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Sodium
136-145 mEq/L
Potassium
3.5-5.1 mEq/L
Chloride
98-107 mEq/L
pH
7.35-7.45
pCO2
35-45 mmHg
Bicarb (HCO3-)
23-29 mEq/L
BUN
6-20 mg/dL
Creatinine
Men: 0.9-1.5 mg/dL
Women: 0.8-1.2 mg/dL
Uric acid
Men: 4.0-8.5 mg/dL
Women: 2.7-7.3 mg/dL
Ammonia
14-45 umol/L
Osmolal gap
Normal: ~0.0 mOsm/kg
Clinically significant if value is > 10 mOsm/kg
Anion gap with K+
16 ± 4 mEq/L; 12-20 mEq/L
Anion gap without K+
12 ± 4 mEq/L; 8-16 mEq/L
Calcium
8.5-10.5 mg/dL
Magnesium
1.9-2.5 mg/dL
Inorganic phosphorus
2.5-4.5 mg/dL
Sodium cation/anion?
Major extracellular cation
Potassium cation/anion?
Major intracellular cation
Chloride cation/anion?
Major extracellular anion
Bicarbonate cation/anion?
Secondary extracellular anion
Magnesium cation/anion?
Secondary intracellular cation
Inorganic phosphorus cation/anion?
Major intracellular anion
Too much ADH
SIADH
Too little ADH
Diabetes Insipidus
Oliguria results in high urine osmolality
SIADH
Polyuria results in low urine osmolality
Diabetes Insipidus
Overhydration results in low plasma osmolality & hyponatremia
SIADH
Dehydration results in high plasma osmolality & hypernatremia
Diabetes Insipidus
What disorder cause patients to have excessive thirst?
SIADH and Diabetes Insipidus
Increased Plasma Osmolality
Excessive amounts of Glucose in plasma
Diabetes Mellitus
Increased Urine Osmolality
Glucose levels above renal thereshold
Diabetes Mellitus
Increased Osmol Gap
Ketoacidosis, increased unmeasured anions
Diabetes Mellitus
Polydipsia, Polyuria, Polyphagia & Unexplained weight loss
Diabetes Mellitus
Decreased renal perfusion pressure…
release of renin
Sympathetic nerve stimulation
release of renin
decreased sodium concentration in distal tubule fluid
release of renin
Renin travels from kidneys to _____ where Angiotensinogen is converted into ________
liver; Angiotensin I
Angiotensin I travels from the liver to the ______ where the angiotensin converting enzyme acts upon it to produce _______
lungs; Angiotensin II
____inhibitor drugs taken for high blood pressure prevent Angiotensin II from being produced and blocking the stimulus for vasoconstriction of blood vessels
ACE
1) Stimulates H2O ____ at Hypothalamus → result: ____
input; thirst
2) Stimulates H2O _____ at Hypothalamus causing the release of ______ → Result: _______
Output; Antidiuretic hormone (ADH); water retention
3) Causes the __________ of blood vessels → Result: ____
Vasoconstriction; increased blood pressure
4) Stimulates the adrenal cortex to release _____ → Result: ______
aldosterone; Distal convoluted tube reabsorb Na+ and secretes K+
Less Sodium reabsorbed at DCT
Less Potassium secreted at DCT
Hypoaldosteronism
Sodium reabsorbed at DCT
Potassium secreted at DCT
Aldosterone normal
More sodium reabsorbed at DCT
More potassium secreted at DCT
Hyperaldosteronism
H+ into cell
K+ out of cell
Lowers H+ in plasma
Acidosis:
Plasma more acidic
pH low
More H+
H+ out of the cell
K+ into cell
Raises H+ in plasma
Alkalosis:
Plasma more basic
pH High
Less H+
Cl- into cell
HCO3- out of cell
More HCO3- to bind free H+ so raises pH
Acidosis:
Plasma more acidic
pH low
More H+
Cl- out of cell
HCO3- into cell
Less HCO3- to bind free H+ so lowers pH
Alkalosis:
Plasma more basic
pH High
Less H+
Depletional
Dilutional
PseuDohyponatremia
Hyponatremia
Depletional hyponatremia
Renal losses: Diuretic use and hypoaldosteronism
Non-renal losses: GI loss (vomiting), skin loss (burns/trauma)
Dilutional hyponatremia
SIADH
Hyperglycemia
Pseudohyponatremia causes
Hyperlipidemia
Hyperproteinemia
Falsely low Na+ due to analytical errors
Water loss
Sodium gain
Hypernatremia
Causes of water loss hypernatremia
GI loss
Excessive sweating
Diabetes insipidus
Causes of Sodium Gain hypernatremia
ingestion or infusion of Na+
Hyperaldosteronism
Increased cellular uptake
Increased renal loss
Excessive GI loss
Hypokalemia
Renal loss causes hypokalemia
Hyperaldosteronism
Diuretic therapy
Licorice ingestion
GI loss hypokalemia
Vomiting
Diarrhea
Laxative abuse
causes of hyperkalemia
increased intake
increased cellular lysis
altered cellular uptake
impaired renal excretion
pseudohyperkalemia
increased intake causes hyperkalemia
transfusion of aged blood
supplementation (banana, meds)
increased in vivo cell lysis causes of hyperkalemia
cellular trauma
cellular injury
in vivo hemolysis
Altered cellular uptake causes hyperkalemia
compensation for acidosis (H+ taken into the cell; K+ put out of cell for electroneutrality)
insulin deficency
causes of renal excretion hyperkalemia
renal insufficiency or failure
hypoaldosteronism
GI losses
Burns
renal loss
Hypochloremia
general causes of hyperchloremia
dehydration
compensation for metabolic alkalosis
Causes of hypomagnesemia
impaired intake
excessive renal loss
causes of hypermagnesemia
renal failure
magnesium intoxication (milk of magnesia, antacids)
Treatment for toxemia of pregnancy
what causes tetany
hypomagnesemia
causes of hypocalcemia
decreased serum protein
hypoparathyroidism
steatorrhea
nephrosis
pancreatitis
Vitmain D deficiency
Heparin given during surgery
causes of hypercalcemia
Metastatic bone disease
hyperparathyroidism
multiple myeloma
causes of hypophosphatemia
rickets
hyperparathyroidism
fanconi syndrome
hemolytic anemia
diabetes mellitus
causes of hyperphosphatemia
glomerular renal failure
hypervitaminosis D
hypoparathyroidism
bone repair
Methods for sodium and potassium
atomic absorption spectroscopy
flame photometry
Potentiometry
Iontophoresis
sweat chloride → Cystic fibrosis
Historical method for calcium precipitation method
Clark and Collip method
precipitation with oxalate
dyes used for historical calcium method
o-cresolphthalein
arsenazo III
reagents used in photometric magnesium method
calmagite, formazan, methylthymol blue
reagent for phosphorus method
ammonium molybdate
causes of an increased anion gap
Increased unmeasured anions
Lactic acidosis
Ketoacidosis
Toxic ingestion of methanol, ethylene glycol, salicylate
Decreased unmeasured cations
decreased calcium
decreased magnesium
Lab error
overestimation of sodium
underestimation of chloride or bicarb
Causes of a decreased anion gap
decreased unmeasured anions
hypoalbuminemia
increased unmeasured cations
increased K+
increased Ca2+
increased Mg2+
presence of paraproteins
lab error
underestimation of sodium
overestimation of chloride or bicarb
increases BUN
febrile illness
corticosteroid or tetracycline therapy
large protein ingestion
GI bleed with blood absorption in gut
elevated thyroid hormone concentration
decrease BUN
low protein diet
increased androgens
growth hormone
pregnancy
Hyperuricemia causes (uric acid)
increased formation/intake
decreased excretion
increased formation/intake causes hyperuricemia
excess dietary purine intake (Gout)
increased nucleic acid turnover (chemo, cancer, trauma)
altered ATP metabolism (alcohol tox and tissue hypoxia)
preeclampsia
down syndrome
decreased excretion causes hyperuricemia
acute or chronic kidney disease
increased renal reabsorption or reduced secretion
lead poisoning
preeclampsia
prescence of orgnaic acids (lactate or acetoacetate)
causes increased ammonia
inherited urea cycle deficencies
advanced liver disease
Reye’s disease
hepatic encephalopathy
specific source of urea
detoxification of ammonia
dietary protein intake
specific source of creatinine
anhydride byproduct of muscle metabolism
specific source of uric acid
purine base metabolism
specific source of ammonia
deamination of amino acids
urea enzymatic methods and ammonia
Berthelot reaction: NH4+ + phenol and hypochlorite → indophenol using nitroprusside as a catalyst → blue product
Coupled enzymatic reaction: NH4+ with 2-oxoglutarate (measure absorbance at 340 nm NADH oxidized to NAD+)
urea chemical method
urea+ diacetyl → (heat) Diazine
thiosemicarbazide and ferric ions added for the color
creatinine method
Jaffe
creatinine + picrate ions under alkaline conditions to form red-orange complex (Janovski complex)
Fuller’s earth
uric acid scientist name
Carraway
oxidation and reduction of phosphotungstic acid to tungsten blue
Enzymatic method for uric acid
uricase → allantion
HPLC → high sensitivity/specificity, but very expensive
prerenal azotemia causes
congestive heart failure
shock
hemorrhage
dehydration
marked decrease in blood volume
renal causes azotemia
renal failure
postrenal azotemia cause
renal lithiasis
tumors of the bladder or prostate
severe infection in the urinary tract
OBSTRUCTION → increased urea in blood