Final Flashcards
1
Q
What is the difference between plasma and serum?
A
Plasma is the liquid portion of whole blood. Serum is the liquid portion of clotted blood.
2
Q
What is the most common specimen used in chemistry testing?
A
Serum.
3
Q
What type of tube will be used for serum and what type for plasma?
A
Serum- red top or serum separator tube SST. Plasma- green top with heparin.
4
Q
How is serum collection done?
A
Blood is allowed to clot for 20-30 minutes and then centrifuged for 5-10 minutes. Serum should be separated from the cells within one hour after collection.
5
Q
What happens if serum is separated from cells after 1 hour?
A
You can get erroneous results like falsely low glucose, and falsely high LDH and K. However this usually takes hours of sitting there.
6
Q
What is hemolysis and what will it lead to?
A
Destruction of RBC’s and this liberates intracellular biochemicals creating falsely high serum LDH and K levels.
7
Q
What is lipemic serum?
A
Serum which is hazy due to the presence of chylomicrons.
8
Q
What causes lipemic serum?
A
Non-fasting specimen or an inherited ipoprotein metablosim abnormality (inability of the liver to clear the chylomicrons).
9
Q
What are metabolites?
A
Toxic waste products that need to be removed.
10
Q
What are substances that are released from cells as a result of cell damage, abnormal permeability, or abnormal cellular proliferation?
A
Enzymes.
11
Q
Name 7 factors that affect glucose control?
A
- Stress. 2. Food consumption. 3. exercise. 4. HORMONES. 5. drugs. 6. Alcoholism. 7. Liver disease.
12
Q
What effects will hormones have on glucose?
A
They all increase serum levels of glucose besides insulin which decreases the levels.
13
Q
What will alcoholism do to glucose levels?
A
Short term- decrease. Long term can lead to diabetes.
14
Q
Why will serum need to be separeted from the cells within one hour?
A
The blood cells will metabolize the glucose resulting in a loss of up to 5 mg/dl (1-2%) of glucose per hour.
15
Q
When can serum go for more than one hour before being separated?
A
If refrigerated or if a gray top (sodium fluoride) tube is used.
16
Q
With a random collected specimen what glucose levels will indicate diabetes mellitus?
A
> 200 mg/dl.
17
Q
With a fasting collected specimen what glucose levels will indicate diabetes mellitus?
A
Greater than or equal to 126 mg/dl.
18
Q
What is the reference value for glucose with a fasting specimen?
A
60-99 mg/dl.
19
Q
How long should you fast before a fasting glucose test?
A
at leaste 8 hours but no more than 12-16.
20
Q
What should not be done prior to glucose testing?
A
No smoking or exercise or undue stress and should be taken first thing in the morning.
21
Q
The fasting glucose test is most useful for what?
A
To indicate overall glucose homeostasis.
22
Q
What is a two-hour postprandial (after a meal) glucose test used for?
A
TO determine the body’s ability to control glucose levels following ingestion of food.
23
Q
What is the two-hour oral glucose tolerance test used for?
A
Used historically to confirm suspected diabetes based upon clinical signs and symptoms.
24
Q
What is the two-hour postload glucose test?
A
A 2 hour specimen alone is used as a single-screening test.
25
What test are recommended by the American Diabetic Association to test for diabetes?
Fasting plasma glucose, two-hour postload glucose.
26
What should be done if you get an abnormal result from a diabetes test?
Should be confirmed by a different test on another day.
27
Which test is best for type II and type I diabetes?
Type II- Fasting plasma glucose. Type I- two-hour postload glucose.
28
What are the names for high and low levels of glucose?
Hyperglycemia and hypoglycemia.
29
What are the most common causes of hyperglycemia?
Uncontrolled DM, Abnormal glucose metabolic states, pancreatic disorders (not making enough insulin), hyper-endocrineopathies (increases hormones and this increases glucose), acute stress, corticosteroid therapy, non-fasting specimen.
30
What are the most common causes of hypoglycemia?
insulinoma, insulin overdose, hypo-endocrinopathies, extensive liver disease, starvation.
31
The formation of urea nitrogen is associated with what?
Protein metabolism (primarily catabolism).
32
How is urea nitrogen made?
Catabolism of proteins liberates amino groups and they are transported to the liver and incorporated into urea.
33
How will urea be excreted?
It diffuses into extracellular fluid and is carried to the kidneys for excretion about 25 grams per day.
34
What is the short name for urea nitrogen?
Blood Urea Nitrogen BUN.
35
What type of product is BUN?
A non-protein nitrogenous waste product.
36
Plasma levels of BUN reflect what?
The balance between production (protein catabolism) and kidney function.
37
What is the name for increased plasma levels of BUN?
Azotemia.
38
What are the 3 types of azotemia?
Pre-renal, renal, post-renal.
39
What pre-renal things can lead to azotemia?
Prolonged high protein intake, dehydration/hypovolemia (decreasd plasma volume), and increased protein catabolism.
40
What are the renal things that can lead to azotemia?
Renal disease.
41
What are the post-renal things that can lead to azotemia?
Lower urinary tract obstructions.
42
What are the things that lead to low levels of BUN?
Expanded plasma volume, liver disease, pregnancy (plasma volume expands).
43
What is the end product of skeletal muscle metabolism?
Creatinine. NOT creatin.
44
Plasma levels of creatinine reflect what?
Skeletal muscle mass only not activity.
45
Creatinine enters the circulation and is removed how?
Removed from the plasma by the kidneys.
46
What type of product is creatinine?
A non-protein nitrogenous waste product.
47
Plasma levels of creatinine are proportional to what?
Skeletal muscle mass of the individual.
48
Increased creatinine and BUN levels are observed in patients with reduced kidney function of how much?
Reduced kidney function of over 50%.
49
Decreased creatinine levels are seen in patients with what?
Reduced muscle mass, most commonly seen in females and children.
50
What are the most common causes of increaed creatinine levels?
Renal disease, increased muscle mass.
51
What is the most common cause of decreased creatinine levels?
Decreased muscle mass.
52
Since creatinine has a steady state of production it is ideal for what?
for a clearance test of kidney function.
53
Clearance is measuered by UV/P which is what?
U- urine concentration of the analyte. V- volume of urine output in 24 hours. P- Plasma concentration of the analyte.
54
Creatinine clearance is considered a sensitive measurement of what?
Overall renal functional impairment.
55
What is the byproduct of purine metabolism?
Uric acid.
56
When will there be purine metabolism?
As RNA and DNA are synthesized and degraded.
57
Uric acid is synthesized where?
In the liver by enzymes.
58
What happens to uric acid as it enters the circulation?
it is filtered, partially reabsorbed and actively secreted into the urine by the kidneys.
59
Plasma levels of uric acid reflect what?
The balance of production and renal function.
60
What results in increased uric acid synthesis?
Increased levels of tissue breakdown.
61
What type of diet has purines in it and a dietary purine intake leads to what?
organ meats, legumes, and yeaste. A low purine diet halves the average daily production.
62
Decreased renal function does what to uric acid levels?
Increases it.
63
How can uric acid exretion be enhanced?
Pharmacologically.
64
What are the names for high and low levels of uric acid?
Hyperuricemia and hypouricemia.
65
What are the most common causes of hyperuricemia (increased production)?
Excess dietary purines, inherited abnormal purine metabolism, certain malignancies (breakdown tissues), chemotherapy.
66
What are the most common causes of hyperuricemia (decreased excretion)?
Idiopathic, renal disease, chemical induced (alcohol, asprin).
67
What are 3 tests for alcoholism?
Increasd Triglycerides and GGT's and hyperuricemia.
68
What are the most common causes of hypouricemia (increased excretion)?
Chemical induced (asprin, estrogen, corticosteroids, warfarin).
69
What are the most common causes of hyouricemia (decreased production)?
Chemical induced (allopurinol).
70
What are the 4 electrolytes?
Sodium, potassium, chloride, CO2
71
Why are electrolytes important?
Water balance, acid-base balance, nerve conductivity and muscle contractility, and many other cellular functions.
72
Why would you order electrolyte tests?
Hospitalized patients: critical care, unstable and surgical patients on intravenous fluids. Outpatients especially those on diuretics and other medications that can alter the electrolyte balance.
73
What is the major intra and extra cellular cations?
Extracelluar- sodium. Intracellular- Potassium.
74
What are the 3 controls of sodium levels?
Dietary intake, renal excretion or retention, endocrine system (ADH, Aldosterone).
75
What are the names for high and low levels of sodium?
Hypernatremia, hyponatremia.
76
What are the most common causes of hypernatremia?
Increased sodium intake from diet (uncommon), decreased sodium loss (increasd aldosterone), excess water loss ( GI loss without rehydration excessive sweating dehydration).
77
What are the most common causes of hyponatremia?
Decreased sodium intake (rare), increased sodium loss (adrenal insufficiency prolonged vomiting/ diarrhea, diuretics, chronic renal insufficiency), increaed free body water (over-hydration congestive heart failure).
78
Hyponatremia can lead to signs and symptoms of what?
hypotension, shock, cardiac abnormalities, mental aberrations such as confusion.
79
What is the plasma level of potassium like?
Very low since it is an intracelluar electrolyte.
80
What function is greately influenced by potassium?
Neuromuscular contractility.
81
Potassium levels are critically important in what?
Patients with heart conditions.
82
How will the kidney regulate pH?
Shift K and H ions.
83
Very slight alterations of potassium serum levels are critical and can reflect what?
major intracellular potassium abnormalites.
84
What happens to potassium in the kidneys?
It is lost and cannot be reabsorbed.
85
Potassium levels are greatly influenced by what?
Aldosterone and sodium reabsorption and loss.
86
What are three things to think of with increased potassium levels?
Hemolysis- will release intracellular K. Venipuncture- can increase if tourniqet is left on too long or if you slap their arm by releasing K from platelets. Thrombocytosis- Platelets are rich in K and K is released into the serum with thrombocytosis.
87
What are the names for high and low levels of potassium?
Hyperkalemia, hypokalemia.
88
What are the most common causes for hyperkalemia?
Exess dietary intake, Dehydration, acute or chronic renal failure (most common), adrenal insufficency, hemolytic diseases, massive tissue injury or infection.
89
What are the most common causes for hypokalemia?
Dieatary deficiency, GI loss (prolonged vomiting/diarrhea, diuretics, hyper-adrenal conditions, licorice overdose.
90
Both hyper and hypo kalemai result in what?
Weakness and loss of deep tendon reflexes, disturbances of GI motility, and also mental aberrations.
91
What are the lethal consequences of hyper- or hypo- kalemia?
paralysis of respiratory muscles and cardiac arrest.
92
What is the major extracellular anion?
Chloride.
93
Chloride is responsible for what?
Maintaining electrical neutrality as a salt in combination with sodium.
94
Chloride is intimately involved in what?
Acid-base balance.
95
It is most common to see chloride changes associated with what?
Altered breathing as part of respiratory compensation for pH.
96
Chloride shifts parallel changes in what?
Sodium.
97
Alone chloride is of what clinical value?
Little always measured in combination with other electrolytes.
98
What are the names for high and low levels of chloride?
Hyperchloremia and hypochloremia.
99
What are the most common causes of hyperchloremia?
Dehydration, acidosis.
100
What are the most common causes of hypochloremia?
Overhydration, GI loss, alkalosis.
101
Why is bicarbonate dissolved not the same as pCO2?
Bicarbonate dissolved is CO2.
102
Bicarbonate has a very similar role as ____ in maintaining electrical neutrality/
Chloride.
103
Bicarbonate is regulated by what to maintain acid-base balance?
Kidneys.
104
What are serum levels of bicarbonate like?
They tend not to be accurate and therefore this test roughly reflects acid-base balance.
105
What are the most common causes of increased and decreased bicarbonate levels?
Increased- metabolic alkalosis. Decreased- metabolic acidosis.
106
CO2 content and related considerations are best evaluated how?
Via arterial blood gases.
107
How much of the total body calcium is stored in bones?
99%.
108
What are the important physiologic activities of clacium?
Blood coagulation, neuromuscular condiction, cell membrane function, regulation of glandular excretions, sekeletal and cardiac muscle contractility.
109
How will calcium circulate in the plasma and what will this mean?
As a cation and as such can be considered an electrolyte. About 50% of the calcium circulates bound to albumin and the other 50% is ionized calcium.
110
A routine serum calcium assay is actually what?
Total serum calcium.
111
What type of circulating calcium is the active portion?
The ionized calcium.
112
What is calcium that is bound to albumin like?
It is not physiologically active.
113
What is more common hypoalbuminemia or hyperalbuminemia?
Hypoalbuminemia.
114
Albumin altering conditions influence what?
The total amount of calcium but not the physiologically active ionized portion.
115
Can ionized calcium be assayed?
Yes via separately ordered test and is not part of a routine biochemical profile.
116
Ionized calcium is most useful in evalutaing what?
Hypocalcemia.
117
What hormone is responsible for controlling plasma levels of calcium?
PTH.
118
What will create an increased amount of PTH?
Hypocalcemia.
119
What will PTH do?
Osteoclastic bony resorption (take calcium from bones), decreases the loss of calcium in the urine, and enhances the absorption of calcium in the intestines. It will also help the kidneys make the active form of vitamin D.
120
What will vitamin D do?
enhances intestinal absorption of calcium and phosphorus and accelerate bony resporption.
121
How will Vitamin D be made from the sun?
Sun changes 7-dehydrocholesterol into cholecalciferol (D3), then D3 goes to the liver (so will Dietary intake of D3 and D2) and will be converted into 25-hydroxyvitamin D3. Then 25-hydroxyvitamin D3 will go to the kidney and with the help of PTH the kidney will convert it inot 1,25-dihydroxyvitamin D3 which maintains calcium balance in the body.
122
How will PTH decrease loss of calcium in the urine?
It promotes excretion of phosphate.
123
Alterations in PTH will affect what portion of calcium?
The ionized calcium.
124
What is the name for high and low levels of calcium?
Hypercalcemia and hypocalcemia.
125
What are the most common causes of hypercalcemia?
parathyroid disease (hyperparathyroidism), malignancies, granulomatous infections (TB, sarcoidosis), hyperthyroidism (thyroid hormone can increse osteoclastic activity), pancreatitis.
126
What are the most common causes of hypocalcemia?
Parathyroid disease (hypoparathyroidism), renal failure, vitamin D deficiency.
127
Hypocalcemia will happen at what level and what is the top limits of calcium?
Hypo- less than 7 mg/dl. Top limit- 10.5 mg/dl.
128
What are the signs of hypocalcemia?
Nervousness, excitability, tetany (uncontrolled total muscle contraction).
129
When will hypercalcemia be something to worry about?
if top limit is 10.5 then you should worry at 10.6.
130
What will happen with calcium levels at 11.5-12.0 mg/dl?
Fatigue, depression, vague GI (nausea, vomit, anorexia, constipation).
131
What will happen with calcium levels at 12.0-13.0 mg/dl?
Calcification of soft tissues.
132
What will happen with calcium levels greater than 13.0 mg/dl?
Medical emergency.
133
In general what will phosphorus do?
The opposite of calcium.
134
How is phosphorus measured?
As inorganic phosphate.
135
what % of total body phosphorus is stored with calcium in bones?
85%.
136
Increased calcium will do what to phosphorus?
Decrease it and decreased calcium will increase phosphorus.
137
What is the name for high and low levels of phosphorus?
Hyperphosphatemia and hypophosphatemia.
138
What are the most common causes of hyperphosphatemia?
parathyroid disease (hypoparathyroidism), renal failure, High phosphate diet, malignancy of bone.
139
What is the most common cause of hypophosphatemia?
Parathyroid disease (hyperparathyroidism).
140
What are the 4 tests for serum proteins?
1. Total protein. 2. Albumin. 3. Globulins. 4. A/g ratio.
141
What are the main types of circulating proteins?
Albumin and globulins.
142
How helpful is a total protein test alone?
Not very you need an albumin or globulins test to go with it.
143
Albumin by weight is the_______________________.
largest single fraction of plasma proteins even though it is a small molecule.
144
Where is albumin made at and what can this be helpful for?
In the liver and it can be used as a liver function test LFT.
145
What is the major responsibility of albumin?
To create osmotic pressure of blood plasma.
146
Albumin acts as a circulating reservoir of what?
Amino acids.
147
What is another role of albumin?
Acts as a carrier protein.
148
How common is hyeralbuminemia and what causes it?
It is rare and is caused by overt clinicla dehydration.
149
Hypoalbuminemia is associated with what?
reduced synthesis, increased loss, increased catabolism.
150
What is the most common cause of hyperalbuminemia?
decreased plasma volume.
151
What are the most common causes of hypoalbuminemia?
Reduced synthesis (liver disease), increased loss (protein-losing nephropathies, protein-losing enteropathies), increased catabolism (widespread cancer).
152
What are globulins?
Total protein minus albumin.
153
How many groups of globulins are there and what are the groups based on?
4 and they are based upon electrophoretic mobility.
154
What will the clinical significance of hypo- and hyper-globulinemai be reatled to?
Which globulin accounts for the increase or decrease.
155
What are the 4 groups of globulins?
Alpha-1-globulins. Alpha-2-globulins. Beta globulins, Gamma globulins.
156
What are the types of alpha-1 globulins and what are there %?
Alpha-1-antitrypsin (AAT)- 90%. Alpha-fetoprotein (AFP)- 10%.
157
What type of protein is the alpha-1-antitrypsin?
Acute phase reactant.
158
What is an acute phase reactant protein?
one that is created as a reaction to the acute phase and they are protease inhibitors.
159
What are protease inhibitors?
they keep inflammatory responses in check.
160
What is the main reason for increased alpha-1-antitrypsin?
Inflammatory diseases.
161
What is the most common cause for decreased levels of alpha-q-antitrypsin?
Inherited deficiencies associated with juvenile pulmonary emphysema.
162
What are plasma levels like for alpha-fetoprotein?
Major plasma protein in the fetus but minute levels in the adult.
163
What are increased levels of alpha-fetoprotein associated with?
certain malignancies or seen during pregnancy with a neural tube defect and down's syndrome.
164
Name the only alpha-2-globulin mentioned in the notes?
Haptoglobin.
165
What is the most common cause for increased alpha-2-globulins?
An acute phase reaction to an acute inflammatory disease.
166
What will haptoglobin do?
Binds and transports free hemoglobin to the RE system and it is an acute phase reactant protein.
167
What is the most common reason for decreased levels of haptoglobin?
hemolysis.
168
Name the 2 beta globulins mentioned in the notes?
Transferrin- transports protein of iron and beta lipoprotein- corresponds to LDL
169
What are the most common causes of increased and decreased beta globulins?
Increased- hypercholesterolemia. Decreased- malnutrition.
170
Name the 5 gamma globulins?
IgA, IgD, IgE, IgG, IgM.
171
IgA is responsible for what?
lining surfaces of tubules and the surface of the respiratory and GI tracts.
172
Where is IgA the perdominant Ig in the body?
Body fluids and secretions.
173
How often is IgA assayed in the the blood and why?
Not often since there is very little in the blood.
174
What is the role of IgD?
B-cell mediated immunity.
175
How often is IgD assayed in the blood and why?
rarely because it is rarely detected in the blood.
176
What is IgE used for?
Allergic reactions like anaphylactic, atopic and asthmatic.
177
IgE assay can be used to identify what?
Existence of allergic reactions or disorders from type I hypersensitivity reactions.
178
What is the test used where the patients IgE is tested to see if it reacts to known allergens?
RAST (radioallergosorent testing).
179
What is the most abundant circulating Gamma globulin?
IgG.
180
What will IgG do?
forms antibodies that may persist for life and give immunity.
181
Increase in IgG is the most common use for what?
Serum protein electrophoresis (SPEP).
182
What is the most common immunoglobulin responsible for the M spike?
IgG.
183
M spike is seen in what?
Multiple myeloma.
184
IgG is commonly responsible for what?
Polyclonal gammopathy associated with inflammatory disorders.
185
IgM does what?
It is the initial humoral response to infection.
186
IgM signals what?
Presence of acute or very recent infection.
187
What is the form of the antibodies in the ABO blood group system?
IgM.
188
What gamma globulins will be present (in what order) for a primary and secondary infection?
primary- IgM first and then followed by a larger IgG. Secondary- IgM first and then almost at the same time a very large IgG response.
189
What is the albumin globulin ratio for?
It serves as an indicator to look closely at the individual levels of albumin and globulins.
190
Why are lipids complexed with proteins?
To transport the insoluble lipids.
191
Name the 4 proteins that carry lipids?
Chylomicrons, low density lipoproteins (LDL), very low density lipoproteins (VLDL), High density lipoproteins (HDL).
192
In general what type of lipids will be in chylomicrons?
mainly triglycerides from diet.
193
In general what type of lipids will be in LDL's?
cholesterol is about half and has some protein and pospholipids.
194
In general what type of lipids will be in VLDL's?
TG.
195
In general what type of lipids will be in HDL's?
VERY LITTLE TG, half is protein, little cholesterol.
196
What happens to lipids from the diet?
They are put into chylomicrons with bile acids and cholesterols help and transported to the capillaries.
197
What happens to chylomicrons in the capillaries?
Lipoprotein lipase (LPL) wil bind to them and burn the lipids as energy or trun them into adipose and spit out lipoprotein remnants full of cholesterol.
198
What happens to lipoprotein remnants?
They go to the liver and release the cholesterol.
199
What happens to cholesterol in the liver?
It can be turned into bile or it can be sent out in VLDL's.
200
What happens to VLDL's?
They go to the capillaries and LPL will burn lipids and make adipose from TG, and then they become LDL's.
201
What happens to LDL's?
1. They can go back to the liver and be recyled. 2. Do to peripheral cells and be used. 3. Macrophages will get them and they undergo oxidation and this leads to atherosclerotic plaque.
202
Where do HDL's come from?
HDL will take cholesterol from tissues and then turn into LDL's.
203
What happens to 70% of the LDL's?
removed by the liver and recyled.
204
Why will LDL's go to peripheral cells?
They need the cholesterol to synthsize hormones, cell membranes.
205
Dyslipoproteinemias can result from what?
dietary supply, liver function, availability of appropriate apoproteins, availability of enzymes, sufficient HDL.
206
What are the 2 catagories of dyslipoproteinemias?
Primary and secondary.
207
What are the causes of primary dyslipoproteinemias?
genetic and lipid levels often need to be controlled via medications.
208
What are the causes of secondary dyslipoproteinemias?
Side effect of another identifiable disorder, if secondary disorder is controlled often lipid levels go back to normal.
209
Where will 25 and 75% of the cholesterol be at?
HDL-25%. LDL-75%.
210
What are the cholestrol levels associated with negative, neutral and positive risk factors for CAD?
Negative- 200 mg/dl.
211
What are the most common causes of hypercholesterolemia?
Dietary indiscreations, hyperlipoproteinemias (type II, III, V), nephrotic syndrome, hypothyroidism, cholestatic hepatobiliary disorders, oral contraceptives.
212
What are the most common causes of hypocholesterolemia?
abetalipoproteinemia, hypobetaliproteinemia, hyperthyroidism, malabsorption, malnutrition.
213
What are the ideal, Optimal and positive risk factor levels of HDL for males and females?
Ideal; males- >45 females- >55. Optimal; males- >60 females- >70. Positive risk; males- < 35.
214
How can HDL's be lowered?
obesity and smoking.
215
How can HDL's be elevated?
Aerobic exercise, moderate alcohol, weight reduction, smoking cessation and niacin (not statins).
216
What is the most common cause of increased HDL's?
Familial high HDL's, exercise (30 minutes 3 times per week).
217
What are the most common causes of decreased HDL's?
Atherogenic lipid profile syndrome, familial low HDL, liver disease, malnutrion.
218
What subclass of HDL has the greatest protective capacity of reverse cholesterol transport?
2b.
219
What HDL levels will have sufficient HDL 2b to provide reverse cholesterol transport?
40-60 mg/dl.
220
What should the Cholesterol/HDL ratio be for females and makes?
Females- >4.4. Males > 5.0.
221
What is the optimal LDL level?
<70 mg/dl in a patient with a high risk of CAD.
222
What are some risk factors for increased LDL's?
cigarete smoking, hypertension, low HDL, family history, 10 year age risk from the framingham algorithm.
223
What are the most common causes of increased LDL's?
Familial lipoproteinemia abnormalites, chronic liver and kidney diseases, hypothyroidism, poor life-styles.
224
What are the most common causes of decreased LDL's?
Familial/ inherited decreased LDL's, hyperthyroidism, hypoprtoeinemic states, good lifestyle states, drugs.
225
What LDL subclasses are most commonly elevated and what are they like?
IIIa and IIIb and they are small enough to migrate into cells and cause atherogenic disease.
226
What are the most dangerous subclasses of LDL's?
Iva dn Ivb because they are very small.
227
What will happen if patients have more than 10% of the type Iva and Ivb LDL's?
They usually display vascular events within months of detection.
228
What will VLDL's primarily reflect?
Endogenously produced TG.
229
Elevated VLDL is a risk factor for what?
CAD because they are made into LD's.
230
Will VLDL's be part of a basic lipid profile?
No.
231
In a fasting state most of the TG circulate how?
VLDL's and a few in LDL's.
232
A non fasting state where will most of the TG be at?
Chylomicrons.
233
Fasting TG is part of a lipid profile used to evaluate what?
The risk of cardiovacular disease.
234
What are the most common causes of hypertrigylceridemia?
familiar hyperlipoproteinemias, DM (poorly controlled), Hypothyroidism, chronic renal disease, alcoholism, OAC/estrogen, high carb diet, non-fasting specimen.
235
What are the most common causes of hypotriglyceridemia?
malabsoprtion/malnutrion, hyperthyroidism, abetalipoprtoeinemia.
236
Elevated plasma levels of lipoprotein "little A" (Lp(a)) is associated with what?
thrombosis development.
237
Lp(a) is a positive risk factor for what?
Cardiovascular disease.
238
What will increase or decrease levels of lP(a)?
It is genetically encoded and cannot be manipulated as easily as HDL or LDL.
239
What happens to hemoglobin when RBC's die?
Globin- goes to AA pool. Heme will turn into unconjugated bilirubin which goes to the liver and then is conjugated bilirubin. Conjugated bilirubin can go to the gallbladder as bile and then goes to the intestines and can be turned into urobilinogen (which is recyled in the liver or excreted in the urine) or it is turned into stercobilin and excreted in the feces. Conjugated bilirubin can also be excreted in the urine but in small amounts.
240
What is total bilirubin?
unconjugated + conjugated.
241
What is the major portion of bilirubin and why?
Unconjugated because conjugated goes into bile.
242
How much unconjugated bilirubin is found in the urine?
None because it is not soluable.
243
Will there be unconjugated hypo and hyperbilirubinemia?
Only hyper.
244
What is the most common causes of unconjugated hyperbilirubinemia?
hematologic conditions involving hemolysis, normal neonatal jaundice, advanced hepatic diseases, gilberts syndrome, crigler-najjar syndrome.
245
What is gilberts syndrome?
Congenital defect in hepatocyte uptake of unconjugated bilirubin resulting in mild unconjugated hyperbilirubinemia; may cause intermittent skin discoloration; no clinical signficance.
246
Increased levels of conjugated bilirubin appear in the circulatino only in the presence of what?
hepatobiliary pathology.
247
Conjugated hyperbilirubinemai will result in bilirubinuria once plasma levels exceed what?
1.5 mg/dl.
248
What are the 3 most common causes of altered conjugated bilirubin levels (and how will it be altered)?
All will be conjugated hyperbilirubinemia. 1. Intrahepatic obstructive disorders. 2. Extrahepatic obstructive disorders. 3. Dubin-Johnson syndrome- congenital defect in transport of conjugated bilirubin into bile; results in a mild conjugate hyperbilirubinemia and may cause skin discoloration.
249
What are 3 types of Jaundice?
Hemolytic, hepatocellular, obstructive.
250
What causes hyemolytic jaundice and what will it be like?
Anemia, increased total bilirubin, increased unconjugated bilirubin, increased serum LDH, increased urobilinogen.
251
What causes obstructive jaundice and what will it be like?
Increased total bilirubin, increased conjugated bilirubin, bilirubinuria, decreased urinary urobilinogen, light clay colored stool.
252
What causes hepatocellular jaundice and what will it be like?
increased total bilirubin, increased conjugated bilirubin, increased unconjugated bilirubin (late), increased serum liver enzymes, bilirubinuria, increased urinary urobilinogen.
253
Why will hepatocellular jaundice have increased urinary urobilinogen?
Less conjugated bilirubin goes to the gall bladder, but urobilinogen that is made (even if small amounts) will not be able to go back to the liver for re-processing and will go out in urine.
254
Where are enzymes located?
Functional ones within the cell. Enzymes in the circulation perform no physiological function.
255
Enzymes in the circulation represent what?
either normal or abnorml cellular metabolism and can reflect altered physiologic or a pathologic state of the cell that the enzyme was derived from.
256
Pathology to a cell will release what enzymes?
Since enzymes are specific to organells a pathology will only release enzymes that affect certain organells.
257
What will location of a cell with a pathology have to do with the amount of enzymes released?
Increased if the cell is by blood vessels or lymphatics.
258
What type of cells will produce more enzymes?
Proliferating cells.
259
Clinically significant enzymes often are derived from where?
More than one organ.
260
Since significant enzymes are often derived from more than on organ how can you tell which organ the enzyme came from?
slighlty different biochemical forms are present and they are referred to as isoenzymes or isozyme.
261
How are enzymes quantified?
By catalytic properties not by weight.
262
Significance of enzymes is judged how?
Relative to how may times over the reference range the activity has risen.
263
Will enzymes normally be increased or decreased in tests?
Normally wont see decreased amounts besides alkaline phosphatase.
264
What is another name for alkaline phosphatase?
ALP.
265
What tissues will be clinically important to ALP?
Bone, liver (hepatobiliary), placenta, intestine.
266
What are some reasons ALP could be elevated do to bones?
Neonatal levels high, Pre-puberty levels high, puberty levels high, Osteoblastic disorders like pagets, osteomalacia, hyperparathyroidism.
267
When would the liver be the cause of elevated ALP?
Cholestatic- stasis of the colon, bile flow is obstructed or sluggish.
268
What are the reasons the ALP levels could be elevated do to the placenta?
the placenta makes ALP and will gradually increase, Some malignancies of the liver, and femal reproductive organs can cause ALP to be in circulation.
269
What is the name of the isozyme that comes from malignancies of the liver or female reproductive organs and is like the placental ALP?
Regan isoenzyme.
270
What are some of the causes of intestinal increase in ALP?
2-3 hours after a fatty meal, bowel or peptic ulcer diseases.
271
What are the most common causes of a mild increase in ALP levels?
hepatobiliary disorders, healing fracutures, growing children, pregnancy, post-menapausal, normal geriatrics.
272
What are the most common causes of a moderatley and a marked increase in ALP levels?
Moderate- hepatobiliary disorders. Marked- primary biliary tract disorders, and bone disorders.
273
What are the transferases aka?
Transaminases.
274
What are the transferases/transaminases and what are all of their names?
1. Serum glutamic-oxaloacetic transaminase (SGOT) aka NEW NAME- aspartate aminotransferase (AST). 2. Serum glutamate-pyruvate transaminase (SGPT) aka NEW NAME alanine aminotransferase (ALT).
275
AST aka SGOT is clinically important to what tissues?
LIVER, heart, skeletal muscle.
276
Will the liver cells contain more AST or ALT?
3.5 times more AST.
277
When will AST and ALT be more sensitive indicators of liver pathologies?
AST- alcholoic liver disease. ALT- acute liver inflammation and extrahepatic biliary tract obstruction.
278
What are the most common causes of a mild increase in AST aka SGOT?
liver- mild inflammation, cirrhosis, neoplasm. Skeletal muscle- myopathy, myositis, trauma.
279
What are the most common causes of a moderate increase in AST aka SGOT?
Liver- moderate inflammation. Heart- myocardil infarction.
280
What are the most common causes of a marked increase in AST aka SGOT?
Liver- acute inflammation (hepatitis).
281
What tissues will be clinically importatant with ALT aka SGPT?
LIVER, heart, skeletal muscle.
282
ALT is clinically used to evaluate what?
Liver damage.
283
When will high and low levels of ALT be seen?
High- inflammatory conditions like hepatitis. Low- skeletal muscle and myocardial pathologies.
284
What are the most common causes of mild ALT increase?
mild hepatic inflammation, infectious mononucleosis.
285
What are the most common causes of moderate and marked ALT increases?
Moderate- actve liver disease, hepatotoxic drugs. Marked- acute active liver disease.
286
A single week of overindulging in fast food leads to what?
Pathological levels of ALT. So heavy fast food eating can cause increased ALT levels.
287
What is the older name for gamma glutamyl transferase (GGT)?
Gamma glutamyl transpeptidase (GGTP).
288
What tissue will be clinically importatn with GGT aka GGTP?
Liver.
289
Large qunatities of GGT are found where?
In similar locations as ALP.
290
GGT tests are most sensitive for what?
indicators of both intra- and extrahepatic obstructive processes.
291
What will increased ALP + increased GGT =?
Liver pathology.
292
What will increased ALP + normal GGT =?
Bone pathology.
293
What will normal ALP + increased GGT= ?
Liver.
294
Will GGT be included in most panels?
No.
295
GGT is released when?
With toxic hepatocellular damage due to acetaminophen, alcohol-very sensitive for consumption.
296
What is the most common cause for increased levels of GGT?
liver- All forms of pathology. Hepatotoxic drugs- ETOH, acetominphen.
297
What enzyme is LD aka LDH?
Lactate dehydrogenase.
298
LDH is present in nearly all tissues but is in greatest abundance in what tissues?
Heart, blood cells, skeletal muscle, liver.
299
How many isozymes are there of LDH and what are the names?
5; LDH1-5.
300
Which LDH is for the lungs?
LDH-3.
301
Which LDH is for the kidney, placenta, and pancrease?
LDH-4.
302
What tissue will LDH-1 be for?
HEART MUSCLE, rbc's
303
Which LDH is for the WBC's?
LDH-2.
304
What tissue will LDH-5 be for?
Liver and skeletal muscle.
305
From greatest levels to leaste what is the order of LDH concentration?
LDH-2 > 1 > 3 > 4 > 5.
306
When concentrations of LDH-2 and LDH-1 flipp this is indicitive of what?
myocardial infarction.
307
How specific will LDH tests be? Why?
Very non specific since LDH is observed in most any condition which tissues are damaged.
308
What are the most common causes of mild, moderate and marked increases in LDH levels?
Mild- liver disorders. Moderate- hematologic conditions, cardiopulmonary conditions, liver inflammation, muscular pathology. Marked- hematologic conditions, hemolytic conditions, acute liver inflammation, disseminated cancer.
309
What is the old name for creatine kinase (CK)?
creatine phosphokinase (CPK).
310
What are the clinically important tissues associated with CK?
heart, skeletal muscle, brain.
311
How many isozymes are there of CK and what are their names (both of them) and what tissues are they associated with?
CK1 aka CK-BB- brain and CNS. CK2 aka CK-MB- myocardial muscle. CK3 aka CK-MM- skeletal muscle.
312
What % of the isozymes of CK will normal serum have?
100% CK3 aka CK-MM.
313
Increased total CK is primarily useful for what?
Myocardial ischemic changes and skeletal muscle abnormalites.
314
What is the GOLD standard for myocardial infarctions?
CK-MB.
315
What will cause increased CK-BB?
Brain traumas.
316
What will cause increased CK-MM?
trauma to skeletal muscle including severe exercise.
317
What are the most common causes of mild, moderate and marked increases in CK levels?
Mild/moderate- severe exercise, skeletal muscle trauma, myocardial infarction. Marked- muscular dystrophy, inflammation of skeletal muscle, myocardial infarction.
318
What enzymes will be elevated with liver pathologies?
AST, ALT, ALP, GGT, LDH.
319
What enzymes will be elevated with heart pathologies?
CK, LDH.
320
What enzmes will be elevated with skeletal muscle pathologies?
CK, LDH.
321
What enzymes will be elevated with bone patholgies/
ALP.
322
What enzymes will be elevated with pancrease pathologies?
amylase and lipase.
323
What is serology?
Diagnostic use of serum antiboides and other globulins to DETECT INFLAMMATION and INFECTIOUS DISEASES.
324
Serolgy is aka?
immunoserolgy or immunodiagnostic testing.
325
ESR is done over how long of a time period?
One hour.
326
Sedimentation is determined by what?
density of RBC's relative to plasma.
327
When will RBC sedementation rates increase? What is this called?
When RBC's aggregate which they want to do. Called Rouleaux.
328
What will help prevent RBC's from aggregating? What is this called?
Negative charges and this is calle dthe Zeta Potential.
329
How is the zeta potential reduced so the RBC can aggregate?
Acute phase reactant proteins from inflammation will lower the zeta potential.
330
What are APP's?
Acute phse reactant proteins.
331
Name 5 APP's?
C-reactive protein (CRP), haptoglobin, fibrinogen, alpha-1-antitrypsin, C3 portion of complement.
332
ESR test is done to detect the existence of what?
Clinically significant inflammation.
333
Name some factors that increase the ESR?
old age, female, pregnancy, anemia, RBC abnormalities- macrocytosis, Elevated APP's from infections, inflammation, malignancy, technical factors.
334
Name some factors that decrease the ESR?
Extreme leukocytosis, polycythemia, RBC abnormalites- spherocytosis, acanthocytosis, microcytosis, technical factors, protein abnormalites.
335
What is the perferred ESR test?
Westergren method.
336
What is the westergren method like and what are the normal results?
200nm tube utilizing diluted anticoagulated blood. Normal patinet > 50= male- age Divided by 2. Female- age + 10 divided by 2.
337
What are the three basic clinical uses of a ESR test?
1. Detect inflammation. 2. monitor a disease. 3. screen for occult inflammatory or neoplastic condition.
338
What will the purpose of a ESR test be?
screening tool but can never rule out the existence of a condition.
339
What are the most common causes of mild, moderate and marked increases of ESR?
Mild- age, menstruating. Moderate- pregnancy, active inflammatory, infectious, neoplatic diseases. Marked- monoclonal gammopathies, Polyclonal gammopathies.
340
What test is better than a ESR?
C-reactive protein (CRP).
341
What is CRP?
A glycoprotein made by the liver in response to inflammation.
342
CRP is what type of protein?
APP that appears early and is very sensitive.
343
What will CRP levels be like in a normal person?
Not present.
344
CRP levels can increase how much after trauma?
100 fold after severe trauma, acute infection/inflammation, surgery, neoplastic proliferation.
345
Will CRP tests be specific?
No but very sensitive.
346
CRP will become detectable how long after pathologies?
18-24 hours.
347
What levels will elevate faster and go down faster with significant inflammatory events ESR or CRP?
CRP elevates faster and returns to normal before ESR.
348
When would CRP levels be almost always present?
Rheumatic fever, rheumatoid arthritis, acute infectious disease.
349
When would CRP levels be frequently present?
active tuberculosis, Gout, advanced malignant tumors.
350
When would CRP levels be sometimes present?
some viral infections, multiple sclerosis, post-surgical.
351
What can CRP be used for that is a non-lipid marker (what are the different names for this)?
cardiovascular disease, aka Highly sensitive CRP, and cardio-CRP.
352
What are the clinical uses of Highly sensitive CRP?
Used to determine the relative risk of cardioascular disease and to assess risk of recurrent cardiovascular events in patients with coronary heart disease.
353
What has midly elevated CRP been linked with?
With risk of CVD including first and recurrent coronary events and stroke, vascular events after stroke, myocardial infarcts or angina in patients with peripheral vascular disease, sudden cardiac death, hypertension, dementia and type II diabetes.
354
Studies have shown that Highly sensitive CRP is a strong predictor of what?
Increased cardiovascular risk in both men and women.
355
Screening with CRP and ____ may provide a better risk assessment than using either test alone.
LDL.
356
What levels of CRP and LDL will suggest that the patient is at greater risk of cardiovascular diseases?
High CRP and normal LDL Vs. those with normal CRP and high LDL.
357
What type of patients should be tested for Highly sensitive CRP?
Those with an intermediate CHD risk.
358
What is Hemostasis?
two things 1. Blood clotts when it is supposed to clott. 2. Blood stays a liquid when it is supposed to be a liquid.
359
How will the endothelial cells of intact vessels prevent thrombin formation?
They secrete tissue plasminogen and inactivate thrombin.
360
What is primary hemostasis?
vascular contraction, platelet adhesion and formation of a soft aggregate plug.
361
With primary hemostasis when will adhesion occur?
When circulating von willebrand factor attaches to the subendotherlium.
362
What part of platelets stick to von willebrand factor?
Glycoproteins.
363
What will activate platelets once they stick to von willebrand factor?
Collagen.
364
The soft plug formed by platelets will form how fast?
In about 20 seconds.
365
What is secondary hemostasis?
the process of stabilizing the soft clott and maintaining vasoconstriction.
366
How is vasoconstriction maintained during secondary hemostasis?
Platelets secrete serotonin, prostaglandin and thrombaxane.
367
The soft plug will solidify through a complex interaction between what?
platelet membrane, enzymes, and coagulation factors.
368
Where are coagulation factors produced at?
The liver.
369
What are the steps of platelet plug formation?
ACTIVATION, adhesion, aggregation, plug formation, consolidation, fibrin stabilization- this is the end-product of coagulation.
370
What are the 3 pathways of coagulation?
Extrinsic, intrinsic and common pathway.
371
What will cause the extrinsic and intrinsic pathways to start the coagulation process?
extrinsic- Vessel injury. Intrinsic- surface contact.
372
Where will the intrinsic and extrinsic pathways merge at?
Factor X.
373
Explain how extrinsic and intrinsic pathways make it to the common pathway?
Extrinsic- vessle injury with tissue factor activates factor VII and activated factor VII (VIIa) will activate factor X which is the start of the common pathway. Intrinsic- surface contact activates a few factors that along with calcium will create (or activate I have no idea) factor VIII which will activate factor X.
374
The liver needs what to make factor VII?
Vitamin K.
375
Von willebrand factor is needed to create what?
Factor VIII.
376
Once factor X is activated into Xa what will happen?
with calcium it will take prothrombin and make thrombin. Thrombin will take fibrinogen and create fibrin, and fibrin will become stable fibrin with cross links.
377
How will heparin prevent coagulation?
It will stop thrombin from turning fibrinogen into fibrin.
378
How many known bleeding conditions are caused by poor vasoconstriction?
None.
379
What kind of tests can be done to assess vasoconstriction?
bleeding time.
380
What tests can be done to assess platelet plug formation?
platelet count, bleeding time.
381
What tests can be done to assess coagulation?
Prothrombin time (PT), Activated partial thromoplastin time (APTT).
382
Will PT or APTT be associated more with Extrinsic and intrinsic pathways?
PT- extrinsic. APTT- intrinsic.
383
As far as different tests that will be run what is the difference in this class between PT and APTT?
Nothing they are the same test for this class.
384
The Bleeding Time (BT) test are done to assess what?
platelet fuction.
385
The bleeding time test is used to evaluate the interaction of what?
platelets with vessel wall and formation of the platelet plug.
386
How will coagulation affect the bleeding time test?
It wont they are independent things.
387
What can prolonge the bleeding time test results?
thrombocytopenia <50K.
388
What needs to be established before the bleeding time test can be done and why?
platelet count. The bleeding time test is to assess the function of platelets so to test function you need to make sure you have a normal amount.
389
Lower platelet numbers equals ______ bleeding.
prolonged or longer time.
390
The bleeding time test is affected by thrombocytopenia and what?
vasoconstriction capabilites.
391
Who will have vasoconstriction problems?
Patients with senile skin changes due to age loss of elasticity in vessels.
392
What are 2 ways to do the bleeding time tests?
1. Duke bleeding time- stab wound to the ear lobe. 2. Ivy bleeding time- more standardized method of incision to the forearm.
393
Name 5 things that can affect bleeding time tests?
Poor vascular function, depth of incision, touching incision, ETOH consumption, asprin consumption.
394
How long will asprin consupmtion still affect bleeding time tests?
5 days after one 300 mg dose.
395
What are 3 of the most common causes of prolonged bleeding times?
1. qualitiative platelet abnormalites- thrombocytopenia. 2. qualitative platelet abnormalities- platelet function. 3. loss of capillary integrity.
396
What can lead to thrombocytopenia?
reduced production in the bone marrow, destruction of platelets outside the bone marrow- intravascular or intrasplenic.
397
What causes reduced production of thrombocytes?
bone marrow malignancies, both primary and metastiasis toxic effects of drugs, chemicals, and microorganisms factor deficiencies (B12 and folate).
398
What causes destruction of platelets outside the bone marrow?
intravascular and intrasplenic immune reactions.
399
What can cause qualitative platelet abnormalites?
Von Willebrands disease.
400
What will be the cause of loss of capillary integrity?
Collagen vascular diseases, senile capillary fragility.
401
Platelet count is done along with bleeding time tests and what is a common test done to determine platelet count?
CBC.
402
What is plasma and serum?
Plasma -the liquid part of blood or lymph, as distinguished from the suspended elements. Serum- the clear, pale-yellow liquid that separates from the clot in the coagulation of blood
403
APTT/PT tests are done with what?
Plasma.
404
What is an APTT/PT test used for?
a test to see the time it takes plasma specimen to yeild a fibrin clot once the intrinsic pathway is initiated.
405
What will prolong the APTT/PT test?
deficiencies in any of the factors involved.
406
The APTT/PT test is used to monitor what?
Patients on therapeutic heparin.
407
Name the 3 most common causes of prolonged APTT?
1. Congenital coagulation factor deficiencies- hemophilia A and B. 2. Acquired coagulation factor deficiencies- chronic liver disease. 3. Anticoagulant medication- heparin and coumarin.
408
How will Coumarin work?
It is a vitamin K antagonist. No vitamin K no factors needed for coagulation (or atleaste less).
409
What is INR?
International normalized ratio. Used to monitor patients on theraputic coumarin.
410
Will hemophilia A and B be more extrinsic or intrinsic pathways?
Intrinsic.
411
What is fibrinolysis?
Physiologically controlled degradation of the clot.
412
How will birinolysis happen?
Fibrinolytic enzymes are deposited into the clot in an inactiveated form during clot production and become activated at the appropriate time and begin to degrade the clot.
413
What is left after a clot undergoes fibrinolysis?
Fibrin degradation products.
414
What is DIC?
Disseminated intravascular coagulopathy. This is a type of disorder of the fibrinolysis system and these are very serious medical emergencies.
