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Apex > Kidney > Flashcards

Kidney Flashcards

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
Q

Where does aldosterone act?

A

Distal tubule and collecting duct

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26
Q

Where does ADH act?

A

Distal tubule and collecting duct

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27
Q

Where in the nephron does parathyroid hormone act to increase Ca reabsorption?

A

Distal tubule

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28
Q

Which aspect of the nephron is impermeable to water?

A

Ascending limb of loop of Henle

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29
Q

What do carbonic anhydrase inhibitors do?

A

Non competitively inhibit carbonic anhydrase in the cells that make up the proximal tubule

***this reduced reabsorption of bicarb, Na, and water

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30
Q

What is the clinical use of carbonic anhydrase inhibitors?

A

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

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31
Q

What are the complications to carbonic anhydrase inhibitors?

A

Metabolic acidosis

Hypokalemia

In patients with COPD, this loss of bicarb (their buffering system) may exacerbate symptoms

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32
Q

What is an osmotic diuretic?

A

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.

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33
Q

Which diuretic is a free radical scavenger?

A

Mannitol

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34
Q

What is the clinical use of osmotic diuretics?

A

Intracranial HTN

Differential diagnosis of acute oliguria (will increase UOP if prerenal injury ~ not intrinsic injury)

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35
Q

What are the complications of osmotic diuretics?

A

CHF
Pulmonary edema
If BBB is disrupted, could cause cerebral edema

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36
Q

What are loop diuretics?

A

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.

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37
Q

What is the clinical use for loop diuretics?

A

Pulmonary edema
Acute kidney injury
CHF
Hypercalcemia
Hypertension
ICP
Anion overdose

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38
Q

What are the complications to loop diuretics?

A

“LOSS OF OUR boy POTASSIUM”

Hypokalemia and hypochloremic metabolic alkalosis

Hypocalcemia

Hypomagnesemia

Hypovolemia

Ototoxicity

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39
Q

What are thiazide diuretics?

A

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
Q

What is the clinical use for thiazide diuretics?

A

HTN
CHF
Osteoporosis
Mobilize edema

41
Q

What are complications of thiazide diuretics?

A

“Sweet cows thia-zide (reside) in the fields”

Hyperglycemia
Hypercalcemia

Hyperuricemia
Hypokalemic, hypochloremic metabolic alkalosis
Hypovolemia
HLD
Sexual dysfunction

42
Q

What are potassium sparing diuretics?

A

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
Q

What is the clinical use of potassium sparing diuretics?

A

Reduce K loss in a patient receiving a loop or thiazide diuretic.

Secondary hyperaldosteronism

44
Q

What are the complications of potassium-sparing diuretics?

A

Hyperkalemia
Metabolic acidosis
Gynecomastia
Libido changes
Nephrolithiasis

45
Q

Which 3 drug classes increase the risk of hyperkalemia in a patient taking a potassium sparing diuretic?

A

NSAIDs
Beta-blockers
Ace Inhibitors

46
Q

What are the two best tests for GFR function?

A

BUN and creatinine clearance

47
Q

What are the two best tests for TUBULAR function?

A

Fractional excretion if sodium and urine osmolality

48
Q

What does a BUN of < 8 indicate?

A

Overhydration

Decreased Urea Production (malnutrition and/severe liver disease)

49
Q

What does a BUN of 20-40 indicate?

A

Dehydration

Increased protein input (high protein diet, GI bleed, hematoma breakdown)

Catabolism (trauma and sepsis)

Decrease GFR

50
Q

What does a BUN > 50 indicate?

A

Decreased GFR

51
Q

What is a normal BUN:Creatinine ration?

A

10:1

52
Q

What does a BUN ratio of > 20:1 indicate?

A

Prerenal azotemia

53
Q

What is the MOST useful indicator of GFR?

A

Creatinine clearance

GFR = (140-age) x (kg) / 72 x serum creatinine (mg/dL)

***in women this is multiplied by 0.85

54
Q

What are the three methods to classify the severity of renal injury?!

A

RIFLE: risk, injury, failure, loss, end-stage

AKIN: Acute Kidney Injury Network

KDIGO: Kidney Disease Improving Global Outcomes

55
Q

What are the three classifications of acute kidney injury?

A

Prerenal

Intrinsic

Postrenal

56
Q

What are the causes and txs to Prerenal Injury?

A

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
Q

What are the causes and txs to intrinsic renal disease?

A

Causes: injury to the tubules, glomerulus, or interstitial space (nephrotoxic drugs, ischemia, NSAIDs, nephrotoxic abx)

Tx: restore renal perfusion/supportive

58
Q

What are the causes and treatments for post renal injury?

A

Causes: result of an obstructive phenomenon (foley catheter clog, ureteral stone, neurogenic bladder)

Tx: relieve obstruction

59
Q

What MAP reduces the risk of prerenal azotemia?

A

MAP> 65

60
Q

What type of anemia results from end-stage renal disease?

A

NORMOCYTIC normochromic anemia

61
Q

What is the MOST common cause of chronic kidney disease?

A

Diabetes mellitus

62
Q

What is the second most common cause of chronic kidney disease?

A

Hypertension

63
Q

What is a normal GFR?

A

> 90

64
Q

What is stage 2 kidney disease? AKA mildly decreased

A

60-89 mL/min

65
Q

What is stage 3 kidney disease? Aka moderately decreased GFR?

A

30-59

66
Q

What is stage 4 kidney disease? Aka severely decreased

A

15-29

67
Q

What is stage 5 kidney disease? Aka kidney failure?

A

< 15

“You hit 15, you kill the bean” 🫘

68
Q

What is the first line therapy for uremic bleeding?

A

Desmopressin

(Uremia causes platelet dysfunction thus increases bleeding time)

69
Q

What is the most common cause of death in patients with chronic kidney disease?

A

CAD

70
Q

What is renal osteodystrophy caused by?

A

Decreased vitamin D production
Secondary hyperparathyroidism

71
Q

What is the cornerstone of treatment?

A

Dialysis

72
Q

What are the 5 indications for dialysis?

A

Volume overload
Hyperkalamia > 6
Severe metabolic acidosis
Symptomatic uremia
Overdose with a drug that is cleared by dialysis

73
Q

What is the leading cause of death in dialysis patients?

A

Infection

74
Q

Which type of dialysis is more efficient?

A

Hemodialysis

BUT peritoneal dialysis is favored in patients who cannot tolerate fluid shifts associated with hemodialysis

75
Q

Is Sux safe in patients with renal failure?

A

YES! IF their potassium is within normal range

**although you should not do a sux drip

76
Q

What are the most suitable NMB for renal failure patients?

A

Benzylisoquinolones

(Aka cisatracurium and Atracurium)

77
Q

Which aminosteriod should you NOT use in renal failure patients?

A

Pancuronium ~ it’s primarily eliminates by kidneys

Pan > Vec > roc

78
Q

Which opioid choices are not good for a renal Failure patient?

A

Morphine ~ metabolite is morphine 6 glucoronide

Meperidine ~ metabolite is normeperidine (can cause seizures!)

79
Q

How does rhabdomyolysis and myoglobinemia affect the kidneys?

A

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
Q

How do amnioglycosides affect the kidneys?

A

Aminos are MEAN to the kidneys

Once they enter the cytosol, they induce free radical damage!

81
Q

What is the risk of using distilled water in a TURP?

A

Hemolysis

“WATER WHIPS ~ the RBCs”

82
Q

What is the risk of using glycine in a TURP?

A

Transient blindness

“Gly-seeing”

83
Q

What is the risk of using Sorbitol in a TURP?

A

Hyperglycemia

“ So Sweet it’s Sorbital”

84
Q

What is the risk of using normal saline in a TURP?

A

Electrocution

“Salty sparks”

85
Q

What is the preferred anesthesia for a TURP?

A

Spinal ~T10

(Allows for early detection of complications ~ can assess patients neurological status through procedure)

86
Q

How long should resection time in a TURP be limited to?

A

1 hour ~ this is due to the increased absorption of irrigation fluid with the increased amount of time

87
Q

Which fluids are contraindicated in a TURP if monopolar electrocautery is used?

A

Normal saline and LR

88
Q

What is TURP syndrome?

A

When a large volume of hypo-osmolar irrigation is absorbed

89
Q

What is the classic TURP triad?

A

Hypertension (increase pulse pressure)

Bradycardia (d/t reflex)

Change in mental status

90
Q

Serum Na less than < 120 causes what?

A

Increases the risk of complications

91
Q

A serum Na < 110 causes what?!

A

Seizure, coma, ventricular dysrhythmias

92
Q

What is the classic presentation to bladder perforation?

A

Abdominal and shoulder pain

93
Q

What is a rough estimate of blood loss during a TURP?

A

2-3 mL per min of resection

94
Q

What are the two absolute contraindications to lithotripsy?

A

Pregnancy and bleeding disorders/anticoagulation.

95
Q

What is nephrotic syndrome?

A

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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