Exam 1 Flashcards

1
Q

What are the functions of the kidneys?

A
  1. Regulate fluid volume in the extracellular space
  2. Excrete waste products from the body
  3. Control blood pressure
  4. Regulate acid-base balance
  5. Produce erythropoietin
  6. Activate vitamin D (need for Calcium absorption in GI)
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2
Q

What do we call the amount of blood filtered each minute by the glomeruli?

What is the normal GFR?

A

Glomerular Filtration Rate (GFR)

125 mL/min (differences based on age)

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3
Q

Which lab measures the end product of protein metabolism in the blood?

What is the normal range for this lab?

A

BUN - Blood, Urea, Nitrogen

6-20 mg/dl

Produced in the liver (ammonia) contains nitrogen

Influenced by protein intake

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4
Q

Which lab measures the serum level of waste product of muscle metabolism and is more specific to renal function than BUN?

What is the normal range for this lab?

A

Serum Creatinine

0.6 - 1.3 mg/dl

Remains fairly constant day to day due to constant muscle mass.

Can see increased levels in men (more muscle) and decreased levels in the elderly.

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5
Q

What test is the most accurate test for kidney function and measures the GFR?

What is the normal range?

What 2 ways measure it?

A

Creatinine clearance

70 - 135 mL/min (>15 mL/min = dialysis)

Measured in 2 ways:

  1. 24 H urine collection (most accurate but time consuming)
  2. A formula using serum Cr, Age, and weight.
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6
Q

What is involved in the formula calculation of GFR?

A

Serum Cr
Age
Weight

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7
Q

There is a range of slight deterioration to severe impairment r/t AKI’s. What do we call it when nitrogenous waste products are found in the blood?

A

Azotemia (“azot” -nitrogen; “emia” -blood condition)

Characterized by abnormally high levels of nitrogen-containing compounds (such as urea, creatinine, various body waste compounds, and other nitrogen-rich compounds) in the blood.

Can lead to uremia or AKI if not controlled.

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8
Q

What do we call it when there is urine in the blood?

A

Uremia (means “urine in the blood”)

This is more progressive than azotemia. The symptoms of renal failure are becoming objective in multiple systems… the backup (not filtering) leads to damage… heart and lungs in particular.

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9
Q

We use RIFLE for staging the severity of injury to the kidneys. What does RIFLE stand for?

What are the determining factors/ranges?

What does it track?

A

R - RISK
(Cr serum x1.5 or GFR down >25%; UO <0.5mL/kg/h x 6h)
I - INJURY
(Cr serum x2.0 or GFR down >50%; UO<0.5mL/kg/h x 12h)
F - FAILURE
(Cr serum >4mg/dl; UO<0.3mL/kg/h x 24h or anuria x 12 h)
L - LOSS
(Persistent AKI=complete loss of kidney function > 4 weeks)
E - END
(End Stage Renal Disease (ESRD)=complete loss of kidney function >3 months)

It tracks urine output (UO) and creatinine, together.

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10
Q

An acute onset of AKI could take hours to days for symptoms to manifest (such as labs). You will see an elevated BUN and a decrease in U.O. Is this reversible?

A

Typically it is reversible. This depends on how long the causing condition persists… and the overall health of the patient.

50% present with oliguria (400 mL/day), that means that 50% don’t!

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11
Q

Burns, thrombus, decreased CO, and hypovolemia are all prerenal, intrarenal, or postrenal causes of AKI?

How is this cause of AKI treated?

A

Prerenal.

Sudden and severe drop in BP (shock) or interruption of blood flow to the kidneys from sever injury or illness.

Tx: correcting the cause of lack of perfusion…
Rehydration.

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12
Q

What type of AKI develops if the prerenal causes prolonged ischemia?

A

Intrarenal (intrinsic) damage.

Direct damage to the kidneys by inflammation, toxins, drugs, infection, or reduced blood supply.

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13
Q

What are some causes of intrarenal injury?

A

Nephrotoxicity (drugs), Rhabdomyolysis (clogging up the kidneys).

Intrarenal is mostly related to the glomerulus due to nephrotoxic drugs such as:
Aminoglycosides
Vancomycin
TB drugs
IV contrast
NSAIDs
Lithium
Methotrexate
Heroin
Cocaine
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14
Q

What type of injury (pre/intra/post) AKI is acute tubular necrosis?

A

Intrarenal.

Pieces of glomerulus start breaking off and clogging tubules… epithelium can regenerate for awhile but then no longer… reversible if basement not destroyed and receive tx.

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15
Q

How do we treat intrarenal AKIs?

A

Flushing with fluids.

We also need to flush patients after contrast treatment.

Special populations need close monitoring!

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16
Q

What is included (organs) post-renaly?

How can these cause an AKI?

How do we tx?

A

Ureters and Bladder.

Obstructions can cause backup of urine. Kidneys can only handle 3-4 mL at a time… leads to injury.

Sudden obstruction of urine flow due to enlarged prostate, kidney stones, bladder tumor, or injury.

17
Q

What are the 3 phases of AKI?

A
  1. Oliguric: happens within 1-2 days of injury
    - - Has onset of 1-7 days of causative agent, a duration of 10-14 days (maybe months), and 50% of patients will not be oliguric.
  2. Diuretic: lasts 1-3 weeks
  3. Recovery: up to 12 months, if unable to recover = chronic kidney failure.
18
Q

What is Acute Tubular Necrosis?

What causes Acute Tubular Necrosis?

A

ATN is the death of tubular epithelial cells that form the renal tubules of the kidneys.

  • Renal ischemia (r/t low blood pressure)
  • Nephrotoxic agents
    tx: flushing with fluids to clear tubules of sloughed cells.
19
Q

Patho of oliguric phase of AKI… Prerenal:

A

R/T low perfusion to kidneys…

Activates the RAAS (Renin-Angiotensin-Aldosterone-System) which controls BP. D/T the low perfusion this triggers the need to hold onto Na and H2O.

This holding onto Na and H2O leads to decreased UO.

Specific gravity then increases (>1.025)

20
Q

Patho of oliguric phase of AKI… Intrarenal:

A

R/T damage in the kidneys…

Na spills out in the urine (so labs will indicate: normal is around 20mEq/L) this is r/t inability to filter.

This leads to a FIXED specific gravity around 1.010.

Acute Tubular Necrosis may develop: will see WBC, RBC, and casts in urine (sloughed cells).

UO <400 mL/day (16mL/hr); fluid retention

May have metabolic acidosis r/t NH3 (ammonia) buildup.

  • Decreased serum Na r/t dumping into urine
  • Excess potassium
  • Increased waste accumulation
21
Q

What does excess potassium look like on an ECG?

A

Peak T waves (hyperacute)

Widened QRS

ST depression

22
Q

What are some manifestations of waste product accumulation r/t kidney dysfunction?

A

Fatigue

Difficulty concentrating urine

Seizures

Asterixis (“flapping” tremor)

23
Q

Patho of diuretic phase of AKI which lasts 1-3 weeks:

A

UO 1-3 liters (up to 5/day)

Osmotic diuresis from high urea amounts in filtrate, causing a fluid shift.

Kidneys are able to rid wastes but not to concentrate leading to severe dehydration and hypovolemia.

*Risk for hypovolemia/hypotension.

24
Q

Which phase of AKI includes an increasing GFR and decreasing BUN, Creatinine labs?

A

Recovery phase.

Can take as long as 12 months (may not ever fully recover)… depends on overall health and any complications… DM, HTN, Elderly

If not adequate recovery = leads to kidney failure.

25
Q

What is used for diagnosing renal issues?

A

History

Urinalysis: Specific gravity, sodium, hematuria, proteinuria, casts

Labs
Renal ultrasound, renal scan, CT/MRI
Renal biopsy (ex: cancer dx)

26
Q

AKI:
Eliminating the cause, considering medication clearance, nutritional therapy, reducing fluid volume (oliguric phase), sodium and potassium balance, maintaining renal perfusion, treating hyperkalemia, and preventing nephrotoxicity are all part of what kind of care?

A

Collaborative Care.

Medication clearance - reducing dose or adjusting timing.

Nutritional therapy: Adequate calories to avoid catabolism, CHO (carbs), fats, very little protein.

Preventing nephrotoxicity: acetylcysteine - Mucomyst, hydration (flushing).

Reducing fluid volume by giving low dose diuretics (Mannitol), and only replacing the fluid that was lost.