Transcript Advanced Renal day 2

ADVANCED RENAL
ANATOMY AND
PHYSIOLOGY
•Urinary
system parts
•How Kidney’s Work
•Kidney Failure
•Transplantation
URINARY SYSTEM PARTS AND
FUNCTION
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Kidneys
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Purple brown organs
• Remove liquid wastes from the blood
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nephrons
• Stabilize balance of salts and substances in blood
• Produce erythropoietin
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Ureters
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Muscles on ureter walls tighten and relax
• Force urine downward
• Small amounts of urine emptied into bladder about every
10-15 seconds
URINARY SYSTEM PARTS AND
FUNCTION
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Bladder
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Hollow organ located in the lower abdomen
Held in place by ligaments
Bladder walls relax and expand to store urine
Can store up to 2 cups urine for 2-5 hours
Sphincter muscles
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Keep urine from leaking
Nerves alert person that it is time to empty the bladder
Urethra
URINARY SYSTEM PARTS AND
FUNCTION
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Facts about urine
• Adults pass about a quart and ½ each day
• Volume formed at night is about ½ that of daytime
• Normal urine is sterile
• Tissues of bladder are isolated from urine and toxic
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substances by a coating that discourages bacteria
growth
Normal urine output is 40-60 mL/hr
Minimum urinary output in the ICU setting is 30 mL/hr
URINARY SYSTEM PARTS AND
FUNCTION
RENAL FAILURE
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Generally due to diseases affecting the
nephron
Most diseases attack both kidneys
simultaneously
Most common diseases of kidney
• Diabetes
• HBP
DISEASES OF THE KIDNEY
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Diabetic neuropathy
• Body unable to use glucose properly
• If glucose stays in the blood, it can be poison
• Unused glucose in the blood causes damage
to nephron
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High Blood Pressure
• Damages the small vessels in the kidneys
• Damaged vessels cannot filter waste
DISEASES OF THE KIDNEY
(2 of 5)
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Glomerular disease
• Auto-immune disease
• Infection related disease
• Sclerotic disease
DISEASES OF THE KIDNEY
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Congenital kidney
diseases
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Polycystic kidney
disease (PKD)
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Cysts replace much of
the mass of the kidney
Autosomal recessive
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Abnormal formation of
the nephron
Signs of kidney disease
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HBP
Anemia
Blood protein in urine
http://content.revolutionhealth.com/contentimages/im
ages-image_popup-r7_kidneyscompared.jpg
DISEASES OF THE KIDNEY
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Trauma
Poisons
Acute renal failure
• Blood loss
• Drugs or poisons
• May lead to permanent renal failure
DISEASES OF THE KIDNEY
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Chronic kidney disease
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Gradual loss of kidney function
Increased risk of stroke or heart disease
End stage renal disease
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Requires dialysis or transplant
Signs of kidney disease
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Frequent urination
Tired or itchy
Nausea or vomiting
Swelling of hands or feet
Skin may darken
Muscle cramps
DIAGNOSTICS FOR RENAL
DISEASE
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HBP measurement
Microalbumineria/proteinuria
• Healthy kidneys remove waste but leave
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protein in blood
Protein in urine is indicator that kidneys
not working adequately
DIAGNOSTICS FOR RENAL
DISEASE
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Glomerular filtration rate (GFR)
• Calculation of how efficiently
kidneys are
filtering waste
• Measurement of creatninine in the blood
• Breakdown of muscle cells during activity (creatine)
• Normal blood creatinine level 0.8-1.4 mL/dL
• Levels can increase 10 X in kidney failure
DIAGNOSTICS FOR RENAL
DISEASE (2 of 2)
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Blood Urea Nitrogen (BUN)
• Manufactured in liver-byproduct of amino
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acids and ammonia
Healthy kidneys remove urea from blood to
urine
Normal 26 mEq/L
Renal imaging
Renal biopsy
TREATMENT FOR RENAL
DISEASE
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Blood pressure
Diet
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Protein
Cholesterol
Sodium
Potassium
Stop smoking
Treat anemia
Dialysis
ALDOSTERONE
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Hormone made by the cortex of the
adrenal gland
Controls the reabsorption of Na+ and
excretion of K+ to control fluid balance,
and electrolytes
Secreted in response to low salt levels
Increases BP
HIGHER THAN NORMAL VALUES
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Primary hyperaldosteronism
Secondary hyperaldosteronism from
cardiac or renal disease
Low sodium diet
Pregnancy
LOWER THAN NORMAL VALUES
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High sodium diet
Congenital adrenal hyperplasia
ROLE IN SECRETION
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Levels of aldosterone increased by
• Decreased serum sodium
• Increased serum potassium
• Increased angiotensin 2
REGULATION OF ACID BASE
BALANCE
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pH equal to (-) log of H+
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Metabolic acidosis
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Main goal of acid-base
homeostasis is to maintain a
normal PH
• Low pH=acidosis
• High pH=alkalosis
• Low pH w/o HCO3- compensation
METABOLIC ACIDOSIS
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Symptoms
• Chest pain
• Palpitations
• Altered mental status
• Dyspnea
• Muscle weakness
• Kussmal’s respirations
• Neurological/cardiac complications
• Seizures
METABOLIC ACIDOSIS
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Diagnosis
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ABG
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ECG
Electrolyte
Glucose
Renal function
CBC
Urinalysis
Possible toxicology
• Low pH/low HCO3-
METABOLIC ACIDOSIS
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Two types:
• Accumulation of fixed acids (ex: lactic acid)
• Will present with a high anion gap
• Hypoxemia can cause lactic acidosis
• Excessive loss of HCO3-
• Will present with a normal anion gap
METABOLIC ACIDOSIS
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Anion gap calculation
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[Sodium + potassium]-[chloride + bicarb]=remaining
anions
• Normal level 8-16 mEq/L
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Metabolic acidosis with increased anion gap
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Lactic acidosis
Ketoacidosis
CRF
Ingestion of acids (salicylate intoxication)
METABOLIC ACIDOSIS
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With a normal anion gap
• Diarrhea (bicarb loss)
• Pancreatic fistula
• Ingestion of ammonium chloride
• Renal failure
• Renal tubular acidosis from failure to reabsorb
bicarb
METABOLIC ACIDOSIS
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Pathophysiology
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Compensatory mechanism
H+ + HCO3- ↔ H2CO3 ↔ CO2 + H2O
Enzyme carbonic anhydrase maintains equilibrium between
bicarbonate and H2CO3
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Converted into carbon dioxide and water
Intracellular buffering of hydrogen atoms
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Proteins
Phosphates
Carbonate in bone
• Respiratory compensation
• Decreasing H by decreasing CO
• Renal compensation
+
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2
Physically removes H+ from the body by retaining HCO3+
METABOLIC ACIDOSIS
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Treatment
• Emergency
• Intravenous bicarbonate
• 50-100 mEq
• ABG monitoring
• Dialysis
ACID BASE BUFFERS
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Respiratory center stimulation
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3-12 minutes to correct
Kidneys excrete acid or alkaline urine
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24-48 hours to correct
With a body PH of 7.40, urine PH = 7.33-7.37
Buffers
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Bicarbonate buffer system
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Carbonic acid (H2CO3) and sodium bicarbonate (NaHCO3)
Phosphate buffer system
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H2PO4 and HPO4
High concentrations in tubular fluid
Protein buffer system
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Amino acids inside cells
RESPIRATORY REGULATION
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Hydrogen ion action on medulla oblongata
Affect rate of alveolar ventilation
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Acidic condition can increase alveolar ventilation rate
4-5 times normal
Alkalotic condition can decrease alveolar ventilation
rate by 50-75%
As pH returns to normal alveolar ventilation
compensatory stimulus lost
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Compensation of hydrogen ion concentration
effectiveness 50-75%
RENAL REGULATION
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Kidneys
• Physically remove H+ from body
• Excrete <100 mEq fixed acid per day
• Also control excretion or retention of HCO3–
• If blood is acidic, then more H+ are excreted
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and all the HCO3– is retained, vice versa
While lungs can alter CO2 in seconds, the
kidneys require hours to days to change
HCO3– and affect pH.
RENAL REGULATION
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Reabsorption of HCO3–
• For every H+ secreted, an HCO3– is reabsorbed.
• They react in the filtrate, forming H2CO3 which
dissociates into H2O and CO2.
• CO2 immediately diffuses into cell, is hydrolyzed
and H+ is secreted into filtrate, HCO3– diffuses into
blood
• Thus, HCO3– has effectively been moved from the
filtrate to the blood in exchange for H+.
• If there is excess HCO3– that does not react with
H+, it will be excreted in urine.
RENAL REGULATION
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Steps of bicarbonate reabsortption
• Tubules not very permeable to bicarbonate
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ion because it is a large ion
Reabsorption begins with reaction of H+
secreted in tubule and HCO3- in tubular fluid
• Carbonic acid
• Carbonic acid dissociates into CO2 and H2O
• Water become part of peritubular fluid
• CO2 diffuses into epithelial cells or into blood
RENAL REGULATION
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Steps of bicarbonate reabsorption (cont)
• CO2 combines with water to form a new
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bicarbonate ion
If patient is acidotic (excess H+) bicarbonate
ion will almost be completely removed from
urine and reabsorbed back into the blood.
RENAL REGULATION
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↑ CO2  ↑ H+ secretion (↑ HCO3reabsorption)
↓ CO2  ↓ H+ secretion (↓ HCO3reabsorption)
TITRATION OF BICARBONATE
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Hydrogen ion secretion =3.5 mmol/min
Bicarbonate ion = 3.49 mmol/min
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Ions combine with each other in tubules
End products of CO2 and H2O
Normal metabolic processes produce slightly
more H+ that is not matched up with HCO3-
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Leftover H+ secreted in urine
In alkalotic state, leftover HCO3- will be secreted in
urine
TITRATION OF BICARBONATE
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Metabolic compensation takes longer
(earliest @ 24-48 hours) but
compensation is complete vs. respiratory
compensation at ~ 75%