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Kidney Flashcards

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1
Q

What 3 things increase renin release?

A

Reduced renal perfusion
Beta 1 stimulation
Decreased sodium and chloride delivery to the distal tubule

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2
Q

Where is ADH PRODUCED?

A

Supraoptic and paraventricular nuclei of the hypothalamus

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3
Q

Where is ADH ReLEASeD?!?

A

Posterior pituitary

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4
Q

What are the two mechanisms that control ADH release?

A

Increased osmolarity ~ increased Na shrinks osmoreceptors
Decreased blood volume ~ baroreceptors stimulate ADH release

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5
Q

What is the ADH V1 receptor?

A

Vasoconstriction ~ increased IP3 > DAG > Ca +

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6
Q

What is the V2 receptor for ADH?

A

Aquaporin 2 channels these are water channels in the collecting duct

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7
Q

What are the three ways to promote renal vasodilation?

A

Prostaglandins
Natriuretic peptide
Dopamine receptors

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8
Q

What is fenoldopam?

A

DA1 receptor agonist that increases renal blood flow

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9
Q

What is normal GFR?

A

125 mL/min

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10
Q

What is the filtration fraction?

A

20% ~ 20% is filtered by the glomerulus and 80% is delivered to the peritubular capillaries

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11
Q

What is the net filtration pressure?

A

Driving force that pushes fluid from the blood (glomerulus) into the Bowman’s capsule

NFP = glomerulae hydrostatic pressure - bowman’s capsule hydrostatic pressure - glomerular oncotic pressure

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12
Q

What are the 3 components of glomerular hydrostatic pressure?

A

Arterial blood pressure
Afferent arteriole resistance
Efferent arteriole resistance

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13
Q

What does constriction of the afferent arteriole cause?

A

Decreased RBF and Decreased GFR

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14
Q

What does construction of the EFFERENT arteriole cause?

A

Decreased in RBF BUT an increase in GFR

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15
Q

What does an increased plasma protein count do to RBF and GFR?

A

RBF ~ nada
GFR ~ decreases (more oncotic pressure)

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16
Q

What does a decreased plasma protein count do to GFR and RBF?

A

RBF ~ nada
GFR ~ increases (less oncotic pressure)

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17
Q

What % of ultrafiltrate is reabsorbed into the peritubular capillaries?

A

99% baby!

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18
Q

What is the autoregulation range for the kidneys?

A

50-180 mmHg (big range)

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19
Q

What is reabsorption in the kidney?!

A

A substance is reabsorbed back into circulation

(from the renal tubule to the peritubular caps)

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20
Q

What is secretion in the kidney?

A

A substance is transferred from the peritubular caps to the tubule!

(Caps to the tub)

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21
Q

What is excretion in the kidney?

A

Substance is removed from the body in the urine

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22
Q

Where does most of the sodium reabsorption happen in the nephron?

A

Proximal tubule

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23
Q

What is the main function of the descending loop of Henle?

A

To form concentrates or dilute urine

(Separates the handling of sodium and water)

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24
Q

What are the two countercurrent systems needed to created the graduates hyperosmotic peritubular interstitium?

A

Loop of Henle: multiplier system that creates an osmotic gradient

Vasa recta: exchanger system that maintain osmotic gradient

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25
Where does aldosterone act?
Distal tubule and collecting duct
26
Where does ADH act?
Distal tubule and collecting duct
27
Where in the nephron does parathyroid hormone act to increase Ca reabsorption?
Distal tubule
28
Which aspect of the nephron is impermeable to water?
Ascending limb of loop of Henle
29
What do carbonic anhydrase inhibitors do?
Non competitively inhibit carbonic anhydrase in the cells that make up the proximal tubule ***this reduced reabsorption of bicarb, Na, and water
30
What is the clinical use of carbonic anhydrase inhibitors?
Open angle glaucoma ~ reduces aqueous humor production and IOP High altitude sickness ~mild metabolic acidosis increases resp drive Central sleep apnea ~ mild metabolic disorder increases resp drive
31
What are the complications to carbonic anhydrase inhibitors?
Metabolic acidosis Hypokalemia In patients with COPD, this loss of bicarb (their buffering system) may exacerbate symptoms
32
What is an osmotic diuretic?
Mannitol/glycerin/Isosorbide Sugars that undergo filtration BUT NOT reabsorption. They inhibit water reabsorption in the proximal tubule (primary site) and the loop of Henle.
33
Which diuretic is a free radical scavenger?
Mannitol
34
What is the clinical use of osmotic diuretics?
Intracranial HTN Differential diagnosis of acute oliguria (will increase UOP if prerenal injury ~ not intrinsic injury)
35
What are the complications of osmotic diuretics?
CHF Pulmonary edema If BBB is disrupted, could cause cerebral edema
36
What are loop diuretics?
Lasix, bumex and ethacrynic acid Loop diuretics disrupt Na-K-2Cl transporter in thick portion of the ascending limb if Henle. This increases the amount of sodium in the tubule and overwhelms the distal tubule’s ability to reabsorb.
37
What is the clinical use for loop diuretics?
Pulmonary edema Acute kidney injury CHF Hypercalcemia Hypertension ICP Anion overdose
38
What are the complications to loop diuretics?
“LOSS OF OUR boy POTASSIUM” Hypokalemia and hypochloremic metabolic alkalosis Hypocalcemia Hypomagnesemia Hypovolemia Ototoxicity
39
What are thiazide diuretics?
Hydrochlorothiazide, chlorthalidone, metolazone, indapamide Inhibit the Na-Cl co transporter in the distal tubule ~ this activates the Na-Ca Antiporter which increases Ca reabsorption ~ increasing serum Ca
40
What is the clinical use for thiazide diuretics?
HTN CHF Osteoporosis Mobilize edema
41
What are complications of thiazide diuretics?
“Sweet cows thia-zide (reside) in the fields” Hyperglycemia Hypercalcemia Hyperuricemia Hypokalemic, hypochloremic metabolic alkalosis Hypovolemia HLD Sexual dysfunction
42
What are potassium sparing diuretics?
Sprironolactone, amiloride, triamterene Spironolactone is a aldosterone antagonist ~ blocking aldosterone at the mineralcorticoid receptor (inhibits K excretion and Na reabsorption) this is in the collecting ducts! Amiloride and triamterene inhibits potassium secretion and sodium reabsorption in the collecting ducts (INDEPENDENT of aldosterone)
43
What is the clinical use of potassium sparing diuretics?
Reduce K loss in a patient receiving a loop or thiazide diuretic. Secondary hyperaldosteronism
44
What are the complications of potassium-sparing diuretics?
Hyperkalemia Metabolic acidosis Gynecomastia Libido changes Nephrolithiasis
45
Which 3 drug classes increase the risk of hyperkalemia in a patient taking a potassium sparing diuretic?
NSAIDs Beta-blockers Ace Inhibitors
46
What are the two best tests for GFR function?
BUN and creatinine clearance
47
What are the two best tests for TUBULAR function?
Fractional excretion if sodium and urine osmolality
48
What does a BUN of < 8 indicate?
Overhydration Decreased Urea Production (malnutrition and/severe liver disease)
49
What does a BUN of 20-40 indicate?
Dehydration Increased protein input (high protein diet, GI bleed, hematoma breakdown) Catabolism (trauma and sepsis) Decrease GFR
50
What does a BUN > 50 indicate?
Decreased GFR
51
What is a normal BUN:Creatinine ration?
10:1
52
What does a BUN ratio of > 20:1 indicate?
Prerenal azotemia
53
What is the MOST useful indicator of GFR?
Creatinine clearance GFR = (140-age) x (kg) / 72 x serum creatinine (mg/dL) ***in women this is multiplied by 0.85
54
What are the three methods to classify the severity of renal injury?!
RIFLE: risk, injury, failure, loss, end-stage AKIN: Acute Kidney Injury Network KDIGO: Kidney Disease Improving Global Outcomes
55
What are the three classifications of acute kidney injury?
Prerenal Intrinsic Postrenal
56
What are the causes and txs to Prerenal Injury?
Causes: hypoperfusion (I.e hypovolemia, decreased CO, systemic vasodilation, renal vasoconstriction) Tx: restoration of renal blood flow, hemodynamic support, PRBCs ***an improvement in UOP following a fluid bolus is confirmation of prerenal azotemia (usually)
57
What are the causes and txs to intrinsic renal disease?
Causes: injury to the tubules, glomerulus, or interstitial space (nephrotoxic drugs, ischemia, NSAIDs, nephrotoxic abx) Tx: restore renal perfusion/supportive
58
What are the causes and treatments for post renal injury?
Causes: result of an obstructive phenomenon (foley catheter clog, ureteral stone, neurogenic bladder) Tx: relieve obstruction
59
What MAP reduces the risk of prerenal azotemia?
MAP> 65
60
What type of anemia results from end-stage renal disease?
NORMOCYTIC normochromic anemia
61
What is the MOST common cause of chronic kidney disease?
Diabetes mellitus
62
What is the second most common cause of chronic kidney disease?
Hypertension
63
What is a normal GFR?
> 90
64
What is stage 2 kidney disease? AKA mildly decreased
60-89 mL/min
65
What is stage 3 kidney disease? Aka moderately decreased GFR?
30-59
66
What is stage 4 kidney disease? Aka severely decreased
15-29
67
What is stage 5 kidney disease? Aka kidney failure?
< 15 “You hit 15, you kill the bean” 🫘
68
What is the first line therapy for uremic bleeding?
Desmopressin (Uremia causes platelet dysfunction thus increases bleeding time)
69
What is the most common cause of death in patients with chronic kidney disease?
CAD
70
What is renal osteodystrophy caused by?
Decreased vitamin D production Secondary hyperparathyroidism
71
What is the cornerstone of treatment?
Dialysis
72
What are the 5 indications for dialysis?
Volume overload Hyperkalamia > 6 Severe metabolic acidosis Symptomatic uremia Overdose with a drug that is cleared by dialysis
73
What is the leading cause of death in dialysis patients?
Infection
74
Which type of dialysis is more efficient?
Hemodialysis BUT peritoneal dialysis is favored in patients who cannot tolerate fluid shifts associated with hemodialysis
75
Is Sux safe in patients with renal failure?
YES! IF their potassium is within normal range **although you should not do a sux drip
76
What are the most suitable NMB for renal failure patients?
Benzylisoquinolones (Aka cisatracurium and Atracurium)
77
Which aminosteriod should you NOT use in renal failure patients?
Pancuronium ~ it’s primarily eliminates by kidneys Pan > Vec > roc
78
Which opioid choices are not good for a renal Failure patient?
Morphine ~ metabolite is morphine 6 glucoronide Meperidine ~ metabolite is normeperidine (can cause seizures!)
79
How does rhabdomyolysis and myoglobinemia affect the kidneys?
Rhabdo and myoglobinemia result from direct muscle trauma. Myoglobin binds to oxygen inside the myoctye ~ this is them freely filtered at the glomerulus. BUT in the presence of acidic urine, myoglobin precipitates ~ this causes obstruction and acute tubular necrosis
80
How do amnioglycosides affect the kidneys?
Aminos are MEAN to the kidneys Once they enter the cytosol, they induce free radical damage!
81
What is the risk of using distilled water in a TURP?
Hemolysis “WATER WHIPS ~ the RBCs”
82
What is the risk of using glycine in a TURP?
Transient blindness “Gly-seeing”
83
What is the risk of using Sorbitol in a TURP?
Hyperglycemia “ So Sweet it’s Sorbital”
84
What is the risk of using normal saline in a TURP?
Electrocution “Salty sparks”
85
What is the preferred anesthesia for a TURP?
Spinal ~T10 (Allows for early detection of complications ~ can assess patients neurological status through procedure)
86
How long should resection time in a TURP be limited to?
1 hour ~ this is due to the increased absorption of irrigation fluid with the increased amount of time
87
Which fluids are contraindicated in a TURP if monopolar electrocautery is used?
Normal saline and LR
88
What is TURP syndrome?
When a large volume of hypo-osmolar irrigation is absorbed
89
What is the classic TURP triad?
Hypertension (increase pulse pressure) Bradycardia (d/t reflex) Change in mental status
90
Serum Na less than < 120 causes what?
Increases the risk of complications
91
A serum Na < 110 causes what?!
Seizure, coma, ventricular dysrhythmias
92
What is the classic presentation to bladder perforation?
Abdominal and shoulder pain
93
What is a rough estimate of blood loss during a TURP?
2-3 mL per min of resection
94
What are the two absolute contraindications to lithotripsy?
Pregnancy and bleeding disorders/anticoagulation.
95
What is nephrotic syndrome?
When kidney diseases injure the glomeruli, which ultimately allows proteins to enter the tubules ~ this allows protein to be lost in the urine

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