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PHAR 255 Exam 1 > Renal 1 > Flashcards

Renal 1 Flashcards

1
Q

What are the functions of the kidneys? Examples?

A

Excretory
Filtration, secretion, (reabsorption), excretion

Endocrine
Renin, prostaglandins, kinins, erythropoeitin

Metabolic
Vitamin D activation, gluconeogenesis, insulin metabolism

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2
Q

What is renal functionsummarized as? (Roles of the kidney)

A

excretion + endocrine + metabolic functions

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3
Q

What are the excretory functions of the kidney?

A

Regulate fluid, electrolyte, and acid-base balance

Remove metabolic waste products & foreign chemicals from blood for urinary excretion

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4
Q

How are the excretory functions of the kidney accomplished?

A

Filtration
Reabsorption
Secretion

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5
Q

Describe glomerular filtration

A

Blood enters the glomerulus through the afferent arteriole

Glomerular filtration: Blood is filtered by hydrostatic pressure through the capillaries that form the glomerulus into the Bowman capsule (Non-selective process)

Blood leaves the kidney through the efferent arteriole

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6
Q

How much of filtrate is composed of the plasma? Composition of Filtrate (Basic)

A

The filtrate is composed of ~20% of the plasma entering the glomerulus

Composed mainly of fluids, electrolytes, small molecules

Excludes proteins and large molecules (e.g., blood cells, albumin)

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7
Q

Composition of Filtrate (Specific). Exceptions?

A

Glucose
Amino acids
(Undergo re-absorption; should see minimal amounts in urine under normal circumstances)

Electrolytes
Water
Urea
Uric acid
Creatinine
Protein (no large proteins; under normal circumstances there will be some proteins)

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8
Q

Describe the process of reabsorption

A

The movement of substances OUT of the renal tubules back INTO the blood capillaries

	FILTRATE → BLOOD
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9
Q

Purpose of Reabsorption

A

Prevents substances needed by the body from being lost in the urine

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10
Q

What molecules are reabsorbed by the kidney?

A

Reabsorption of water and solutes including:

NaCl, K+, HCO3-, urea, amino acids, glucose

100% of glucose and amino caids should be reabsorbed

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11
Q

Describe glucose reabsorption in diabetics

A

Under normal physiological conditions 100% of glucose should be reabsorped

In diabetics, the amount of glucose in the blood and ultimately filtrate exceeds the capacity to be reabsorped

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12
Q

Describe the process of Na+ and H20 reabsorption

A

Water reabsorption occurs through an osmotic gradient

Where Na+ goes, H2O will go with it

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13
Q

How much of the filtrate is excreted in the urine?

A

Less than 1% of the filtrate is excreted

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14
Q

Describe the process of secretion

A

Substances move OUT of the blood and INTO the tubules where they mix with the water and other wastes and are converted into urine

BLOOD → FILTRATE

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15
Q

What substances undergo secretion?

A

Substances secreted include: H+, K+, uric acid, certain drugs

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16
Q

How are substances secreted?

A

Active transport mechanism (e.g., P-glycoprotein)

Diffusion across the membranes

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17
Q

Where in the kidney does reabsorption occur?

A

Bulk reabsorption, which is not under hormonal control, occurs largely in the proximal tubule.

Regulated reabsorption occurs in the collecting duct

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18
Q

Where does secretion occur in the kidney?

A

Proximal Tubule

Regulated Secretion Collecting Duct

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19
Q

Describe acid base balance in the body?How is this accomplished by the kidneys?

A

Body maintains pH within a narrow range (7.35-7.45) by regulating H+ concentration

Accomplished through filtration, reabsorption, secretion in kidney

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20
Q

What are some mechanisms of H+ concentration regulation in the body?

A

Mechanisms of H+ concentration regulation:
Lungs: alveolar ventilation of carbon dioxide

Kidney: hydrogen ion excretion, bicarbonate reabsorption, phosphate and ammonia buffer systems

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21
Q

Kidneys Regulation of acid base balance

A

Kidney is responsible for secreting acids (H+)

Kidney is responsible for reabsorbing bicarbonate (HCO3-)

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22
Q

How does the kidney respond to acidosis?

A

In response to excess acid, kidneys reabsorb all filtered bicarbonate and produces new bicarbonate

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23
Q

How does the kidney respond to alkalosis?

A

In response to too little acid, kidneys excrete bicarbonate to restore H+ concentration to normal

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24
Q

Examples of of specific substance excretion by the kidney

A

Responsible for the excretion of waste products produced from protein metabolism (uric acid) and from muscle contraction (creatinine)

Renal elimination of certain drugs

Removed by filtration and/or secretion

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25
Q

Briefly describe the endocrine functions of the kidney

A

Produces hormones involved in:

Blood pressure control

RBC production

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26
Q

What are some key mechanisms of renal blood pressure mechanisms?

A

Renin-Angiotensin-Aldosterone System (RAAS)

Antidiuretic hormone (ADH)

Atrial natriuretic peptide (ANP)

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27
Q

What is the main mechanims by which kidneys control blood pressure?

A

RAAS System

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28
Q

Describe the RAAS system?

A

Main mechanism by which the kidneys control blood pressure

For filtration to occur, hydrostatic blood pressure must be at a certain value

Renin is released from renal juxtaglomerular cells in response to decreased blood pressure

Indirectly, renin leads to:
Vasoconstriction
Sodium and water retention

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29
Q

Draw out the RAAS system?

A
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30
Q

What is the role angiotensin II?

A

Angiotensin II evokes vasoconstriction of the efferent arteriole, to increase glomerular hydrostatic pressure

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31
Q

What other important endogenous compounds maintain blood pressure? How?What do they also promote?

A

Prostaglandin E2 and I2

Produced by the kidney in response to decreased blood flow

Cause vasodilation, specifically of the afferent arteriole, to increase renal perfusion

Also promote the secretion of renin

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32
Q

Describe the relationship between renal function and NSAIDs?

A

Prostaglandin E2 and I2

Cause vasodilation, specifically of the afferent arteriole, to increase renal perfusion

–> Why NSAIDs decrease kidney function
–> NSAIDS limit the vasodilation leading to less blood flow

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33
Q

What is aldosterone? What is its mechanism?What are some other functions?

A

Secreted by the adrenal cortex in response to Angiotensin II

Primary role is to stimulate tubule reabsorption of sodium

This means sodium (salt) moves OUT of the kidney/renal tubule and INTO the blood/body
Wherever salt goes, water follows –> BP goes up

Indirectly:
Increases potassium excretion
Increases H+ excretion

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34
Q

What is antidiuretic hormone (ADH)? Mechanism?

A

Secreted by the posterior pituitary in response to increased blood sodium levels / low blood volume

Increases water permeability of the collecting ducts, promoting water reabsorption

Means water is going BACK into the BLOOD instead of being peed out

Thus, the kidney excretes a more concentrated urine (antidiuresis)

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35
Q

What is atrial naturietic peptide (ANP)?

A

Stored in the right atrium of the heart

Released in response to increased stretch of the heart muscle

Indicative of fluid overload

Elevated in heart failure

Opposes the actions of RAAS by causing vasodilation and increased renal excretion of sodium (opposite effect of aldosterone)

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36
Q

How do the kidneys regulate RBC production?

A

ERYTHROPOIETIN

Stimulates production of red blood cells (increase oxygen-carrying capacity of the blood)

90% produced in the kidneys by peritubular interstitial cells

Produced by the kidneys in response to decreased blood oxygen levels (anemia, hypoxia, etc.)

Deficient/lack of erythropoeitin production in chronic kidney disease (CKD) leads to anemia

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37
Q

What are the metabolic functions of the kidney?

A

Metabolism of endogenous compounds (e.g., insulin)
Vitamin D activation
Gluconeogenesis

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38
Q

Describe the process of vitamin D synthesis in the kidneys?

A
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39
Q

Describe vitamin D activation by the kidneys?

A

Vitamin D has to be activated by the liver and then the kidney before it can exert its effect

Cholecalciferol → calcidiol → calcitriol

In CKD, vitamin D activation is impaired

Leads to disruption of the calcium-phosphorus-parathyroid hormone balance and renal bone disease

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40
Q

Describe the process of gluconeogenesis in the kidney?

A

To make glucose from amino acids

Most of gluconeogenesis occurs in the liver, but some also occurs in the cortex of the kidney

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41
Q

Why do pharmacists check renal function?

A

Monitoring and early recognition of CKD
–> Monitoring the effect of drugs on slowing progression
–> Predict the time to onset of ESRD
–> Evaluating risk of complications

To adjust doses of medications excreted by the kidneys (renal dose adjustments)

Monitoring nephrotoxic medications

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42
Q

What is creatinine?

A

a by-product of muscle metabolism that is primarily eliminated by glomerular filtration

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43
Q

What is serum creatinine?

A

Concentration of creatinine in the blood

Endogenous substance

A way to measure the filtration rate

When GFR is low, SCr is increased

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44
Q

What does MDRD measure?

A

measures the GFR

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45
Q

What does CKD-EPI measure?What is it used for?

A

Glomerular filtration rate, new improved version of MDRD, more accurate estimates especially when GFR is >60 ml/min

Used for classifying the severity of kidney dx

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46
Q

What does the cockcroft-gault equation measure?

A

Creatinine Clearance; not GFR

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47
Q

What does the salazar corcoran measure?

A

Creatinine Clerance for Obese patients

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48
Q

What equation is used for making renal dose adjustments for medications?

A

Cockcroft-Gault most common measure for renal dose adjustments; increasing popularity to use eGFR for renal dose adjustments (more accurate estimate of someone’s true ability to eliminate drugs through the kidneys)

Need to be manually calculating when using Cockcroft-gault

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49
Q

T/F: The CKD-EPI equation is used to estimate kidney function in a patient receiving dialysis

A

False

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50
Q

What are some sources of error in GFR estimating using creatinine?

A
51
Q

What equations are used to calculate stable renal function?

A

Most patients with stable renal function = CKD-EPI and Cockcroft-Gault equation

–> To calculate CrCl for the purpose of DRUG/DOSE ADJUSTMENT, use COCKROFT-GAULT
–> To calculate eGFR to STAGE CKD, use CKD-EPI

In practice, check the drug monograph to see what equation to use for dose adjustments

52
Q

Are all kidney measurements 100% accurate?

A

NO KIDNEY MEASUREMENTS are 100% accurate –> all are estimates

53
Q

What is a new major update to the CKD-EPI equation?

A

Have removed ‘race’ from the equation

Impact: lower eGFR in patients who self-identify as Black race and higher eGFR in patients who self-identify as non-Black race

54
Q

In a new update to the CKD-EPI equation, what is the difference between indexed and non-indexed?

A

Indexed or Normalized
- Standardized to a BSA of 1.73m2
- Units: mL/min/1.73m2
- Recommended for CKD staging/progression

Non-indexed or Without Normalization
- Adjusted (calculated) according to the patient’s BSA
- Units: mL/min
- Consider for drug dosing (caution in morbidly obese patients, as can lead to overdosing)

55
Q

What is the Bedise Schwartz equation?

A

Pediatrics GFR

56
Q

An alternative to creatinine for calculation GFR is….

A

Cystatin C

57
Q

Urea as a test of kidney function

A
  • AKA Blood Urea Nitrogen (BUN) - produced as a break down product of protein
  • Filtered by the kidney but is also reabsorbed, therefore measurement underestimates GFR
  • Not strictly regarded as a renal function test, but increases in renal impairment
58
Q

What can elevate BUN?

A

dietary protein (falsely elevated BUN that has nothing to due with kidney function)

GI bleeding(Increased BUN due to ingestion of blood; protein)

hydration status (HIGH urea means LOW water; dehydration) – independent of kidney function

59
Q

Whatis BUN dependent on? BUN and GFR relationship

A

The production of urea depends on good liver function (liver for conversion piece) and the availability of protein

When GFR decreases, BUN goes up. However a high BUN may be indicative of something else

60
Q

Is protein often lost in the urine?

A

Normally, no/minimal protein is lost in the urine

61
Q

Anothermarker of kidney damage is…. What is this particularily indicative of?

A

Persistent ↑ in urine protein is a marker of kidney damage (“proteinuria” = bad) –> More specificially glomerular damage (filter)

62
Q

What does the type of protein lost in the urine depend on?

A

Type of protein lost in the urine depends on type of kidney damage:

↑ albumin excretion sensitive to kidney damage from diabetes, hypertension, glomerular diseases

↑ excretion of low molecular weight globulins in tubulointerstitial kidney diseases (kidney injury from toxins)

63
Q

What is proteinuria?What proteins does oit measure?

A

General term for presence of increased amounts of protein in the urine

Nonspecific: Albumin +/or other proteins

64
Q

What is albuminuria?What does it predict?

A

A small amount of albumin in the urine is normal

↑ levels are an early predictor of glomerular dysfunction (especially diabetic kidney disease)

65
Q

What test can be used to evaluate albuminuria?

A

Screening test is the urine albumin : creatinine ratio (ACR)

Mostly evaluating for albumin (the standard) rather than measuring proteinuria as a whole

WILL SEE INCREASE HERE (ESPECIALLY IN DIABETES) WITHOUT Decreases IN GFR

66
Q

Albumin Categoreiesin CKD and Values

A
67
Q

Are increases in proteinuria always associated with kidney dx?What is required here?

A

Transient increases not associated with kidney dx

NEED A REPEATED TEST IN 3 MONTHS TO SHOW THAT THESE ELEVATIONS ARE CONSISTENT SINCE ONE MEASURE CAN BE HIGH DUE TO A TRANSIENT CAUSE

68
Q

What are some potential causes for transient albuminuria?

A

Recent Major Exercise
Urinary Tract Infection
Febrile Illness
Decompensated Congestive Heart Failure
Menstruation
Acute Severe Elevation in Blood Glucose
Acute Severe Elevation in Blood Pressure

69
Q

What is urinanalysis?

A

Urinalysis – ”routine & microscopic” (R&M)
–> Provides info about the physical and chemical composition of urine

70
Q

What does urinalysis measure?

A

Colour, turbidity

Presence of cells, micro-organisms, “casts,” crystals
–> Granular casts, RBC casts, WBC casts

Urinary eosinophils → interstitial nephritis

pH analysis, specific gravity

Glucose, ketones → indicative of diabetes/DKA

Leukocyte esterase and nitrite → positive in UTIs

71
Q

What is urinanalysisused for?Example?

A

Narrow down the cause of kidney dx and detect things that may not have been found as they are asymptomatic

RBC’s that are dysmorphic –> As pass through structure of kidneys become disformed
–> If not dismorphic, mor elikely to be in later urinary tract (e.g. bladder)

72
Q

What urinary electrolytes used for?

A

Used to differentiate causes of AKI

73
Q

Urinanalysis criteria for CKD

A
74
Q

what are CASTS?

A

Cylindrical protein structure, assume this shape as formed in the tubules of the kidneys, found in the urine under a microscope

DO not always indicate kidney diseases (e.g. hytaline cast, granular cast in dehydrated healthy people)

WBC, RBC –> ANY CELLS –> pathological condition Should not see cells being filtered

75
Q

Define acute kidney injury (AKI)

A

A sudden decline in renal function (hours or days) as evidenced by changes in laboratory values (SCr, BUN, and urine)

76
Q

Can the CKD-EPI equation be used to estimate kidney function in someone experiencing an acute kidney injury?How is an AKI diagnosed?

A

NO

Developped in individuals with stable kidney function, not acutely changing
–> A lag time before serum creatinine rise in AKI

AKI diagnosed based off of urine output and serum creatinine

Urine production decreases with AKI

77
Q

How ca an acute kidney injury be classified?Can urine production always be used to diagnose AKI?

A

Anuric
less than 50 mL/day urine output

Oliguric
less than 500 mL/day urine output

Non-Oliguric
greater than 500 mL/day urine output

Urine Production decrease —> Dehydration
Urine Production Increase –> Diuretics

Urine volume can be misleading and not indicative of AKI in all cases

78
Q

What is the RIFLE criteria of an AKI?

A
79
Q

What is the AKIN criteria of an AKI?

A
80
Q

In regards to the classification of an AKI, what takes precedence?

A

Urine output takes precedence in RIFLE and AKIN criteria

81
Q

What do all staging systems depend on?

A

All staging systems depend on SCr and urine output as the main diagnostic criteria

Associated with the same inherent weaknesses

82
Q

Describe the changes noted in AKI regarding SCr and urine output. Why is this critical? How can we detect changes in SCr?

A

After development of AKI, may take up to 4 days before an ↑ in SCr is observed

The lag time may significantly delay the diagnosis of AKI and impact outcomes

↓ in urine output emerges earlier in AKI but is a non-specific marker

All criteria based on detecting CHANGE in SCr
Therefore, need to know the patient’s baseline!

83
Q

How does an AKI present sx wise?

A

Most patients with AKI are asymptomatic

Diagnosed based on laboratory data (↑SCr, BUN)
~50% are oliguric

Patients may present with:

Signs and symptoms of dehydration (pre-renal)
Malaise, anorexia, nausea, vomiting, pruritis (uremia)
Severe abdominal or flank pain (kidney stone?)
Decreased force of urine stream (obstruction)
Cola-coloured urine (blood?)
Excessive foaming of urine (protein in urine)
Sudden weight gain, edema

84
Q

What are some risk factors for an AKI?

A

Anything that ↓ blood flow to the kidneys

Pre-existing renal dysfunction (acute-on-chronic)

85
Q

Drugs account for what percentage of AKI’s?

A

DRUGS account for ~ 20% AKI cases!

86
Q

How are the causes of an AKI classfied?

A

Most commonly the cause is classified based on the location of the problem:

1) Pre-renal:
blood supply (including renal artery)

2) Intra-renal or Intrinsic:
tubules, glomerulus, interstitium, vasculature

3) Post-renal:
collecting tubule, ureter, bladder, urethra

87
Q

What is the most common cause of an AKI (classfication wise)?

A

Pre-renal - Most common cause of AKI (~60% cases)

88
Q

What is another name for pre-renal AKI’s?

A

prerenal azotemia

89
Q

What is the reason for the development of a pre-renal AKI?

A

Kidney not getting adequate blood supply to filter the blood (“hypo-perfusion”)

Kidneys themselves are healthy

Kidneys can modify the rate of filtration based of vasoconstriction or dilation of efferent/afferent

90
Q

In a pre-renal AKI, decreased kidney perfusion may be from:

A

Intravascular volume depletion (e.g., hemorrhage, dehydration, burns, diuretic therapy)
Decreased effective circulating volume (e.g., HF, cirrhosis)
Hypotension (e.g., vasodilating medications, septic shock)
Decreased glomerular filtration pressure (ACEi/ARBs + NSAIDs)

91
Q

How much of AKI’s are Intrinsic AKI’s?

A

25-35% AKI cases

92
Q

An intrinsic AKI is a result of…..due to….

A

Results from direct damage to the kidney

Due to ischemia, toxins, or disease

93
Q

What are the main types of an intrinsic AKI?

A

Acute tubular necrosis (tubule damage) – damage tubular endothelial cells – e.g., endogenous (myoglobin - Rhabomyolysis) or exogenous (aminoglycosides) toxins, ischemia

Acute interstitial nephritis- injury to interstitium around the tubules e.g., idiopathic hypersensitivity immune reaction to drugs (NSAIDs, penicillin), infection

Acute glomerulonephritis – glomerulus injury e.g., post-strep antigen-antibody complexes

Vascular kidney injury – e.g., renal artery stenosis, HTN

94
Q

Post-renal AKI’s account for how many AKI cases?

A

< 5% of all cases

Least common AKI

95
Q

What is a post-renal AKI? Where?

A

Obstruction to urinary flow anywhere in the urinary tract:

Urethral obstruction
Ureter obstruction (Would need both ureters)
Bladder neck obstruction

96
Q

What are some causes of a post-renal AKI?

A

Nephrolithiasis (kidney stones)

Prostate enlargement

Cervical cancer tumors

Drugs that crystallize (sulfonamides, acyclovir, MTX)

97
Q

Whatis the process for diagnosing an AKI?

A

History
Laboratory Data
Serum Creatinine
Urinary Sodium Concentration
Fractional Excretion of Na+ (FeNa)
Urinanalysis
Renal Ultrasound
Kidney Biopsy

98
Q

In a history for the diagnosis of an AKI, considerations are….

A

(so many potential causes, what drugs, sick, how long drugs, dehydrated, etc.)

99
Q

In the laboratory data for the diagnosis of an AKI, one would expect…..

A

↑SCr,↑BUN, acidosis, hyperkalemia

100
Q

Serum Creatinine consideration for the diagnosis of an AKI

A

Changes in SCr will lag behind the decrease in kidney function due to slow accumulation, increased tubular secretion, and increased extra-renal clearance

101
Q

What is the difference between urinary sodium concentration and FENa?

A

The fractional excretion of sodium (FENa) is the percentage of the sodium filtered by the kidney which is excreted in the urine. It is measured in terms of plasma and urine sodium, rather than by the interpretation of urinary sodium concentration alone, as urinary sodium concentrations can vary with water reabsorption.

102
Q

What is FENa? Consequences?

A

FENa (Fractional Excretion of Sodium) = % sodium filtered by the kidneys that is excreted in urine

↓ with pre-renal AKI
↑ with tubular damage- intrinsic

Decrease in pre-renal AKI because RAAS system activated, the reabsorption of Na+ to increase H2O reabsorption to increase blood pressure to maintain perfusion –> LESS NA+ excreted

Tubular damage because reabsorption process impaired

103
Q

Is FENa a specific measure for kidney damage? Why or why not? Example?

A

Not specific to kidney damage – can be affected by other factors (e.g. furosemide, blocks Na+ in loop of henle, may increase NA+ levels requiring interpretation)

104
Q

Urinanalysis Findings for the Diagnosis of an AKI

A

Cellular debris (“casts”) → seen with acute tubular necrosis

Hematuria, proteinuria → indicate glomerular injury

↑ WBC → UTI/pyelonephritis

Pyuria, urinary eosinophils → acute interstitial nephritis

Crystals → post-renal AKI (can also see hematuria with kidney stones)

Pre-renal AKI –> generally few WBCs, casts, etc., but ↓ FENa (All due with hemodynamic as kidney itself is healthy)

105
Q

Are kidney biopsies common?

A

Invasive, only used if necessary

106
Q

What are the goals of therapy for an AKI?

A

Prevent further renal injury (detect and remove the cause)

Minimize extra-renal complications

Facilitate recovery of renal function back to baseline

107
Q

Describe the treatment of an AKI?

A

Treatment is largely supportive

108
Q

Treatment of pre-renal failure

A

Hydration with IV fluids (e.g., isotonic sodium chloride) if hypovolemic - stop diuretics

BP support with vasopressors (dopamine, norepinephrine, vasopressin as applicable)
Sepsis, septic shock, vasomotor shock

Fluid removal in volume overload states (e.g., heart failure) with diuretics

Stop (or “hold”) drugs that impair kidney function/urine flow (e.g., NSAIDs)

109
Q

Treatment of intrinsic renal failure

A

Discontinue offending agent

Manage underlying autoimmune disease

110
Q

Treatment of post-renal failure

A

Catheter to restore urine flow

Identify and remove obstruction

Adequate hydration when giving drugs with potential to crystallize

111
Q

What is hyperkalemia?How is K+ managed? Kidneys role?

A

Serum K+ levels maintained in a narrow range (3.5-5mmol/L) by several mechanisms (e.g., insulin, aldosterone, epinephrine)

The kidney is the primary route of K+ elimination
↑ serum K+ seen with AKI and CKD

112
Q

Mild-moderate hyperkalmeia is defined as….. SX?

A

Mild-Moderate (K+ 5.1-7mmol/L)

weakness, confusion, muscle twitches, ECG changes (peaked T-waves)

113
Q

Severe hyperkalemia is defined as…. Sx?

A

Severe (K+ > 7mmol/L)

ECG changes like widened QRS complex, small amplitude P waves, sine waves → heart block, ventricular tachycardia, death  CAN HAPPEN FAST

114
Q

What is considered a high K+ level? Why is this bad?

A

Can cause sudden arrythmias and death to occur

  • Over 5 mmol/L is considered high
115
Q

Treatment of Mild Hyperkalemia

A

May not require therapy or can use Kayexalate® (sodium polystyrene sulfonate); delayed onset of effect (~1 hour)
–> 15-60g po BID-QID until K+ concentration normalizes

Furosemide (IV) administration to increase urinary excretion

116
Q

MOA of Kayexalate

A

Cation exchange resin  passe through he GI tract and exchanges K+ for Na+ ions  Passes out into the stool (K+)

117
Q

Monitoring of Furosemide

A

Furosemide  Monitor for hypokalameia, loop diuretics

Eliminate potassium through the kidney

need functional kidneys for furosemide to have an effect

118
Q

Tx of Severe Hyperkalemia

A

If severe: (K+ >7 mmol/L or ECG changes) → Medical emergency!

  1. Calcium gluconate to stabilize myocardium

To drive K+ into cells (combo of these may be used):
- Rapid-acting/Regular insulin +/- glucose (depending on BG levels)
- Sodium bicarbonate IV infusion (if metabolic acidosis present)
- Salbutamol via nebulizer (if pulmonary congestion)

  1. Kayexalate → eliminate excess K+ from the body (slower onset)

If refractory → dialysis

119
Q

Tx of Severe Hyperkalemia Mechanims Simple

A

Move from the bloodstream into the tissues; not necessarily trying to get out of the body

120
Q

Tx of Fluid overload in an AKI

A

Leads to pulmonary congestion and edema

Diuretics (furosemide +/- metolazone)

121
Q

Tx of metabolic acidosis in an AKI

A

Treat with sodium bicarbonate IV

122
Q

Uremia AKI Consequences

A

May cause nausea, vomiting, anorexia
If severe can progress to mental status changes, coma

123
Q

When to dialyze in an AKI?

A

More likely to start dialysis in AKI with hyperkalemia and metabolic acidosis

CKD is mainly uremia

PHAR 255 Exam 1 (8 decks)

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