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Summer Patho > Kidneys > Flashcards

Kidneys Flashcards

1
Q

How much of the cardiac output do the kidneys receive

A

15-20%

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2
Q

How much RBF is directed to renal cortex

A

95%

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3
Q

How much RBF is directed to medulla

A

5%

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4
Q

What is the rate of blood flow through renal arteries

A

1-2.5 L/min

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5
Q

What is the autoregulation range for kidneys

A

60-160mmhg

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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

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7
Q

What is the glomerulus

A

It separates the afferent and efferent arterioles and finsteres the blood

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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

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9
Q

What are the capillaries of the glomerulus lined with

A

Endothelial cells called podocytes

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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

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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
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12
Q

A decrease in BP will stimulate?

A

RAAS

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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
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14
Q

Where does ADH come from?

A

Sunthesized in hypothalamus and released from post pituitary gland

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15
Q

What’s the half life of ADH

A

16-24 mins

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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

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17
Q

What are the periop causes of ADH release

A 
Hemorrhage
PPV
Upright position
Nausea
Meds
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18
Q

What is renin

A

Enzyme secreted by the kidneys that converts angiotensinogen to angiotensin 1

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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

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20
Q

How is Ang 1 converted to ang 2

A

Ang 1 is converted in the lungs by ACE to ang 2

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21
Q

What is ang 2

A

A portent vasoconstrictor and stimulates the hypothalamus to secrete ADH

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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

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23
Q

What is a drug that blocks aldosterone receptors

A

Spironolactone

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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

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25
Q

Pre-renal kidney failure

A

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

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26
Q

Renal or acute tubular necrosis

A

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

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27
Q

Post renal renal dx

A

Obstruction, surgical ligation, edema are causes

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28
Q

What is oliguria?

A

UOP of < 0.5 ml/kg/hr

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29
Q

What is Polyuria?

A

UOP of > 2.5L/day of NON CONCENTRATED urine

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30
Q

What are the risk factors for acute renal failure/injury

A 
Increasing age
Pre-existing renal dysfunction
Certain surgeries 
Sepsis
Use of nephrotoxic agents
Diabetes, HTN
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31
Q

How much dose renal reserve decrease with age

A

For each year after age 50, creatinine clearance decreases by 1.5mls and renal plasma flow by 8ml

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32
Q

What surgical procedures are high risk for acute renal injury

A 
Cardiac bypass > 2h
Aortic aneurysm (Supra-renal aortic clamping)
Ventricular dysfunctions
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33
Q

Contrast induced nephropathy

A

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

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34
Q

What is the treatment for contrast induced nephropathy

A

Mainly supportive
Careful fluid and electrolyte management
Dialysis may be required in some cases

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35
Q

Prevalence of CIN

A

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

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36
Q

CIN patho

A

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

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37
Q

CIN treatment

A

Supportive, prevention, weight risks and benefits

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38
Q

Oliguria in OR

A

Can be a sign of poor perfusion
Monitors - catheter, TEE, CVP, BP, SVV
Assume prerenal oliguria is related to fluid until proven otherwise

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39
Q

Diuretics and oliguria in the OR

A

Do not give them in the setting of intravascular hypovolemia

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40
Q

Dopamine agonists

A

Causes renal arteriolar vasodilation which will increase urine output

Fenoldopam or low dose dopamine

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41
Q

Hispanic Americans and CKD incidence

A

1.5x greater risk for developing kidney failure than non-hispanics

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42
Q

African Americans and CKD

A

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

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43
Q

Native Americans and CKD

A

They are about 1.8x more likely to be diagnosed with kidney failure, with diabetes being the leading cause

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44
Q

Renal replacement therapy and geographics

A

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

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45
Q

Chronic renal failure

A

Slow, progressive, irreversible
Decreased functioning nephrons and RBF
Decreased GFR, tubular function, reabsorptive capacity

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46
Q

Common causes of chronic renal failure

A

Glomerulonephritis, pyelonephritis, diabetes, vascular or hypertensive insults, congenital defects

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47
Q

Stages of chronic renal failure

A

Decreased renal reserve
Renal insufficiency
End stage or uremia

48
Q

Decreased renal reserve patients are asymptomatic until

A

<40% or normal nephron remain

49
Q

Renal insufficiency

A

10-40% of functioning nephrons remain

Compensate, little reserve

50
Q

End-stage or uremia

A 
>95% of nephrons are not functioning, 
GFR is 5-10% of normal
Severely compromised lytes
Uremia is eventually lethal
Dialysis dependent
51
Q

Manifestations of chronic renal failure

A 
Hypervolemia
Academia
Hyperkalemia
Cardioresp dysfunction
Anemia
Bleeding disturbance
52
Q

Treatment for chronic renal fail

A

Hemodialysis
Peritoneal dialysis
Kidney transplant

53
Q

Specific gravity

A

Measurement of solutes int the urine - indicates teh kidneys ability to excrete concentrate urine - reflects tubular function

54
Q

Urine osmolality

A

Moles of solute/kg solvent - more specific than specific gravity - ability to excrete concentrated urine indicates good tubular function

55
Q

Proteinuria

A

When >150mg is excreted per day

> 750mg is indicative of severe glomerular damage

Failure of renal tubules to reabsorb protein

56
Q

Urinary pH

A

The inability to excrete acid urine in the presence of acidosis is indicative of renal insufficiency

57
Q

Glucose and the kidneys

A

Freely filtered at glomerulus

Reabsorbed in proximal tubule

58
Q

Glycosuria

A

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
Q

Blood urea nitrogen

A

Not a direct renal function - influenced by exercise, bleeding, steroids, and tissue breakdown

Elevated in kidney disease once GFR is reduced to 75%

60
Q

Serum creatinine

A

Muscle tissue turnover and dietary intake of protein

Creatinine is freely filtered at glomerulus and is neither reabsorbed nor secreted

61
Q

Creatinine clearance

A

Good measure of GFR

62
Q

GFR

A

Best measure of glomerular function

Normal is 125ml/min

63
Q

Patients are asymptomatic until GFR

A

Is less than 30-50% of normal

64
Q

ECG in renal disease

A

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
Q

Blood storage and K

A

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
Q

Severe hyperkalemia following transfusion risk can be minimized by

A

Selecting blood no more than 5d old, wash any blood before transfusion, use of k absorption filters, and keep rate and volume low

67
Q

Ultrasound imaging and renal patients

A

Noninvasive, minimal patient prep, assess kidney size, hydronephrosis, vasculature, obstructions, and masses

68
Q

CT imaging and renal disease

A

Detects stones of al kinds, masses may be evaluated with contrast

69
Q

MRI and renal disease

A

Detailed tissue characterization, nice alternative to a contrast CT, reduced radiation exposure

70
Q

What is the IV contrast agent commonly used in MRI

A

Gadolinium - paramagnetic IV contrast agent

71
Q

GA effect on renal function

A

PPV and decreased CO - depression of RBF, GFR, urinary flow, and electrolyte secretion

72
Q

Regional and renal function

A

Parallels with degree of SNS blockade, decreased venous return, decrease in BP

73
Q

Indirect effects of periop on renal function

A

Circulatory, endocrine, SNS, positioning

74
Q

Direct effects on renal function

A

Meds that target renal cell function

75
Q

Surgical effects on renal function

A

Stress and catecholamine release, fluid shift, secretion of vasopressin and angiotensin

76
Q

Morphine and renal function

A

Active metabolites that depend on renal clearance mechanisms for elimination

Metabolites excreted via kidney

77
Q

Meperidine and renal failure

A

Active metabolite normeperidine depends on renal excretion and accumulation can lead to CNS toxicity and seizures

78
Q

Fentanyl and renal failure

A

Not grossly altered, but decrease in plasma protein binding may result in higher free fraction

79
Q

CKD and ketamine

A

8% of ketamine is metabolized in liver to norketamine and then excreted by liver

Most people believe dose modification is not necassary

80
Q

Gabapentinoids and kidney disease

A

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
Q

Inhalational agents and renal

A

All can decrease BP and kidneys respond with compensatory increase in renal vascular resistance leading to decreased renal blood flow

82
Q

Isoflurane and renal

A

Decreases BP (dose dependent)

83
Q

Desflurane and renal

A

Increased heart, may maintain a greater degree of CO and therefore renal perfusion

84
Q

Sevo and renal

A

Free fluoride ion metabolite and compound A risk

85
Q

Compound A

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
Q

Amsorb

A

Replaces soda lime is non caustic and can be disposed of in domestic waste no production of compound A

87
Q

Propofol and renal

A

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
Q

Succ and renal

A

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
Q

How much does suc raise K

A

Rapid transient increase of 0.5 mEq/l

Can be exaggerated in patient with renal failure

90
Q

Duration of muscle relaxants and renal failure

A

MAY BE PROLONGED

91
Q

Sugammadex and renal fail

A

Sug-roc compound is excreted by kidney, but no evidence of probs with accumulation

92
Q

Sodium nitroprusside and kidney

A

Thiocyanate toxicity is a possibility especially with long term infusions

S&S = hypoxia, nausea, tinnitus, muscle spasm, disorientation, and psychosis

93
Q

Albumin and renal

A

Protective of renal perfusion, binding of endogenous toxins and nephrotoxic drugs and preventing oxidative damage

94
Q

Hetastarch/dextran and renal

A

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
Q

Dopaminergics

A

Dopamine and fenoldapam are dopa 1 agonists that dilate afferent and efferent arterioles to increase renal perfusion

96
Q

Anti-dopaminergics

A

Metclopramide, phenothizines, droperidol may impair renal response to dopamine

97
Q

What is the most common renal malignancy

A

Renal cell carcinoma (>80% off all solid renal masses)

98
Q

Renal cell carcinoma

A

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
Q

Bigger problem with renal cell carcinoma

A

When the tumor extends into renal vein and IVC and RA

May require CPB

100
Q

Renal dysplasia

A

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
Q

Polycystic kidney disease

A

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
Q

Wilms tumor

A

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
Q

Stages of wilms tumor

A

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
Q

Total nephrectomy

A

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
Q

Partial nephrectomy

A

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
Q

Anesthetic considerations for nephrectomy

A 
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
107
Q

PTH increased what in exchange for phosphate

A

Calcium reabsorption

108
Q

Erythropoietin

A

Release by kidney in response to anemia, hypoxia

109
Q

Aldosterone

A

Secreted from adrenal cortex causes reabsorption of na

110
Q

ADH/vasopressin

A

Constricts efferent arteriole and causes reabsorption of water

111
Q

ANP

A

Atrial distention (fluid overload) stimulates excretion of Na and water

112
Q

Dopamine

A

DA1 receptor in renal vascular - vasodilation and Na excretion

113
Q

Kidneys filter blood in our body how much

A

20-25 x per day

114
Q

How many nephrons per kidney

A

1 mill

115
Q

In nephrons in 2 kidneys are removed and laid out end to end they cover a distance of

A

10 miles

116
Q

What is kidney awareness month

A

March

117
Q

If you lose 1 kidney, how much kidney function do you lose

A

Only 25%

Summer Patho (10 decks)

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