Kidney Flashcards
(215 cards)
1
Q
What structures are found in the renal medulla?
A
loops of henle and collecting ducts
2
Q
what is found in the renal cortex?
A
everything else that makes up the nephron
3
Q
the pyramids are part of the renal cortex or medulla?
A
medulla
4
Q
which two organs are the primary regulators of acid base balance? which acids do they excrete?
A
kindeys (excrete non volatile acids)
lungs (excrete volatile acids CO2)
5
Q
decreased O2 delivery to the kidneys has what effect on EPO production?
A
increased EPO production
6
Q
severe kidney dz has what effects on EPO production leading to what?
A
decreased EPO production leading to anemia
7
Q
what hormones are produced by the kidneys?
A
EPO
calcitrol (active Vit D)
prostaglandins
8
Q
low blood Ca has what effect on PTH levels?
A
low blood Ca causes an increase in PTH
9
Q
increased PTH does what to calcitriol?
A
^PTH>^Calcitriol (active Vit D)
10
Q
what does aldosterone cause? what does it primarily control?
A
Na and H20 reabsorption and K and H excretion.
primarily controls extracellular fluid volume
11
Q
what does ADH do and what does it primarily control?
A
only H20 reabsorption. so it primarily controls plasma oxmolarity
12
Q
long term BP control mechanism?
A
thirst and Na / H20 excretion
13
Q
intermediate BP control
A
RAAS
14
Q
where is renin produced?
A
JGA cells
15
Q
where is aldosterone produced?
A
adrenal cortex
16
Q
short term BP control?
A
baroreceptor reflex
17
Q
what to know about phase 1 and phase 2 reactions in regards to the kidney and liver?
A
both the kidney and liver can do phase 1 and phase 2 biotransformation reactions
18
Q
what does EPO cause?
A
stem cells in the bone marrow to produce more RBCs
19
Q
what prostaglandins are produced by the kindeys and what is their function?
A
PGE2 & PGI2 vasodilate renal arteries
Thromboxane A2 constricts renal arteries
20
Q
what are the three effects of increased serum calcitriol levels?
A
- ^ intestinal Ca absoprtion
- decreased Renal Ca and phosphate excretion
- ^ deposition of Ca into bones and ^ resorption of old bone. (this just helps turn bone over)
remember: calcitriol levles raise serum Ca levels.
21
Q
increasing serum Ca levels has what effect on PTH levels?
A
as Ca increases PTH decreases
22
Q
can the kidneys create glucose?
A
yes, can sythesize glucose from amino acids like the liver.
23
Q
do the kindeys or the liver make more gluocse?
A
Kidney’s rival the livers ability to perform gluconeogenesis.
24
Q
Kidneys get what percent of CO?
A
20-25%
25
how is renal blood flow divided?
90% goes to cortex and 10% goes to renal medulla and juxtamedullary nephrons
26
what is the average PaO2 in the renal cortex vs renal medulla? why is this importnat?
PaO2 is about 50 in renal cortex and only 10 in renal medulla. This is why renal medulla and juxtamedullary nephrons are so sensitive to ischemia
27
how much blood is filtered at the glomerulus?
about 20%
28
what happens to the other 80% of blood that is not filtered through the glomerulus?
just circulates through the peritubular capillaries
29
how much of the ultrafiltrate is reabsorbed into the peritubular capillaries?
99%
30
how much urine is produced each day?
about 1-1.5L urine excreted each day
31
how much does renal blood flow decrease for each decade of life after age 50?
decrease by 10% for each decade after 50yrs
32
explain renal blood flow ammount in a neonate
RBG doubles in the first 2 weeks of life, and reaches acult levels by age 2yr.
33
RBF is autoregulated in what range?
texts varry widely, but apex likes MAP 50-180
34
is urine output autoregulated?
No, it is linearly related to MAP > 50
35
what are the two most important mechanims for renal autoregulation?
myogenic mechanisms and tubuloglomerular feedback
36
explain the myogenic mechanism of renal autoregulation?
increased renal artery pressure > afferent arteriole constriction to protect glomerulus from excessive pressure.
decreased renal artery perfusion > afferent arteriole dilation to increase blood flow to nephron
37
describe tubuloglomerular feedback mechanism of renal autoregulation
JGA is in the distal tubule between afferent and efferent arterioles.
Na and Cl concentrations in the distal tubule affect afferent arteriolar tone
38
explain nervous system innervation of the kidney
very limited PNS innervation
SNS innervation of the afferent and efferent arterioles. This typically overridden by internal autoregulation. However, during extreme stress or excessive catecholamines SNS can cause decreased renal blood flow.
39
explain the surgical stress response effects on the kidneys
surgical stress an cause transient state of vasoconstriction and Na retention for up to several days which leads to oliguria and edema, predisposing the kidney to ischemic injury and effects of nephrotoxic drugs.
40
Where is the JGA located?
in distal tubule between afferent and efferent arterioles
41
explain the effect of decreased RBF on the JGA
decreased RBF > decreased GFR > decreased Na and Cl delivery to to JGA (sensed by the macula densa) > dilation of afferent arterioles to ^ GFR
42
how do low Cl levles in ultrafiltrate affect the JGA cells?
low Cl levels in ultrafiltrate > Renin release from JGA cells > RAAS activation. RAAS activation > efferent arteriole constriction which also ^ GFR.
43
what three systems control BP?
SNS
RAAS
Vasopression system
44
what triggers RAAS?
decreased renal perfusion
45
where is angiotensionogen made?
the liver
46
explain steps of RAAS
Renin converts angiotensinogen to angiotension 1
ACE in the lungs converts angiotension 1 to angiotension 2
angiogensin 2 has 5 effects
47
what else does ACE do besides convert angiotensin 1 to angiotensin 2?
also breaks down brandykinin into inactive proteins.
48
increased bradykinin from ACE inhibitors can cause what sysmptoms?
cough
allergy symptoms
angioedema
bronchospasm
49
what are the 5 effects of angiotensin 2
vasoconsctriction (very potent)
^ aldosterone
SNS activation
^ ADH
^ Thirst
50
What 3 things increase Renin release and give examples of each
1. Decreased Renal perfusion (hemorrhage, PEEP, CHF, liver failure with ascities, sepsis, diuresis)
2. B1 / SNS activation
3. Tubuloglomerulur feedback ( decreased Na or Cl in distal tubule)
51
effects of aldosterone and mech of action
Na and H2O retention with K and H excretion.
this happens via Na/K ATPase in principal cells of distal tubule and collecting ducts
52
what three things increase aldosterone release?
RAAS
hyperkalemia
hyponatremia
53
sodium retaining effects of angiotension 2 happen how quickly?
almost immediately
54
how soon do physiologic effects of aldosterone kick in after aldosterone release?
1-2hr delay between release and physiologic effects
55
what is Conns disease? What does it cause?
excess aldosterone. Leads to Na retention and K loss
56
when do we see inadequete aldosterone release?
very rare to seee inadequete aldosterone in isolation
most commonly seen as a result of addisions disease or adrenocortical insufficiency.
57
what is addisions disease?
usually the result of adrenocortical insufficiency.
Inadequate production of adrenal hormones, mainly cortisol and aldosterone.
58
what is normal plasma osmolarity?
280-290mOsm/L
59
what is the main determinant of plasma osmolarity?
Na concentration
60
what is the formula to calculate plasma osmolarity?
plasma osmolarity = 2Na + glucose/18 + BUN/2.8
61
another name for ADH
arginine vasopressin or vasopressin
62
what two things increase ADH release?
^ osmolarity of ECT
decreased blood volume
63
ADH mech of action
1. V1 receptors cause peripheral vasoconstriction
2. V2 receptors cause ^ H20 reabsorption (increased aquaporin channels inserted into the wall of the collecting ducts)
64
ADH half life
5-15min
65
where is ADH systhesized?
primarily in the supraoptic nuclei of the hypothalamus, but small amount is also synthesized in the paraventricular nuclei.
66
what are the three pathways of renal vasodilation?
1. prostaglandins
2. naturetic peptides
3. Dopamine receptors
67
pathophys of renal vasodilation from prostaglandins
leukotrines cause vasoconstriction
when hypoxic pathway goes to vasoconstrictors from cyclic endoperoxides instead of the other way
68
what 4 things can increase phospholipase A2 leading to renal vasodilation?
ischemia
hypotension
NorEpi
angiotensin 2
Basically the stress response will triggers events that are designed to preserve renal blood flow
69
how do NSAIDs affect renal vasodilation pathway from prostaglandins
inhibit cycloxygenase resulting in renal vasoconstriction
70
describe pathophys of naturetic peptide pathway for renal vasodilation
ANP > inhibits renin release > causes vasodilation, Ha and H2O excretion in the collecting ducts
71
name the dopamine receptors and their location
DA1 in renal vasculature and tubules
DA2 in pre-synaptic SNS nerve terminals
72
list the function of DA1 and DA2 receptors
DA1 ^ cAMP > vasodilation, ^ RBF, ^ GFR, diuresis, and Na excretion
DA2 decrease cAMP > decreased NorEpi release
73
how does renal dose dopamine effect the kidneys?
dopamine does increase Urine output, but no solid evidence supports dopamine as a treatment or prevention of AKI
74
Fenoldopam med class
selective DA1 receptor agonist
75
Fenoldopam effects
^ RBF
76
Fenoldopam dose and effects
0.1-0.2 mcg/kg/min ^ RBF, ^GFR, ^ Na excretion with no effect on arterial BP
77
during which surgeries does fenoldopam offer renal protection? when does it affect mortality rates?
aortic surgery and CPB
also decreases the need for dialysis and in-hospital mortality in cardiac surgery patients.
78
what is the normal glomerular filtration rate?
125ml/min
79
what percent of renal blood flow is filtered through the glomerulus? What percent is delivered straight to the peritubular capillaries
20% filtered through glomerulus
80% delivered to peritubular capillaries
80
what substances are freely filtered at the glomerulus and what substances are not?
H20, electrolytes, and glucose are freely filtered
plasma proteins are not filtered
81
when can plasma proteins enter the tubules?
in kidney disease the basement membrane is destroyed which allows proteins to enter the tubules and can lead to hypoalbuminemia
82
two examples of kidney disease where proteins are lost in the urine
nephrotic syndrome
interstitial nephritis
83
what is the main determinant of GFR?
glomerular hydrostatic pressure
84
what are the 3 determinants of glomerular hydrostatic pressure
1. Arterial BP
2. Afferent arteriole resistance
3. Efferent arteriole resistance
85
how do increased and decreased plasma protein concentration affect GFR and filtration fraction?
increased plasma proteins > decreased GFR, and decreased filtration fraction
decreased plasma proteins > ^ GFR and ^ filtration fraction
86
explain the affects of efferent arteriole constrction on RBF and GFR
biphasic pattern
mild constriction decreased flow to peritubular capillaries and ^ GFR
excessive constriction: decreased RBF and decreased GFR
87
explain maximum transport in regards to renal function
for some substances there is a max amount that can be reabsorbed into peritubular capillaries, once the max level is reached the rest is excreted regardless of plamsa concentration
example: hyperglycemia
88
urine excretion rate formula
urine excretion = filtration - reabsorption + secretion
89
what does reabsoprtion of water and elctrolytes require?
reabsorption of electrolytes requires ATP (energy)
while water reabsorption is via osmosis and does not require energy
90
where is the body does the rule, "water follows salt" not always hold up?
in the nephron
91
main functions of proximal convoluted tubule?
65% of Na, H20, K, Cl, and bicarb reabsoprtion
organic bases, acids, and H ions are secreted into the PCT from peritubular capillaries
92
main functions of descendign loop of henle?
20% of H20 reabsorbed > concentrates NaCl in the tubular fluid
separates the handling of water and salt
highly permeable to water and only mildly permable to ions
progressive ^ in oxmolarity down the descending loop, starts at 300mOsm/L and gets down to 1,500 mOsm/L in renal pelvis
93
main function of ascending loop of henle
reabsorbs 20% of tubular sodium
not permeable to H20
this is the countercurrent mechanism
94
Distal convoluted tubule function
5% of sodium, K, Cl, bicarb reabsorbed
late DCT is imperable to H20 except for in the presence of Aldosterone or ADH
adjusts urea concentration
PTH induced Ca reabsorption occurs here
95
collecting duct function
5% sodium reabsorption
ADH and aldosterone also work here
ANP inhibits H20 and Na reabsorption
adjusts hydrogen concentration
96
list some carbonic anhydrase inhibitors
acetazolamide and dorzolamide
97
carbonic anhydrase mech of action
decreased reabsorption of H20, Na, K and HCO3 in PCT > alkaline urine and mild hyperchloremic metabolic acidosis
98
clinical uses to carbonic anhydrase inhibitors?
open angle glaucoma: decreased aqueous humor production
high altitude sickness and central sleep apnea: mild metabolic acidosis to increase resp drive.
99
name some osmotic diuretics
mannitol, glycerin, isosorbide
100
osmotic diuretics mech of action
sugars that undergo filtration but not reabsorption. Inhibit h20 reabsorption in proximal tubule (primary site) and loop of henle.
101
what is an extra effect of mannitol and its consequences?
mannitol is also a free radical scavenger which may limit cellular edema and obstruction of renal tubules.
102
name loop diuretics
lasix, bumetanide, ethacrynic acid
103
loop diuretics mech of action
disrupt Na-K-2Cl transportor in TAL of henle and ^ Na in tubule. > large volume of dilute urine. K, Ca, Mag, and Cl lost in urine as well.
104
with loop diuretic is the most ototoxic
ethacrynic acid
105
unique medication interaction consideration of loop diuretics
decreased lithium clearance
106
list some thiazide diuretics
hydrocholorothiazide, chlorthalidone, metolazone, indapamide
107
thiazide diuretics mech of action
inhibit NaCl con trasnporter in distal tubule > ^ Na, Cl, and H20 excretion
^ Ca reabsporption
108
which diuretics can cause hyperglycemia
thiazide diuretics
109
name the K sparing diuretics
spironolactone, amiloride, triamterene
110
mech of action of k sparing diuretics
amiloride and triamterene: inhibit K secretion and Na reabsorption in collecting duct. they function independently of aldosterone.
spironolactone: aldosterone antagonist: inhibits K secretion and Na reabsoprtion in collecting ducts
111
some medications can increase the risk of hyperkalemia from K sparing diuretics. what medications?
NSAIDs, BBs, ACEi
112
other SE of loop diuretics
gynecomastia
lilbido changes with spironolactone
triamterene: nephrolithiasis
113
what tests are best for glomerular function?
BUN
serum creatine
creatine clearance
114
what tests are best for tubular function?
fraction excretion of Na
urine osmolality
urine sodium concentration
urine specific gravity
115
where does urea come from?
primary metabolite of protein metabolism.
amino acids > ammonia > urea
116
why is BUN a better indicator of uremic symptoms than as a measurement of GFR?
because urea is filtered at glomerulus and also reabsorbed.
117
where does creatine come from?
produced by skeltal muscle and is a by product of creatine breakdown
118
how does creatine production relate to muscle mass?
directly proportional
119
why is creatinine a good indicator or GFR?
it undergoes renal filtration but not reabsoprtion
120
if creatine increases by 100% how much has GFR changed?
50% decrease in GFR
121
what is a normal BUN:creatine ration
10:1
122
BUN:creat of 20:1 suggests what?
pre-renal azotemia
123
what is the best indicator of GFR?
creatine clearance
124
what does Fractional excretion of Na help us do clinically?
relate Na clearance to creatine clearance
125
what does FeNa <1% indicate?
more Na donserved relative to creatine cleared, suggests pre-renal azotemia
126
what does FeNa >3% indicate?
more Na excreted relative to creatine cleared, suggests impaired tubular function
127
what does urinary sodium tell us about the kidneys?
working kidneys can conserve sodium
failing kidneys waste sodium
128
what does lots of protein in urine indicate?
glomerular injury
(>750mg/day or 3+ by urinalysis)
129
urine osmolality is a better test what than specific gravity?
tubular function
130
lab findings you would expect in pre-renal oligura
FeNa < 1%
urinary Na <20
urine osmolality >500
BUN:Creat >20:1
131
lab findings you would expect in acute tubular necrosis
FeNa > 3
urinary Na >20
urine osmolality < 400
BUN:Creat 10-20:1
132
what is the most common cause of periop kidney injury
ischemia-repurfusion injury
133
oliguria is usually blank in origin
pre-renal
134
why can't oliguria be used as a marker for renal perfusion in perioperative setting?
because oliguria is often caused by the perioperative stress response (^ADH secretion)
135
what are the three methods to calssify severity of renal injury?
RIFLE, AKIN, KDIGO
136
what do RIFLE, AKIN, and KDIGO actually tell you? or not tell you?
only tell you after injury has occured, dont predecit or give heads up about an injury occuring in the future
137
how do you treat pre-renal injury
fluids and hemodyanamic suppport
avoid NSAIDS
138
what are the different types of intrinsic renal injury?
injury to tubules, glomerulus, or interstitial space. ATN is the most important
139
how do you treat intrinsic renal injury?
restore perfusion
140
fluid mgmt goals to avoid AKI
keep MAP > 65
hydroxl starches are the highest risk of renal injury
141
what happens if you try to convert oliguiric aki to non-oliguric aki?
increases the risk of additional renal injury and mortality
142
how to alpha 1 agonists affect RBF in healthy patients?
decrease RBF
143
can you use alpha 1 agonists in increase renal perfusion in septic patients?
yes, the increase in MAP outweights the renal vasoconstrictive effects
144
which pressor is best for AKI?
vaso preferentially constricts efferent arteriole to maintain GFR better than Neo or NorEpi
145
list the KDIGO guidlines to prevent AKI in high risk patients
only use diuretics for volume overload
avoid aminoglycoside ABXs
target BG 110-149 in critically ill
don't opt for off pump CPB only as a way to decrease risk of AKI.
146
what are the first and second most common cuases of CKD?
1st: DM
2nd: HTN
147
main issues that come with CKD
uremic syndrome
uremic bleeding
anemia
CV effects
acid base disturbances
Resp effects
Hyperkalemia
neurologic effects
osteodystrophy
148
explain uremic bleeding
uremia messes up platelet function and vWF. this leads to bleeding with normal PT, PTT, and platelets levels.
DDAVP is 1st line tx.
149
what kind of anemia is caused by CKD?
normochromic normocytic from decreased EPO
150
SE of EPO
HTN
151
why is blood tranfusion not first line for anemia in CKD?
because it can increase risk of HLA sensitization and ^ risk of future transplant rejection
152
what is most common cause of death in CKD pts?
CAD
assume everyone with CKD has CAD
153
K > what is an indication for dialysis
6
154
5 indications for dialysis
1. volume overload
2. hyperkalemia >6
3. severe metabolic acidosis
4. symptomatic uremia
5. drug OD that can be cleared by dialysis
155
which form of HD is most effecienct?
HD is more efficeint that PD
156
when should PD be used over HD?
patients that can't tolerate fluid shifts
157
what is the most common event during dialysis
HoTN
158
what is the leading cause of death in dialysis patients?
infection! Strict aseptic technique is important.
159
what was the risk of methoxyflurane use in renal failure?
caused high output renal failure from lots of fluoride ions
160
what are renal patients at risk of hemodyanically?
risk of exaggerated hemodynamic effects
161
why can't you use sux drip in renal failure?
sux-monocholine (active metabolite) ex excred by the kidneys and could lead to prolonged paralysis
162
name the benzilisoquinollines
cixatracurium
atracurium
163
what does laudenosine cause?
CNS stimulant could cause seizures
164
what creates more laudenosine, atracurium or cisatracurium?
atracurium
165
what benylixoquinoline releases histamine?
atracurium,
166
which NDNMBs undergo organ independent elimination?
benzylisoquinolines
167
name the amino steroids
roc
vec
pancuronium
168
how is roc eliminated?
hepato-billiary elimination
169
is Vec good choice in renal failure? why or why not?
no, has 3-OH-Vec active metabolite that will prolong its action
170
Roc effects in renal failure
unpredictable increase in DOA
171
can you use pancuronium in renal failure? why or why not
no bad choice, it is primarily eliminated by the kidneys.
172
how should traditional reversal agents be dosed in renal failure?
simillar increae in DOA of both anticholinesterases and anticholinergics so no dose adjustment needed
173
can you use sugammadex in renal failure?
not recommended. WE still did in clinical though..
174
propofol dosing consideratiosn in renal failure
may need dose increase becasue of hyperdynamic circulation and BBB disruption from uremia
175
is precedex okay in renal failure? why or hwy not?
yes, liver biotransformation so safe in renal patients
176
which opiods have active metabolites
morphine : morphine-6-glucuronide
meperidine : normeperidine
hydromorphone : contraversial, but some texts say hydromorphone-6-glucuronide
177
which opioids are best for renal failure
fentanyl, remifentanil, and sufentanil because no active metabolites.
178
morphine-6-glucuronide effects
more potent than morphine
179
normeperidine effects
accumulation can cause seizures
180
hydromorphone-6-glucuronide effects
can prolong resp depression and casue myoclonus
181
list some ways to mitigate nephrotoxicity from contrast. Something else to consider about contrast
use non-ionic iso- or hypo-osmolar contrast instead of hyperosmolar contrast
lowest volume possible of contrast
sodium bicarb to alkalize urine
contrast can also cause anaphylaxis
182
how does myoglobin hurt the kidney
in acidic urine myoglobin precipitates in the proximal tubule, > tubular obstruction > acute tubular necrosis
183
tx for myoglobinuria & hemolysis from hemolytic reaction
IV hydration to maintain renal blood flow
osmotic diuresis with mannitol
keep UOP > 100-150ml/hr
sodium bicarb or acetazolamind to alalize urine
184
what condidtions can increase ammount of compound A formed by sevo?
low FGF
high sevo vol%
warm soda lime
^ CO2 production
185
list some other drugs that are nephrotoxic
aminoglycosides
calcinerurin inhibitors (immuno supressants)
other ABXs
186
what are some aminoglycosides
gentamycin
tobramycin
amikacin
187
what are some calcineruin inhibitors
cyclosporine
tacrolimus
188
other abx besides aminoglycosides that are nephrotoxic
amphotercin B
vaco
sulfonamide
tetracyclines
cephalosporins
189
5 conditions that can cause rhabdomyolysis and myoglobinemia
1. direct muscle trauma
2. muscle ischemia
3. prolonged immobilization
4. MH
5. sux in pt with duchene muscular dystrophy
190
which anesthetic technique is most common for TURP?
spinal need level to T10
191
why is spinal preffered for TURP?
can assess mental status
192
how much resection fluid is absobred during turp?
estimated to be 10-30ml/min
193
how high to keep irrigation fluid above OR table?
no more than 60cm above, some texts suggest lowering height at the end because there will be more open venus sinuses
194
resection time during turp should be limited to how long?
limited to 1hr
195
when is it okay or not okay to use NS or LR for the irrigation fluid during TURP?
if bipolar cautery is used okay to use NS and LR, if monocautery is used it is too high risk for electric shock
196
pros and cons of glycine containing irrigation fluid during turp
decreased risk of TURP syndrome but risk of transiet blindness for 24-48hrs
197
what does glycine normally do in the eye
it is an inhibitory neurotransmitter
198
turp syndrome symptoms
HTN, bradycardia (reflex), and changes in mental status.
199
what causes turp syndrome
large volume of hypoosmolor irrigation solution absorption
200
Na < what increases risk of complications in turp?
Na<120
201
Na < what is associated with seizure, coma, and lethal ventricular dysrhythmias
Na <110
202
how do you treat TURP
have surgeon abort procedure
get electrolytes, hematocrit, creatine gluocose levels and 12 lead EKG
if Na >120 restrict fluids and give loop diuretic
if Na<120 3% Nacl @100ml/hr and DC after Na >120
203
s/s of bladder perforation from TURP
abd pain and shoulder pain
decreased irrigation fluid return is a sign of bladder perforation
204
how to tx bladder perforation
treatmetn is supportive care
205
what is nephrolithiasis
kidney stone
206
what is ureterolithiasis
ureter stone
207
what is cystolithasis
bladder stone
208
absoulute CI to ESWL
pregnancy
coagulopathy
209
relative CI to ESWL
pacemaker/ICD
calcified aneurysm of aorta or renal artery (density problem)
untreated UTI
obstruction beyond renal stone
morbid obesity (energy source to far away from stone)
210
possible ESWL complications
shock can cause R on T, must be synced with EKG
any organ in the shock path is at risk of perforation
skin bruising and petechiae may occur
hematuria is a common side effect
211
when is percutaneous nephrolithotripsy used? How is the stone accessed?
when ESWL has been ineffective
urethreal sten placed > nephrostomy tube placed to access the stone
212
what type of anesthesia and position typically for percutaneous nephrolithotripsy?
GETA in prone position
213
possible complications of percutaneous nephrolithotripsy?
irrigation fluid is used so TURP considerations apply
pneumothorax is a possible complication
214
anesthetic considerations for laser lithotripsy
usually in lithotomy position
follow laser precatuions
irrigation fluid used, so TURP considerations apply
215
explain osteodystrophy caused by CKD
CKD > decreased vit D > decreased Ca absorption > ^PTH release
at the same time, decreased GFR > ^phosphate levels. ^phosphate > low Ca levels.
