Blood Analytes Flashcards
1
Q
Major source of energy in the body
A
Glucose
2
Q
Chemical structure of glucose
A
mono, di and polysaccharides
3
Q
Glucose Metabolism?
A
- Glycolysis, Glycogenesis, etc.
- Enzymes
4
Q
Regulates glucose by increasing cellular uptake and promoting glycogenesis
A
Insulin
5
Q
Regulates glucose by stimulating glycogenolysis and gluconeogenesis
A
Glucagon
6
Q
Regulates glucose by elevating glucose levels
A
Epinephrine
7
Q
Function to elevate glucose levels
A
GH, ACTH, Cortisol, and Thyroid hormones
8
Q
Person has this when fasting blood sugars are greater than or equal to 120 mg/dL
A
Hyperglycemia
9
Q
Causes of Hyperglycemia
A
Diabetes mellitus (type 1, 2, and gestational)
Liver Failure
10
Q
Symptoms of Hyperglycemia
A
- Glucosuria
- nausea/vomiting
- malaise
- diarrhea
11
Q
Person has this when fasting blood sugars are less than or equal to 50 mg/dL
A
Hypoglycemia
12
Q
Causes of Hypoglycemia
A
- hormone deficiency
- drug reaction
- insulin excess
- genetic disorder
13
Q
Symptoms of Hypoglycemia
A
- nausea
- trembling/sweating
- rapid pulse
- lightheadedness
- watch CNS symptoms
14
Q
Diabetes mellitus type 1 (insulin dependent)
A
Caused by autoimmune destruction of pancreatic beta cells, juvenile onset
- hyperglycemia
- ketosis
15
Q
Diabetes mellitus Type 2 (non-insulin dependent
A
Caused by insulin resistance and insulin deficiency
- obesity
16
Q
Lab tests for blood glucose
A
Direct measurement
Urine
Glucose tolerance test (GTT)
- evaluates insulin response challenge
Glycosalated Hgb (Hgb A1c)
17
Q
nitrogen-containing metabolite of protein catabolism
A
Urea
18
Q
Blood urea nitrogen is synthesized in ____ (CO2 + NH3) and excreted in kidney
A
Liver
19
Q
Urea (BUN) is dependent on
A
exogenous nitrogen intake and endogenous protein catabolism
20
Q
Disorder of elevated urea
A
Azotemia
21
Q
Causes of prerenal azotemia
A
- decreased renal blood flow; CHF,
shock, dehydration - increased protein breakdown
- high protein diet
- GI hemorrhage
- Obstruction
22
Q
Azotemia brought on by renal failure
A
Renal azotemia
23
Q
toxic condition; high serum urea accompanied w/renal failure
A
Uremia
24
Q
Causes of Decreased BUN
A
- Liver failure
-Overhydration (SIADH)
-Negative nitrogen balance (protein depletion)
-Pregnancy
-Nephrotic syndrome
25
Creatinine levels in the blood
Relative to muscle mass and body weight
Low variance
Primarily measured for Glomerular Filtration Rate (GFR), # of functioning nephrons
Associated with BUN
26
BUN/Creatinine ratio
12-20 mg urea/mg creatinine.
Helps determine cause of azotemia
Both BUN & Creatinine elevated indicate post renal obstruction or prerenal azotemia superimposed on kidney disease
27
High BUN/Creatinine ratio
Indicates prerenal cause for azotemia
28
Low BUN/Creatinine ratio
Indicate acute tubular necrosis, low protein intake, starvation or liver disease
29
eGFR
Indicates renal function
eGFR (mL/min/1.73m3) = 1.86 x
(Pcr)^-1.154 x(age)^-0.203 x (0.742 if female)
x (1.210 if AA)
> 60mL/min/1.73m^3
30
Total Protein Lab study
Measures numerous classes of proteins;
- Albumin
- Alpha-1 (AAT, A1-Fetoprotein)
- Alpha-2 (Haptoglobin, Ceruloplasmin)
- Beta (CRP, Transferrin, Complement)
- Gamma (Immunoglobulins)
31
Main protein in our bladder?
Albumin
32
Causes of Hyperproteinemia
Dehydration
Excess immunoglobulins - Multiple Myeloma, Waldenstrom's macroglobulinemia
33
Causes of Hypoproteinemia
Kidney disease
Blood loss
Malnutrition
Liver disease
34
Causes of Hypoalbuminemia
Inflammation - negative APP (acute phase protein)
Hepatic
Urinary loss
GI loss
Poor diet
35
Compounds that are soluble in organic solvents and insoluble in water
- fats
- steroids
lipids
36
Synthesized in the liver and intestine
Constituent of cell membranes
Precursor for hormones
Transported by LDL and HDL
Cholesterol
37
Partially synthesized in liver
Transported by chylomicrons and VLDL
Provides energy to cells
Insulates organs
Triglycerides
38
Transport vehicles for lipids
- Chylomicrons
- VLDL; degrades to LDL in circulation
- LDL; "bad" - cholesterol into cells
- HDL; "good" - remove excess cholesterol from cells
Lipoproteins
39
Remove excess cholesterol from cells
High Density Lipoproteins
40
Transport cholesterol into cells
Low Density Lipoproteins
41
Hyperlipidemia may be caused by __________ via diet, diabetes, ETOH, hormone defect in pancreas, hypothyroidism
Increased Triglycerides
42
Hyperlipidemia may be caused by ________ via genetic defects in liver, lack of specific receptor on cells, diet
Increased Cholesterol
43
Causes of Hypolipoproteinemia
Genetic defect - low LDL/HDL
Absent LDL (w/low cholesterol)
- failure to thrive
- steatorrhea
- CNS degeneration
- malabsorption of fats and vitamins
44
Decreased LDL
- increased life expectancy
- decreased risk of CAD/AMI
45
Reduced HDL
- increased risk of atherosclerosis/CAD
46
Absent HDL (Tangier's disease)
- increased accumulation of cholesterol in tonsils, adenoids and spleen
47
Included in Lipid Panel
Cholesterol
Triglycerides
HDL
LDL
48
Produced by catabolism of heme (RBC's)
Bilirubin
49
_______ bilirubin is bound to glucuronide
Conjugated (direct)
50
Free bilirubin that has not been attached to a glucuronide molecule
Unconjugated (indirect) bilirubin
51
a yellow color in the skin, the mucous membranes, or the eyes
Due to -
Newborn (HDN)
Inherited
Hepatic dysfunction
Jaundice
52
Affects about 30% of breast-fed babies. Due to B-glucuronidase in breast milk
(deconjugates bilirubin)
Breast-milk jaundice
53
Inadequate milk supply
Breast-feeding jaundice
54
Thought to be caused by a deficiency in the enzyme glucuronosyltransferase. Inherited bilirubin disorder causing jaundice
Gilbert's syndrome
55
Absence or deficiency of uridine diphosphate (UDP) glucuronyl transferase. Inherited bilirubin disorder causing jaundice.
Crigler-Najjar syndromes
56
Types of Liver disorders
Prehepatic
Hepatic
Posthepatic
-urinalysis can affect
57
Function of Creatine Kinase (CK)
Production of ATP needed for muscle contraction
58
____ is needed as a cofactor for creatine kinase (CK)
Mg2+
59
Inhibitors of Creatine Kinase (CK)
Mn2+, Ca2+, Zn2+, Cu+
(Mg2+ in excess)
60
Occurs as a dimer with two subunits (isoenzymes)
Creatine Kinase structure
61
Brain type creatine kinase
CK-1(BB)
62
hybrid type, cardiac tissue creatine kinase
CK-2(MB)
63
muscle type (cardiac and skeletal) creatine kinase
CK-3 (MM)
64
Percentage of serum CK fraction that is MM from skeletal muscle
98-100%
65
Skeletal muscle CK distribution
CK-3 and CK-2
66
Brain CK distribution
CK-1
67
Heart CK distribution
CK-3 and CK-2
68
Smooth muscle CK distribution
CK-1
69
Devoid of CK
Liver and RBC's
70
May be indicated as increased CK-2. Can detect reinfarction soon after initial episode. Testing being replaced by troponins
Myocardial infarction
71
can separate CK-MB into isoforms 1 & 2
- Clinical sensitivity @ 6hrs 90-95%
- Diagnostic specificity 89-100%
high voltage electrophoresis
72
Muscle disease indicated by increased CK-3
Muscular dystrophy (Duchenne type)
73
CNS disease indicated by increased CK-1 (70x)
Reye's Syndrome
74
Indicated by increased CK-3 (5x)
Hypothyroid
75
CK is unstable above ____ degrees C. Best stored refrigerated or frozen. Not affected by slight hemolysis.
37
76
Protein that regulates muscle contraction
Troponins
77
How many subunits are there for Troponins?
3 - T,I,C
78
94-97% of troponins are located in ______.
Myofibrils
79
T and I subunits of troponins are useful in the diagnosis of _____.
AMI
80
Troponins are more specific than CK-MB and are ______ in the serum of healthy and non-cardiac patients
Absent
81
Levels become elevated 2-3 hrs after AMI
Can remain increased up to for 7-10 days after AMI
Clinical sensitivity of 50 - 75% up to 4-6 hours after onset of chest pain
High clinical sensitivity (>90%) up to 4-7 days after AMI
Troponins T and I
82
Function of Lactate Dehydrogenase (LD/LDH)
H+ ion transfer enzyme w/ NAD as acceptor
Catalyzes the reversible reaction of pyruvate to lactate (based on pH)
L->P (pH 8.8-9.8)
P->L (pH 7.4-7.8)
83
Fractions of LD. Present in all cells cytoplasm. Tissue levels are 500x higher than serum
5 major + LD-X and LD-6
84
Isoenzyme of LD in mitochondria, 20-40% activity
LD-1 (HHHH)
85
Isoenzyme of LD - major form in serum. 35-46%
LD-2 (HHHM)
86
Isoenzyme of LD - 17-33%
LD-3 (HHMM)
87
Isoenzyme of LD - 9-18%
LD-4 (HMMM)
88
Isoenzyme of LD - major fraction in skeletal muscle (6-17%)
- Force conversion of pyruvate to lactate, regeneration of NAD
- Anaerobic glycolysis (cytoplasm)
LD-5 (MMMM)
89
Cardiac tissue and RBC's have the highest concentration of which lactate dehydrogenase isoenzyme
LD-1
90
During AMI - LD rise within 12-24 hrs, peak within 48-72, may be elevated for 10 days
"______________"- 80% seen
Hemolysis (2 and 1 would flip flop to indicate MI)
Flipped pattern
91
Elevated LD 1 and 2 indicates
Megaloblastic anemia
92
10x total LD indicates
Liver; toxic hepatitis - lower in viral hepatitis
10x total LD indicates
93
normal - 2x total LD indicates
Cirrhosis/Obstructive jaundice
94
Germ cell tumors
elevated LD-1 indicates
95
elevated total LD indicates
Malignant Diseases
96
Elevated LD 2, 3 and 4 indicate
PLT destruction (ITP) (3 highest)
- Lymphatic system;
- Mono
- Lymphomas and leukemias
97
Elevated LD 5 indicates
- Liver disease
- Passive congestion (CHF)
- Skeletal injuries or disorders
98
Increase in all levels but normal pattern
- Hypoxia
- Hyperthermia
- Congestive heart failure
- Renal Disease
99
High LD activities will be seen in the _________ in 90% of bacterial infections
10% of viral infections
Specimen - free of hemolysis, separate from cells immediately
Cerebrospinal fluid
100
Functions of Alkaline Phosphatase
nonspecific enzyme
- catalyzes the hydrolysis of many phosphomonoesters at an alkaline pH
- movement of substances across cell membranes
- lipid transport in GI
- calcifying process in bone
101
Forms of Alkaline Phosphatase
Located at or in cell membranes
Major isoenzymes derived from liver, bone, intestine, placenta, spleen, and kidney (*most common elevation causes)
Placental (2nd and 3rd trimester)
102
Primary areas where you'll see elevated phosphate
Liver and Bone
103
Present in most tissue
Liver - hepatocytes and biliary tract cells
Bone - osteoblasts (children and geriatrics)
Intestine - blood groups B or O who are secretors
Placenta; increased 1 - 1 ½ upper limit
- 16 - 20 weeks
Kidney
Distribution of Alkaline Phosphatase
104
alkaline phosphatase abnormality of bone disease- osteoblast involvement (highest) 10-25x UL
Paget's disease
105
alkaline phosphatase abnormality of bone disease- moderate (2-4x UL)
Osteomalacia
106
alkaline phosphatase abnormality of bone disease- normal to slight increase
Osteoporosis
107
alkaline phosphatase abnormality of bone disease - high
Bone cancer
108
alkaline phosphatase abnormality of liver disease ( >3x UL)
Extrahepatic obstruction
109
alkaline phosphatase abnormality of liver disease (< 3x UL)
Intrahepatic obstruction
110
alkaline phosphatase abnormality of liver disease (<3x to normal)
Viral hepatitis
111
______ causes of increased synthesis of alkaline phosphatase -
pregnancy, healing fractures, infections
Transient
112
alkaline phosphatase abnormality causing slight to moderate increase in levels.
Secondary Hyperparathyroidism
113
The _____ type of amylase breaks 1,4 alpha linkages of sugars (random). This requires calcium and chloride.
Alpha
114
Amylase is readily _____ by the kidneys and has a pH optimum at 6.9 - 7.0
Filtered
115
Hydrolase; breakdown of polysaccharides, different rates
Functions of Amylase
116
- synthesized by acinar cells
- involved in major digestion of starches
Pancreatic (p-type) amylase
117
- In the mouth
- neutralized by stomach pH
Salivary (s-type) amylase
118
Distribution of amylase
Small conc. in other tissues (ovaries, testes, tears, colostrum, lungs, adipose tissue)
Salivary glands (greatest conc.)
Pancreas
119
Hyperamylasemia is seen in ______ in which serum levels rise w/in 5 - 8 hours of symptom onset
- 4-6x UL normal
- max conc. @ 12 - 72 hours
- RTN by day 3 - 4
Acute Pancreatitis
120
Hyperamylasemia seen in this - up to 4x UL.
Cholesystitis
121
Causes of Hyperamylasemia (levels not mentioned)
Obstruction
Salivary gland inflammation
122
Hyperamylasemia seen in this - 50x UL
Carcinomas; lung and ovary
123
Testing for hyperamylasemia can also detect
- pseudocyst
- ascites
- pleural effusion
- trauma
- alcoholism
124
Functions of Lipase
Hydrolyzes ester linkage of triglycerides to glycerol and fatty acids (carbons 1 & 3)
Bile salt and colipase assist in emulsification
Emulsification - fat to small sizes
125
Lipase sources
Pancreas
Tongue
126
Lipase increased levels seen in _______. Serum levels rise in 4-8hrs (2-50xUL), peak @ ~24hrs, decreases 8-14 days
Other causes;
- obstructions
More specific for pancreatitis than amylase levels.
Pancreatitis
127
Transaminases
Catalyze the reversible transfer of an amine from an alpha-amino acid to an alpha-keto acid
Participate in amino acid catabolism and biosynthesis
128
Alanine aminotransferase (ALT)
Catalyzes the reversible transfer of an amine group
Alanine + Oxoglutarate Pyruvate + glutamate
Widely distributed in tissues
Predominate source, liver & kidney
129
ALT is _________ and indicates Liver cell damage (Hepatocellular disorders, ie. Hepatitis)
Liver Specific
130
Aspartate + Oxoglutarate <-> oxaloacetate + glutamate
Tissue sources - widely distributed
- Heart and liver
- Skeletal muscle
- Kidney
Located in cytoplasm and mitochondria
Aspartate (AST)
131
Significance of AST
Could be use to determine if pt was having AMI. Rise 6-8 hrs, peak at 18-48, normal 4-5 days (ALT usually normal)
- avg. increase 4-5x, 10-15x = fatal infarct
Muscular dystrophy - ~8x UL
Liver Diseases
132
Gamma glutamyltransferase (GGT)
Transfer of gamma-glutamyl group from one peptide to another amino acid
Acts on glutamate residue
All cells (membrane) except muscle
133
Function of Gamma glutamyltransferase (GGT)
Transport of amino acids through cell membrane
Serum levels originates in the liver
Kidney shows highest activity
Can be liver function test
134
Significance of Gamma glutamyltransferase (GGT)
Elevated in all forms of Liver disease
- Hepatitis - moderate
- Liver cancer - high
- Cirrhosis - variable
Pancreatitis - 5-15x UL
Prostate malignancy
Anticonvulsant drugs
135
Intrahepatic or posthepatic biliary obstruction (highest) 5-30x normal
More sensitive of an indicator than ALP, ALT, AST for obstructive jaundice, cholecystitis & cholangitis (occurs earlier and persists longer)
GGT and Biliary Obstruction
136
Liver function tests (LFTs)
ALT
AST
GGT
Albumin/Total Protein
Bilirubin
ALP
PT
137
Cardiac Panel
Troponin T and/or I
CK-MB
Total CK
Myoglobin
LD (1/2)?
AST?
138
Pancreatic panel
Amylase
Lipase
Calcium
Triglycerides
Glucose
