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CPR > Test 6 - Renal > Flashcards

Test 6 - Renal Flashcards

1
Q

What CNS disease can hyponatremia cause?

A

Critical cerebral edema

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2
Q

What is pseudohyponatremia?

A

When there is a presence of other osmotically active substances in the serum (glucose, for example), causing serum osmolality to be normal while [Na+] is low.

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3
Q

What is the treatment for symptomatic hyponatremia?

A

Hypertonic saline

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4
Q

What is the diagnostic criteria for syndrome of inappropriate ADH (SIADH)?

A
  1. Hyponatremia (<135mmol/L)
  2. Decreased serum osmolality (<270mOsm/kg)
  3. Urine sodium >20 mmol/L
  4. Inappropriate urine concentration (urine osmolality >100mOsm/kg)
  5. Exclusion of renal or endocrine causes
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5
Q

Over-rapid correction of hyponatremia can cause __________?

A

Central pontine myelinolysis

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6
Q

What is the difference between central diabetes insipidus and nephrogenic diabetes insipidus.

A

Central DI is due to a lack of ADH from the hypothalamus, whereas nephrogenic DI is due to a lack of response to ADH by the kidneys.

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7
Q

What is the treatment for hypernatremia?

A

Give the patient hypotonic fluids:

  • 5% dextrose in water
  • oral water
  • half-normal saline
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8
Q

What are the five characteristics of nephrotic syndrome?

A
  1. Proteinuria 3.5g/day or higher
  2. Hypoalbuminemia
  3. Hyperlipidemia
  4. Lipiduria
  5. Edema
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9
Q

What is the calculation to estimate total body water in a male, and female, respectively?

A

TBW = 60% of body weight for men and 50% for women

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10
Q

Describe the proportions body water amongst the various compartments.

A

2/3 of TBW is ICF
1/3 TBW is ECF
-3/4 of ECF is interstitial
-1/4 of ECF is intravascular (plasma)

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11
Q

What is a BUN:creatinine ratio of 20 or higher indicative of?

A

Pre-renal AKI

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12
Q

Name 4 things that can cause K+ to shift into the intracellular compartment.

A
  1. Insulin
  2. Beta agonists
  3. Catecholamines
  4. Alkalosis
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13
Q

People should be emergently treated for hypokalemia if their serum [K+] is below ______.

A

2.5mEq/L

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14
Q

What is the treatment for severe hypokalemia?

A

Dilute KCl in normal saline and give intravenously. Monitor serum [K+] closely.

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15
Q

Name four things that can cause K+ to shift out of cells.

A
  1. Hyperglycemia
  2. Metabolic acidosis
  3. Cell necrosis
  4. Beta blockers
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16
Q

What is the name of the disease that is characterized by hypoaldosteronism?

A

Addison’s disease

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17
Q

What are the characteristic ECG findings of hypokalemia?

A

Reduced amplitude T waves and prominent U waves.

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18
Q

What are the characteristic ECG findings of hyperkalemia?

A
  1. Hyperacute T waves
  2. 1st degree AV block
  3. Loss of P waves
  4. Widening of the QRS complex
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19
Q

People should be emergently treated for hyperkalemia if their serum [K+] is above ______.

A

6.5 mEq/L

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20
Q

What is the emergency treatment for hyperkalemia? How does it work?

A

calcium gluconate to stabilize cell membrane potentials at -70mV

21
Q

Other than calcium gluconate, name three other things you could give to a hyperkalemic patient to shift K+ into cells. How quickly does each one work and for how long does each last?

A
  1. Insulin: takes 30 min to work and lasts 2 hours
  2. Beta agonists (albuterol): 30 min to work and lasts 2 hours
  3. Sodium bicarb: takes 2 hours to work at lasts a day
22
Q

What is a normal anion gap?

A

12

23
Q

What is the treatment for diabetic ketoacidosis?

A

IV fluids, insulin, K+ replacement, maybe phosphate replacement

24
Q

What is the treatment for alcoholic ketoacidosis?

A

IV dextrose

25
Q

What is the treatment for methanol or ethylene glycol poisoning?

A

IV fluids, fomepizole or ethanol with hemodialysis

26
Q

Specifically which acids are responsible for metabolic acidosis from aspirin poisoning?

A

Organic acids like lactic acid and ketoacids.

27
Q

What is the treatment for metabolic acidosis from aspirin poisoning?

A

Alkali therapy (sodium bicarb) + hemodialysis

28
Q

What is the treatment for metabolic alkalosis due to vomiting?

A

Normal saline + KCl

29
Q

What is the treatment for diuretics overdose?

A

NaCl and KCl in normal saline

30
Q

What is the cutoff blood pressure value for stage 1 hypertension?

A

140/90 (avg. of 2 consecutive readings)

31
Q

Define resistant hypertension.

A

BP > 140/90 despite being on 3+ classes of BP meds, including a diuretic

32
Q

You are treating a young, otherwise healthy woman for resistant hypertension. You suspect something is causing her RAAS to be chronically activated, maybe coarctation or something. CT angiography shows no coarctation, but some stenosis of the right renal artery. What is the likely Dx?

A

Fibromuscular dysplasia

33
Q

How do you treat hypertension?

A 
ABCD!
A = angiotensin blockers (include ACE-inhibitors and angiotensin receptor blockers)
B = beta blockers
C = calcium channel blockers
D = diuretics
34
Q

Describe how a patient’s kidney function dictates the effectiveness of different types of diuretics.

A

Thiazides don’t work at GFRs below 30ml/min

Loop diuretics work when GFR is low

35
Q

What is first line BP treatment for patients with hypertension and diabetic kidney disease?

A

ACE inhibitors or angiotensin receptor blockers

36
Q

What BP meds to black patients typically respond best to? What typically doesn’t work as well?

A

Diuretics or calcium channel blockers.

ACE inhibitors don’t work as well

37
Q

What is first line BP treatment for patients with HTN and heart failure?

A

ACE inhibitors or angiotensin receptor blockers.

Aldosterone receptor blockers (spironolactone) and beta blockers are also good.

38
Q

What should you not give to a pregnant person with hypertension?

A

ACE inhibitors, they are teratogenic!

39
Q

Name two ways to differentiate chronic kidney disease from acute kidney injury.

A

Urine output: AKD = oliguria and CKD = polyuria due to an inability to concentrate urine

Kidney size: CKD kidneys will be small

40
Q

What is a BUN:creatinine ratio of 10-15:1 suggestive of?

A

ATN

41
Q

Can a high BUN:creatinine ratio be caused by other things?

A

Yeah, catabolism (wasting diseases) or GI bleeds, or steroid use

42
Q

Describe how urine electrolytes allow you to differentiate ATN from pre-renal AKI.

A

In pre-renal AKI, renal function is intact, so kidneys will be reabsorbing Na+ and free water in collecting ducts (via ADH) –> low urine [Na+] (<10mmol/L) and high urine osmolality.

In ATN, kidneys are busted, so they can’t reabsorb Na+ and they can’t reabsorb free water, so urine [Na+] will be high (>20 mmol/L) and urine osmolality will be similar to plasma (300mOsm).

43
Q

Buzz word: muddy brown casts in urine sediment

A

Acute tubular necrosis

44
Q

What is the mechanism by which CKD causes anemia?

A

No mo EPO!

45
Q

What is the mechanism by which CKD causes osteopenia?

A

No more hydroxylation of 25-hydroxycholecalciferol into active calcitriol –> decreased Ca2+ gut absorption and no more negative feedback on the parathyroid by calcitriol –> increased PTH levels –> increased phosphate secretion in the kidneys and increased osteoclast activity

46
Q

What does it mean when you see RBCs in urine sediment analysis that are all spiky?

A

Its chill, they do that from being in a hypertonic solution

47
Q

What are dysmorphic RBCs and RBC casts on urine sediment analysis pathognomonic for?

A

Glomerular disease

48
Q

What type of proteins does a UA pick up? Does this help if you think your patient has multiple myeloma?

A

Albumin only.

It will not help for multiple myeloma cuz it won’t sense Bence Jones proteins (Ig light chains) in urine

49
Q

What is the first sign of diabetic kidney disease and when should you screen for it?

A

Microalbuminuria - not picked up on UA so you gots to do albumin:creatinine ratio (ACR).

For type 1 DM, start screening 5 years after Dx and every year after that.

For type 2 DM, screen every year.

CPR (27 decks)

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