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(Amanda's)FINAL-Physical & Health Assessment (Spring 2025) > Renal Assessment (Exam III) '25 > Flashcards

Renal Assessment (Exam III) '25 Flashcards

1
Q

What percentage of total body water (TBW) is water?

A

60%

This percentage varies with gender, age, and body fat percentage

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2
Q

What is the extracellular fluid (ECF) composed of?

A

Interstitial fluid (ISF) + Plasma

ECF is less than half the volume of TBW

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3
Q

What role do osmolarity sensors in the anterior hypothalamus play?

A

Stimulate thirst, release Vasopressin (ADH)

This leads to increased water and sodium retention

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4
Q

What role does ANP have on osmolar homeostasis?

A

Cardiac atria will release ANP that will act on kidney to DECREASE Na and H20 reabsorption if its overdoing it.

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5
Q

What is the function of the juxtaglomerular apparatus (JGA)?

A

Volume homeostasis:
Sense changes in volume and trigger RAAS when volumes are low

This results in sodium and water reabsorption

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6
Q

At what Na levels would we want to cancel the case?

A

Serum sodium levels ≤125 or ≥155 mEq/L

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7
Q

What is typically the underlying cause of hypervolemia in hyponatremia patients

A

ARF/CKD, heart failure

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8
Q

15% of hospitalized patients are hyponatermic due to…

A

Over fluid resucitation and increased endogenous vasopressin

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9
Q

What is the maximum recommended correction rate for sodium levels?

A

1.5 mEq/L/hr

Rapid correction can cause osmotic demyelination syndrome (permanent neuro damage)

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10
Q

What are treatment options for hyponatremia

A
  1. treat underlying cause
  2. Electrolyte drinks
  3. Diuretics
  4. Hypertonic/3% NaCl

Slow on the fluids unless they are having seizures r/t low Na. then it is best to correct the Na faster

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11
Q

How often should you check the Na level when treating hyponatremia?

A

Q4h

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12
Q

The clinical presentation of hyponatremia is _____

A

Neurological. Starts w headache and confusion

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13
Q

The most severe consequences of hyponatremia include

A

Seizures, coma, death.

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14
Q

What are common causes of hypernatremia? (6)

A
  1. Excessive evaporation
  2. Poor oral intake
  3. Overcorrection of hyponatremia
  4. Diabetes Insipidus
  5. GI losses
  6. Excessive Na Bicarb

DI- Loss of dilute urine

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15
Q

What is the most common cause of hypovolemic hypernatremia?

A

Renal or GI loss

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16
Q

What are the symptoms of hypernatremia?

A
  1. Orthostasis
  2. Restlessness
  3. Lethargy
  4. Tremor/muscle twitching/spasticity
  5. Seizures
  6. Death
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17
Q

Treatment of Hypernatremia:
Hypovolemic-
Euvolemic-
Hypervolemic-

A

Hypovolemic- NS
Euvolemic- H2O replacement
Hypervolemic- Diuretics

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18
Q

What do we want the Na reduction rate to be when we are treating hypernatremia to avoid cerebral edema, seizures, and neurologic damage

A

less than or equal to 0.5 mmol/L/hr
and less than or equal to 10 mmol/L/day

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19
Q

What is the normal range for serum potassium (K+)?

A

3.5-5.5 mmol/L

Potassium is the major intracellular cation (<1.5% in ECF)

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20
Q

Aldosterone and K are _____ releated

A

Inversely

Aldo causes distal nephron to secrete K (and reabsorb Na)

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21
Q

Why do renal failure patients typically have chronicly high K levels?

A

Because the excretion declines and shifts to the GI system which takes longer to get rid of it

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22
Q

What are the three major categories for hypokalemia?

A
  1. Renal loss (diuretics, hyperaldosteronism)
  2. GI loss (N/V/D)
  3. Intracellular shift (alkalosis, insulin)

Excessive licorice isnt a major category but is a common cause and is a board question

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23
Q

What are symptoms of hypokalemia?

A

Generally cardiac (U wave) and muscle (Muscle weakness/cramping)

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24
Q

What is the preferred treatment for hypokalemia?

A

PO potassium. it will fix it way faster!

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25
What are considerations for giving IV potassium? How much do we give and how much will it raise the K?
Given through CVC. Dose: 10-20 mEq/L/hr Each 10 mEq will raise by 0.1 mmol/L (takes forever)
26
What should we avoid with hypokalemia
1. Excessive insulin 2. B agonists 3. bicarb 4. Diuretics ## Footnote Also hyperventilation
27
What are causes of hyperkalemia?
* Renal failure * Hypoaldosteronism * Drugs inhibiting RAAS (specifically second A-aldo) * Succs ## Footnote Succs will increase serum K by 0.5-1 mEq/L
28
What are EKG symptoms of hyperkalemia?
* Cardiac dysrhythmias 1. peaked T wave 2. P wave gone 3. prolonged QRS ## Footnote If we see a peaked T wave, check K level
29
Hyperkalemia treatment
Dialyze within 24hrs prior to surgery. 1. Ca++ first initial treatment 2. Hyperventilation 3. Insulin (w or w/o glucose) ## Footnote Dialysis ALSO initially causes hypovolemia
30
What is the normal ionized calcium (iCa++) level?
1.2-1.38 mmol/L ## Footnote Only ionized plasma Ca++ is physiologically active
31
___% of Ca is in ECF and _____% is stored in bones
1% ECF 99% Bones
32
60% of plasma Ca is PB to albumin and rendered inactive. What can change the binding between Ca and albumin?
pH changes. ## Footnote increase pH/alkalosis = increase Ca binding to albumin = less iCa
33
What 3 hormones regulate Ca
1. PTH 2. Vit D 3. Calcitonin ## Footnote -PTH- increase Ca absorption (via bones kidneys & GI) -Vit D - helps GI absorption
34
What is required for PTH production
Mag
35
When should we check iCa++ when giving PRBCs?
After 4+ units. May need to give Ca++
36
What are common causes of hypocalcemia?
* Decreased PTH secretion * Magnesium deficiency * Low Vitamin D * Renal failure * Massive blood transfusion ## Footnote Blood transfusion bc it has citrate preservative that binds to Ca
37
When would we be worried about hypocalcemia and laryngospasm?
during thyroid/PT surgery can cause decreased PTH which can lead to laryngospasm
38
Majority of pts with hypercalcemia have _____ or ____. what are the serum Ca levels for these two.
1. hyperparathyroid <11 2. Cancer >13
39
What EKG changes can we see with hypomagnesium?
Polymorphic V-tach/Torsades De Pointes ## Footnote 2g mag sulfate is the tx
40
What are common causes of hypermagnesium?
* Over treatment for pre-eclampsia/eclampsia * Pheochromocytoma
41
Where are the kidneys located? (give location in regards to spinal level)
retroperitoneal between T12-L4. Right is slightly caudal (lower) than left to accomodate liver
42
The kidney receives ____% of CO. The outer layer (Cortex) receives majority of this blood flow, ______%
20% 85-90% ## Footnote Inner layer - medulla necrosis in response to HoTN
43
What is the normal glomerular filtration rate (GFR)?
125-140 mL/min ## Footnote It is the best measure of renal function over time (is we look at trends)
44
What does an increase in serum creatinine indicate?
A decrease in GFR ## Footnote A doubling of serum creatinine can indicate a 50% drop in GFR
45
What is a normal BUN? Normal BUN:Creatinine ratio?
10-20 mg/dL 10:1
46
What does a BUN:Creatinine ratio of >20:1 suggest?
Pre-renal azotemia ## Footnote Indicates a volume issue
47
What is acute kidney injury (AKI)?
Deterioration of kidney function over hours to days ## Footnote It affects 20% of hospitalized patients and 50% of ICU patients
48
What are the risk factors for AKI?
* Pre-existing renal disease * Advanced age * CHF * PVD * DM * Sepsis * Hypotension
49
What is the hallmark of AKI?
Azotemia ## Footnote It is the buildup of nitrogenous products such as urea and creatinine
50
What are the three main categories for AKI?
1. Prerenal Azotemia 2. Renal Azotemia 3. Postrenal Azotemia
51
What is happening in: 1. Prerenal Azotemia 2. Renal Azotemia 3. Postrenal Azotemia Which one is the easiest to treat?
1. Prerenal: decrease renal prefusion 2. Renal: nephron injury 3. Postrenal: outflow obstruction Postrenal easiest to treat
52
What is the most common form of AKI?
Pre renal azotemia ## Footnote 1/2 of hospital-aquired AKI cases
53
What is the most common cause of acute tubular necrosis?
Pre-renal azotemia if it isnt reversed
54
Neurological complications of AKI are related to ________ build up in the blood.
protein/amino acid
55
What are the cardiovascular complications of AKI in the order of incidence?
1. Systemic HTN 2. LV hypertrophy 3. CHF ## Footnote pulmonary edema, uremic cardiomyopathy and arrhythmias
56
What is the primary function of the renal system regarding blood glucose?
Regulates blood glucose homeostasis through gluconeogenesis and glucose filtration/reabsorption
57
What medication can improve coagulation in uremic patients?
Prophylactic DDAVP and Factor 8. ## Footnote DDAVP --> tachyphylaxis so dont give it willy nilly
58
What are the metabolic effects of chronic kidney disease?
* Water & Sodium imbalances * Hyperkalemia * Hypoalbuminemia * Metabolic acidosis * Malnutrition * Hyperparathyroidism
59
What is the preferred fluid for renal patients during anesthesia?
Normal Saline (NS). ## Footnote Because no K
60
True or False: Vasopressin constricts the afferent arteriole better than alpha-agonists.
False. Vasopressin constricts the efferent arteriole better. ## Footnote Pressor of choice in AKI
61
What are the leading causes of chronic kidney disease?
* Diabetes Mellitus (DM) * Hypertension (HTN) ## Footnote DM most common at 38%. HTN 26%
62
GFR decreases by _____ per decade starting from age _____.
10; 20
63
What is the first-line treatment for systemic hypertension in chronic kidney disease?
Thiazide Diuretics. ## Footnote May need ACE-i and ARB
64
Which populations are high risk for silent MI?
women and diabetics
65
What is the risk associated with blood transfusions in patients with chronic kidney disease?
Excess hemoglobin can lead to sluggish circulation, acidosis, and hyperkalemia.
66
What are the indications to consider dialysis?
* Volume overload * Severe hyperkalemia * Metabolic acidosis * Symptomatic uremia * Failure to clear medications
67
True or False: Hemodialysis is more efficient than peritoneal dialysis.
True. However, OD is slower and less dramatic fluid shifts so might be preferred for these patients
68
What are the anesthetic agents that should be avoided in patients with chronic kidney disease?
* Agents with active metabolites * Morphine * Demerol
69
What is normeperidine?
An active metabolite of Demerol that can cause neurotoxicity.
70
Why would you avoid morphine in kidney injury
40% cleared through kidneys and has active metabolite. build up can lead to resp depression

(Amanda's)FINAL-Physical & Health Assessment (Spring 2025) (31 decks)

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