Kidneys Flashcards
1
Q
How much of the cardiac output do the kidneys receive
A
15-20%
2
Q
How much RBF is directed to renal cortex
A
95%
3
Q
How much RBF is directed to medulla
A
5%
4
Q
What is the rate of blood flow through renal arteries
A
1-2.5 L/min
5
Q
What is the autoregulation range for kidneys
A
60-160mmhg
6
Q
How do kidneys autoregulate?
A
An intrinsic mechanism that causes vasodilation and vasoconstriction of renal afferent arterioles regulates the regulation of renal blood flow
***THIS IS INTACT EVEN IN DENERVATED KIDNEYS
7
Q
What is the glomerulus
A
It separates the afferent and efferent arterioles and finsteres the blood
8
Q
How does the glomerulus work
A
The resistance in the efferent arterioles creates hydrostatic pressure within the glom to provide force for ultrafiltration
9
Q
What are the capillaries of the glomerulus lined with
A
Endothelial cells called podocytes
10
Q
Wha this the glomerular filtration rate
A
The rate at which blood is filtered through all of the glomeruli measure of overall kidney function
11
Q
What does SNS activation do to the kidney
A
Reduce renal blood flow
- blood is shunted to skeletal muscle
- stimulation can increase vascular resistance
- adrenal medulla stimulated = catecholamine release
12
Q
A decrease in BP will stimulate?
A
RAAS
13
Q
What simulates release of ADH
A
Released in response to
- decreased stretch receptors in atrial and arterial wall
- increased osmolality of the plasma monitored by the hypothalamus
14
Q
Where does ADH come from?
A
Sunthesized in hypothalamus and released from post pituitary gland
15
Q
What’s the half life of ADH
A
16-24 mins
16
Q
What are the 2 primary functions of ADH
A
Increases reabsorption of water in the kidneys
Causes vasoconstriction and PVR to increase BP
17
Q
What are the periop causes of ADH release
A
Hemorrhage PPV Upright position Nausea Meds
18
Q
What is renin
A
Enzyme secreted by the kidneys that converts angiotensinogen to angiotensin 1
19
Q
Where is renin released from and in response to what
A
Released from JG cells located near afferent arterioles in response to a decrease in arterial BP or a decrease in sodium load delivered to the distal tubules or SNS stimulation via B1
20
Q
How is Ang 1 converted to ang 2
A
Ang 1 is converted in the lungs by ACE to ang 2
21
Q
What is ang 2
A
A portent vasoconstrictor and stimulates the hypothalamus to secrete ADH
22
Q
What is aldosterone?
A
A mineralcorticoid hormone released from the adrenal gland that simulates epithelial cells in the distal tubule and collecting ducts to reabsorb sodium and water and exchanges K to maintain electro neutrality
23
Q
What is a drug that blocks aldosterone receptors
A
Spironolactone
24
Q
Acute kidney injury/acute renal failure
A
The sudden inability of kidneys to vary urine volume and content appropriately
50% mortality rate - develops rapidly but may resolve
25
Pre-renal kidney failure
Hemodynamic or endocrine factors that impair PERFUSION
- aka hypoperfusion or hypovolemia
Will activated mechanism to conserve salt and water and can progress to permanent parenchymal damage
26
Renal or acute tubular necrosis
A form of intrinsic renal disease
There is tissue damage d/t prolonged ischemia or nephrotoxic injury, or glomerulonephritis
Patients will have trouble concentrating urine - high Na, low osmolality
27
Post renal renal dx
Obstruction, surgical ligation, edema are causes
28
What is oliguria?
UOP of < 0.5 ml/kg/hr
29
What is Polyuria?
UOP of > 2.5L/day of NON CONCENTRATED urine
30
What are the risk factors for acute renal failure/injury
```
Increasing age
Pre-existing renal dysfunction
Certain surgeries
Sepsis
Use of nephrotoxic agents
Diabetes, HTN
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31
How much dose renal reserve decrease with age
For each year after age 50, creatinine clearance decreases by 1.5mls and renal plasma flow by 8ml
32
What surgical procedures are high risk for acute renal injury
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Cardiac bypass > 2h
Aortic aneurysm (Supra-renal aortic clamping)
Ventricular dysfunctions
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33
Contrast induced nephropathy
3rd most common causes of HA acute renal injury and represents about 12% of cases
You are at higher risk after renal hypoperfusion and post op renal injury
Results from admin of iodinated contrast dye
Transient and reversible
34
What is the treatment for contrast induced nephropathy
Mainly supportive
Careful fluid and electrolyte management
Dialysis may be required in some cases
35
Prevalence of CIN
Most common with CT, angiography, pyelography
Incidence is low in patients with normal renal function
12-27% in patients with pre-existing renal impairment
50% in patients with diabetic nephropathy
36
CIN patho
Not well understood, but worsened by hypoxia and hypoperfusion
Direct toxicity of contrast media could cause free radicals and oxidative stress causing harm potentially via cytokine release
Contrast media causes increased osmotic force which increases sodium and water excretion which will increase intratubular pressure and reduce GFR leading to acute renal failure
37
CIN treatment
Supportive, prevention, weight risks and benefits
38
Oliguria in OR
Can be a sign of poor perfusion
Monitors - catheter, TEE, CVP, BP, SVV
Assume prerenal oliguria is related to fluid until proven otherwise
39
Diuretics and oliguria in the OR
Do not give them in the setting of intravascular hypovolemia
40
Dopamine agonists
Causes renal arteriolar vasodilation which will increase urine output
Fenoldopam or low dose dopamine
41
Hispanic Americans and CKD incidence
1.5x greater risk for developing kidney failure than non-hispanics
42
African Americans and CKD
ESRD rates nearly 4-fold higher among African Americans as well has hypertension being most prevalent among African Americans which is a major cause of ESRD
43
Native Americans and CKD
They are about 1.8x more likely to be diagnosed with kidney failure, with diabetes being the leading cause
44
Renal replacement therapy and geographics
80% live in Europe, japan, or North America
But less than 10% of Indian ESRD patients receive RRT or they have to stop within the 1st 3 months because they either die or just can’t afford it and then die
Transplant is rare in LMICs
45
Chronic renal failure
Slow, progressive, irreversible
Decreased functioning nephrons and RBF
Decreased GFR, tubular function, reabsorptive capacity
46
Common causes of chronic renal failure
Glomerulonephritis, pyelonephritis, diabetes, vascular or hypertensive insults, congenital defects
47
Stages of chronic renal failure
Decreased renal reserve
Renal insufficiency
End stage or uremia
48
Decreased renal reserve patients are asymptomatic until
<40% or normal nephron remain
49
Renal insufficiency
10-40% of functioning nephrons remain
| Compensate, little reserve
50
End-stage or uremia
```
>95% of nephrons are not functioning,
GFR is 5-10% of normal
Severely compromised lytes
Uremia is eventually lethal
Dialysis dependent
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51
Manifestations of chronic renal failure
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Hypervolemia
Academia
Hyperkalemia
Cardioresp dysfunction
Anemia
Bleeding disturbance
```
52
Treatment for chronic renal fail
Hemodialysis
Peritoneal dialysis
Kidney transplant
53
Specific gravity
Measurement of solutes int the urine - indicates teh kidneys ability to excrete concentrate urine - reflects tubular function
54
Urine osmolality
Moles of solute/kg solvent - more specific than specific gravity - ability to excrete concentrated urine indicates good tubular function
55
Proteinuria
When >150mg is excreted per day
>750mg is indicative of severe glomerular damage
Failure of renal tubules to reabsorb protein
56
Urinary pH
The inability to excrete acid urine in the presence of acidosis is indicative of renal insufficiency
57
Glucose and the kidneys
Freely filtered at glomerulus
| Reabsorbed in proximal tubule
58
Glycosuria
Signifies that the ability of the renal tubules to reabsorb glucose has been exceeded by an abnormally heavy glucose load and is usually indicative of DM
59
Blood urea nitrogen
Not a direct renal function - influenced by exercise, bleeding, steroids, and tissue breakdown
Elevated in kidney disease once GFR is reduced to 75%
60
Serum creatinine
Muscle tissue turnover and dietary intake of protein
Creatinine is freely filtered at glomerulus and is neither reabsorbed nor secreted
61
Creatinine clearance
Good measure of GFR
62
GFR
Best measure of glomerular function
| Normal is 125ml/min
63
Patients are asymptomatic until GFR
Is less than 30-50% of normal
64
ECG in renal disease
Reflects toxic effects of potassium excess more closely than determination of the serum k concentration
You will see tall peaked t waves and small or indiscernible P waves
65
Blood storage and K
During storage, there is a slow but constant leak of K from cells into surrounding plasma along a concentration gradient as a result of na-k ATPase pump failure
Plasma K may increase by 0.5-1 mmol/L per day of refrigerator storage
66
Severe hyperkalemia following transfusion risk can be minimized by
Selecting blood no more than 5d old, wash any blood before transfusion, use of k absorption filters, and keep rate and volume low
67
Ultrasound imaging and renal patients
Noninvasive, minimal patient prep, assess kidney size, hydronephrosis, vasculature, obstructions, and masses
68
CT imaging and renal disease
Detects stones of al kinds, masses may be evaluated with contrast
69
MRI and renal disease
Detailed tissue characterization, nice alternative to a contrast CT, reduced radiation exposure
70
What is the IV contrast agent commonly used in MRI
Gadolinium - paramagnetic IV contrast agent
71
GA effect on renal function
PPV and decreased CO - depression of RBF, GFR, urinary flow, and electrolyte secretion
72
Regional and renal function
Parallels with degree of SNS blockade, decreased venous return, decrease in BP
73
Indirect effects of periop on renal function
Circulatory, endocrine, SNS, positioning
74
Direct effects on renal function
Meds that target renal cell function
75
Surgical effects on renal function
Stress and catecholamine release, fluid shift, secretion of vasopressin and angiotensin
76
Morphine and renal function
Active metabolites that depend on renal clearance mechanisms for elimination
Metabolites excreted via kidney
77
Meperidine and renal failure
Active metabolite normeperidine depends on renal excretion and accumulation can lead to CNS toxicity and seizures
78
Fentanyl and renal failure
Not grossly altered, but decrease in plasma protein binding may result in higher free fraction
79
CKD and ketamine
8% of ketamine is metabolized in liver to norketamine and then excreted by liver
Most people believe dose modification is not necassary
80
Gabapentinoids and kidney disease
Liberal admin may increases risk of over sedation and even coma
These agents do not undergo hepatic metabolism and are excreted soley by kidney
Reduction of 50% of the dose for each 50% decline in GFR or CCr and increase in time interval of dosing
81
Inhalational agents and renal
All can decrease BP and kidneys respond with compensatory increase in renal vascular resistance leading to decreased renal blood flow
82
Isoflurane and renal
Decreases BP (dose dependent)
83
Desflurane and renal
Increased heart, may maintain a greater degree of CO and therefore renal perfusion
84
Sevo and renal
Free fluoride ion metabolite and compound A risk
85
Compound A
CO2 absorbents containing soda lime degrade sevo resulting in a vinyl ether called compound A
Risk higher wiht closed circuit anesthesia, long duration of exposure, low fresh gas flow, high concentration of sevo
86
Amsorb
Replaces soda lime is non caustic and can be disposed of in domestic waste no production of compound A
87
Propofol and renal
Does not adversely affect renal tubular function
Prolong induction may result in green urine due to phenolic metabolites
PRIS can result in renal failure secondary to rehab do, myoglobinuria, hypotension, met acidosisq
88
Succ and renal
Can be used carefully
Metabolism is catalyses by pseudocholinesterase to yield the nontoxic end products of succinic acid and chline - precursor excreted by kidneys
Ok to give if patient has received dialysis within 24 h and serum k is normal
89
How much does suc raise K
Rapid transient increase of 0.5 mEq/l
| Can be exaggerated in patient with renal failure
90
Duration of muscle relaxants and renal failure
MAY BE PROLONGED
91
Sugammadex and renal fail
Sug-roc compound is excreted by kidney, but no evidence of probs with accumulation
92
Sodium nitroprusside and kidney
Thiocyanate toxicity is a possibility especially with long term infusions
S&S = hypoxia, nausea, tinnitus, muscle spasm, disorientation, and psychosis
93
Albumin and renal
Protective of renal perfusion, binding of endogenous toxins and nephrotoxic drugs and preventing oxidative damage
94
Hetastarch/dextran and renal
Has been associated with AKI secondary to breakdown of synthetic carbs and degradation products that cause direct tubular injury and plugging of tubules
Worsened by decreased renal perfusion
95
Dopaminergics
Dopamine and fenoldapam are dopa 1 agonists that dilate afferent and efferent arterioles to increase renal perfusion
96
Anti-dopaminergics
Metclopramide, phenothizines, droperidol may impair renal response to dopamine
97
What is the most common renal malignancy
Renal cell carcinoma (>80% off all solid renal masses)
98
Renal cell carcinoma
Originates in the lining of proximal tubules, refractory to chemo/rad,
Surgical resection is curative
Triad of presentation of hematuria, flank pain, and renal mass
Although often found incidentally
99
Bigger problem with renal cell carcinoma
When the tumor extends into renal vein and IVC and RA
May require CPB
100
Renal dysplasia
Malformation of tubules following fetal development
Kidney consist of irregular cysts
Dx made in uterine by US
May also have ureteropelvic junction obstruction and vesicoureteral reflux
Linked to genetic mutation and illicit drug use by mom
Bilateral is incompatible with survival
Can lead to CKD, dialysis, and transplant
101
Polycystic kidney disease
Inherited massive enlargement of kidney with compromised renal function
Painful
Most cases are bilateral by adulthood
Complications include HTN, cyst infection, bleeding, decline in renal function
Treatment - symptom manage, dialysis, transplant
102
Wilms tumor
Unilateral, painless, palpable mass
Most common malignancy in children (1/3 occur under age 1)
Requires resection and chemo - rapid growth
Metastasis usually to the lungs
103
Stages of wilms tumor
1-limited to kidney, completely excised
2-extends beyond tumor, completely excised
3-inoperable primary tumor or lymph node metastasis
4-lymph node metastases outside of abdomino pelvic region
5-bilateral renal involvement
104
Total nephrectomy
The renal artery adn veins re lighted and then it involves removal of the kidney, the ipsilateral adrenal gland, perinephric fat, and surrounding fascia
**the other kidney needs to be functional
105
Partial nephrectomy
Nephron sparing surgery considered for patients with a solitary functional kidney, small lesions, or bilateral tumors, or for patients with increased risk because of other disease such as DM or hypertension
106
Anesthetic considerations for nephrectomy
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Standard risk assessment
ID risk factors
Note any renal dysfunction
Many are anemic - CBC - T&C
Get BMP
Regional include T8-L3
ERAS
Opioid sparing
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107
PTH increased what in exchange for phosphate
Calcium reabsorption
108
Erythropoietin
Release by kidney in response to anemia, hypoxia
109
Aldosterone
Secreted from adrenal cortex causes reabsorption of na
110
ADH/vasopressin
Constricts efferent arteriole and causes reabsorption of water
111
ANP
Atrial distention (fluid overload) stimulates excretion of Na and water
112
Dopamine
DA1 receptor in renal vascular - vasodilation and Na excretion
113
Kidneys filter blood in our body how much
20-25 x per day
114
How many nephrons per kidney
1 mill
115
In nephrons in 2 kidneys are removed and laid out end to end they cover a distance of
10 miles
116
What is kidney awareness month
March
117
If you lose 1 kidney, how much kidney function do you lose
Only 25%
