Renal/Electrolytes Flashcards
Main functions of the kidneys:
- Cleanse and detoxify blood
- Filtration
- Reabsorption of water, electrolytes, amino acids
- Secretes water and wastes
- Acid/base balance
- BP regulation
- Erythropoietin production
- Electrolyte embalance
Approximately, what percent of cardiac output goes to the kidneys?
~ 20%
Name the 5 parts of the nephron:
- Glomerulus: the major filter of the nephron, the workhorse
- Proximal convoluted tubule: Reabsorption
- Loop of Henle: Job is to concentrate urine
- Distal convoluted tubule: “Fine tunes” by regulating pH, Na, K, Ca, and amino acids
- Collecting duct:
The glomerulus is a network of capillaries that does what?
Filters blood.
“Workhorse” of the nephron
The Proximal Convoluted Tubule reabsorbs what 4 things?
Reabsorbs water, sodium, amino acids and glucose.
The Loop of Henle reabsorbs what 2 things?
Concentrates urine.
Reabsorbs water and sodium.
Where loop diuretics work (Lasix) by preventing urine concentration, thus diuresing… also, leading to loss of electrolytes
What 4 things are regulated in the Distal Convoluted Tubule?
“Fine tunes.”
Regulates pH, K, Na and Calcium
What is collected in the collecting duct?
Collects urine from the nephrons.
The two major hormones involved in fluid balance?
ADH and Aldosterone
Thirst, ANP, RAAS, ADH and &Aldosterone all help regulate what?
Fluid balance
What hormone causes retention of Na and H2O?
( It is also released if hyperkalemic )
Aldosterone
Again, hyperkalemia leads to aldosterone excretion. The aldosterone triggers potassium excretion via the kidneys.
This peptide triggers the kidneys to excrete water when the atria are overstretched:
Atria-natriuretic peptide (ANP)
When this system is triggered, it leads to the kidneys to hold onto water:
Renin Angiotensin Aldosterone System (RAAS)
Where is aldosterone synthesized?
What 2 triggers cause adrenal gland to make aldosterone?
Cortex portion of adrenal gland on top of kidneys; aldosterone is made from cholesterol.
Triggers:
1. When angiotensin II comes around (The conversion of angiotensin I to angiotensin II is catalyzed by an enzyme called angiotensin-converting enzyme (ACE). ACE is found primarily in the vascular endothelium of the lungs and kidneys. [To start the system or cycle, when blood pressure falls, your kidneys release the enzyme renin into your bloodstream. Renin splits angiotensinogen, a protein made in your liver and releases the pieces. One piece is the hormone angiotensin I.])
- When an elevated level of potassium ions are detected
What do we call it when urine output is less than 100 mLs a day?
Anuria
What is it called when urine output is between 100-400 mL/day?
Oliguria
What is it called when urine output is about 1500 mLs per day?
Normal
0.5 mL/kg/hr
Ex 1: 45 kg/ 100 lbs ~ 23 mL/hr
Ex 2: 82 kg/ 180 lbs ~ 41 mL/hr
If someone puts out >2500 mL/day, what is it called?
Polyuria
What is azotemia?
Acute rise in BUN (blood urea nitrogen)
(BUN-usually ranging 7 to 21 mg/dL), creatinine in the blood, and other secondary waste products within the body
Will cause altered mental status if it gets too high (~90 peds, 150 adults? not hard # out there)
What (r/t kidneys) is used to evaluate kidneys’ ability to remove waste products?
GFR: Glomerular Filtration Rate
- Measurement of how much filtrate is made by the kidney (mL/min)
- Estimated by assessing creatinine clearance. (males have slightly higher creatinine clearance than females)
- Isolated plasma creatinine is NOT a sensitive marker for GFR in early stages of kidney injury
What are the cylindrical structures formed by the kidneys in certain disease states, such as ?
Where are they released from?
How are they detected, diagnosed?
- Urine casts. Sign of tubular distress/damage.
- Distal tubules and collecting ducts.
- Urinalysis
What is the following a definition of:
an abrupt decrease in the GFR?
Acute Kidney Injury (AKI)
Pt will begin to experience metabolic acidosis r/t build up of waste… may also have accompanying respiratory acidosis r/t pulmonary edema 2/2 to fluid overload.
What % of hospitalized pts have some degree of AKI?
What % of ICU pts have some degree of AKI?
Avg hosp cost of AKI event?
~5%
~30%
17K
What is the mortality rate for those who develop ATN?
~50%
Drops to 30% if they survive the first year.
Classic sign of ATN in the hospital?
acute tubular necrosis
Someone who gets hemodialysis for the first time.
What are the following risk factors for?
Elderly
Female > Male
HF
Existing renal insufficiency
Elevated BMI (>32)
COPD
Liver disease (HRS: hepatorenal syndrome)
Sepsis
GI Bleeding
Burns
Medications (vanco, Gent, antivirals)
AKI
Also:
Multi-system organ dysfunction
Hypotension
Trauma injury
Rhabdomyolysis
Contrast
kidneys and liver works side by side, if one fails, the other may start to fail.
RIFLE Criteria. What does RIFLE stand for?
FYI: This criteria can assist with preventing further kidney injury by assessing Cr levels prior to giving nephrotoxic Rx such as contrast… as well as diligent prevention of hypotension that decrease perfusion, etc.
Risk: Is the pt oliguric x 6 hr ( <0.5mg/kg/hr)? If not, 1-7 day decrease >25% in GFR, or serum creatinine x 1.5 sustained.
Injury: Oliguric x 12 hr OR GFR decrease >50% serum creatinine x 2
Failure: Adjust Cr or GFR decrease >75% or Anuric x 12 hr
Loss: Irreversible AKI or persistent AKI >4 wks
ESRD: > 3 months
Normal creatinine clearance?
80-120 ml/min
Note: Creatinine level has up to a 12 hr lag time.
Normal BUN/Creatinine ratio?
What is the most sensitive indicator of kidney function?
10:1 to 15:1
Urine output. BUN levels increase for quite a few reasons, Cr has the 12 hr lag time so we just track trends… urine output will be most accurate assessment.
What 3 main things are needed for treating AKI pts? (and protecting their kidneys)
- Adequate hydration
- Adequate perfusion
- Stop nephrotoxic meds
Common labs for AKI evaluation?
- BUN
- Creatinine
- BUN/Cr ratio (normal 10:1)
- GFR
- UA — casts (tubular cell death)
- Urine electrolytes
- Urine glucose
Causes of post-renal AKI?
OBSTRUCTION
- Stone
- Prostate
- Infection
- Neurogenic bladder
Can have a normal BUN/Cr ratio but will be elevated, ex: BUN 80, Cr 7.
Causes of PRE-renal AKI?
PERFUSION
- Sepsis
- HF
- Trauma
- Severe hypovolemia
BUN/Cr ratio in pre-renal AKI?
25:1
BUN elevates quicker than the Creatinine. If it isn’t properly address, the Cr will continue to rise and may lead to ATN.
In early AKI, what will the urine sodium levels be?
What would their urine osmolality and specific gravity be like?
Low; < 10 mEq/L
(This is bc kidney’s are holding onto Na and H2O)
Osmo and specific gravity will be high, urine will be concentrated.
Acute Tubular Necrosis (ATN), aka?
What are some causes?
Intrarenal Kidney Injury: damage w/in the nephron
mostly will always need some form of dialysis
Causes:
1. Hypotension
2. Glomerulonephritis
3. Diabetes
4. Rhabdomyolysis
5. Nephrotoxic medications
6. Shock states
What would BUN, Cr, BUN/Cr ratio, and treatment look like in ATN?
BUN: > 25 mg/dL
Cr: > 1.2 mg/dL
BUN/Cr ratio: Both elevated but still 10:1
- Treatment often requires renal replacement therapy (almost always need some form of dialysis).
- Prevent acidosis.
- Prevent electrolyte imbalances and uremia
- Stop nephrotoxic meds
What are the 2 types of ATN?
Causes of each?
- Toxic ATN: better to have toxic than ischemic.
Causes:- Drugs, bacteria
(Vanco, Gent, Aminoglycosides, antivirals)
- Drugs, bacteria
- Ischemic ATN
Causes: low perfusion
Differences between toxic and ischemic ATN?
Toxic is uniform and widespread damage. Recovery is quicker ( < 8 days) and is REVERSIBLE (as long as the cause is ID’d and stopped).
Ischemic has irregular damage along tubular membranes, tubular damage and cast formation. Cause: poor to no kidney perfusion. Recovery is longer ( >8 days ).
