Apex- Renal Flashcards
At what vertebral levels do the kidneys lay
between T12-L3 in the retroperitoneal space
The kidney can be divided into what 2 parts and what does each contain (4/2)
Renal Cortex
- Glomerulus, bowmans capsule
- Proximale and distal tubules
Renal Medulla
- loop of henle
- collecting duct
(the two things that drop down)
functional unit of the kidney
nephron
What substance is produced by the juxtaglomeular apparatus
renin
Where is erythropoietin synthesized and what is it secreted in response to?
In the kidney
-secreted in response to hypoxia
The kidney produces : (select 3)
- Calcitrol:
- ADH:
- Aldosterone:
- Renin:
- Erythropoietin:
- Angiotensinogen:
-Calcitrol: parathyroid tells kidneys to convert inactive vitamin D3 to active vitamin D3 (calcitrol)
- ADH: supraoptic nuclei and paraventricular nuclei in the hypothalmus- released from posterior pitutiary gland
- Aldosterone: adrenal cortex
-Renin: by the juxtaglomerular apparatus in response to decreased perfusion
-Erythropoietin: secreted in response to hypoxia
-Angiotensinogen: liver
Where is angiotensinogen manufactured
in the liver
Where is aldosterone synthesizied
in the adrenal cortex
Where is ADH produced/released from
produced in the hypothalmus (supraoptic and paraventricular nuclei)
released from posterior pitutiary gland
Where is erythropoietin syntheized
in the kidney
(in response to hypoxia)
What is calcitrol
the active form of vitamin D3
synthesized in the kidney under influence of parathyroid hormone
where is renin produced from?
the kidney - the juxtaglomerular apparatus
What organs are the regulators of acid base balance
lungs and kidney
lungs- rid body of volatile acids (CO2)
kidneys- rid body of non-volatile acids (Bicarb)
someone is anemic bc of chronic kidney diseae - why are they anemic?
bc the kidney produces erythropoietin (stimulates RBC production), less RBCs = less hgb
Renal blood flow decreases ____% per decade after the age of ____
10% /decade after 50yo
In the neonate, RBF doubles when and reaches adult function when
*rule of 2’s
- RBF doubles in first 2 weeks of life
- adult levels by 2 years
Difference between aldosterone and ADH (vasopressin)
aldosterone controlls extracellular fluid volume (sodium and water reabsorption)
ADH manipulates plasma osmolarity (water is absorbed by sodium is not)
T/F- the kidney is capable of phase 1 and phase 2 metabolism
true
Why do people hgb become elevated when “dry”
bc if they are intravascularly dry, the kidneys sense reduced o2 delivery to them, they secrete erythropoietin to make more RBCs, more RBCs = more hemoglobin to try and carry more o2 to the kidneys
Why cant you give NSAIDs to people with impaired renal function
bc they block prostagladins and prostagladins control blood flow to the renal arteries
- PGE2 and PGI2 vasodilate the renal arteries (afferent)
- Thromboxane A2 consticts the renal arteries (efferent)
- blocking this, impairs filtration time
____ & ____ vasodilate the afferent arterioles
_____constricts the efferent arterioles
(prostagladins subtypes)
PGE2 & PGI2 vasodilate
Thromboxane A2- constricts
What is the vitamin D3 that is sythesized by the skin upon exposure to ultraviolet light?
Calciferol (like a feral cat outside)
-it’s INACTIVE
2 ways we get vitamin D
-how does it become activated?
Sunlight (calciferol, skin) & Diet
(both inactive forms)
- liver converts calciferol to 25-hydroxycholecalciferol (biotransformation- makes orginal word root longer)
25-hydroxychloecalciferol is converted to
1,25- dihydroxycholecalciferol (calcitriol) - active form of vitamin D 3
PTH regulates this process - increase serum PTH, increases serium calcitrol level
Active form of Vitamin D3
Calcitriol
T/F- the renal medulla receives 90% of the renal blood flow
FALSE- renal cortex
-think - cortex = higher level functions = more o2 needed
How do the kidneys prevent hypoglycemia during fasting?
by synthesizing glucose from amino acids
How does active vitamin D3 increase serum calcium levels? (3 ways)
- stimulates intenstines to absorb more CA++ from food
- instructs kidney to reduce CA++ and phos exretion
- Increases deposition of CA++ into the bone (increases bone turnover time- no clue)
What hormone controls plasam osmolarity?
ADH
What hormone controls extracellular fluid volume?
Where do the kidneys receive SNS innervation from?
T8-L1
(Lies at T12-L3)
How much of the CO do the kidneys receive
20-25%
1,000 - 1250ml/min
Of the blood flow delivered to the kidney, only ____% is filtered at the glomerulus
20%
Renal blood flow is (directly/inversely) propotional to the difference between MAP and renal venous pressure and (directly/inversely) propotional to renal vascular resistance
directly proportional to difference between MAP and renal venous pressure (greater pressure gradient = greater RBF)
-inversel ypropotional to RVR (increases resistance = decreased RBF)
Autoregulation maintains renal blood flow between a MAP of ____ - _____
50- 180mmHg
the blood in the peritubular capillaries returns to the IVC by way of what?
the renal veins
How to calculate RBF
(MAP-Renal venous pressure)/ Renal vascular esistance
Renal cortex recieves ___% of RBF (PO2)
Renal medulla recieves ___% of RBF (PO2)
which is more sensitive to ischemia?
Cortex - 90% renal blood flow (PO2 50)
Medulla - 10% RBF (PO2 10)
*medulla is most sensitive to ischemia
T/F - UOP is autoregulated
false- it is linearly related to a MAP > 50
What is the myogenic mechanism and how does it relate to RBF
If pressure is too high through the renal artery, the myogenic mechanism constricts the afferent arteriole to protect the glomerulus from excessive pressure
-
-when the pressure is too low, the mygoenic mechanism dilates the afferent arteriole to increase blood flow going to the nephron
Where in the kidney specifically is the juxtaglomerular apparatus located?
in the distal tubule (specifically the region that passes through the afferent and efferent arterioles)
What renal structures are innervated by the SNS?
The afferent and efferent arterioles
Which factor increases renin release?:
A. PEEP
B. Hypervolemia
C. Angiotensinogen
D. Increased chloride delivery to the macula densa
A. PEEP
Increase or decrease renin release:
-Beta 1 stimulation
Increase (Beta receptors on the juxtaglomerular apparatus)
(Increased/decreased) sodium and chloride delivery to the distal tubule increases renin release
decreased
(decreased solutes, release renin > vasoconstriction)
Aldosterone is a ______ hormone that is produced by the zona ________ of the adrenal gland.
steroid hormone, zona glomerulosa
NA+ reabsorption, K+ and H+ excretion
T/F- Aldosterone does not meaningully affect serum os
true- it manipulates absopriton and excretion of solutes; whereas ADH mainpulates reabsopriton of water (osmolarity) and not solutues
Aldosterone facilitates reabsoprtion and exretion of what?
absorpiton of sodium (and water)
exretion of K & H
think NA has two ++ , so in addition to K+ , it also excretes H+ to balance the scale
Angiotension 2 causes constriction of the (efferent/afferent) arteriole, which (increases/decreases) GFR
efferent
increases
What happens when renin is released
it converts angiotensinogen from the liver to angiotension 1
angiotension 1 is converted to angiotension 2 by ACE in the lungs (also breaks down bradykinins)
- angiotension 2 is the most potent vasoconstrictor in the body: peripheral vessels, efferent arteriole, triggers release of aldosterone (na and water reabosprtion, k & H extretion- DT), relase of ADH (post. pit) - water reabsorption (CD) ; signals sodium to be reabsoprtied in the proximal tubule, and triggers thirst
- wow that was extra
6 mechanisms by which angiotension 2 increases BP
- peripheral vasoconstriction
- constriction of the efferent arteriole
- aldosterone release
- from the adrenal gland (zona glomerulosa)
- steroid hormone
- promotes NA+ reabsoprtion, K+ exretion
- distal tubule
- ADH release
- Posterior pituitary
- water reabsoprtion
- collecting duct
- Na+ reabsoprtion
* proximal tubule - Thirst
What causes aldosterone to be released (3) things
RAAS activation
Hyperkalemia (takes sodium, gets rid of K)
Hyponatremia (takes sodium, gets rid of K)
Conn’s disease occurs with (too much/too little) aldosterone production
too much
- causes sodium retention and potassium loss
- aldosterone = conn man, takes sodium for k
*too little aldosterone production is uncommon
ADH agonizes the (V1/V2) receptor and (increases/decreases) cAMP
agonizes the V2 receptor (increases aquaporin channels in the CDs)
increases cAMP
T/F ADH increases water reabsorption in the proximal tubules
false- collecting ducts
What is the principle determinate of osmolarity
What 2 other things play a role?
Sodium concentration
Glucose and BUN
Normal serum osmolarity
280-290mOsm/L
In what 2 instances is ADH released into the systemic circ?
- increased osmolarity of ECF (will promote water reabsoprtion to dilute solutes)
- decreased blood volume/ RAAS activation
2 ways by which ADH restores blood pressure
1. V1 receptor stimulation in vasculature causes vasoconstriction (increased SVR)
- Gq ⇒ increased IP3, DAG, CA +
2. V2 receptor stimulation in the collecting ducts causes water retention
(Osmolality/Osmolarity) measures the number of osmoles per (liter/kg) of solvent
Osmolality - osmoles per kg
OsmolaRity- osmoles per liteR
(differences are so minuscule that they can be used interchangably but just incase you get questions on this bullshit)
Half life of ADH
5-15 minutes
All of hte following enhance renal perfusion EXCEPT:
- fenoldopam
- PGE2
- Naturitic peptide
- Thromboxane A2
Thromboxane A2
(vasoconstrictor and increases in time of ischemia)
What do naturitic peptides do to the kideny
- well they are released in response to increased blood volume
- so they inhibit RAAS, promoting sodium and water exretion
What does the stimulation of D1 vs D2 receptors result in
D1 ⇒ vasodilation, increased renal blood flow, increased GFR, diuresis, sodium exretion
D2 ⇒ decreased NE release from the presynaptic SNS nerve terminal
3 things that promote renal vasodilation
- prostagladins
- naturitic peptide
- dopamine receptors
Where are prostagladins produced?
inthe afferent arteriole of the kidney
When is arachidonic acid liberated from the cell membrane (4) & How
in response to
- ischemia
- hypotension
- NE
- Angiotension 2
(well thats confusing)
Phospholiapse A2 convers phospholipid in the cell membrane to arachidonic acid
What two things are produced by arachidonic acid and by what 2 pathways
1. Cyclic endoperoxides: (Cyclooxygenase pathway)
- Vasodilators: PGI2 ♦ PGE2 ♦ PGD2
- Vasoconstrictors: Thromboxane A2 ♦ PGF2
2. Leukotrienes (Lipooxygenase pathway)
How do NSAIDS reduce renal blood flow?
By inhibiting cyclooxygenase and the production of vasodilating prostagladins
Vasodilator or vasoconstrictor:
PGI2
Vasodilator
Vasodilator or vasoconstrictor:
PGE2
Vasodilate
(D2, I2,E2)
-when you DIE, you vasodilate
Vasodilate or constrict
PGD2
Vasodilate
(D2, I2, E2)
-when you DIE, you vasodilate
Vasodilate or vasoconstrict:
Thromboxane A2
Vasoconstrict
(+PGF2)
Vasodilate or constrict: PGF2
Constrict
(D-I-E = vasodilate)
(F = fuck that, i’m gonna try to help you not die and constrict)
(+thromboxane A2)
Where are D1 receptors located (2 places)
on the kidney and in splanchic circulation
Where are D2 recpetors present
on the presynaptic adrenergic nerve terminal
(D1/D2) receptor stimulation results in (increased/decreased) cAMP
D1 = increased cAMP (vasodilation, increased RBF, increased GFR, diuresis (bc of the increased RBF), sodium exretion
D2 = decerased cAMP (decreased NE release from presynaptic nerve terminals)
i’m confused
What is Fenoldopam
a selective D1 agonist that increases renal blood flow
- low doses 0.1-0.2mcg/kg/min
- may offer renal protection during aortic surgery and during CPB
2 effects natruetic peptide has on the kidneys
- inhibits renin release
- promotes sodium and water exretion in the collecting ducts
Normal GFR
125mL/min
3 determinants of glomerular hydrostatic pressure
- Arterial pressure
- afferent arteriole resistance
- efferent arteriole resistance
T/F - The Glomerular hydrostatic pressure if the most important determinant of GFR
True
Constriction of the efferent arteriole (increases/decreases) RBF and GFR
decreased RBF but increases GFR
Where does MOST of hte sodium reabsopriton occur in the nephron?
- proximal tubule
- distal tubule
- collecting duct
- ascending loop of henle
Proximal tubule
Define:
Reabsoprtion:
Secretion:
Excretion:
Reabsoprtion - substance is transfered from the tubule > peritubular capillaries
Secretion - substance transferred from the peritubular capillaries > tubules
Excretion - substance is removed fromo the body in the urine
Which part of the loop of henle (ascending vs descending) is highly permeable vs impermeable to water
Descending = highly permeable (think taking a deep dive into a pool of water)
Ascending - impermeable to water
Primary site of reabsorption in the nephron
proximal convuluted tubule
T/F - reabsorption of solutes and water is proportional in the proximal convuluted tubule
True
65% sodium, (followed by) 65% water
+ 65% K, Cl-, HCO3-
Primary goal of the loop of henle
handles sodium and water to form concnetrated or dilute urine
What part of the nephron “fine-tunes” solute concentration
the distal convoluted tubule
T/F- the late distal tubule is impermeable to water
True - except i nthe presence of aldosterone or ADH which fine-tune the final urine concentration
What does the collecting duct do?
regulates the final concentration of the urine
Where does aldosterone act on the nephron?
In the DCT & collecting ducts
Where does ADH act on the nephron?
in the DCT and collectin ducts
Where in the nephron does parathyroid hormone promote CA+2 reabsoprtion?
Distal tubules
Which part of hte nephron is impermeable to water?
The ascending loop of henle
match
What specifically in the kidney do most diuretics target?
The NA/K- ATPase pumps that allows sodium to move from the tubule to the peritubular capillaries that allows for maintenance of the concnetration gradient
What is the function of carbonic anhydrase in the proximal tubule?
So
- CO2 and water diffuse into the PCT where carbonic anhydrase is
- Carbonic anhydrase facilitates the formation of carbonic acid (H2CO3)
- H2CO3 then dissocitates into:
H+ (Stays in the tubular lumen)
HCO3 - (Diffuses back into the blood)
-so with people on carbonic anhydrase inhibitors, HCO3- stays in the urine, making it more basic, and produces a mild hyperchloremic metabolic acidosis
Why wouldn’t you want to give acetazolamide (diamox) to a COPD patient or someone with an elevated CO2 level
elevated CO2 level = hydrogen ion excess /acidosis
if you give diamox - your going to lose HCO3- in the urine and take away the kidneys ability to try and buffer that excess H+ in the blood (worsens hypercapnia/sleepiness)
What diuretic may be given for those with central sleep apnea and why?
acetazolamide (diamox) - bc it will prodice a mild metabolic acidosis and the excess H++ ions will stimulate respiratory drive
Dose of acetazolamide
250-500mg
Which diuetic can be used to treat open-angle glaucoma
acetazolamide (diamox)
-inhibition of carbonic anhydrase reduces aqueous humor production and decreases IOP
T/F- carbonic anhydrase inhibitors can produce hypokalemia
True - not sure why though….
Where do osmotic diuretics work?
in the proximal tubule (primary) and loop of henle
Why is mannitol thought to protect the kidney
Bc it’s going to enhance renal blood flow by pulling fluid into the intravascular space
If your giving mannitol, what should you think of in terms of pt history
mycoardial function - if poor; it can preciptate heart failure and pulmonary edema bc the heart cant handle the increase in volume
What is isosorbide
an osmotic diuretic
What diuretics inhibit water reabsoprtion in the proximal tubule and loop of henle?
Osmotic diuretics
-mannitol, glycerin, isosorbide
what is glycerin
an osmotic diuretic
- i think this is what they are talking about with TUR syndrome and using glycerin as the fluid - if it gets into a venous sinus, it can increase intravascular volume and lead to pulm edema? maybe? lol who knows
Dose of mannitol
0.25-1g/kg
Mannitol can be used as a differential diagnosis of acute oliguria - how?
if the issue is pre-renal, UOP will increase (kindey still works fine)
if the issue is intrinsic- there will be no increase in UOP (kidney is damaged and not fucntioning as it should)
Mannitol in TBI- yes or no
NO - the BBB can be disrupted and if mannitol enters the brain it will worsen cerebral edema
Loop diuretics disrupt the __________ transporter in the medullary region of the (thick/thin) portion of the (ascending/descending) loop of henle.
- NA-K-2CL transporter
- Thick portion of ASCENDING loop (impermeable to water)
- increased amount of sodium remains in the tubule
…idk i dont get it
Dose of furosemide
20-200mg
What is Bumetanide?
Dose?
Bumex - loop diuretic
0.5-2mg
What is ethracrynic acid ?
Edecrin
-loop diuretic
What diuretics inhibit the Na-Cl co-transporter in the distal tubule
Thiazides
Which type of diuretics can cause hyperglycemia?
Thiazide diuretics
-speculated poss decrease insulin release from pancreas or impair glucose utilization in the body .
What is chlorthalidone
Thiazide diuetic
(DCT)
What is metolazone
thiazide diuretic
(DCT)
What is indapamide
thiazide diuretic
(DCT)
What is spironolactone?
K-sparing diuretic
aldostone antagonist
-inhibits K secretion and NA reabsportion in the collecting ducts
What is amiloride?
K-Sparing diuretic
(collecting duct)
What is triamterene?
K-Sparing diuretic
(Collecting duct)
Why would K-sparing diuretics be used in someone with secondary hyperaldosteronism?
increased aldosterone = hypernatremia, hypokalemia
-K-sparing diuretics do the opposite.
Which K-sparing diuretic antagonizes aldosterone at the mineralocorticoid receptors?
Spironolactone
3 drug classes the increase the risk of hyperkalemia in a patient on K-sparing diuretics
- NSAIDS
- betablockers
- ACE inhibitors
What does the tubular function of the kidney assess?
concentrating ability
3 tests of glomerular function
Normal BUN
10-20mg/dL
Normal serum creatinine
0.7-1.5mg/Dl
normal creat clearance
110-150ml/min
4 tests of tubular function (concentrating ability)
- Fractional excretion of sodium (1-3%)
- Urine os (70-1400mOm/L)
- Urine sodium concentration (130-260mEq/day)
- urine SG (1.003- 1.030)
what is creatinine?
a metabolic byproduct of creatine breakdown
(levels should be normal if your kidneys functioning normally, they can filter it out)
Best indicator of GFR
creatine clearance
(110-150ml/min)
Normal fractional exretion of sodium
1-3%
Normal urine os
70-1400 mOsm/L
Normal urine sodium concentration
130-260 mEq/day
normal urine SG
1.003- 1.030
What is the primary metabolite of protein metabolism in the liver?
urea
(amino acids ⇒ ammonia ⇒ urea)
Why would somone have a BUN < 8mg/dL
(2 causes)
- overhydration (diluted out)
- Decreased urea production
- malnutrition - not taking in enough protein (gets broken down to ammonio > urea)
- severe liver disease - liver can’t metabolize ammonia into urea
What BUN level would signify to you that your patient may be dehydrated
20-40 range
Why would a BUN of 20-40 be something present in a patient with a GIB?
because BUN increases after a high digestion of protein or blood
creatine production is constant and (directly/inversely) proportional to muscle mass
directy propotional
women and elderly have lower creat levels bc they have decreased muscle mass
a 100% increase in creatinine indicates a ___% reduction in GFR
50%
Normal BUN:Cr ratio
10:1
What does a BUN:Cr ratio of > 20:1 suggest?
PRE-renal azotemia
If Fe(NA+) [fractional exretion of sodium] is <1% - what does that suggest?
what if it’s > 3%?
<1% - prerenal (more sodium is conserved relative to amount of creatinine cleared)
>3% = imparied tubular function )more sodium is excreted relative to the amount of creatinine cleared
T/F- failing kidneys waste sodium
True
What does a large amount of protein in the urine indicate?
Glomerular injury
(>750mg/day or +3 by UA)
T/F- specific gravity is a better test of tubular function than urine osmolality
false
urine os is superior
T/F- prerenal azotemia can canuse acute tubular necrosis
True
T/F- hydroxyethyl startches are assoicated with an increased risk of renal mobidity
True
-whatever the fuck that is
What is the most common cause of perioperative kidney injury?
ischemia-reperfusion injury
Your argument if somone is saying they arent making much urine
- well surgical stress increases ADH release and the body will hold onto fluid
- just because they arent making a huge amount of urine doesn’t indicate that their kidneys are taking a hit; MAP is >65, they are being perfused, its fine lol
Cause of prerenal injury
decreased perfusion to the kidneys
*restore RBF with IVF, blood, and pressors to halt progression to ATN
What can cause ATN? (2)
ischemia and nephrotoxic drugs
-supportive treatment
What is postrenal injury do to?
an obstruction between anywhere between collecting system and urtethra
t/f- efforts should be made to convert oliguric to nonoliguric aki with diuretics
false- increases renal injury and mortality
t/f- renal dose dopamine does not prevent or treat aki
true
T/F- vasopressin maintains GFR and UOP better than NE or neo
true
Vasopressin preferentially constricts the (afferent/efferent) arteriole
efferent
What are the 2 most common causes of CKD?
- Diabetes
- HTN
Pathophysiologic considerations for ESRD include (select 3):
- Secondary hyperparathyroidism
- Increased PT
- Megoblastic anemia
- Obstrictive ventilatory defect
- Gap metabolic acidosis
- Increased bleeding time
-
Secondary hyperparathyroidism
- From impaired active vitamin D3 production and hyperphosphatemia
- Increased PT
- PT, PTT, and platelets are normal
- Megoblastic anemia
- erythropoietin production is reduced
- contribut4es to normocytic normochromic anemia
- megoblastic anemia is associated with nitrous oxide
- Obstrictive ventilatory defect
- Fluid overload creates a restrictive ventilatory defect (not obstructive)
-
Gap metabolic acidosis
- from the accumulation of non-volatile acids
-
Increased bleeding time
- uremia increases bleeding time
What is bleeding time a measure of?
Platelet function
-it is elevated by uremia and is the most accurate predictor of bleeding risk
What is demopressin?
why would it be given?
von Willebrand factor 8
(first line treatment to decrease risk of bleeding in the uremic patient)
What is the first line treatment in the anemic patient with CKD?
Erythopoietin + iron
*NOT PRBC - increases risk of HLA sensitization and future rejection of a transplanted kindey
Why are you not suprised if a CKD patient has a pericardial effusion and/or tamponade?
bc elevated uremic levels in the blood can lead to pericarditis (inflmattion of the heart sac) - the irritation can lead to fluid accumulation
gap acidosis is the result of accumulation of ___________;
non-gap acidosis is hte result of a loss of __________.
gap acidosis - accumulation of non-volatile acids
non-gap - results from loss of HCO3 ions
Normal GFR
>/= 90
Drugs to avoid in the patietn on HD (select 2):
- Vecuronium
- Meperidine
- Sux
- Dex
Vec ⇒ 3-OH Vec
Meperidine ⇒ Normeperidine (accumulation > seizures)
Sux is only contraindicated if the K is high
Which is better for the renal patient, atracurium or cistatricurium
Cisatracurium
(AHHHHtracurium produces more laudanosine - CNS stimulant and also releases histamine - risk of hypotension)
Why is fluids and bicarb indicated in rhabdo patients
fluids bc myglobin is nephrotic and can cause ATN
sodium bicarb to alkalize the urine
- Aciditic urine causes myoglobin to precipitate in the proximal tubule causing tubular obstruction and ATN
Where is compound A vs free fluride ions produce with sevo?
compound A is produced in the breathing circuit (soda lime)
free flouride ions are produced by the liver
5 heavy hitters abx on renal fx
gentamycin
vancomycin
tobramycin
amikacin
amphotericin B
3 Aminoglycoside antibiotics
Gentamycin, tobramycin and amikacin
*give plenty of fluids with these agents
match
Their in the correct order
Why should you limit your fluid with TURP procedures
bc the irrigation fluid is abosrbed through the open venous sinuses of the prostate > risk of overload of toxicity from the irrigation solutes
How much irrigant can be absorbed into systemic circulation during a TURP?
-recetion time should be limited to what?
10-30ml/min
30 mins - 300mls -900mls of fluid
60 minutes - 600 - 1080mls of fluid
limited to 1 hour
Which fluid irrigant for TURPs is associated with TURP syndrome ?
what is the classic triad of sxs
hypo-osmolar irrigant (distilled water)
*HTN, bradycardia (reflex), and change in MS
which irrigant for TURP can lead to transient blindness?
Glycine
- it’s an inhibitory neurotransmitter in the eye
- no treatement is required (transient)
Treatment for TURP syndrome
hemodynamic support
- correct sodium levels (will be diluted down)
- monitor for seizures and treat with midaz
Your main concerns for TURPs (4)
- TURP syndrome (htn,brady, change ms)
- Bladder perforation (abdominal and shoulder pain)
- bleeding
- hypothermia (need bair hugger)
What level is required for a spinal for a TURP
T10
The height of the irrigating soluation should be no more than ____cm above the OR table
60cm
(60/2.54 = 24inches/2feet)
Why aren’t NS or LR used for TURP irrigation?
bc they are highly ionized, making them good conductors of electricity
-ok for bipolar but not okay for monopolar
Which TURP irrigant fluid increases ammonia levels and can lead to decreased LOC?
which irrigant solution for TURP can lead to hyperglycemia
Sorbitol
What should you do if your suspect TURP syndrome (pt becomes HTN and bradycardic?)
- support hemodynamics
- tell surgeon
- get labs: sodium, hct, creat, glucose, ekg
- if NA > 120, restrict fluids and give furosemide
if NA < 120, give 3% saline at < 100mls/hr and d/c once NA 120
What’s your concern during a TURP if the surgon is saying he’s not getting return of irrigation fluid
-early sign of bladder rupture
*monitor hemodynamics, open fluids, H&H
*prepare for emergent suprpubic systostomy or possible ex. lap
how do you figure out blood loss with TURPs since it mixes with the irrigation fluid
rough estimate = 2-5ml/min of resection time
30 mins = 60-150mls of blood
At what serum sodium concentration are seizures likely to occur?
<110
2 Absolute contraindication to extracorporeal shock wave lithotripsy
Pregnancy & bleeding disorders/anticoagulation
*VERYIFY NEGATIVE URINE HCG FOR FEMALES
What is lithotripsy?
a procedure that breaks up stones in the kidney, urteter, or bladder
What the ESWL shock wave timed with
the R-wave to minimize R-on-T phenomonon
Nephrolithiasis =
Ureterolithasis =
Cystolithiasis =
Nephrolithiasis = kidney stone
Ureterolithasis = ureter stone
Cystolithiasis = bladder stone
Relative contraindications to ESWL (5)
- Pacemaker/ICD
- Calcified aneurysm of the aorta or renal artery (can break off?)
- UTI (untreated)
- obstruction beyond the renal stone (cant elminate fragments)
- morbid obesity (further distance from energy source to stone
Why is it super important to keep the patient still during ESWL
bc any internal organ in the path of the shock wave is at risk for perforation
T/F: hematuria is a common side effect of ESWL
True
How is a percutaneous nephrolithotripsy done?
pt is prone- surgeon places urtetheral stents
neph tube is placed to access the stone
- irrigation considerations
- PTX is a possible complication
concern with perc nephrolithotripsy
-irrigation fluids and PTX
4 complications assoicated with ESWL
arrhythmias
organ perforation
skin bruising
hematuria
Which of the following are increased in the serum of the patient with renal osteodystrophy (select 2)
- phosphate
- PTH
- calcitrol
- calcium
Phosphate and PTH
“Two P’s increased in pts with renal osteodystoPhy”
- Calcitrol - the active form of vitamin D3 is protuced by the kidney; when kidney fails to produce calcitrol, the body absorbs less calcium from the GI tract and serum CA falls
- Decreased calcium levels signal the anterior pituitary to release PTH in attempt to correct calcium levels via:
- demineralization of the bone ⇒ increased risk of fxs
- As GFR declines, phosphate clearance is reduced –> increased serum phosphate concentration
What are the MOST potent stimulators of ADH secretion (2):
- Hypernatremia
- Hypovolemia
- Hyponatremia
- hypovolemia
- hypovolemia
- hypernatremia
BUN/Crt ratio of 30 most likely suggests (select 2):
- Acute tubular necrosis
- intersistial nephritis
- UGIB
- dehydration
-UGIB & Dehydration
- creatinine is a waste product of muscle metabolism
- urea is a waste product of protein metabolism
- ratio distinguishes between pre-renal and intrinsic kindey injury
- normal = 10:1
- BUN and creat both freely filtered at glomerulus
- BUN can undergoreabsorption in the renal tubules & creat does not
- When kidneys conserve more water, they pull BUN back into the blood
- Because BUN is returned to the blood but creat is not, the BUN/Creat ratio increases
Normal GFR:
-125ml/min
-275ml/min
-450ml/min
-650ml/min
125ml/min
Renal blood flow to each kidney in ml/min
650ml/min
- kidney gets 20%-25% of cardiac output
- 1,000-1,250ml/min to BOTH
- 500-650ml/min to each kidney
normal filtration fraction
20% of renal blood flow
(125GFR/650 RBF to each kidney)
T/F: The fraction of ultrafiltrate excreted as urine is 10%
False- 1%
Creat clearence
- Normal =
- Mild dysfx=
- Mod dysfx=
- Severe dysx=
- Normal = 95- 150ml/min
- Mild dysfx= 50-80ml/min
- Mod dysfx=10-25ml/min
- Severe dysx= <10ml/min
How to calculate creat clearance for a man
vs woman 8
Man: (140-age) x (weight kg) / (Serum creatinine x 72)
Woman: 0.85 x [(140- age) x (weight kg) / (Serium creat x 72)]
What is the BEST method of renal protection following major muscle trauma?
- mannitol
- norepi
- acidyfing the urine
- N-Acetylcystine
Mannitol
- The best way to prevent AKI is to maintain UOP between 100-150mls/hr
- Best accomplished with osmotic diuresis with mannitol
NSAIDS inhibit _____________ which reduces __________ leading to increased renal vascular resistance and decreased renal blood flow
inhibit cyclooxygenase
> reduced renal prostaglandin synthesis
T/F: When antagonizing Roc in a patient with ERSD, the dose of neostigmine should be decreased by 25%
False - same as non-ERSD pt
Presence of U waves on an EKG - what 2 drugs are the MOST likely cause for this finding (select 2):
- Amiloride
- Metolazone
- Bumetanide
- Spironolactone
Metolazone & Bumetanide
- amiloride and spironolactone = K sparing
- Bumetanide = bumex = loop - yes
- Metolazone = zaroxyln = thiazide = yes
What kind of diuretic is zaroxolyn?
Generic?
Does it cause hypokalemia?
Metolazone
- Thiazide
- yes
Pt presents for b/l mastectomy and has n/v/polyuria and short QTc, which of the following agents will worsen this patient’s condition?
A. Mannitol
B. Hydrochlorothiazide
C. Furosemide
D. Triamterene
B. Hydrochlorothiazide
- Symptoms suggestive of high calcium levels
- Also makes sense bc b/l mastectomy = breast cancer
- cancer = cause of hypercalcemia
- other EKG changes = prolonged PR, wide QRS, short QTc
- TX = IV hydration with NSS and furosemide
- Thiazide diruetics inhibit the NA-Cl exchangeer in the distal tubule which activates the NA-Ca antiporter and increases CA reasoprtion
which of the following should be avoided in the diabetic patient?
A. Spironolactone
B. Triamterene
C. HCTZ
D. Ethacrynic acid
C. HCTZ
-thazides cause hyperglycemia (mechanism not completely understood- poss decreased insulin realease from pancrease or imparied glucose utilization in body)
What class of diuretic is triameterene
potassium sparing
What class of diuretic is indapamide?
Thiazide diuretic
(Distal tubule)
3 unique side effects of thiazide diruetics
- Hyperglycemia (caution in diabetics)
- Hypercalcemia (caution in hypercalcemia)
- Hyperuricemia (caution in gouty arthritis)
