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Assessment '24 - Mordecai > T3 - Renal Assessment > Flashcards

T3 - Renal Assessment Flashcards

1
Q

~_____% TBW is water (varies w/ _____, ______, _____ %)

A
  • 60%
  • gender, age, body fat

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2
Q

ECF- fluid outside of cells ( _____ + _______) = < 1/2 volume of TBW

A

ISF +Plasma

Slide 3

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3
Q

How is osmolar homeostasis primarily mediated?

A

Osmolality sensors in the anterior hypothalamus

Slide 3

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4
Q

What is the path created by the hypothalamus to regulate osmolar homeostasis?

A
  • Stimulate thirst
  • Cause pituitary release of vasopressin (ADH) (To retain fluid)
  • Cardiac atria release ANP (will act on kidney to decrease Na/H2O reasbsorption) (to get rid of fluid)

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5
Q

How is volume homeostasis mediated?

A

Mediated by juxtaglomerular apparatus

Slide 3

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6
Q

What are the changes caused by the JGA?

A
  • JGA senses a decrease in volume
  • JGA triggers Renin-Angiotensinogen-Aldosterone system
  • RAAS causes Na+/H2O reabsorption

Slide 3

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7
Q

What would be concerning when it comes to Na levels and surgery?

A

Acute changes

≤125 or ≥155

Correct prior to elective cases

Slide 4 notes

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8
Q

In hypovolemia, what fluid and Na abnormality would you expect?

What could be some causes?

A
  • Na and H2O loss
  • Diuretics, GI loss, burns, trauma
    Slide 4 notes
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9
Q

What could cause sodium decrease in a euvolemic state?

A
  • Salt restriction
  • Endocrine-related: hypothyroid, SIADH (retaining H2O more than Na)

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10
Q

What could be the cause of hyponatremia in a hypervolemic state with a urine Na >20?

A
  • ARF/CKD
  • Heart failure

Slide 4 notes

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11
Q

What percentage of hospitalized patients are considered hyponatremic?

What could be a cause?

A
  • 15%
  • Over fluid-resuscitation
  • ↑ endogenous vasopressin

Slide 4 notes

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12
Q

Clinical neurological presentation of hyponatremia: 130-135 mEq/L

A
  • Asymptomatic
  • Headache
  • Nausea
  • Vomiting
  • Fatigue
  • Confusion
  • Muscle cramps
  • Depressed reflexes

*Bold are individual to this category and are not repeated in the next category

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13
Q

Clinical neurological presentation of hyponatremia: 120-130 mEq/L:

A
  • Malaise
  • Unsteadiness
  • Headache
  • Nausea
  • Vomiting
  • Fatigue
  • Confusion
  • Muscle cramps

*Bold are individual to this category and are not repeated in the other categories

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14
Q

Clinical neurological presentation of hyponatremia: <120 mEq/L

A
  • Headache
    - Restlessness
    - Lethargy
    - Seizures
    - Brain-stem herniation
    - Respiratory arrest
    - Death

*Bold are individual to this category and are not repeated in the other categories

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15
Q

Which are the most severe consequences of hyponatremia:

A
  • Seizures
  • Comma
  • Death

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16
Q

What is the single most important for the treatment of hyponatremia?

What are some treatment options?

A
  • Treat underlying cause (look at volume status)
  • Electrolyte drinks
  • Normal saline
  • Diuretics
  • Hypertonic saline/3% NaCl

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17
Q

What should the infusion rate be when treating hyponatremia with 3% NaCl hypertonic solution?

What should the Na correction not exceed?

A
  • 80 ml/hr over 15h
  • Correction should not exceed 1.5 mEq/L/hr

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18
Q

What could happen with rapid correction of hyponatremia?

How fast would you have to correct in order to achieve this adverse effect?

Is this a serious or reversible adverse effect?

A
  • Osmotic Demyelination Syndrome
  • You’d have to correct >6 mEq/L in 24h
  • Serious - often permanent neuro damage

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19
Q

Are hyponatremic seizures a medical emergency?

How would you treat this?

A
  • Yes! neurological damage could occur
  • 3-5 ml/kg of 3% over 20 min until seizures resolve

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20
Q

What are some causes of HYPERnatremia?

A
  • Diabetes insipidus
  • Excessive evaporation
  • Poor oral intake (very young, very old, altered mental status)
  • Overcorrection of hyponatremia
  • GI losses
  • Excessive sodium bicarb (treating acidosis)

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21
Q

HYPERnatremia diagnostic algorithm

Hypovolemia

S/S:

  • Urine Na >20:
  • Urina Na <20:

Treatment:

A

PPT notes: Renal or GI loss

S/S: Decreased skin turgor, flat neck veins, dry mucous membranes, orthostatic hypotension, tachycardia, oliguria

Urine Na >20: Renal salt and water loss
- Osmotic diuretic
- Loop diuretic
- Postrenal obstruciton
- Intrinsic recall disease
- Profound glycosuria

Urine Na <20: Extrarenal salt and water loss
- Diarrhea
- GI fistulas
- Sweating

Treatment: Normal saline

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22
Q

HYPERnatremia diagnostic algorithm

Euvolemia
- Urine Na ______?

Treatment:

A

Urine Na variable

Renal water loss:
- Diabetes insipidus: Central, nephrogenic, gestational

Extrarenal water loss:
- Insensible losses: Respiratory tract; Skin

Treatment: water replacement (po or D5W)

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23
Q

HYPERnatremia diagnostic algorithm

Hypervolemia

S/S

Urine Na >20:

Treatment:

A

S/S: Peripheral edema, rales, ascites

Urine Na >20: Sodium gains
- Hyperaldosteronism
- Cushing’s syndrome
- Hypertonic dialysis
- IV NaHCO3
- NaCl tablets
- Hyperalimentation
- Salt water drowning

Treatment: diuretics

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24
Q

What are common symptoms of HYPERnatremia?

A

LORDTS (Madea’s voice)

  • Lethargy
  • Orthostasis
  • Restlessness
  • Death
  • Tremor/muscle twitching
  • Seizures
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25
Q

How would you treat HYPERnatremia in hypovolemic, euvolemic, or hypervolmeic states?

A

Root cause, Assess volume status (VS, UOP, Turgor, CVP)
- Hypovolemic: normal saline
- Euvolemic: water replacement (po or D5W)
- Hypervolemic: diuretics

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26
Q

How fast do you want to reduce Na levels for correction?

Why would you want to correct at this rate?

A

≤ 0.5 mmol/L/hr and ≤ 10 mmol/L/day

  • To avoid cerebral edema, seizures, and neurological damage
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27
Q

What is the percentage of the major intracellular fluid (ICF) cation (K+) that is present in the extracellular fluid (ECF)?

A

Less than 1.5% of the major intracellular fluid cation is present in the extracellular fluid.

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28
Q

Does serum potassium (K+) reflect transmembrane K+ regulation or total body K+ more accurately?

A

Serum potassium (K+) reflects transmembrane K+ regulation more than total body K+.

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29
Q

What is the effect of aldosterone on potassium and sodium in the distal nephron?

A

Aldosterone causes the distal nephron to secrete potassium (K+) and reabsorb sodium (Na+).

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30
Q

How does renal failure affect potassium excretion?

A

In renal failure, potassium excretion declines and excretion shifts towards GI system.

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31
Q

When renal potassium excretion declines, where does the excretion shift towards?

A

When renal potassium excretion declines, excretion shifts towards the gastrointestinal (GI) system.

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32
Q

What dietary issue can cause low serum potassium?

A

Low PO intake

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33
Q

By which 2 ways mentioned in the PPT can we lose K+ through the kidneys?

A

Diuretics use and hyperaldosteronism can cause renal loss of potassium.

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34
Q

How can gastrointestinal issues lead to low potassium?

A

Nausea, vomiting, diarrhea, and malabsorption can cause gastrointestinal loss of potassium.

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35
Q

Which conditions lead to an intracellular shift of potassium?

A

Alkalosis, the use of β-agonists, and insulin administration can cause an intracellular shift of potassium.

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36
Q

Which medical condition related to diabetes can cause low serum potassium? How?

A

Diabetic ketoacidosis (DKA) can lead to low serum potassium due to osmotic diuresis.

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37
Q

Which type of blood pressure medication can lead to a decrease in potassium?

A

Hydrochlorothiazide (HCTZ) found in some blood pressure medications.

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38
Q

What unusual dietary source can lead to low potassium levels?

A

Excessive consumption of licorice.

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39
Q

What are general types of symptoms seen in hypokalemia?

A

Generally cardiac and neuromuscular symptoms.

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40
Q

What muscular symptoms can hypokalemia cause?

A

Muscle weakness and cramps.

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41
Q

What is ‘Ileus’ in the context of hypokalemia?

A

A disruption of the normal propulsive gastrointestinal motor activity due to hypokalemia.

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42
Q

How does hypokalemia affect the heart?

A

It can cause dysrhythmias and U waves on an EKG.

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43
Q

What is the typical rate for IV potassium replacement?

A

Generally 10-20 mEq/L per hour IV.

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44
Q

What is the preferred route of potassium administration for treating hypokalemia?

A

Potassium orally is preferred over intravenous; central venous catheter (CVC) may be used; treatment may require several days.

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45
Q

What is the effect of 10 mEq IV potassium on serum levels?

A

Each 10 mEq of IV potassium can raise the serum potassium by approximately 0.1 mmol/L.

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46
Q

What treatments or actions should be avoided in hypokalemia?

A

Avoid excessive insulin, β-agonists, bicarbonate, hyperventilation, and diuretics.

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47
Q

What are renal-related causes of hyperkalemia?

A

Renal failure and hypoaldosteronism (causes K+ secretion and excretion)

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48
Q

Which type of drugs affecting the renin-angiotensin-aldosterone system (RAAS) can cause hyperkalemia?

A

Drugs that inhibit RAAS and drugs that inhibit K+ excretion

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49
Q

How can neuromuscular blocking agents affect potassium levels?

A

Depolarizing NMBs like Succinylcholine (Succs) can cause hyperkalemia by increasing serum K+ by 0.5 to 1 mEq/L

*mEq is used interchangibly in monovalent ions just fyi

ChatGPT:
For monovalent ions (those with a charge of +1 or -1), like potassium (K+), sodium (Na+), chloride (Cl-), and bicarbonate (HCO3-), 1 mmol/L is equivalent to 1 mEq/L because their valence is 1.

However, for divalent ions (those with a charge of +2 or -2), like calcium (Ca2+), magnesium (Mg2+), and sulfate (SO4^2-), the situation is different. For these ions, 1 mmol/L is equivalent to 2 mEq/L because their valence is 2. Therefore, when converting concentrations for divalent ions, the concentration in millimoles is multiplied by 2 to get the concentration in milliequivalents.

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50
Q

What role does acidosis play in potassium balance?

A

Both respiratory and metabolic acidosis can lead to hyperkalemia.

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51
Q

Which conditions associated with cell damage can lead to hyperkalemia?

A

Cell death from trauma, use of tourniquets, and massive blood transfusion.

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52
Q

What are the symptoms of chronic hyperkalemia?

A

Chronic hyperkalemia may cause minimal symptoms like malaise and gastrointestinal upset.

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52
Q

What neuromuscular symptoms can occur with hyperkalemia?

A

Skeletal muscle paralysis and decreased fine motor skills.

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53
Q

How does hyperkalemia affect the heart?

A

It can cause cardiac dysrhythmias.

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54
Q

What are the EKG progression signs of hyperkalemia?

A
  • Peaked T waves
  • P wave disappearance
  • Prolonged QRS complex
  • Sine wave formation
  • Asystole
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55
Q

When should you dialyze a hyperkalemic patient before surgery?

A

Dialyze within 24 hours prior to surgery.

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56
Q

What is the first initial treatment for hyperkalemia and why?

A

Calcium is given to quickly stabilize the cell membrane.

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57
Q

How does hyperventilation affect serum potassium levels?

A

Increasing the pH by 0.1 can decrease K+ by 0.4-1.5 mmol/L.

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58
Q

What is the role of insulin and glucose in treating hyperkalemia?

A

Insulin, given with glucose (10 units IV: 25g D50), can lower K+ levels, working in 10-20 minutes.

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59
Q

What is the role of bicarbonate in managing hyperkalemia?

A

Bicarbonate can help shift potassium into cells by increasing blood pH, reducing serum levels.

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60
Q

Which diuretics are useful in treating hyperkalemia?

A

Loop Diuretics can be used to increase renal excretion of potassium.

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60
Q

How does Kayexalate work in treating hyperkalemia?

A

Kayexalate binds to K in digestive tract and removes potassium from the body, working over hours to days.

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61
Q

What should be avoided in the management of hyperkalemia?

A
  • Avoid using Succinylcholine (0.5-1 mEq/L increase)
  • Hypoventilation (decreased pH=increased K)
  • Lactated Ringer’s solution (will also decrease pH=increased K)
  • Potassium-containing IV fluids.
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62
Q

What is the distribution of calcium in the body?

A

Only 1% of the body’s calcium is in the extracellular fluid (ECF); 99% is stored in bones.

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63
Q

Which form of plasma calcium is physiologically active?

A

Only ionized plasma calcium (Ca++) is physiologically active, not protein-bound calcium.

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64
Q

What are the normal levels of ionized calcium (iCa++) in the blood?

A

Normal iCa++ levels range from 1.2 to 1.38 mmol/L.

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65
Q

How are ionized calcium levels affected by albumin and pH?

A

Ionized calcium levels are influenced by albumin levels and pH.

  • 60% plasma Ca++ is protein bound (mainly to albumin)
  • pH changes influence the binding of Ca++ to albumin

Increase in pH/alkalosis=Increased Ca++ binding to albumin, therefore a decrease in plasma Ca++

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66
Q

Which hormone increases gastrointestinal absorption, renal reabsorption of calcium, and pulls calcium from bone?

A

Parathyroid hormone (PTH) increases GI absorption, renal reabsorption, and mobilizes calcium from bone.

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67
Q

What role does vitamin D play in calcium regulation?

A

Vitamin D augments intestinal calcium absorption.

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68
Q

How does calcitonin affect calcium levels?

A

Calcitonin promotes bone resorption, which decreases plasma calcium levels.

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69
Q

Aldosterone _________ effects K+

A

inversely

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70
Q

3 major categories of cause of hypokalemia?

A

Renal loss
GI loss
Transcellular shift

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71
Q

Aldosterone causes K+ ________ & ________

A

secretion & excretion

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72
Q

Succinylcholine increases serum K+ by __________

A

0.5-1 mEq/L

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73
Q

Dialysis ALSO initially causes ___________

A

Hypovolemia

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74
Q

pH Δ’s influence the ____________ of Ca++ to albumin

A

binding

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75
Q

___% plasma Ca++ is protein bound (mainly to _________)

A
  • 60
  • Albumiin
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76
Q

↑pH/Alkalosis leads to ↑Ca++ binding to albumin

Therefore, there will be a ________ in plasma iCa++

A

decrease

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77
Q

What can cause a decrease in parathyroid hormone (PTH) secretion leading to hypocalcemia?

A

Hypocalcemia can result from reduced PTH secretion, often as a complication of thyroid or parathyroid surgery.

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78
Q

How does magnesium deficiency affect calcium levels?

A

Magnesium deficiency can lead to hypocalcemia as magnesium is required for PTH production

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79
Q

What role does vitamin D play in calcium levels?

A

Low vitamin D or disorders of vitamin D metabolism can lead to hypocalcemia due to reduced calcium absorption from the gut.

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80
Q

How does renal failure contribute to hypocalcemia?

A

Renal failure can cause hypocalcemia due to the kidneys not responding to PTH effectively.

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81
Q

Why can massive blood transfusions lead to hypocalcemia?

A

The citrate preservative in blood products can bind calcium, leading to hypocalcemia.

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82
Q

What are the target sites of PTH action to increase calcium absorption?

A

PTH acts on:

  • The bones to mobilize calcium
  • The kidneys to increase calcium reabsorption
  • The gastrointestinal system to enhance calcium absorption
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83
Q

Why is magnesium important for PTH function?

A

Magnesium is essential for the production and secretion of PTH.

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84
Q

What is the role of Vitamin D in calcium homeostasis?

A

Vitamin D facilitates gastrointestinal absorption of calcium.

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85
Q

When should ionized calcium (iCa++) levels be checked in the context of blood transfusions?

A

Check iCa++ after transfusing 4 or more units of packed red blood cells (PRBCs), as you may need to administer calcium to counteract the binding effects of citrate in transfused blood.

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86
Q

What are neurological symptoms of hypercalcemia?

A

Confusion and lethargy.

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87
Q

How does hypercalcemia affect muscle tone and reflexes?

A

Causes hypotonia and decreased deep tendon reflexes (↓DTR).

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88
Q

What are gastrointestinal symptoms of hypercalcemia?

A

Abdominal pain and nausea/vomiting (N/V).

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89
Q

What is a characteristic EKG change in hypercalcemia?

A

Short QT interval (QT-I).

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90
Q

What chronic condition can result from elevated calcium levels?

A

Chronic high calcium levels can lead to hypercalciuria and nephrolithiasis.

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91
Q

What sensations are typical in hypocalcemia?

A

Paresthesias.

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92
Q

What behavioral changes might indicate hypocalcemia?

A

Irritability.

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93
Q

How can hypocalcemia affect blood pressure?

A

Hypocalcemia can cause hypotension (HoTN).

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94
Q

What are severe neurological symptoms of hypocalcemia?

A

Seizures and myocardial depression.

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95
Q

What is a characteristic EKG change in hypocalcemia?

A

Prolonged QT interval (QT-I).

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96
Q

What is a life-threatening complication of hypocalcemia post-parathyroidectomy?

A

Hypocalcemia-induced laryngospasm, which can be a life-threatening complication.

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97
Q

Extra caution when extubating parathyroidectomy, always have ____________ plan

A

Larangospasm

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98
Q

What dietary issues can lead to hypomagnesemia?

A

Low dietary intake or poor absorption can cause hypomagnesemia.

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99
Q

How can renal function affect magnesium levels?

A

Renal wasting can lead to hypomagnesemia.

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100
Q

What are muscular symptoms of hypomagnesemia?

A

Muscle weakness or excitation can occur.

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101
Q

What are the neurological effects of hypomagnesemia?

A

Seizures may be a symptom of hypomagnesemia.

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102
Q

What cardiac dysrhythmia is associated with hypomagnesemia?

A

Polymorphic V-tach or
Torsades De Pointes

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103
Q

Where are the kidneys located?

A

Retroperitoneal T12-L4

Right is slightly caudal to the left to accommodate liver

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104
Q

How common is hypermagnesemia and what are its usual causes?

A

Hypermagnesemia is very uncommon and is generally due to:

Overtreatment
- Pre-eclampsia/eclampsia
- Pheochromocytoma

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105
Q

What symptoms are associated with magnesium levels of 4-5 mEq/L?

A

Lethargy, nausea/vomiting (N/V), and flushing.

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106
Q

What symptoms appear when magnesium levels exceed 6 mEq/L?

A

Hypotension (HoTN) and decreased deep tendon reflexes (↓DTR).

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107
Q

What are the severe symptoms of magnesium levels over 10 mEq/L?

A

Paralysis, apnea, heart blocks, and cardiac arrest.

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108
Q

What are the treatment options for hypermagnesemia?

A

Treatment includes diuresis, intravenous calcium (to stabilize cell membranes), and dialysis.

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109
Q

What is the nephron?

A

The nephron is the primary structural and functional unit of the kidney. Each kidney contains approximately 1 million nephrons.

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110
Q

What are the main components of a nephron?

A

A nephron consists of the:
* glomerulus, tubular system
* Bowman’s capsule
* proximal tubule (PCT)
* loop of Henle
* distal tubule (DCT)
* collecting duct.

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111
Q

What percentage of cardiac output does the kidney receive?

A

The kidneys receive 20% of the cardiac output (COP).

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112
Q

How much blood do the kidneys filter per minute?

A

The kidneys filter 1 to 1.25 liters of blood per minute (L/min).

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113
Q

What is the outer layer of the kidney called and what percentage of renal blood flow (RBF) does it receive?

A

The outer layer is called the cortex, and it receives the majority of renal blood flow, about 85-90%.

114
Q

What is the inner layer of the kidney called?

A

The inner layer of the kidney is called the medulla.

115
Q

Which part of the kidney is particularly vulnerable to necrosis due to hypotension?

A

The Loop of Henle (LOH) in the medulla is particularly vulnerable to developing necrosis in response to hypotension (decreased kidney perfusion).

116
Q

What do the kidneys regulate in terms of extracellular fluid?

A

The kidneys regulate extracellular (EC) volume, osmolarity, and composition.

117
Q

How do the kidneys contribute to blood pressure regulation?

A

he kidneys regulate blood pressure both intermediately and long-term via the renin-angiotensin-aldosterone system (RAAS) and atrial natriuretic peptide (ANP).

118
Q

What is the role of the kidneys in excretion?

A

The kidneys excrete toxins and metabolites from the body.

119
Q

How do the kidneys maintain acid/base balance?

A

The kidneys regulate the balance of acids and bases by excreting hydrogen ions and reabsorbing bicarbonate.

120
Q

What hormones are produced by the kidneys?

A

The kidneys produce several hormones including renin, erythropoietin, calcitriol, and prostaglandins.

121
Q

How do the kidneys assist in blood glucose homeostasis?

A

The kidneys contribute to blood glucose homeostasis by producing glucose through gluconeogenesis and filtration and reabsorption of glucose

122
Q

What is the normal range for the glomerular filtration rate (GFR)?

A

The normal GFR range is 125-140 mL/min. It is the best measure of renal function over time and is heavily influenced by hydration status.

123
Q

What is the creatinine clearance range and how is it performed?

A

Creatinine clearance measures 110-140 mL/min and is obtained from a 24-hour urine test.

Creatinine is freely filtered and not reabsorbed, making this the most reliable measure of GFR.

124
Q

What is the normal range for serum creatinine and what does it indicate?

A

The normal range for serum creatinine is 0.6-1.3 mg/dL, and it correlates with muscle mass. It can be influenced by high protein diet, supplements, and muscle breakdown.

125
Q

Why is having a baseline serum creatinine important in acute monitoring?

A

It is important for acute monitoring as serum creatinine (SC) is inversely related to GFR.

In acute cases, a doubling of SC can mean a drop in GFR by 50%.

126
Q

What is the role of the Renin-Angiotensin-Aldosterone system (RAAS)?

A

RAAS increases sodium and water reabsorption, which helps regulate volume and blood pressure.

127
Q

How does Atrial Natriuretic Peptide (ANP) function in the kidneys?

A

ANP is secreted from cardiac atria and binds to receptors in the kidney, leading to increased sodium and water excretion to decrease blood volume and pressure.

128
Q

How do the kidneys regulate pH balance?

A

The kidneys regulate pH balance by the reabsorption and excretion of bicarbonate (HCO3-) and hydrogen ions (H+).

129
Q

What is Erythropoietin’s (EPO) role in renal function?

A

EPO is involved in red blood cell (RBC) production, and renal patients often require EPO supplementation due to kidney dysfunction.

130
Q

What role does Calcitriol play in renal function?

A

Calcitriol is crucial for maintaining serum calcium levels.

131
Q

What is the role of prostaglandins (PGs) in the kidneys?

A

Prostaglandins act as inflammatory modulators and have vasodilatory effects that help maintain renal blood flow.

132
Q

How are the kidneys involved in glucose regulation?

A

The kidneys contribute to gluconeogenesis and are responsible for the filtration and reabsorption of glucose.

133
Q

What is the normal range for Blood Urea Nitrogen (BUN)?

A

The normal range for BUN is 10-20 mg/dL.

134
Q

What does a low BUN indicate?

A

Low BUN could indicate malnutrition or a volume-diluted state.

135
Q

What could cause a high BUN level?

A

High BUN could be due to a high protein diet, dehydration, GI bleed, trauma, or muscle wasting.

136
Q

What is the normal BUN:Creatinine ratio and what does it signify?

A

The normal BUN:Creatinine ratio is 10:1, and it’s a good measure of hydration status because BUN is reabsorbed and creatinine is not.

137
Q

What does proteinuria indicate and what is the normal range?

A

Normal proteinuria is less than 150 mg/dL. More than 750 mg/day could suggest glomerular injury or a urinary tract infection (UTI).

138
Q

What does the specific gravity of urine measure and what is the normal range?

A

Specific gravity (1.001-1.035) compares the weight of 1ml urine to 1ml distilled water and measures the nephron’s ability to concentrate urine.

139
Q

What should be considered when assessing a patient’s hydration status?

A

Consider the big picture, including history and physical exam, along with orthostatic pressure changes.

140
Q

Which lab changes might you see with dehydration?

A

Decreased base excess (↓BE) and increased lactate levels may be indicative of volume loss.

141
Q

What is a late sign of volume loss in renal assessment?

A

A drop in urine output (UOP) is a late sign of volume loss.

142
Q

What is the normal range for urine output?

A

Normal UOP is 30 ml/hr or 0.5-1 ml/kg/hr.

143
Q

How is oliguria defined?

A

Oliguria is defined as less than 500 mL of urine produced in 24 hours.

144
Q

What does a compressed/collapse IVC indicate?

What other way could you have to patient do to determine fluid responsiveness?

A

50% collapse = Dehydration

Passive leg raise to determine fluid responsiveness

145
Q

How can ultrasound (US) be used in assessing volume status?

A

Ultrasound is used to assess the inferior vena cava (IVC) for changes in diameter that correlate with volume status.

Slide 28 - extra info added by ChatGPT

146
Q

What do CVP and RAP indicate in volume monitoring?

A

Central venous pressure (CVP) and right atrial pressure (RAP) are indicators of right-sided heart pressures and can reflect fluid status.

Slide 28 - extra info added by ChatGPT

147
Q

Why are LAP and PCWP important in renal assessment?

A

Left atrial pressure (LAP) and pulmonary capillary wedge pressure (PCWP) are important as they can be powerful stimuli for renal vasoconstriction, affecting kidney function.

Slide 28 - extra info added by ChatGPT

148
Q

What does pulmonary artery pressure (PAP) indicate?

A

Pulmonary artery pressure (PAP) can indicate fluid overload, especially in the context of heart failure.

Slide 28 - extra info added by ChatGPT

149
Q

What does stroke volume variation (SVV) measure?

A

SVV compares inspiratory vs. expiratory pressure to assess fluid responsiveness, particularly in ventilated patients with sinus rhythm.

Slide 28 - extra info added by ChatGPT

150
Q

Over what time period does acute kidney injury develop?

A

AKI develops over hours to days.

151
Q

What percentage of hospitalized and ICU patients are affected by AKI?

A

AKI affects 20% of hospitalized patients and 50% of ICU patients.

152
Q

What are common causes of AKI?

A

AKI can be caused by hypotension/hypovolemia and nephrotoxins.

153
Q

What is azotemia and its significance in AKI?

A

Azotemia is the buildup of nitrogenous waste products such as urea and creatinine and is a hallmark of AKI.

154
Q

What is the mortality rate of AKI with multi-system organ failure (MSOF) requiring dialysis?

A

AKI with MSOF requiring dialysis carries a mortality rate greater than 50%.

155
Q

Can AKI be reversible and what intervention may be used?

A

AKI is reversible with timely interventions and may be managed with Continuous Venovenous Hemodiafiltration (CVVHD) to get through temporary insults.

156
Q

Risk Factors of AKI:

A
  • Pre-existing renal disease
  • Advanced age
  • CHF
  • PVD
  • Diabetes
  • Sepsis (hypotension)
  • Jaundice
  • Major operative procedures
  • IV Contrast
157
Q

What serum creatinine changes meet the AKI diagnostic criteria?

A

An increase in serum creatinine by 0.3 mg/dL within 48 hours or an increase by 50% within 7 days.

158
Q

What changes in creatinine clearance indicate AKI?

A

A decrease in creatinine clearance by 50%.

159
Q

Is oliguria always present in AKI?

A

Abrupt onset of oliguria is a diagnostic criterion, although it is not always seen in AKI.

160
Q

Can AKI be asymptomatic?

A

Yes, AKI can be asymptomatic.

161
Q

What general symptoms might a person with AKI experience?

A

Malaise and hypotension (HoTN) can be symptoms of AKI.

162
Q

What are the volume status symptoms associated with AKI?

A

Patients may present as hypovolemic or hypervolemic.

163
Q

Prerenal Azotemia Causes:

A

Pre-renal= ↓ renal perfusion

Hemorrhage
GI fluid loss
Trauma
Surgery
Burns
Cardiogenic shock
Sepsis
Aortic clamping
Thromboembolism

164
Q

Renal Azotemia Causes:

A

Renal = nephron injury

Acute glomerulonephritis
Vasculitis
Interstitial nephritis
Acute Tubular Necrosis (ATN)
Contrast dye
Nephrotoxic drugs
Myoglobinuria

165
Q

Postrenal Azotemia Causes:

A

Post-renal = outflow obstruction (easiest to treat)

Nephrolithiasis
Benign Prostatic Hyperplasia (BPH)
Clot retention
Bladder carcinoma

166
Q

What is the prevalence of pre-renal azotemia in AKI cases?

A

Pre-renal azotemia is the most common form of AKI, accounting for half of hospital-acquired AKI cases.

167
Q

How can anesthesia medications affect renal blood flow?

A

Anesthesia medications, along with volume and blood loss, can lead to decreased renal blood flow (RBF).

168
Q

What is the typical BUN:Cr ratio in pre-renal AKI?

A

In pre-renal AKI, the BUN:Creatinine ratio is greater than 20:1.

169
Q

Is pre-renal azotemia reversible?

A

Yes, pre-renal azotemia is usually reversible as it’s often a volume issue.

170
Q

: What is the relationship between pre-renal azotemia and acute tubular necrosis (ATN)?

A

Pre-renal azotemia is the most common cause of ATN if not reversed, as the condition can progress from pre-renal to renal azotemia.

171
Q

What happens to sodium and water reabsorption in pre-renal azotemia?

A

In pre-renal azotemia, the body is still reabsorbing sodium and water efficiently.

172
Q

What is renal azotemia?

A

Renal azotemia is intrinsic renal disease and is a potentially reversible condition along a continuum of renal injury

Renal AKI BUN:Cr decreased from pre-renal AKI (>20)

173
Q

What are the treatments for pre-renal azotemia?

A

Treatment includes restoring renal blood flow with fluids, mannitol, diuretics, maintaining mean arterial pressure (MAP), and possibly using pressors.

174
Q

What are late symptoms of renal azotemia related to glomerular filtration rate?

A

Decreased GFR is a late symptom in renal azotemia, indicating significant impairment in kidney function.

175
Q

How does renal azotemia affect blood urea nitrogen (BUN) levels?

A

There is decreased urea reabsorption in the proximal tubule, leading to decreased BUN.

176
Q

What happens to blood creatinine levels in renal azotemia?

A

Decreased creatinine filtration leads to increased blood creatinine levels.

177
Q

What is the typical BUN:Creatinine ratio in renal azotemia?

A

The BUN:Creatinine ratio often falls below 15:1 in cases of renal azotemia.

178
Q

What is the primary cause of post-renal azotemia?

A

Post-renal azotemia is caused by outflow obstruction of urine from the kidneys.

179
Q

What effect does post-renal azotemia have on nephron tubular pressure?

A

It leads to increased nephron tubular hydrostatic pressure.

180
Q

Which diagnostic tool is useful for post-renal azotemia?

A

Renal ultrasonography is useful for identifying the cause and location of the obstruction.

181
Q

How does the duration of obstruction affect reversibility in post-renal azotemia?

A

The reversibility of post-renal azotemia is inversely related to the duration of the obstruction.

182
Q

What is the treatment for post-renal azotemia?

A

The treatment involves removing the obstruction if possible.

183
Q

What can prolonged obstruction lead to in post-renal azotemia?

A

Persistent obstruction can lead to damage in the tubular epithelium.

184
Q

What causes prerenal AKI and what are its features?

A

Prerenal AKI is due to true volume loss or decreased effective arterial blood volume. Causes include hypovolemia, decreased arterial supply due to conditions like cardiorenal or hepatorenal syndrome, and certain drugs.

It’s characterized by a

BUN/Cr ratio > 20:1
FeNa (fractional excretion of Na) < 1%
FEurea (Fractional excretion of Urea) < 35%.
Urine [Na] <20
Seditment: Bland and hyaline casts

Slide 38

185
Q

What causes intrinsic AKI and what are its features?

A

Intrinsic AKI is due to damage to the glomeruli, tubules, or interstitium. Causes include ATN, ischemia, toxic substances, and inflammation.

It’s characterized by a
BUN/Cr ratio < 20:1
FeNa > 2% for ATN (varies for other causes)
FEurea > 50% for ATN.
Urine [Na] >20
Sediment - ATN=Muddy, brown casts; AIN= WBC casts+ Neg Ucx; GN= RBC casts; Abx/chol. emboli= urine E.O.s; NSAIDS= lymphocytes

Slide 38

186
Q

What are the key diagnostic markers for different types of AKI?

A

Urine sediment in

-prerenal AKI is typically bland with hyaline casts.
-In intrinsic AKI, the urine sediment can show muddy brown casts for ATN and White blood cell casts for acute interstitial nephritis (AIN), among others.
- postrenal AKI urine sediment might contain blood.

187
Q

Neurological complications of AKI

A

Related to protein/amino acids buildup in blood
Uremic Encephalopathy (Dialysis improves)
Mobility disorders
Neuropathies
Myopathies
Seizures
Stroke

188
Q

What are the cardiovascular complications associated with AKI?

A

Cardiovascular complications can include systemic hypertension, left ventricular hypertrophy (LVH), congestive heart failure (CHF), pulmonary edema, uremic cardiomyopathy, arrhythmias, and pericarditis with or without effusion.

189
Q

What is the typical progression of cardiovascular complications in AKI?

A

The typical order of incidence is hypertension (HTN) → LVH → CHF → ischemic heart disease → anemic heart failure → rhythm disturbances → pericarditis with or without effusion → cardiac tamponade → uremic cardiomyopathy.

190
Q

What type of anemia is associated with AKI?

A

Anemia related to AKI is due to decreased erythropoietin (EPO) production, reduced red blood cell production, and decreased red blood cell survival.

191
Q

How does AKI affect platelet function?

A

AKI can lead to platelet dysfunction; platelet function assays or thromboelastography (TEG) are valuable for assessing this condition.

192
Q

What role does von Willebrand factor (vWF) play in AKI?

A

vWF is disrupted by uremia in AKI, which can affect coagulation.

193
Q

What is the role of DDAVP in the management of hematological complications in AKI?

A

Prophylactic Desmopressin (DDAVP) can increase vWF and Factor VIII levels, which helps improve coagulation in patients with AKI.

194
Q

Why might coagulation factors be affected in AKI?

A

Uremic conditions in AKI disrupt normal coagulation factor function, necessitating interventions like DDAVP to restore effective coagulation.

195
Q

What electrolyte imbalance is commonly seen in AKI?

A

Hyperkalemia is a common electrolyte imbalance in AKI due to decreased excretion by the kidneys.

196
Q

What fluid and electrolyte imbalances are associated with AKI?

A

Water and sodium imbalances are frequent in AKI, leading to conditions such as fluid overload or depletion.

197
Q

Why might hypoalbuminemia occur in AKI?

A

Hypoalbuminemia can occur if the kidneys allow albumin to escape, which may happen in AKI due to altered glomerular permeability.

198
Q

What type of acid-base imbalance is often seen in AKI?

A

Metabolic acidosis is common in AKI because the kidneys cannot excrete acid effectively.

199
Q

How does AKI contribute to malnutrition?

A

AKI can lead to malnutrition due to losses of nutrients and protein through impaired kidney function.

200
Q

What is the connection between AKI and hyperparathyroidism?

A

Hyperparathyroidism may develop as the parathyroid glands go into overdrive in an attempt to stimulate the kidneys to reabsorb calcium, often a compensatory response to the kidneys’ impaired function in AKI.

201
Q

What initial management steps should be taken for AKI in the context of anesthesia?

A

Correct fluid, electrolyte, and acid/base status to prevent further renal injury.

202
Q

What type of fluid is preferred for AKI management during anesthesia and why?

A

Normal Saline (NS) is preferred due to the absence of potassium, which is important for patients at risk of hyperkalemia.

203
Q

What should be considered when using colloids in AKI?

A

Be cautious with colloids due to the risk of exacerbating fluid overload and affecting osmolarity.

204
Q

What is the target for mean arterial pressure (MAP) maintenance during anesthesia in AKI?

A

Maintain MAP at least 20% of baseline to ensure adequate renal blood flow.

205
Q

What role do vasopressors play in managing AKI during anesthesia?

A

Vasopressors, such as Vasopressin and Alpha-agonists, may be used to maintain MAP and renal perfusion.

206
Q

Why is prophylactic sodium bicarbonate administered during anesthesia in the context of AKI?

A

It helps decrease the formation of free radicals and prevents acute tubular necrosis (ATN) from progressing to renal failure.

207
Q

How does Vasopressin aid in managing AKI compared to alpha agonists?

A

Vasopressin preferentially constricts the efferent arteriole, which is more effective than alpha agonists for maintaining renal blood flow.

208
Q

What consideration should be given to hemodynamic monitoring in patients with kidney issues?

A

There should be a low threshold for invasive hemodynamic monitoring to closely track and manage blood pressure and fluid status.

208
Q

What is the preference regarding dialysis before surgery?

A

Prefer preoperative dialysis to optimize fluid and electrolyte balance, especially if the patient is already on a dialysis regimen

209
Q

What lab values are particularly important to have before anesthesia in patients with kidney issues?

A

Recent laboratory values, especially potassium (K+), should be reviewed to manage risks of electrolyte imbalance during anesthesia.

210
Q

```

What equipment should be readily available for patients with kidney issues undergoing anesthesia?

A

Point-of-care (POC) equipment should be available for immediate lab testing and monitoring during the perioperative period.

211
Q

How should drug dosing be approached in these patients?

A

Drug dosing should be tailored to the individual’s renal function, avoiding drugs with active metabolites, those that decrease renal blood flow (RBF), and renal toxins.

212
Q

```

What may be required if the patient is unable to clear drugs on their own?

A

Post-op dialysis

213
Q

What is CKD?

A

CKD stands for chronic kidney disease. It’s a progressive condition where kidney function declines over time.

214
Q

How does CKD commonly present?

A
  • CKD patients often undergo surgeries for dialysis access
  • May require procedures like toe/foot surgeries due to diabetes complications.
  • They might also have non-healing wounds and frequent healthcare visits.
215
Q

CKD chart to look at:

A
216
Q

What is the GFR range for Stage 1 CKD?

A

Stage 1 CKD is characterized by kidney damage with normal or increased GFR (>90 mL/min/1.73m²).

217
Q

What is the GFR range for Stage 2 CKD?

A

Stage 2 CKD involves kidney damage with mildly decreased GFR (60-89 mL/min/1.73m²).

218
Q

What is the GFR range for Stage 3 CKD?

A

Stage 3 CKD indicates moderately decreased GFR (30-59 mL/min/1.73m²).

219
Q

What is the GFR range for Stage 4 CKD?

A

Stage 4 CKD is characterized by severely decreased GFR (15-29 mL/min/1.73m²).

220
Q

What is the GFR range for Stage 5 CKD?

A

Stage 5 CKD represents kidney failure with a GFR of less than 15 mL/min/1.73m².

221
Q

What happens to GFR with age?

A

GFR decreases by 10 per decade starting from age 20.

222
Q

What cardiovascular effects are associated with CKD?

A

CKD commonly leads to systemic hypertension, which is both a cause and consequence of the disease.

223
Q

What contributes to the development of systemic hypertension in CKD?

A
  • Retention of sodium and water, leading to volume overload leading to the activation of the renin-angiotensin-aldosterone system (RAAS).
224
Q

What are the first-line treatments for hypertension in CKD?

A

Thiazide diuretics are often the first-line treatment for hypertension in CKD patients.

Additionally, ACE inhibitors (ACE-I) or angiotensin II receptor blockers (ARBs) may be necessary.

225
Q

How do ACE inhibitors (ACE-I) and angiotensin II receptor blockers (ARBs) affect CKD?

A

ACE-I and ARBs are often used in CKD to:

  • Decrease systemic blood pressure and glomerular pressure
  • Reduce proteinuria by decreasing glomerular hyperfiltration
  • Slow the progression of glomerulosclerosis
226
Q

Why are ACE-I/ARBs typically withheld on the day of surgery for CKD patients?

A

ACE inhibitors (ACE-I) and angiotensin II receptor blockers (ARBs) are withheld on the day of surgery in CKD patients to reduce the risk of profound hypotension during anesthesia induction.

227
Q

What interventions may be necessary if ACE-I or ARBs are continued up to the day of surgery in CKD patients?

A

If ACE inhibitors (ACE-I) or angiotensin II receptor blockers (ARBs) are continued up to the day of surgery in CKD patients:

  • Vasopressin
  • Norepinephrine
  • Epinephrine

may be needed to counteract the potential risk of hypotension.

228
Q

What cardiovascular effects are associated with CKD?

A

CKD is associated with dyslipidemia, often characterized by elevated triglycerides (>500 mg/dL) and LDL cholesterol (>100 mg/dL).

229
Q

What is a common risk associated with dyslipidemia in CKD?

A

CKD patients are predisposed to “silent MI” (silent myocardial infarction), which may occur without typical symptoms due to peripheral and autonomic neuropathy, leading to blunted sensation.

230
Q

Which populations are at high risk for silent MI in CKD?

A

Women and individuals with diabetes are high-risk populations for silent myocardial infarction in the context of CKD.

231
Q

What hematologic effects are associated with CKD?

A

CKD commonly leads to anemia, which is often responsive to exogenous erythropoietin therapy. The target hemoglobin level for CKD patients is typically around 10 g/dL.

232
Q

What are the considerations for platelet dysfunction in CKD?

A

CKD patients may experience platelet dysfunction, which can impact their coagulation status.

233
Q

What should be considered before transfusing blood in CKD patients?

A

Transfusion in CKD patients requires careful consideration of risks versus benefits. Excess hemoglobin can lead to sluggish circulation.

Acidosis and hyperkalemia is also associated with blood transfusions.

234
Q

Indications to consider dialysis:

A
  • Volume overload
  • Severe hyperkalemia
  • Metabolic acidosis
  • Symptomatic uremia
  • Failure to clear medications
235
Q

What should be considered regarding dialysis modalities?

A

Hemodialysis (HD) is more efficient than peritoneal dialysis (PD).

However, PD may be more suitable for patients who can’t tolerate fluid shifts, such as those with poor cardiac function.

236
Q

What is the most common side effect of hemodialysis?

A

Hypotension is the most common side effect of hemodialysis, which may occur due to rapid fluid removal during the procedure.

237
Q

What is a leading cause of mortality in dialysis patients?

A

Infection is a leading cause of mortality in dialysis patients due to their impaired immune system and delayed wound healing.

238
Q

What considerations are important for anesthesia in patients with end-stage renal disease (ESRD)?

A

Anesthesia in ESRD patients requires:

  • Assessing stability
  • Monitoring body weight pre/post dialysis (within 24 hours of surgery)
  • Evaluating blood pressure control
  • Determining whether medications should be continued
  • Managing glucose levels and A1C
  • Taking aspiration precautions, especially in patients with diabetes and obesity.
239
Q

What precautions should be taken for uremic bleeding in ESRD patients undergoing anesthesia?

A

Uremic bleeding risk in ESRD patients requires:

  • Assessing normal platelet count & function, PT, and PTT

Treatment options may include:
- Cryoprecipitate
- Factor VIII
- von Willebrand factor (vWF)
- Desmopressin, which peaks at 2-4 hours and lasts 6-8 hours

  • Tachyphylaxis should also be considered.
240
Q

How are many anesthetic agents eliminated in patients with renal impairment?

A

Many anesthetic agents are lipid-soluble and are reabsorbed by renal tubular cells, leading to prolonged effects in patients with renal impairment.

241
Q

What type of anesthetic agents are preferred in patients with renal impairment?

A

In patients with renal impairment, it is preferable to use anesthetic agents that are not dependent on renal elimination to avoid potential toxicity and prolonged effects.

242
Q

What characteristics make for the best neuromuscular blocking agents (NMB) in patients with renal impairment?

A

The best neuromuscular blocking agents (NMB) for patients with renal impairment are those that do not rely on renal elimination, as they can be safely used without the risk of accumulation and prolonged effects.

243
Q

Which 2 analgesic medications mentioned in the PPT should be avoided in patients with renal impairment?

A

avoid analgesic medications such as morphine and Demerol (meperidine) due to the risk of accumulation of active metabolites and potential toxicity.

244
Q

How are lipid insoluble drugs eliminated in patients with renal impairment?

A

Some medications are eliminated unchanged in urine, leading to prolonged duration of action (DoA) and increased risk of accumulation in patients with renal impairment.

245
Q

How is renal dosing typically determined for medications?

A

Renal dosing of medications is usually based on glomerular filtration rate (GFR)

246
Q

Give examples of medications that require renal dosing.

A
  • Thiazide diuretics
  • Loop diuretics
  • Digoxin
  • Many antibiotics
247
Q

Name 2 induction drugs that are primarily eliminated by the kidneys.

A

Phenobarbital

Thiopental

248
Q

Give 2 examples of muscle relaxants eliminated by the kidneys.

A

Pancuronium

Vecuronium

249
Q

What are 2 cholinesterase inhibitors that undergo renal excretion?

A

Edrophonium

Neostigmine

250
Q

Name 5 cardiovascular drugs that are excreted renally.

A

Atropine
Digoxin
Glycopyrrolate
Hydralazine
Milrinone

251
Q

Name 4 antimicrobials are primarily excreted by the kidneys?

A

Aminoglycosides
Cephalosporins
Penicillins
Vancomycin

252
Q

What morphine metabolites are excreted in the urine? by how much?

A
  • morphine-3 glucuronide
  • morphine-6 glucuronide
  • 40%
253
Q

What is normeperedine?

What are the main adverse effects of Normeperidine?

A

Active metabolite of meperedine

The main adverse effect of Normeperidine is neurotoxicity, which can manifest as nervousness, tremors, muscle twitches, and seizures.

254
Q

How does Normeperidine accumulate in the body?

What is its parent drug elimination half-life?

What is normeperedine’s elimiation half-life?

A

Multiple doses of meperidine result in the accumulation of Normeperidine due to its long elimination half-life (15-30 hours) compared to meperidine (2-4 hours).

255
Q

What is the recommended potassium level for elective surgery?

A

Potassium should be less than 5.5 mEq/L for elective surgery.

256
Q

What is the recommendation for dialysis patients before elective surgery?

A

Dialysis patients should undergo dialysis within 24 hours preceding elective surgery.

257
Q

Why is aspiration prophylaxis important, especially in patients with diabetes mellitus (DM)?

A

Aspiration prophylaxis is crucial, especially in patients with diabetes mellitus (DM), to prevent the risk of aspiration during surgery.

258
Q

How does anesthesia and surgery affect renal blood flow (RBF) and glomerular filtration rate (GFR)?

A

Anesthesia and surgery decrease renal blood flow (RBF) and glomerular filtration rate (GFR).

259
Q

How does blood loss affect renal blood flow (RBF)?

A

Blood loss activates baroreceptors, leading to increased sympathetic nervous system (SNS) outflow.

Catecholamines activate α1-receptors, causing afferent arteriole constriction and decreased renal blood flow (RBF).

260
Q

What are the consequences of longer periods of hypotension during surgery?

A

Longer periods of hypotension, such as during cross-clamping, hemorrhage, or sepsis, lead to decreased renal blood flow (RBF).

261
Q

What clinical signs indicate hypovolemia in the context of hyponatremia?

A

Decreased skin turgor, flat neck veins, dry mucous membranes, orthostatic hypotension, tachycardia, and oliguria.

262
Q

With a urinary sodium concentration greater than 20 in a hypovolemic patient, what is the likely cause of hyponatremia?

A

Renal losses, which can be due to:

  • Salt-losing nephritis
  • Diuretic excess
  • Osmotic diuresis
  • Mineralocorticoid deficiency
  • Ketonuria
  • Renal tubular acidosis
  • Metabolic alkalosis
263
Q

What does a urinary sodium concentration less than 20 indicate in a hyponatremic and hypovolemic patient?

A

Extrarenal losses, such as those from vomiting, diarrhea, third space losses (like burns, pancreatitis, or muscle trauma).

264
Q

What are the clinical signs of euvolemia in hyponatremia?

A

The absence of signs of volume depletion or volume overload; patients appear clinically normal in terms of volume status.

265
Q

In euvolemic hyponatremia, what does a urinary sodium concentration above 20 suggest?

A

Causes such as:

  • Glucocorticoid deficiency
  • Hypothyroidism
  • High sympathetic drive
  • Drugs
  • Syndrome of Inappropriate Antidiuretic Hormone secretion (SIADH).
266
Q

For euvolemic hyponatremia with a urinary sodium concentration less than 20, what is the probable cause?

A

Salt-restricted diet.

267
Q

What are the signs of hypervolemia in a patient with hyponatremia?

A

Peripheral edema, rales (crackles heard in the lungs), and ascites.

268
Q

In hypervolemic hyponatremia, what does a urinary sodium concentration above 20 indicate?

A

Renal losses due to conditions like acute renal failure or chronic renal failure.

269
Q

With a urinary sodium concentration less than 20 in a hypervolemic patient, what could be the causes of hyponatremia?

A

Avid sodium reabsorption due to conditions such as nephrotic syndrome, cardiac failure, or cirrhosis.

270
Q

In the context of hypovolemia and hyponatremia, what does a urinary sodium (UNa) concentration less than 20 mmol/L suggest?

A

It suggests extrarenal losses due to conditions such as vomiting, diarrhea, third-space losses (like burns, pancreatitis, or muscle trauma).

271
Q

When assessing a euvolemic patient with hyponatremia, what does a urinary sodium (U_Na) concentration less than 20 mmol/L suggest when paired with symptoms like decreased skin turgor and dry mucous membranes?

A

It suggests a salt-restricted diet

272
Q

What does a urinary sodium (U_Na) concentration greater than 20 mmol/L indicate in a hypervolemic patient with hyponatremia and signs like peripheral edema and ascites?

A

Renal losses due to acute renal failure or chronic renal failure.

273
Q

In a hypervolemic patient with hyponatremia, what does a urinary sodium (U_Na) concentration less than 20 mmol/L indicate?

A

Avid sodium reabsorption, which can be seen in conditions such as nephrotic syndrome, cardiac failure, or cirrhosis.

274
Q

What clinical signs suggest hypovolemia in the context of hypernatremia?

A
  • Decreased skin turgor
  • Flat neck veins
  • Dry mucous membranes
  • Orthostatic hypotension
  • Tachycardia
  • Oliguria.
275
Q

In a hypovolemic patient with hypernatremia, what does a urinary sodium (U_Na) concentration greater than 20 mmol/L indicate?

A

Renal salt and water loss due to causes such as
- Osmotic diuretics
- Loop diuretics
- Postrenal obstruction
- Intrinsic renal disease
- Pofound glycosuria

276
Q

For a hypovolemic patient with hypernatremia, what does a urinary sodium (U_Na) concentration less than 20 mmol/L suggest?

A

Extrarenal salt and water loss, potentially from diarrhea, GI fistulas, burns, or sweating.

277
Q

What does euvolemia in a patient with hypernatremia indicate about their water loss?

A

It suggests renal water loss due to diabetes insipidus (central, nephrogenic, or gestational)

or

extrarenal water loss from insensible losses through the respiratory tract or skin.

278
Q

What are the signs of hypervolemia in a patient with hypernatremia?

A

Peripheral edema, rales, and ascites.

279
Q

In a hypervolemic patient with hypernatremia and a urinary sodium (U_Na) concentration greater than 20 mmol/L, what is the likely cause?

A

Sodium gains due to conditions such as
- Hyperaldosteronism
- Cushing’s syndrome
- Hypertonic dialysis
- Intravenous sodium bicarbonate
- Sodium chloride tablets
- Hypertonic saline enemas
- Hypertonic alimentation
- Salt water drowning

280
Q

What are the possible causes of renal salt and water loss leading to hypovolemic hypernatremia with a urinary sodium concentration greater than 20 mmol/L?

A
  • Osmotic diuretic use
  • Loop diuretic use
  • Postrenal obstruction
  • Intrinsic renal disease
  • Profound glycosuria
281
Q

What are some causes of extrarenal salt and water loss leading to hypernatremia with a urinary sodium concentration less than 20 mmol/L in a hypovolemic patient?

A
  • Diarrhea
  • Gastrointestinal fistulas
  • Burns
  • Excessive sweating
282
Q

In the context of euvolemia with hypernatremia, what are the causes of renal and extrarenal water loss when the urinary sodium concentration is variable?

A

Renal water loss can be due to diabetes insipidus (central, nephrogenic, or gestational), and extrarenal water loss can be due to insensible losses from the respiratory tract or skin.

Assessment '24 - Mordecai (10 decks)

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