Exam 3 Flashcards
pH reference range
normal: 7.35
acidosis: <7.35
Alkalosis: >7.35
pCO2 reference range
normal: 35-45 mmHg
pO2 reference range
80-100 mmHg
HCO3 reference range
22-26 mmol/L
HCO3 : H2O2
20:1
pH/HCO3/H2CO3 equation (HH)
ph=pka + log (HCO3/pCO2*0.0301)
pH measurement
Glass membrane
H+ exchange causing potential to develop
pCO2 measurement
Serveringhaus electrode
pH buffer lowered in presence of CO2 (proportional)
pO2 measurement
Clark electrode
change in electrical current occurs as O2 diffuses from blood
HCO3/H2CO3 buffer
CO2 + H2O are converted into H2CO3 by carbonic anhydrase which is broken down into H+ and HCO3-
HCO3 decrease (pH)
pH decreases
HCO3 increase (pH)
pH increase
Hyperventilation
CO2 removed, pH increase
Hypoventilation
CO2 retained, pH decrease
Metabolic acidosis
Decreased pH
Decreased pCO2
Decreased HCO3
Diabetes
Metabolic alkalosis
pH increased
pCO2 increased
HCO3 increased
Vomiting
Respiratory acidosis
Decreased pH
Increased pCO2
Increased HCO3
Emphysema
Respiratory alkalosis
Increased pH
Decreased pCO2
Decreased HCO3
Hyperventilation
Metabolic Acidosis (increased AG)
Ketoacidosis
Lactic acid
Toxic ingestion of aspirin
ethylene glycol
Metabolic Acidosis (normal AG)
renal diseases
Metabolic Acidosis (MUDPILES)
Methanol Uremia Diabetes Paraldehyde Isoniazid Lactic acidosis Ethylene glycol Salicylate toxicity
metabolic alkalosis causes
base excess
cushing’s disease
vomitting
full compensation
20:1 balance bicarb/carbo
pH normal
partial compensation
balance off
pH normal or approaching
uncompensated
pH off
compensatory mechanism is still normal
specimen collection (ABG)
arterial blood
radial
STAT
heparin syringe
bubbles in syringe (ABG)
increased pH
decreased pCO2
increased pO2
Syringe at room temp (ABG)
decreased pH
increased pCO2
decreased pO2
glycolysis (ABG)
decreased pH, pO2
increased pCO2
pH and temperature
per 1 degree rise pH decreased 0.015
Amount of O2 bound to Hemoglobin
availability of O2
fever
type of hemoglobin
pH
Alkalosis (Hemoglobin)
O2 readily bound to hemoglobin
Acidosis (hemoglobin)
O2 will not bind to hemoglobin
Function of Lipids
energy
hormone precursors
cell membranes
insulators
fatty acids
linear chain of C-H bonds
part of triglycerides/phospholipids
Saturated fatty acids
contain CH3 without double bonded C-C atoms
Monounsaturated fatty acids
one double bond
polyunsaturated fatty acids
more than one double bond
triglycerides
3 fatty acids and glycerol
synthesized by body
hydrophobic
phospholipids
2 fatty acids
hydrophillic/hydrophobic
cell membranes
synthesized in liver
cholesterol
produced in liver from acetyl-CoA (500-1000mg)
dietary cholesterol recommendation
<300 mg / day
cholesterol functions
cell membranes
precursor to steroids
conversion of bile acids
not a fuel source
cholesteryl esters
hydrophobic
center of lipid drops/lipoproteins
lipoproteins
lipids+proteins
Transportation of insoluble fats through blood
apolipoprotein
outer layer of proteins around lipid drop
large lipoprotein
increased lipid
decreased density
small lipoprotein
increased protein
increased density
chylomicron
largest/least dense lipoprotein
high % triglycerides
produced in intestines
VLDL, LDL, HDL
chylomicron function
transport dietary fat to adipose/muscle cells
chylomicron specimen
creamy layer upon plasma
reflect light
cause turbidity
VLDL
-Very Low Density Lipoproteins
LDL
-Low Density Lipoprotein
VLDL function
endogenous triglycerides to adipose tissue
made by liver
LDL function
transport cholesterol from liver to cells
bad cholesterol
few LDL receptors
blood cholesterol rises, excess deposited into arteries
HDL
High Density Lipoprotein
HDL function
transport cholesterol from peripheral tissue TO the liver, to be incorporated into bile salts
“scavenger of excess cholesterol”
Friedwald
LDL=Tot - HDL - (tri/5)
HDL reference range
good: >60 mg/dl
okay: 40-59 mg/dl
bad: <40 mg/dl
Cholesterol range
140-200 mg/dl
LDL range
50-130 mg/dl
triglyceride range
60-150 mg/dl
Non-HDL calculation
130 mg/dl
good predictor of heart disease
no fasting
counts LDL and VLDL
Apo A-I
Major protein on HDL
Apo B
protein on LDL, VLDL, chylomicrons
100: LDL, associated with CVD
48: chylomicrons
Apo C
Breakdown triglycerides
Lipid absorption
Micelles contact membranes of intestinal cells, enter circulation, picked up by albumin and taken to liver
micelles
lipid aggregates with bile acids
pancreatic lipase
cuts off fatty acids and converts to more polar compounds (amphipathic)
form micells
exogenous pathway
transport of dietary lipids
Chylomicron remnants taken up by liver, broken down by lysosomal enzymes
released from exogenous pathways
fatty acids, free cholesterol, amino acids
endogenous pathway
transport of hepatic derived lipids
VLDL endogenous pathway
loses core lipids, converts to remnants, half are converted to LDL, half are taken in by liver
Reverse cholesterol transport
HDL
excess cholesterol transported to liver. Cholesteryl esters to chylomicrons. VLDL to liver.
Conversion of cholesterol into bile acids
Thyroxine/Cholesterol
Hypothyroid: hyper cholesterol
Hyperthyroid: hypocholesterol
Estrogen/Cholesterol
Post-menopausal: increased LDL
Pregnancy/cholesterol
Increased cholesterol
Arteriosclerosis
Deposition of lipids in artery walls
Hyperlipoproteinemia
Elevated lipoproteins
Hypercholesterolemia
Linked to heart disease
Lacking/deficient LDL receptors (LDL build up)
Hypercholesterolemia symptoms
heart attacks
xanthomas
300-1000mg/dl
Hypertriglyceridemia
imbalance between synthesis and clearance of VLDL.
deficience of apo-C and LPL
can cause pancreatitis
Hypertriglyceridemia/hormones
hormones trigger lipase
insulin, glucagon, GH, ACTH, thyrotropin, epinephrine, norepinephrine
Hypolipoproteinemia
Low lipoproteins,
decrease in HDL
Disease/Hypolipoproteinemia
Tangier disease
Metabolic syndrome
increased trig. obesity. high blood pressure. low HDL. Glucose intolerance.
Elevated lipid treatment
Treat secondary cause first (i.e diabetes)
treat by exercise/diet
drug treatment (statins)
Lipid analysis specimen collection
Serum
Fasting
Cholesterol testing
Cholesterol oxidase coupled reaction
NCEP ranges
Tot. Cho: <200 mg/dl
Trig: <150 mg/dl
LDL: <100 mg/dl
HDL: >40 mg/dl
3 major renal functions
Glomerular filtration
Tubular reabsorption
Tubular secretion
Nonprotein Nitrogen Compounds
Products of catabolism of proteins and nucleic acids
Major Non-protein Nitrogen Analytes
Urea
Uric Acid
Creatinine
Ammonia
BUN origin
Formed in liver when ammonia is removed and combined with CO2
BUN reference range
Plasma/Serum: 6-20 mg/dl
24h Urine: 12-20 g/d
BUN Clinical sig
Evaluation of renal function
Hydration
Nitrogen balance
Dialysis
BUN/Glomerular function
Increased BUN = decreased glom. function
Azotemia
elevated urea concentration
Uremia
increased urea accompanied by renal failure
BUN/Creatinine Ratio
20:1
Prerenal azotemia
Congestive heart failure Shock Burns Increased protein Dehydration
Renal azotemia
Disease of nephron
ex. glomerulonephritis, nephrotic syndrome
Post renal azotemia
Obstruction to urine outflow
ex. kidney stones
Prerenal Azotemia ratio
Elevated BUN
Elevated ratio
Normal creatinine
Renal Azotemia ratio
Normal ratio
Elevated BUN
Elevated creatinine
Post renal azotemia ratio
Elevated BUN
Elevated ratio
Elevated creatinine
Decreased BUN/ low ratio
Decreased protein
Liver disease
Tubular necrosis
Dialysis
Specimen collection BUN
Plasma, Serum, Urine
BUN methodology
Urease catalyzes urea and produced ammonia
Uris Acid formation
Product of catabolism of nucleic acids
majority reabsorbed by glomerulus
Uric Acid clinical significance
Gout Purine metabolism Renal calculi Chemotherapy kidney dysfunction
Uric acid reference range
Men: 3.5-7.2 mg/dl
Women: 2.6-5.5 mg/dl
Child: 2.0-5.5 mg/dl
Gout
Uric acid crystals
older males
Monosodium urate: >6.0 mg/dl
Hyperuricemia
Gout
Purine-rich diet
Chronic renal disease
Hyperuricemia disease
Lesch-Nyhan syndrome
Hypouricemia
Hepatocellular disease
Fanconi syndrome
<2.0 mg/dl
Uric Acid specimen collection
- Plasma
- Serum removed ASAP
- Urine
Uric Acid Methedology
Uricase method
Caraway method
Uric acid interferences
hemolysis
bilirubin
Vitamin C
Decrease results
Creatinine formation
Creatine in muscle loses phosphoric acid and water
Creatinine (Plasma)
Inversely related to glomerular filtration rate
Creatinine advantages
Formed at constant rate
Identify fluid as urine
kidney function before cat scan
Creatinine clinical significance
renal function/kidney damage
–> increased creatinine = decreased GFR
Creatine clinical significance
increased associated with muscle disease
Creatinine specimen collection
plasma/serum
24 h urine
Specimen requirements Creatinine
Avoid hemolysis/icterus
Creatinine methedology
Jaffe: creatinine reacts with picric acid (red-orange)
Kinetic Jaffe: picrate
enzymatic: creatinase
Creatinine clearance reference ranges
Males: 97-137 ml/min
Females: 88-128 ml/min
Creatinine disadvantages
- 24 h collection
- correction
- drugs inhibit secretion
- elevated blood levels increase creatinine
- bacterial breakdown
GFR/Creatinine
Decerased GFR = Increased serum creatinine
Ammonia formation
Breakdown of amino acids
Bacterial metabolism
Ammonia disease
Reye’s syndrome
Renal failure
Liver disease
Ammonia reference range
Adult: 19-60 ug/dl
Child: 68-136 ug/dl
Ammonia specimen collection
Whole blood -EDTA, Heparin STAT no tourniquet on ice
Ammonia error
No smoking prior to collection
Ammonia methodology
Glutamate dehydrogenase
eGFR advantages
indicate impaired renal function
eGFR disadvantages
GFR can remain normal until extensive kidney damage has occured