injury.
False because it may be changing rapidly and other waste products build up faster.
196
List two examples of community acquired AKI
Prerenal azotemia (hypoperfusion) and postrenal obstruction (kidney stone)
197
List three examples of hospital acquired AKI
Multiple organ failure, sepsis, bleeding, liver disease, mechanical ventilator
198
What is functional acute renal failure?
A decrease in glomerular hydrostatic pressure which leads to decreased GFR (often caused by NSAIDs, ACE inhibitors)
199
What is are helpful measures of acute renal function?
Urine output and FEna
200
What UOP characterizes acute anuria?
<50mL / 24 hours
201
What UOP characterizes oliguria?
<400 ml / 24 hours
202
What UOP characterizes non-oliguria?
>400 mL / 24 hours
203
A FENa of <1% indicates what potential cause?
Prerenal or functional renal failure
204
A FENa of >1% indicates what potential cause?
Renal injury
205
What is the goal of acute renal injury treatment?
Remove cause then supportive therapy
206
What are the most common nephrotoxic drug classes?
NSAIDs (and acetaminophen), ACE inhibitors, contrast media, and proton pump inhibitors
207
What does the AEIOU abbreviation stand for when determining indications for renal replacement therapy?
Acid/base balance, Electrolytes, Intoxication, Overload, Uremia
208
When should you initiate dialysis?
When BUN >100 and/or SCr >10. Look at S/Sx too.
209
What kinds of molecules are you trying to pull out of the blood in dialysis?
BUN, creatinine, middle molecules like beta2microglobulin, uric acid
210
Which dialysis vascular access has the longest survival rate?
AV fistula
211
Which dialysis vascular access takes the shorter time to mature?
AV graft
212
Which dialysis vascular access is associated with more complications?
AV graft
213
Which dialysis vascular access might not be good for patients with poor circulation to extremities?
AV fistula
214
What four types of substances are not removed from the blood during dialysis?
1. High Vd (volume of distribution) -- mostly in tissues
2. High lipophilicity
3. Large molecular weight
4. Highly protein bound
215
What two measures are used to analyze the effectiveness of a dialysis session?
Kt/V and URR
216
What is Kt/V? What is your Kt/V goal?
Measure of the fraction of total body water that is cleared of urea. K is clearance, t is time, V is Vd. Goal = 1.4
217
What is urea reduction ratio? What is a goal URR?
Measure of reduction of patient's BUN. Goal is >70% reduction.
218
What complications can arise during hemodialysis?
Hypotension, pruritus, muscle cramps
219
What types of patients usually receive peritoneal dialysis?
Patients with bigger abdomens, residual kidney function, pediatric patients
220
True or false: Peritoneal dialysis requires at least three sessions a week.
False -- peritoneal dialysis is continuous
221
What is the time between loading fluid into peritoneum and draining it out called?
Dwell time
222
What is the reasoning for dwell times of different duration?
Different molecules take different times to equilibrate
223
Describe the schedule of CAPD (continuous ambulatory peritoneal dialysis).
Patient switches waste out and puts new dialysate in three times during the day and dwells overnight.
224
Describe the schedule of CCPD (continuous cyclic peritoneal dialysis).
Patient dwells during the day and a cycler drains and refills throughout the night.
225
Describe the schedule of NIPD (nocturnal intermittent peritoneal dialysis).
Patient is "empty" throughout the day and cycler runs throughout the night. Unfortunately, no long dwell.
226
Describe the schedule of NTPD (nocturnal tidal peritoneal dialysis).
Patient is "empty" throughout the day and cycler runs throughout the night, but does not fully drain the fluid, leaving a reserve volume in the entire time.
227
What signs and symptoms can indicate peritonitis?
Cloudy effluent, abdominal pain, fever, N/V, chills, tenderness
228
What should you use to treat peritonitis?
Empiric therapy (covers gram + and -) before organism identified, then modify once cultures obtained.
229
What is unique about treatment of peritonitis?
Antibiotics can be administered intraperitoneally, directly to the infection site. Especially good when PO not an option or poor vascular access.
230
What is the primary use for continuous renal replacement therapies?
Acute renal failure, especially if pt critically ill or hemodynamically unstable.
231
What drug should be used in conjunction with CAVH (continuous arteriovenous hemofiltration)? Why?
Heparin. Because the heart is pumping the blood through at a slow rate that can lead to clotting.
232
What force is removing waste in CVVH (continuous venovenous hemofiltration)? How?
Convection -- addition of ultrafiltrate fluid before dialyzer increases blood volume, which must be forced out through dialysis.
233
Do continuous renal replacement therapies work at slower or faster rates than hemodialysis?
Slower -- they can work on the blood 24/7 but hemodialysis must happen over 4 hours per session.
234
What force is removing waste from the blood in CVVHD (continuous venovenous hemodialysis)? How?
Diffusion. In this method, dialysate is being run opposite the blood so substances can diffuse from the blood to dialysate just like regular hemodialysis except longer period of time/slower rate.
235
What force is removing waste from the blood in CVVHDF (continuous venovenous hemodiafiltration)? How?
Convection AND diffusion. This is done by running the blood opposite dialysate just like hemodialysis, but there is also ultrafiltrate added to the blood before it reaches the dialyzer so that excess volume is also spilling over into the dialysate and waste.
236
What is a normal hemoglobin range?
Target range 10-11 g/dL
Normal male: 13-17.5 g/dL
Normal female: 12-15.5 g/dL
237
What is a normal phosphorus range?
2.5 - 4.5 mg/dL
238
What is a normal calcium range?
8.5 - 10.5 mg/dL
239
What is a normal iPTH range?
Non-dialysis: 11-54 pg/mL
| Dialysis: 100-500 pg/mL
240
What is a normal TSAT range?
>30% is target
241
What is a normal ferritin range?
>500 ng/mL is target
242
What is a normal MCV range?
80-96 um^3
243
What is a target inactive vitamin D value?
30 ng/mL
244
What is a normal red cells distribution width?
11.5-14.5%
