Test #1 Flashcards
Azotemia
Elevated BUN/Creatinine
The buildup of abnormally large amounts of nitrogenous waste products in the blood
Types of azotemia
Pre-renal failure
Intrinsic renal failure
Post-renal obstruction
Oliguria
Urine output < 400 mL/day
Urine output < 20 cc/hr
Anuria
Urine output < 100 mL/day
Glomerular filtration rate (GFR)
The sum filtering rate of all functioning neurons
-Kidney filtration rate
Measure Creatinine, Urea, or Inulin clearance
GFR Normals by gender
Men = 130 mL/min/173 m2
Women = 120 mL/min/173 m2
Decrease normally w/ age
Influenced by age, sex, body size, and renal blood flow
Creatinine clearance
Assess GFR
Normals: Men = 107-139
-Women = 87-107
Can overestimate the GFR by 40%, especially with decreased renal function
Major body cations and normal values
Sodium: 135-145
Potassium: 3.8-5.5
Major body anions and normal values
Chloride: 98-106
Bicarbonate: 21-28
Total CO2: 23-30
Typically secreted electrolytes
Hydrogen
Potassium
Urate
Odors indicate:
Ammonia-like
Foul/offensive
Sweet
Fruity
Maple syrup-like
Ammonia-like: Urea-splitting bacteria
Foul/offensive: Old, pus, inflammation
Sweet: Glucose
Fruity: Ketones
Maple syrup-like: Maple syrup urine disease
Colors indicate:
Colorless
Deep yellow
Yellow-green
Red
Brownish-red
Brownish-black
Colorless: Dilute urine
Deep yellow: Concentrated urine
Yellow-green: Bilirubin
Red: Blood/Hemoglobin
Brownish-red: Acidified blood (acute glomerulonephritis)
Brownish-black: Homogentisic acid (Melanin)
Globulinuria DDx
Glomerulonephritis
Tubular dysfunction
Bence Jones proteinuria DDx
Multiple myeloma
Leukemia
Fibrinogen proteinuria DDx
Severe renal disease
Types of ketone bodies
Acetoacetic acid
Acetone
Betahydroxybutyric acid (most common)
Nephrotic syndrome vs nephritic syndrome
Lots of protein loss w/ nephrotic
Lots of blood loss w/ nephritic
Acute renal failure
Heath’s intro
Abrupt kidney function loss w/in 7 days
Pre-renal, intrinsic, or post-renal
Chronic kidney disease
Heath’s intro
Progressive renal function loss over months/years
End-stage renal disease
Heath’s intro
Chronic kidney disease at stage 5 progression
GFR <15
Glomerulopathy
Heath’s intro
Disease of glomeruli or nephron
Can be inflammatory or non-inflammatory
Nephritic syndrome, IgA nephropathy, Nephrotic syndrome
Hydrostatic vs osmotic pressure
Hydrostatic pressure pushes fluid into the interstitium
Osmotic pressure pushed fluid from interstitium back into capillary/tubule
Fluid and electrolyte intake and output regulation
Fluid intake - hypothalamus regulates thirst
Electrolyte intake - dietary habits regulate
Output of both is regulated by kidneys
Mechanisms to stimulate hypothalamic thirst center
Increased plasma osmolality (Dry mouth and osmoreceptors stimulated)
Decreased plasma volume (RAAS and decreased BP)
ADH stimulation and mechanism
Stimulated by dehydration, increase in osmolality, or RAAS
Increases water absorption by increasing the number of aquaporins in the collecting tubule
Kidney blood vessel order
Aorta - renal artery - segmental artery - interlobar artery - arcuate artery - cortical radiate artery - afferent arteriole - glomerulus
Glomerulus - efferent arteriole - peritubular capillaries and vasa recta - cortical radiate vein - arcuate vein - interlobar vein - renal vein - inferior vena cava
Renal clearance
Volume of plasma completely cleared of waste by kidneys per minute
Clearance = (Urine concentration * urine flow rate) / plasma concentration
Can be used to estimate GFR if substance excreted is freely filtered w/o absorption
Renal autoregulation
Allows GFR to remain stable in spite of arterial blood pressure changes
Afferent and efferent arterioles change resistance to modify GFR and blood flow
Myogenic response and tubuloglomerular feedback (macula densa)
Feedback that triggers an increase in GFR
Prostaglandins
Fever/pyrogens
Glucocorticoids
Hyperglycemia (DM)
Macula densa senses low NaCl
Feedback that triggers a decrease in GFR
NSAIDs
Aging (10% decline/decade after 40 years)
PCT
Most reabsorption of vital substances - glucose, aa, bicarb, Na, Cl, water
Ammonia is generated and secreted here
Mannitol and acetazolamide diuretics work here
Angiotensin II increases sodium and water reabsorption
PTH increases phosphate excretion
Transport maximum
Some substances (glucose) can only be absorbed to a certain threshold, and all excess gets excreted
Loop of Henle - thin descending loop
Water is passively absorbed here
Loop is impermeable to sodium and solutes (medulla hypertonicity)
Loop of Henle - ascending loop
Not permeable to water, but active electrolyte reabsorption occurs here w/ Na/K/Cl pump
Loop diuretics (Lasix) work here to shut down pump and produce very dilute urine
The high osmotic gradient created here allows for urine concentration later
DCT
Subjected to hormonal control (Aldosterone, ADH, Angiotensin II, ACEI, ANP)
Early DCT only electrolytes permeable
Late DCT and CT - ADH controls water permeability
-principal and intercalated cells assist w/ concentration here
Aldosterone
Secreted from adrenal gland
Increases sodium absorption and potassium secretion in order to maintain blood volume and pressure
Triggered by RAAS
Angiotensin II
End of RAAS
Causes Aldosterone, ADH release
Also causes arterial constriction, increases GFR and increases thirst
Results in BP increase, water retention, and increased fluid intake
ACEI/ARB effect on kidneys
Inhibits RAAS - decreased aldosterone and ADH secretion
Decreases efferent arteriolar resistance and directly inhibits sodium reabsorption
Results in natriuresis, diuresis, and decreased BP
ANP
Secreted by atrial BP increase
Inhibits sodium and water reabsorption to reduce BP and volume
Inhibits RAAS while increasing the GFR
Common secreted by the tubule
Bile salts
Oxalate
Urate
Creatinine
Catecholamines
Collecting duct
Concentrates the urine according to the ECF osmolality and ADH levels
Cockcroft-Gault Formula
GFR/CrCl = [(140-age)*kg] / (72-SCr)
Multiply by 0.85 for women
MDRD
Takes gender and race into account for eGFR
Normal: >60mL/min/1.73 m2
Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI)
Measure creatinine w/ external filtration markers in order to provide a more accurate eGFR in patients w/ normal/mildly reduced GFR
BUN
Normal: 6-20 mg/dL
Waste of protein breakdown - urea that becomes BUN as soon as its in the blood
Increased BUN DDx
Renal disease
Excess protein breakdown
High protein diet
GI bleed
Decreased BUN DDx
Liver disease
Starvation
Creatinine
Muscle breakdown byproduct
Normal: 0.8-1.4 (men) 0.6-1.2 (women)
Steady-state relationship w/ GFR
Used w/ BUN to distinguished types of azotemia
Increased Creatinine DDx
Renal failure
High protein diet
Meds (ACEI, NSAIDs, diuretics)
Muscular disease
Decreased Creatinine DDx
Pregnancy - normal effect 0.4-0.6 mg/dL
Occurs because GFR and volume increase
Creatinine and BUN filtration dynamics
BUN can be absorbed over time w/ a decreased GFR
Creatinine is not absorbed, is secreted into CT for excretion
-Any Creatinine increase may be caused by blocked secretion (cimetidine (antacid, antihistamine), trimethoprim (Bactrim)
BUN:Creatinine increases
Both should increase proportionally to indicate intrinsic or post-renal disease
Increased BUN w/ normal creatinine DDx
Pre-renal azotemia
Catabolic state (increased breakdown)
GI bleed
High protein diet
Drugs (tetracyclines, steroids)
Decreased BUN:Creatinine DDx
ATN
Low protein/starvation
Liver disease
Dialysis
SIADH
Pregnancy
Decreased BUN w/ Increased Creatinine DDx
Rhabdomyolysis
Muscular patient in renal failure