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GU > Acid/Base AKI - Exam 1 > Flashcards

Acid/Base AKI - Exam 1 Flashcards

1
Q

a drop in osmotic pressure will lead to an increase in what 4 things? _____ will be decreased

A

Increased:
Sympathetic nervous system output
RAAS activity
ADH levels
Thirst

decrease: ANP

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2
Q

an increase in osmotic pressure will lead to an decrease in what 4 things? _____ will be decreased

A

decreased:
Sympathetic nervous system output
RAAS activity
ADH levels
Thirst

increased: ANP -> Atrial natriuretic peptide (ANP)

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3
Q

What is the net goal of normal balance of sodium and water?

A

Net Goal = Modify (1) water intake, (2) water and Na retention by the kidney, and (3) vasoconstriction

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4
Q

loss of body fluids
often accompanied by decreased fluid intake

What am I?

A

isotonic fluid volume deficit

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5
Q

What is the treatment for isotonic fluid volume deficit? What can happen if tx is given in excess? What do you give to combat this?

A

0.9% NS

NS in excess can lead to hyperchloremic metabolic acidosis. Avoid being overly aggressive with administration!

Use bicarb solution if needed

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6
Q

inability to get rid of water and/or sodium, or excess water/sodium intake usually due to overadministration of IV fluids.
edema
bounding pulses

What am I?
What is the tx?

A

Isotonic Fluid Volume Excess

IV Loop diuretics
persistent: dialysis
restrict fluid and sodium intake

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7
Q

fatigue
SOB
N/V
Hyperreflexia
carpopedal spasm
+ Trousseau or Chvostek sign

What am I? What is the underlying cause? What is also commonly seen in conjuction?
What is the tx?

A

Hyperphosphatemia

impaired renal excretion of phosphate

low calcium

limit phoshate intake
phosphate binders
avoid processed foods
restore renal function

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8
Q

What are some causes of hypokalemia? What organ system does it effect the most?

A

poor intake
**insulin
beta-agonists
**loop diuretics
alkalosis

muscles!! skeletal, smooth and CARDIAC

muscle weakness, fatigue, cramps, constipation, hypotension, palpitations, dysrhythmias

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9
Q

**What will the EKG look like on a pt with hypokalemia?

A

ECG - flattened T waves → prolonged QT → U wave → ST depression

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10
Q

When thinking about low potassium what other electrolyte do you also want to check? What are 2 other contributing factors towards hypokalemia?

A

always check magnesium level!!

Metabolic alkalosis
Medication adjustments

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11
Q

_____ is a very common complication of both AKI and CKD. Name some common causes

A

hyperkalemia

inadequate renal excretion
cellular breakdown
excessive/severe muscle contraction
ACE/ARB, Beta-blockers, excessive intake

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12
Q

**What does the EKG look like on a pt with hyperkalemia? What is a highlighted GI s/s?

A

ECG - peaked T waves → loss of P waves → widened QRS → sine wave

Diarrhea

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13
Q

What is the treatment for hyperkalemia? (IN ORDER)

A
  1. If cardiac/arrhythmia present: 10 mL of 10% calcium gluconate IV over 2-3 minutes with cardiac monitoring
  2. IV 10 U of regular insulin IV followed immediately by 40mL of 50% dextrose (D50W)- can add on inhaled albuterol
  3. remove K through 1 of 3 options:

GI cation exchangers Sodium polystyrene sulfonate (SPS, Kayexelate), zirconium cyclosilicate (Lokelma), patiromer (Veltassa)

Loop or thiazide diuretics if also volume overloaded

hemodialysis

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14
Q

You give 10 mL of 10% calcium gluconate IV over 2-3 minutes with cardiac monitoring to help reduce _____. How long does it take to go into effect? How long should it last?

A

hyperkalemia

Takes effect in 1-3 min

lasts 30-60 min

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15
Q

IV calcium gluconate potentiates cardiac toxicity of _____; consider
_____ of calcium if it must be used

A

digoxin

slower infusion

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16
Q

Why do you give insulin in hyperkalemia? How long does it take to go into effect? ______ is common to see after insulin is given. How do you combat this?

A

Rapid reduction of plasma K+ by forcing into cells

takes effect in 10-20 minutes, peaks in 30-60 minutes and lasts 4-6 hours

Hypoglycemia is common

Usually follow with 10% dextrose at 50-75 mL/h, glucose monitoring
Not necessary to give if glucose 250+ mg/dL

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17
Q

What is the MOA for GI cation exchangers? name the 3 common ones. Which one works the fastest? Which one is the cheapest?

A

Exchanges Na+ for K+ in GI tract, ￪ fecal K+ excretion

Sodium polystyrene sulfonate (SPS, Kayexelate) -> cheapest
zirconium cyclosilicate (Lokelma)- > fastest
patiromer (Veltassa)

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18
Q

What is the major SE of GI cation exchangers?

A

constipation, decreases magnesium and potassium

19
Q

for hyperkalemia tx which drug class diuretics is preferred? What is the most effective and reliable removal of potassium method?

A

LOOP!!

Hemodialysis

20
Q

_____ is low Na in the context of normal Sosm. What is the tx?

A

isotonic hyponatremia

tx: mainly focused on gradually correcting underlying cause and monitoring for changes in osmolality/tonicity

21
Q

____ is low Na in the context of high serum osmo. Why does this occur? What is the tx?

A

Hypertonic hyponatremia

Another osmotically active molecule is present (Glucose, radiocontrast, mannitol)

tx: mainly focused on gradually correcting underlying cause and monitoring for changes in osmolality/tonicity

22
Q

_____ is caused by inappropriate salt loss. What is the major medication contributor? What is an extrarenal cause? What is the tx? What is the tx for SEVERE?

A

Hypovolemic hyponatremia

V/D, burns, dehydration

diuretics

if not severe, IV rehydration with isotonic 0.9% NS will correct - raises serum Na by 1 mEq per L

severe: increase Na by 4-6 mEq/L as soon as possible. Hypertonic saline (3% saline in 100 mL IV bolus)

23
Q

______ in sodium is retained, but H2O retention is disproportionately larger than Na retention. Commonly seen in ______

A

Hypervolemic hyponatremia

nephrotic syndrome

24
Q

________ is commonly seen in SIADH, hypothyroidism, psychogenic polydipsia, beer potomania. ____ and ___ can help us have an idea of ADH activity

A

Euvolemic hyponatremia

UNa+ and Uosm

25
Q

What are s/s of hyponatremia? What will you see in chronic hyponatremia?

A

neuro in nature due to cerebral edema!

N/V, HA, confusion, lethargy
seizure, brainstem herniation, coma, death
May see muscle cramps or weakness, third spacing of fluid

If chronic hyponatremia (>48 h) LESS likely to have severe s/s

26
Q

in severe acute hyponatremia, what 2 additional things can be given alongside 3% saline. Give rationale behind each medication

A

May co-administer with a loop diuretic to avoid volume overload and/or desmopressin (dDAVP) to avoid osmotic demyelination syndrome

27
Q

What is the nonemergent tx of hyponatremia?

A

May use NS, slower infusion of hypertonic saline, and/or oral salt tablets

fluid restriction

Vasopressin receptor antagonists: conivaptan (Vaprisol) - IV
tolvaptan (Samsca) - oral

28
Q

Should a pt fluid restrict while on a vasopressin receptor antagonists? What are the 2 medications in this drug class? When should they be started? What is the monitoring?

A

NO!! fluid restriction is CI

conivaptan (Vaprisol) - IV
tolvaptan (Samsca) - oral

need to start/change dose in the hospital

**LFTs (due to hepatotoxicity), renal function, electrolytes

29
Q

______ loss of body water or inability to retain water appropriately, and/or excessive sodium intake

A

hypernatremia

30
Q

What does hypernatremia with low urine osmo suggest?

A

suggestive of diabetes insipidus (neurogenic or nephrogenic)

31
Q

What is the tx of hypernatremia?

A

correct underlying cause!!

fluid replacement- 1/2NS or D5W

restore renal function

32
Q

______ of sodium correction depends on _____ of abnormal labs. Acute? Chronic?

A

speed

duration

If acute (<48 hrs) - try to correct within 24 hours to avoid CNS damage

If chronic (>48 hrs) - correct more gradually at 6-12 mEq/L per 24 hrs

33
Q

What are the major causes of metabolic alkalosis?

A

increased acid loss due to vomiting

excess bicarb

abnormal renal excretion/absorption

34
Q

increased neuronal excitability
dizziness
panic
light-headedness
seizures
Muscle tetany
numbness/tingling
Chvostek and Trosseau signs
dysrhythmias
increased protein-binding to calcium

What am I?
What is the tx?

A

Metabolic Alkalosis

Antiemetics, decreasing or discontinuing GI suctioning
Reducing bicarbonate administration
Supplementing with fluids and electrolytes as needed
Tx of adrenal disease (Cushing’s or hyperaldosteronism) if present
Restoration of renal function

35
Q

What are the major causes of metabolic acidosis?

A

increased acid generation (ketoacidosis, acid ingestion)

loss of bicarb (diarrhea)

decreased renal acid excretion

36
Q

decreased neuronal excitability confusion
weakness
drowsiness
increased depth and rate of respiration
dysrhythmias
muscle weakness
increased thirst
decreased protein-binding to calcium

What am I?
What is the tx?

A

metabolic acidosis

bicarb: if pH is less than 7.2 IV bicarb

37
Q

What is chronic metabolic acidosis due to? give 3 examples. What is the tx?

A

GI loss, CKD, renal tubular acidosis

bicarb replacement and decreasing animal products especially animal proteins

38
Q

_____ hinders the kidney’s ability to excrete acid and regenerate ____

A

Low GFR

HCO3-

39
Q

a pt has AKI and metabolic acidosis, what is the tx?

A

dialysis or bicarb

40
Q

When is dialysis indicated in metabolic acidosis with AKI?

A

Severe oligouric or anuric AKI, volume overload, and severe metabolic acidosis (pH <7.1)

AKI and organic acidosis (lactic or keto) and pH < 7.1

41
Q

**The worse the _____ symptoms are, the greater the indication for at least _______

A

uremic

temporary dialysis

see screenshot for s/s of uremia

42
Q

What are the expanded indications for dialysis in AKI? What is highlighted factor to remember?

A

Hyperkalemia >6.5 or rapidly rising, refractory to therapy

aka hyperkalemia will kill them the fastest!!

43
Q
A

GU (13 decks)

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