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Clin Lab > Final > Flashcards

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.

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2
Q

What is the most common specimen used in chemistry testing?

A

Serum.

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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.

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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.

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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.

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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.

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7
Q

What is lipemic serum?

A

Serum which is hazy due to the presence of chylomicrons.

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8
Q

What causes lipemic serum?

A

Non-fasting specimen or an inherited ipoprotein metablosim abnormality (inability of the liver to clear the chylomicrons).

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9
Q

What are metabolites?

A

Toxic waste products that need to be removed.

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10
Q

What are substances that are released from cells as a result of cell damage, abnormal permeability, or abnormal cellular proliferation?

A

Enzymes.

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11
Q

Name 7 factors that affect glucose control?

A
  1. Stress. 2. Food consumption. 3. exercise. 4. HORMONES. 5. drugs. 6. Alcoholism. 7. Liver disease.
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12
Q

What effects will hormones have on glucose?

A

They all increase serum levels of glucose besides insulin which decreases the levels.

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13
Q

What will alcoholism do to glucose levels?

A

Short term- decrease. Long term can lead to diabetes.

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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.

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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.

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16
Q

With a random collected specimen what glucose levels will indicate diabetes mellitus?

A

> 200 mg/dl.

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17
Q

With a fasting collected specimen what glucose levels will indicate diabetes mellitus?

A

Greater than or equal to 126 mg/dl.

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18
Q

What is the reference value for glucose with a fasting specimen?

A

60-99 mg/dl.

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19
Q

How long should you fast before a fasting glucose test?

A

at leaste 8 hours but no more than 12-16.

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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.

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21
Q

The fasting glucose test is most useful for what?

A

To indicate overall glucose homeostasis.

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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.

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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.

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24
Q

What is the two-hour postload glucose test?

A

A 2 hour specimen alone is used as a single-screening test.

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25
Q

What test are recommended by the American Diabetic Association to test for diabetes?

A

Fasting plasma glucose, two-hour postload glucose.

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26
Q

What should be done if you get an abnormal result from a diabetes test?

A

Should be confirmed by a different test on another day.

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27
Q

Which test is best for type II and type I diabetes?

A

Type II- Fasting plasma glucose. Type I- two-hour postload glucose.

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28
Q

What are the names for high and low levels of glucose?

A

Hyperglycemia and hypoglycemia.

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29
Q

What are the most common causes of hyperglycemia?

A

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.

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30
Q

What are the most common causes of hypoglycemia?

A

insulinoma, insulin overdose, hypo-endocrinopathies, extensive liver disease, starvation.

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31
Q

The formation of urea nitrogen is associated with what?

A

Protein metabolism (primarily catabolism).

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32
Q

How is urea nitrogen made?

A

Catabolism of proteins liberates amino groups and they are transported to the liver and incorporated into urea.

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33
Q

How will urea be excreted?

A

It diffuses into extracellular fluid and is carried to the kidneys for excretion about 25 grams per day.

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34
Q

What is the short name for urea nitrogen?

A

Blood Urea Nitrogen BUN.

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35
Q

What type of product is BUN?

A

A non-protein nitrogenous waste product.

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36
Q

Plasma levels of BUN reflect what?

A

The balance between production (protein catabolism) and kidney function.

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37
Q

What is the name for increased plasma levels of BUN?

A

Azotemia.

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38
Q

What are the 3 types of azotemia?

A

Pre-renal, renal, post-renal.

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39
Q

What pre-renal things can lead to azotemia?

A

Prolonged high protein intake, dehydration/hypovolemia (decreasd plasma volume), and increased protein catabolism.

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40
Q

What are the renal things that can lead to azotemia?

A

Renal disease.

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41
Q

What are the post-renal things that can lead to azotemia?

A

Lower urinary tract obstructions.

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42
Q

What are the things that lead to low levels of BUN?

A

Expanded plasma volume, liver disease, pregnancy (plasma volume expands).

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43
Q

What is the end product of skeletal muscle metabolism?

A

Creatinine. NOT creatin.

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44
Q

Plasma levels of creatinine reflect what?

A

Skeletal muscle mass only not activity.

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45
Q

Creatinine enters the circulation and is removed how?

A

Removed from the plasma by the kidneys.

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46
Q

What type of product is creatinine?

A

A non-protein nitrogenous waste product.

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47
Q

Plasma levels of creatinine are proportional to what?

A

Skeletal muscle mass of the individual.

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48
Q

Increased creatinine and BUN levels are observed in patients with reduced kidney function of how much?

A

Reduced kidney function of over 50%.

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49
Q

Decreased creatinine levels are seen in patients with what?

A

Reduced muscle mass, most commonly seen in females and children.

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50
Q

What are the most common causes of increaed creatinine levels?

A

Renal disease, increased muscle mass.

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51
Q

What is the most common cause of decreased creatinine levels?

A

Decreased muscle mass.

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52
Q

Since creatinine has a steady state of production it is ideal for what?

A

for a clearance test of kidney function.

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53
Q

Clearance is measuered by UV/P which is what?

A

U- urine concentration of the analyte. V- volume of urine output in 24 hours. P- Plasma concentration of the analyte.

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54
Q

Creatinine clearance is considered a sensitive measurement of what?

A

Overall renal functional impairment.

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55
Q

What is the byproduct of purine metabolism?

A

Uric acid.

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56
Q

When will there be purine metabolism?

A

As RNA and DNA are synthesized and degraded.

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57
Q

Uric acid is synthesized where?

A

In the liver by enzymes.

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58
Q

What happens to uric acid as it enters the circulation?

A

it is filtered, partially reabsorbed and actively secreted into the urine by the kidneys.

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59
Q

Plasma levels of uric acid reflect what?

A

The balance of production and renal function.

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60
Q

What results in increased uric acid synthesis?

A

Increased levels of tissue breakdown.

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61
Q

What type of diet has purines in it and a dietary purine intake leads to what?

A

organ meats, legumes, and yeaste. A low purine diet halves the average daily production.

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62
Q

Decreased renal function does what to uric acid levels?

A

Increases it.

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63
Q

How can uric acid exretion be enhanced?

A

Pharmacologically.

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64
Q

What are the names for high and low levels of uric acid?

A

Hyperuricemia and hypouricemia.

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65
Q

What are the most common causes of hyperuricemia (increased production)?

A

Excess dietary purines, inherited abnormal purine metabolism, certain malignancies (breakdown tissues), chemotherapy.

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66
Q

What are the most common causes of hyperuricemia (decreased excretion)?

A

Idiopathic, renal disease, chemical induced (alcohol, asprin).

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67
Q

What are 3 tests for alcoholism?

A

Increasd Triglycerides and GGT’s and hyperuricemia.

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68
Q

What are the most common causes of hypouricemia (increased excretion)?

A

Chemical induced (asprin, estrogen, corticosteroids, warfarin).

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69
Q

What are the most common causes of hyouricemia (decreased production)?

A

Chemical induced (allopurinol).

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70
Q

What are the 4 electrolytes?

A

Sodium, potassium, chloride, CO2

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71
Q

Why are electrolytes important?

A

Water balance, acid-base balance, nerve conductivity and muscle contractility, and many other cellular functions.

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72
Q

Why would you order electrolyte tests?

A

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.

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73
Q

What is the major intra and extra cellular cations?

A

Extracelluar- sodium. Intracellular- Potassium.

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74
Q

What are the 3 controls of sodium levels?

A

Dietary intake, renal excretion or retention, endocrine system (ADH, Aldosterone).

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75
Q

What are the names for high and low levels of sodium?

A

Hypernatremia, hyponatremia.

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76
Q

What are the most common causes of hypernatremia?

A

Increased sodium intake from diet (uncommon), decreased sodium loss (increasd aldosterone), excess water loss ( GI loss without rehydration excessive sweating dehydration).

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77
Q

What are the most common causes of hyponatremia?

A

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).

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78
Q

Hyponatremia can lead to signs and symptoms of what?

A

hypotension, shock, cardiac abnormalities, mental aberrations such as confusion.

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79
Q

What is the plasma level of potassium like?

A

Very low since it is an intracelluar electrolyte.

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80
Q

What function is greately influenced by potassium?

A

Neuromuscular contractility.

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81
Q

Potassium levels are critically important in what?

A

Patients with heart conditions.

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82
Q

How will the kidney regulate pH?

A

Shift K and H ions.

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83
Q

Very slight alterations of potassium serum levels are critical and can reflect what?

A

major intracellular potassium abnormalites.

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84
Q

What happens to potassium in the kidneys?

A

It is lost and cannot be reabsorbed.

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85
Q

Potassium levels are greatly influenced by what?

A

Aldosterone and sodium reabsorption and loss.

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86
Q

What are three things to think of with increased potassium levels?

A

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.

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87
Q

What are the names for high and low levels of potassium?

A

Hyperkalemia, hypokalemia.

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88
Q

What are the most common causes for hyperkalemia?

A

Exess dietary intake, Dehydration, acute or chronic renal failure (most common), adrenal insufficency, hemolytic diseases, massive tissue injury or infection.

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89
Q

What are the most common causes for hypokalemia?

A

Dieatary deficiency, GI loss (prolonged vomiting/diarrhea, diuretics, hyper-adrenal conditions, licorice overdose.

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90
Q

Both hyper and hypo kalemai result in what?

A

Weakness and loss of deep tendon reflexes, disturbances of GI motility, and also mental aberrations.

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91
Q

What are the lethal consequences of hyper- or hypo- kalemia?

A

paralysis of respiratory muscles and cardiac arrest.

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92
Q

What is the major extracellular anion?

A

Chloride.

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93
Q

Chloride is responsible for what?

A

Maintaining electrical neutrality as a salt in combination with sodium.

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94
Q

Chloride is intimately involved in what?

A

Acid-base balance.

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95
Q

It is most common to see chloride changes associated with what?

A

Altered breathing as part of respiratory compensation for pH.

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96
Q

Chloride shifts parallel changes in what?

A

Sodium.

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97
Q

Alone chloride is of what clinical value?

A

Little always measured in combination with other electrolytes.

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98
Q

What are the names for high and low levels of chloride?

A

Hyperchloremia and hypochloremia.

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99
Q

What are the most common causes of hyperchloremia?

A

Dehydration, acidosis.

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100
Q

What are the most common causes of hypochloremia?

A

Overhydration, GI loss, alkalosis.

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101
Q

Why is bicarbonate dissolved not the same as pCO2?

A

Bicarbonate dissolved is CO2.

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102
Q

Bicarbonate has a very similar role as ____ in maintaining electrical neutrality/

A

Chloride.

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103
Q

Bicarbonate is regulated by what to maintain acid-base balance?

A

Kidneys.

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104
Q

What are serum levels of bicarbonate like?

A

They tend not to be accurate and therefore this test roughly reflects acid-base balance.

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105
Q

What are the most common causes of increased and decreased bicarbonate levels?

A

Increased- metabolic alkalosis. Decreased- metabolic acidosis.

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106
Q

CO2 content and related considerations are best evaluated how?

A

Via arterial blood gases.

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107
Q

How much of the total body calcium is stored in bones?

A

99%.

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108
Q

What are the important physiologic activities of clacium?

A

Blood coagulation, neuromuscular condiction, cell membrane function, regulation of glandular excretions, sekeletal and cardiac muscle contractility.

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109
Q

How will calcium circulate in the plasma and what will this mean?

A

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.

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110
Q

A routine serum calcium assay is actually what?

A

Total serum calcium.

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111
Q

What type of circulating calcium is the active portion?

A

The ionized calcium.

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112
Q

What is calcium that is bound to albumin like?

A

It is not physiologically active.

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113
Q

What is more common hypoalbuminemia or hyperalbuminemia?

A

Hypoalbuminemia.

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114
Q

Albumin altering conditions influence what?

A

The total amount of calcium but not the physiologically active ionized portion.

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115
Q

Can ionized calcium be assayed?

A

Yes via separately ordered test and is not part of a routine biochemical profile.

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116
Q

Ionized calcium is most useful in evalutaing what?

A

Hypocalcemia.

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117
Q

What hormone is responsible for controlling plasma levels of calcium?

A

PTH.

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118
Q

What will create an increased amount of PTH?

A

Hypocalcemia.

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119
Q

What will PTH do?

A

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.

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120
Q

What will vitamin D do?

A

enhances intestinal absorption of calcium and phosphorus and accelerate bony resporption.

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121
Q

How will Vitamin D be made from the sun?

A

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.

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122
Q

How will PTH decrease loss of calcium in the urine?

A

It promotes excretion of phosphate.

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123
Q

Alterations in PTH will affect what portion of calcium?

A

The ionized calcium.

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124
Q

What is the name for high and low levels of calcium?

A

Hypercalcemia and hypocalcemia.

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125
Q

What are the most common causes of hypercalcemia?

A

parathyroid disease (hyperparathyroidism), malignancies, granulomatous infections (TB, sarcoidosis), hyperthyroidism (thyroid hormone can increse osteoclastic activity), pancreatitis.

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126
Q

What are the most common causes of hypocalcemia?

A

Parathyroid disease (hypoparathyroidism), renal failure, vitamin D deficiency.

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127
Q

Hypocalcemia will happen at what level and what is the top limits of calcium?

A

Hypo- less than 7 mg/dl. Top limit- 10.5 mg/dl.

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128
Q

What are the signs of hypocalcemia?

A

Nervousness, excitability, tetany (uncontrolled total muscle contraction).

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129
Q

When will hypercalcemia be something to worry about?

A

if top limit is 10.5 then you should worry at 10.6.

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130
Q

What will happen with calcium levels at 11.5-12.0 mg/dl?

A

Fatigue, depression, vague GI (nausea, vomit, anorexia, constipation).

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131
Q

What will happen with calcium levels at 12.0-13.0 mg/dl?

A

Calcification of soft tissues.

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132
Q

What will happen with calcium levels greater than 13.0 mg/dl?

A

Medical emergency.

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133
Q

In general what will phosphorus do?

A

The opposite of calcium.

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134
Q

How is phosphorus measured?

A

As inorganic phosphate.

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135
Q

what % of total body phosphorus is stored with calcium in bones?

A

85%.

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136
Q

Increased calcium will do what to phosphorus?

A

Decrease it and decreased calcium will increase phosphorus.

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137
Q

What is the name for high and low levels of phosphorus?

A

Hyperphosphatemia and hypophosphatemia.

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138
Q

What are the most common causes of hyperphosphatemia?

A

parathyroid disease (hypoparathyroidism), renal failure, High phosphate diet, malignancy of bone.

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139
Q

What is the most common cause of hypophosphatemia?

A

Parathyroid disease (hyperparathyroidism).

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140
Q

What are the 4 tests for serum proteins?

A
  1. Total protein. 2. Albumin. 3. Globulins. 4. A/g ratio.
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141
Q

What are the main types of circulating proteins?

A

Albumin and globulins.

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142
Q

How helpful is a total protein test alone?

A

Not very you need an albumin or globulins test to go with it.

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143
Q

Albumin by weight is the_______________________.

A

largest single fraction of plasma proteins even though it is a small molecule.

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144
Q

Where is albumin made at and what can this be helpful for?

A

In the liver and it can be used as a liver function test LFT.

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145
Q

What is the major responsibility of albumin?

A

To create osmotic pressure of blood plasma.

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146
Q

Albumin acts as a circulating reservoir of what?

A

Amino acids.

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147
Q

What is another role of albumin?

A

Acts as a carrier protein.

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148
Q

How common is hyeralbuminemia and what causes it?

A

It is rare and is caused by overt clinicla dehydration.

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149
Q

Hypoalbuminemia is associated with what?

A

reduced synthesis, increased loss, increased catabolism.

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150
Q

What is the most common cause of hyperalbuminemia?

A

decreased plasma volume.

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151
Q

What are the most common causes of hypoalbuminemia?

A

Reduced synthesis (liver disease), increased loss (protein-losing nephropathies, protein-losing enteropathies), increased catabolism (widespread cancer).

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152
Q

What are globulins?

A

Total protein minus albumin.

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153
Q

How many groups of globulins are there and what are the groups based on?

A

4 and they are based upon electrophoretic mobility.

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154
Q

What will the clinical significance of hypo- and hyper-globulinemai be reatled to?

A

Which globulin accounts for the increase or decrease.

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155
Q

What are the 4 groups of globulins?

A

Alpha-1-globulins. Alpha-2-globulins. Beta globulins, Gamma globulins.

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156
Q

What are the types of alpha-1 globulins and what are there %?

A

Alpha-1-antitrypsin (AAT)- 90%. Alpha-fetoprotein (AFP)- 10%.

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157
Q

What type of protein is the alpha-1-antitrypsin?

A

Acute phase reactant.

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158
Q

What is an acute phase reactant protein?

A

one that is created as a reaction to the acute phase and they are protease inhibitors.

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159
Q

What are protease inhibitors?

A

they keep inflammatory responses in check.

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160
Q

What is the main reason for increased alpha-1-antitrypsin?

A

Inflammatory diseases.

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161
Q

What is the most common cause for decreased levels of alpha-q-antitrypsin?

A

Inherited deficiencies associated with juvenile pulmonary emphysema.

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162
Q

What are plasma levels like for alpha-fetoprotein?

A

Major plasma protein in the fetus but minute levels in the adult.

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163
Q

What are increased levels of alpha-fetoprotein associated with?

A

certain malignancies or seen during pregnancy with a neural tube defect and down’s syndrome.

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164
Q

Name the only alpha-2-globulin mentioned in the notes?

A

Haptoglobin.

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165
Q

What is the most common cause for increased alpha-2-globulins?

A

An acute phase reaction to an acute inflammatory disease.

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166
Q

What will haptoglobin do?

A

Binds and transports free hemoglobin to the RE system and it is an acute phase reactant protein.

167
Q

What is the most common reason for decreased levels of haptoglobin?

A

hemolysis.

168
Q

Name the 2 beta globulins mentioned in the notes?

A

Transferrin- transports protein of iron and beta lipoprotein- corresponds to LDL

169
Q

What are the most common causes of increased and decreased beta globulins?

A

Increased- hypercholesterolemia. Decreased- malnutrition.

170
Q

Name the 5 gamma globulins?

A

IgA, IgD, IgE, IgG, IgM.

171
Q

IgA is responsible for what?

A

lining surfaces of tubules and the surface of the respiratory and GI tracts.

172
Q

Where is IgA the perdominant Ig in the body?

A

Body fluids and secretions.

173
Q

How often is IgA assayed in the the blood and why?

A

Not often since there is very little in the blood.

174
Q

What is the role of IgD?

A

B-cell mediated immunity.

175
Q

How often is IgD assayed in the blood and why?

A

rarely because it is rarely detected in the blood.

176
Q

What is IgE used for?

A

Allergic reactions like anaphylactic, atopic and asthmatic.

177
Q

IgE assay can be used to identify what?

A

Existence of allergic reactions or disorders from type I hypersensitivity reactions.

178
Q

What is the test used where the patients IgE is tested to see if it reacts to known allergens?

A

RAST (radioallergosorent testing).

179
Q

What is the most abundant circulating Gamma globulin?

A

IgG.

180
Q

What will IgG do?

A

forms antibodies that may persist for life and give immunity.

181
Q

Increase in IgG is the most common use for what?

A

Serum protein electrophoresis (SPEP).

182
Q

What is the most common immunoglobulin responsible for the M spike?

A

IgG.

183
Q

M spike is seen in what?

A

Multiple myeloma.

184
Q

IgG is commonly responsible for what?

A

Polyclonal gammopathy associated with inflammatory disorders.

185
Q

IgM does what?

A

It is the initial humoral response to infection.

186
Q

IgM signals what?

A

Presence of acute or very recent infection.

187
Q

What is the form of the antibodies in the ABO blood group system?

A

IgM.

188
Q

What gamma globulins will be present (in what order) for a primary and secondary infection?

A

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
Q

What is the albumin globulin ratio for?

A

It serves as an indicator to look closely at the individual levels of albumin and globulins.

190
Q

Why are lipids complexed with proteins?

A

To transport the insoluble lipids.

191
Q

Name the 4 proteins that carry lipids?

A

Chylomicrons, low density lipoproteins (LDL), very low density lipoproteins (VLDL), High density lipoproteins (HDL).

192
Q

In general what type of lipids will be in chylomicrons?

A

mainly triglycerides from diet.

193
Q

In general what type of lipids will be in LDL’s?

A

cholesterol is about half and has some protein and pospholipids.

194
Q

In general what type of lipids will be in VLDL’s?

A

TG.

195
Q

In general what type of lipids will be in HDL’s?

A

VERY LITTLE TG, half is protein, little cholesterol.

196
Q

What happens to lipids from the diet?

A

They are put into chylomicrons with bile acids and cholesterols help and transported to the capillaries.

197
Q

What happens to chylomicrons in the capillaries?

A

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
Q

What happens to lipoprotein remnants?

A

They go to the liver and release the cholesterol.

199
Q

What happens to cholesterol in the liver?

A

It can be turned into bile or it can be sent out in VLDL’s.

200
Q

What happens to VLDL’s?

A

They go to the capillaries and LPL will burn lipids and make adipose from TG, and then they become LDL’s.

201
Q

What happens to LDL’s?

A
  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
Q

Where do HDL’s come from?

A

HDL will take cholesterol from tissues and then turn into LDL’s.

203
Q

What happens to 70% of the LDL’s?

A

removed by the liver and recyled.

204
Q

Why will LDL’s go to peripheral cells?

A

They need the cholesterol to synthsize hormones, cell membranes.

205
Q

Dyslipoproteinemias can result from what?

A

dietary supply, liver function, availability of appropriate apoproteins, availability of enzymes, sufficient HDL.

206
Q

What are the 2 catagories of dyslipoproteinemias?

A

Primary and secondary.

207
Q

What are the causes of primary dyslipoproteinemias?

A

genetic and lipid levels often need to be controlled via medications.

208
Q

What are the causes of secondary dyslipoproteinemias?

A

Side effect of another identifiable disorder, if secondary disorder is controlled often lipid levels go back to normal.

209
Q

Where will 25 and 75% of the cholesterol be at?

A

HDL-25%. LDL-75%.

210
Q

What are the cholestrol levels associated with negative, neutral and positive risk factors for CAD?

A

Negative- 200 mg/dl.

211
Q

What are the most common causes of hypercholesterolemia?

A

Dietary indiscreations, hyperlipoproteinemias (type II, III, V), nephrotic syndrome, hypothyroidism, cholestatic hepatobiliary disorders, oral contraceptives.

212
Q

What are the most common causes of hypocholesterolemia?

A

abetalipoproteinemia, hypobetaliproteinemia, hyperthyroidism, malabsorption, malnutrition.

213
Q

What are the ideal, Optimal and positive risk factor levels of HDL for males and females?

A

Ideal; males- >45 females- >55. Optimal; males- >60 females- >70. Positive risk; males- < 35.

214
Q

How can HDL’s be lowered?

A

obesity and smoking.

215
Q

How can HDL’s be elevated?

A

Aerobic exercise, moderate alcohol, weight reduction, smoking cessation and niacin (not statins).

216
Q

What is the most common cause of increased HDL’s?

A

Familial high HDL’s, exercise (30 minutes 3 times per week).

217
Q

What are the most common causes of decreased HDL’s?

A

Atherogenic lipid profile syndrome, familial low HDL, liver disease, malnutrion.

218
Q

What subclass of HDL has the greatest protective capacity of reverse cholesterol transport?

A

2b.

219
Q

What HDL levels will have sufficient HDL 2b to provide reverse cholesterol transport?

A

40-60 mg/dl.

220
Q

What should the Cholesterol/HDL ratio be for females and makes?

A

Females- >4.4. Males > 5.0.

221
Q

What is the optimal LDL level?

A

<70 mg/dl in a patient with a high risk of CAD.

222
Q

What are some risk factors for increased LDL’s?

A

cigarete smoking, hypertension, low HDL, family history, 10 year age risk from the framingham algorithm.

223
Q

What are the most common causes of increased LDL’s?

A

Familial lipoproteinemia abnormalites, chronic liver and kidney diseases, hypothyroidism, poor life-styles.

224
Q

What are the most common causes of decreased LDL’s?

A

Familial/ inherited decreased LDL’s, hyperthyroidism, hypoprtoeinemic states, good lifestyle states, drugs.

225
Q

What LDL subclasses are most commonly elevated and what are they like?

A

IIIa and IIIb and they are small enough to migrate into cells and cause atherogenic disease.

226
Q

What are the most dangerous subclasses of LDL’s?

A

Iva dn Ivb because they are very small.

227
Q

What will happen if patients have more than 10% of the type Iva and Ivb LDL’s?

A

They usually display vascular events within months of detection.

228
Q

What will VLDL’s primarily reflect?

A

Endogenously produced TG.

229
Q

Elevated VLDL is a risk factor for what?

A

CAD because they are made into LD’s.

230
Q

Will VLDL’s be part of a basic lipid profile?

A

No.

231
Q

In a fasting state most of the TG circulate how?

A

VLDL’s and a few in LDL’s.

232
Q

A non fasting state where will most of the TG be at?

A

Chylomicrons.

233
Q

Fasting TG is part of a lipid profile used to evaluate what?

A

The risk of cardiovacular disease.

234
Q

What are the most common causes of hypertrigylceridemia?

A

familiar hyperlipoproteinemias, DM (poorly controlled), Hypothyroidism, chronic renal disease, alcoholism, OAC/estrogen, high carb diet, non-fasting specimen.

235
Q

What are the most common causes of hypotriglyceridemia?

A

malabsoprtion/malnutrion, hyperthyroidism, abetalipoprtoeinemia.

236
Q

Elevated plasma levels of lipoprotein “little A” (Lp(a)) is associated with what?

A

thrombosis development.

237
Q

Lp(a) is a positive risk factor for what?

A

Cardiovascular disease.

238
Q

What will increase or decrease levels of lP(a)?

A

It is genetically encoded and cannot be manipulated as easily as HDL or LDL.

239
Q

What happens to hemoglobin when RBC’s die?

A

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
Q

What is total bilirubin?

A

unconjugated + conjugated.

241
Q

What is the major portion of bilirubin and why?

A

Unconjugated because conjugated goes into bile.

242
Q

How much unconjugated bilirubin is found in the urine?

A

None because it is not soluable.

243
Q

Will there be unconjugated hypo and hyperbilirubinemia?

A

Only hyper.

244
Q

What is the most common causes of unconjugated hyperbilirubinemia?

A

hematologic conditions involving hemolysis, normal neonatal jaundice, advanced hepatic diseases, gilberts syndrome, crigler-najjar syndrome.

245
Q

What is gilberts syndrome?

A

Congenital defect in hepatocyte uptake of unconjugated bilirubin resulting in mild unconjugated hyperbilirubinemia; may cause intermittent skin discoloration; no clinical signficance.

246
Q

Increased levels of conjugated bilirubin appear in the circulatino only in the presence of what?

A

hepatobiliary pathology.

247
Q

Conjugated hyperbilirubinemai will result in bilirubinuria once plasma levels exceed what?

A

1.5 mg/dl.

248
Q

What are the 3 most common causes of altered conjugated bilirubin levels (and how will it be altered)?

A

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
Q

What are 3 types of Jaundice?

A

Hemolytic, hepatocellular, obstructive.

250
Q

What causes hyemolytic jaundice and what will it be like?

A

Anemia, increased total bilirubin, increased unconjugated bilirubin, increased serum LDH, increased urobilinogen.

251
Q

What causes obstructive jaundice and what will it be like?

A

Increased total bilirubin, increased conjugated bilirubin, bilirubinuria, decreased urinary urobilinogen, light clay colored stool.

252
Q

What causes hepatocellular jaundice and what will it be like?

A

increased total bilirubin, increased conjugated bilirubin, increased unconjugated bilirubin (late), increased serum liver enzymes, bilirubinuria, increased urinary urobilinogen.

253
Q

Why will hepatocellular jaundice have increased urinary urobilinogen?

A

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
Q

Where are enzymes located?

A

Functional ones within the cell. Enzymes in the circulation perform no physiological function.

255
Q

Enzymes in the circulation represent what?

A

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
Q

Pathology to a cell will release what enzymes?

A

Since enzymes are specific to organells a pathology will only release enzymes that affect certain organells.

257
Q

What will location of a cell with a pathology have to do with the amount of enzymes released?

A

Increased if the cell is by blood vessels or lymphatics.

258
Q

What type of cells will produce more enzymes?

A

Proliferating cells.

259
Q

Clinically significant enzymes often are derived from where?

A

More than one organ.

260
Q

Since significant enzymes are often derived from more than on organ how can you tell which organ the enzyme came from?

A

slighlty different biochemical forms are present and they are referred to as isoenzymes or isozyme.

261
Q

How are enzymes quantified?

A

By catalytic properties not by weight.

262
Q

Significance of enzymes is judged how?

A

Relative to how may times over the reference range the activity has risen.

263
Q

Will enzymes normally be increased or decreased in tests?

A

Normally wont see decreased amounts besides alkaline phosphatase.

264
Q

What is another name for alkaline phosphatase?

A

ALP.

265
Q

What tissues will be clinically important to ALP?

A

Bone, liver (hepatobiliary), placenta, intestine.

266
Q

What are some reasons ALP could be elevated do to bones?

A

Neonatal levels high, Pre-puberty levels high, puberty levels high, Osteoblastic disorders like pagets, osteomalacia, hyperparathyroidism.

267
Q

When would the liver be the cause of elevated ALP?

A

Cholestatic- stasis of the colon, bile flow is obstructed or sluggish.

268
Q

What are the reasons the ALP levels could be elevated do to the placenta?

A

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
Q

What is the name of the isozyme that comes from malignancies of the liver or female reproductive organs and is like the placental ALP?

A

Regan isoenzyme.

270
Q

What are some of the causes of intestinal increase in ALP?

A

2-3 hours after a fatty meal, bowel or peptic ulcer diseases.

271
Q

What are the most common causes of a mild increase in ALP levels?

A

hepatobiliary disorders, healing fracutures, growing children, pregnancy, post-menapausal, normal geriatrics.

272
Q

What are the most common causes of a moderatley and a marked increase in ALP levels?

A

Moderate- hepatobiliary disorders. Marked- primary biliary tract disorders, and bone disorders.

273
Q

What are the transferases aka?

A

Transaminases.

274
Q

What are the transferases/transaminases and what are all of their names?

A
  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
Q

AST aka SGOT is clinically important to what tissues?

A

LIVER, heart, skeletal muscle.

276
Q

Will the liver cells contain more AST or ALT?

A

3.5 times more AST.

277
Q

When will AST and ALT be more sensitive indicators of liver pathologies?

A

AST- alcholoic liver disease. ALT- acute liver inflammation and extrahepatic biliary tract obstruction.

278
Q

What are the most common causes of a mild increase in AST aka SGOT?

A

liver- mild inflammation, cirrhosis, neoplasm. Skeletal muscle- myopathy, myositis, trauma.

279
Q

What are the most common causes of a moderate increase in AST aka SGOT?

A

Liver- moderate inflammation. Heart- myocardil infarction.

280
Q

What are the most common causes of a marked increase in AST aka SGOT?

A

Liver- acute inflammation (hepatitis).

281
Q

What tissues will be clinically importatant with ALT aka SGPT?

A

LIVER, heart, skeletal muscle.

282
Q

ALT is clinically used to evaluate what?

A

Liver damage.

283
Q

When will high and low levels of ALT be seen?

A

High- inflammatory conditions like hepatitis. Low- skeletal muscle and myocardial pathologies.

284
Q

What are the most common causes of mild ALT increase?

A

mild hepatic inflammation, infectious mononucleosis.

285
Q

What are the most common causes of moderate and marked ALT increases?

A

Moderate- actve liver disease, hepatotoxic drugs. Marked- acute active liver disease.

286
Q

A single week of overindulging in fast food leads to what?

A

Pathological levels of ALT. So heavy fast food eating can cause increased ALT levels.

287
Q

What is the older name for gamma glutamyl transferase (GGT)?

A

Gamma glutamyl transpeptidase (GGTP).

288
Q

What tissue will be clinically importatn with GGT aka GGTP?

A

Liver.

289
Q

Large qunatities of GGT are found where?

A

In similar locations as ALP.

290
Q

GGT tests are most sensitive for what?

A

indicators of both intra- and extrahepatic obstructive processes.

291
Q

What will increased ALP + increased GGT =?

A

Liver pathology.

292
Q

What will increased ALP + normal GGT =?

A

Bone pathology.

293
Q

What will normal ALP + increased GGT= ?

A

Liver.

294
Q

Will GGT be included in most panels?

A

No.

295
Q

GGT is released when?

A

With toxic hepatocellular damage due to acetaminophen, alcohol-very sensitive for consumption.

296
Q

What is the most common cause for increased levels of GGT?

A

liver- All forms of pathology. Hepatotoxic drugs- ETOH, acetominphen.

297
Q

What enzyme is LD aka LDH?

A

Lactate dehydrogenase.

298
Q

LDH is present in nearly all tissues but is in greatest abundance in what tissues?

A

Heart, blood cells, skeletal muscle, liver.

299
Q

How many isozymes are there of LDH and what are the names?

A

5; LDH1-5.

300
Q

Which LDH is for the lungs?

A

LDH-3.

301
Q

Which LDH is for the kidney, placenta, and pancrease?

A

LDH-4.

302
Q

What tissue will LDH-1 be for?

A

HEART MUSCLE, rbc’s

303
Q

Which LDH is for the WBC’s?

A

LDH-2.

304
Q

What tissue will LDH-5 be for?

A

Liver and skeletal muscle.

305
Q

From greatest levels to leaste what is the order of LDH concentration?

A

LDH-2 > 1 > 3 > 4 > 5.

306
Q

When concentrations of LDH-2 and LDH-1 flipp this is indicitive of what?

A

myocardial infarction.

307
Q

How specific will LDH tests be? Why?

A

Very non specific since LDH is observed in most any condition which tissues are damaged.

308
Q

What are the most common causes of mild, moderate and marked increases in LDH levels?

A

Mild- liver disorders. Moderate- hematologic conditions, cardiopulmonary conditions, liver inflammation, muscular pathology. Marked- hematologic conditions, hemolytic conditions, acute liver inflammation, disseminated cancer.

309
Q

What is the old name for creatine kinase (CK)?

A

creatine phosphokinase (CPK).

310
Q

What are the clinically important tissues associated with CK?

A

heart, skeletal muscle, brain.

311
Q

How many isozymes are there of CK and what are their names (both of them) and what tissues are they associated with?

A

CK1 aka CK-BB- brain and CNS. CK2 aka CK-MB- myocardial muscle. CK3 aka CK-MM- skeletal muscle.

312
Q

What % of the isozymes of CK will normal serum have?

A

100% CK3 aka CK-MM.

313
Q

Increased total CK is primarily useful for what?

A

Myocardial ischemic changes and skeletal muscle abnormalites.

314
Q

What is the GOLD standard for myocardial infarctions?

A

CK-MB.

315
Q

What will cause increased CK-BB?

A

Brain traumas.

316
Q

What will cause increased CK-MM?

A

trauma to skeletal muscle including severe exercise.

317
Q

What are the most common causes of mild, moderate and marked increases in CK levels?

A

Mild/moderate- severe exercise, skeletal muscle trauma, myocardial infarction. Marked- muscular dystrophy, inflammation of skeletal muscle, myocardial infarction.

318
Q

What enzymes will be elevated with liver pathologies?

A

AST, ALT, ALP, GGT, LDH.

319
Q

What enzymes will be elevated with heart pathologies?

A

CK, LDH.

320
Q

What enzmes will be elevated with skeletal muscle pathologies?

A

CK, LDH.

321
Q

What enzymes will be elevated with bone patholgies/

A

ALP.

322
Q

What enzymes will be elevated with pancrease pathologies?

A

amylase and lipase.

323
Q

What is serology?

A

Diagnostic use of serum antiboides and other globulins to DETECT INFLAMMATION and INFECTIOUS DISEASES.

324
Q

Serolgy is aka?

A

immunoserolgy or immunodiagnostic testing.

325
Q

ESR is done over how long of a time period?

A

One hour.

326
Q

Sedimentation is determined by what?

A

density of RBC’s relative to plasma.

327
Q

When will RBC sedementation rates increase? What is this called?

A

When RBC’s aggregate which they want to do. Called Rouleaux.

328
Q

What will help prevent RBC’s from aggregating? What is this called?

A

Negative charges and this is calle dthe Zeta Potential.

329
Q

How is the zeta potential reduced so the RBC can aggregate?

A

Acute phase reactant proteins from inflammation will lower the zeta potential.

330
Q

What are APP’s?

A

Acute phse reactant proteins.

331
Q

Name 5 APP’s?

A

C-reactive protein (CRP), haptoglobin, fibrinogen, alpha-1-antitrypsin, C3 portion of complement.

332
Q

ESR test is done to detect the existence of what?

A

Clinically significant inflammation.

333
Q

Name some factors that increase the ESR?

A

old age, female, pregnancy, anemia, RBC abnormalities- macrocytosis, Elevated APP’s from infections, inflammation, malignancy, technical factors.

334
Q

Name some factors that decrease the ESR?

A

Extreme leukocytosis, polycythemia, RBC abnormalites- spherocytosis, acanthocytosis, microcytosis, technical factors, protein abnormalites.

335
Q

What is the perferred ESR test?

A

Westergren method.

336
Q

What is the westergren method like and what are the normal results?

A

200nm tube utilizing diluted anticoagulated blood. Normal patinet > 50= male- age Divided by 2. Female- age + 10 divided by 2.

337
Q

What are the three basic clinical uses of a ESR test?

A
  1. Detect inflammation. 2. monitor a disease. 3. screen for occult inflammatory or neoplastic condition.
338
Q

What will the purpose of a ESR test be?

A

screening tool but can never rule out the existence of a condition.

339
Q

What are the most common causes of mild, moderate and marked increases of ESR?

A

Mild- age, menstruating. Moderate- pregnancy, active inflammatory, infectious, neoplatic diseases. Marked- monoclonal gammopathies, Polyclonal gammopathies.

340
Q

What test is better than a ESR?

A

C-reactive protein (CRP).

341
Q

What is CRP?

A

A glycoprotein made by the liver in response to inflammation.

342
Q

CRP is what type of protein?

A

APP that appears early and is very sensitive.

343
Q

What will CRP levels be like in a normal person?

A

Not present.

344
Q

CRP levels can increase how much after trauma?

A

100 fold after severe trauma, acute infection/inflammation, surgery, neoplastic proliferation.

345
Q

Will CRP tests be specific?

A

No but very sensitive.

346
Q

CRP will become detectable how long after pathologies?

A

18-24 hours.

347
Q

What levels will elevate faster and go down faster with significant inflammatory events ESR or CRP?

A

CRP elevates faster and returns to normal before ESR.

348
Q

When would CRP levels be almost always present?

A

Rheumatic fever, rheumatoid arthritis, acute infectious disease.

349
Q

When would CRP levels be frequently present?

A

active tuberculosis, Gout, advanced malignant tumors.

350
Q

When would CRP levels be sometimes present?

A

some viral infections, multiple sclerosis, post-surgical.

351
Q

What can CRP be used for that is a non-lipid marker (what are the different names for this)?

A

cardiovascular disease, aka Highly sensitive CRP, and cardio-CRP.

352
Q

What are the clinical uses of Highly sensitive CRP?

A

Used to determine the relative risk of cardioascular disease and to assess risk of recurrent cardiovascular events in patients with coronary heart disease.

353
Q

What has midly elevated CRP been linked with?

A

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
Q

Studies have shown that Highly sensitive CRP is a strong predictor of what?

A

Increased cardiovascular risk in both men and women.

355
Q

Screening with CRP and ____ may provide a better risk assessment than using either test alone.

A

LDL.

356
Q

What levels of CRP and LDL will suggest that the patient is at greater risk of cardiovascular diseases?

A

High CRP and normal LDL Vs. those with normal CRP and high LDL.

357
Q

What type of patients should be tested for Highly sensitive CRP?

A

Those with an intermediate CHD risk.

358
Q

What is Hemostasis?

A

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
Q

How will the endothelial cells of intact vessels prevent thrombin formation?

A

They secrete tissue plasminogen and inactivate thrombin.

360
Q

What is primary hemostasis?

A

vascular contraction, platelet adhesion and formation of a soft aggregate plug.

361
Q

With primary hemostasis when will adhesion occur?

A

When circulating von willebrand factor attaches to the subendotherlium.

362
Q

What part of platelets stick to von willebrand factor?

A

Glycoproteins.

363
Q

What will activate platelets once they stick to von willebrand factor?

A

Collagen.

364
Q

The soft plug formed by platelets will form how fast?

A

In about 20 seconds.

365
Q

What is secondary hemostasis?

A

the process of stabilizing the soft clott and maintaining vasoconstriction.

366
Q

How is vasoconstriction maintained during secondary hemostasis?

A

Platelets secrete serotonin, prostaglandin and thrombaxane.

367
Q

The soft plug will solidify through a complex interaction between what?

A

platelet membrane, enzymes, and coagulation factors.

368
Q

Where are coagulation factors produced at?

A

The liver.

369
Q

What are the steps of platelet plug formation?

A

ACTIVATION, adhesion, aggregation, plug formation, consolidation, fibrin stabilization- this is the end-product of coagulation.

370
Q

What are the 3 pathways of coagulation?

A

Extrinsic, intrinsic and common pathway.

371
Q

What will cause the extrinsic and intrinsic pathways to start the coagulation process?

A

extrinsic- Vessel injury. Intrinsic- surface contact.

372
Q

Where will the intrinsic and extrinsic pathways merge at?

A

Factor X.

373
Q

Explain how extrinsic and intrinsic pathways make it to the common pathway?

A

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
Q

The liver needs what to make factor VII?

A

Vitamin K.

375
Q

Von willebrand factor is needed to create what?

A

Factor VIII.

376
Q

Once factor X is activated into Xa what will happen?

A

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
Q

How will heparin prevent coagulation?

A

It will stop thrombin from turning fibrinogen into fibrin.

378
Q

How many known bleeding conditions are caused by poor vasoconstriction?

A

None.

379
Q

What kind of tests can be done to assess vasoconstriction?

A

bleeding time.

380
Q

What tests can be done to assess platelet plug formation?

A

platelet count, bleeding time.

381
Q

What tests can be done to assess coagulation?

A

Prothrombin time (PT), Activated partial thromoplastin time (APTT).

382
Q

Will PT or APTT be associated more with Extrinsic and intrinsic pathways?

A

PT- extrinsic. APTT- intrinsic.

383
Q

As far as different tests that will be run what is the difference in this class between PT and APTT?

A

Nothing they are the same test for this class.

384
Q

The Bleeding Time (BT) test are done to assess what?

A

platelet fuction.

385
Q

The bleeding time test is used to evaluate the interaction of what?

A

platelets with vessel wall and formation of the platelet plug.

386
Q

How will coagulation affect the bleeding time test?

A

It wont they are independent things.

387
Q

What can prolonge the bleeding time test results?

A

thrombocytopenia <50K.

388
Q

What needs to be established before the bleeding time test can be done and why?

A

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
Q

Lower platelet numbers equals ______ bleeding.

A

prolonged or longer time.

390
Q

The bleeding time test is affected by thrombocytopenia and what?

A

vasoconstriction capabilites.

391
Q

Who will have vasoconstriction problems?

A

Patients with senile skin changes due to age loss of elasticity in vessels.

392
Q

What are 2 ways to do the bleeding time tests?

A
  1. Duke bleeding time- stab wound to the ear lobe. 2. Ivy bleeding time- more standardized method of incision to the forearm.
393
Q

Name 5 things that can affect bleeding time tests?

A

Poor vascular function, depth of incision, touching incision, ETOH consumption, asprin consumption.

394
Q

How long will asprin consupmtion still affect bleeding time tests?

A

5 days after one 300 mg dose.

395
Q

What are 3 of the most common causes of prolonged bleeding times?

A
  1. qualitiative platelet abnormalites- thrombocytopenia. 2. qualitative platelet abnormalities- platelet function. 3. loss of capillary integrity.
396
Q

What can lead to thrombocytopenia?

A

reduced production in the bone marrow, destruction of platelets outside the bone marrow- intravascular or intrasplenic.

397
Q

What causes reduced production of thrombocytes?

A

bone marrow malignancies, both primary and metastiasis toxic effects of drugs, chemicals, and microorganisms factor deficiencies (B12 and folate).

398
Q

What causes destruction of platelets outside the bone marrow?

A

intravascular and intrasplenic immune reactions.

399
Q

What can cause qualitative platelet abnormalites?

A

Von Willebrands disease.

400
Q

What will be the cause of loss of capillary integrity?

A

Collagen vascular diseases, senile capillary fragility.

401
Q

Platelet count is done along with bleeding time tests and what is a common test done to determine platelet count?

A

CBC.

402
Q

What is plasma and serum?

A

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
Q

APTT/PT tests are done with what?

A

Plasma.

404
Q

What is an APTT/PT test used for?

A

a test to see the time it takes plasma specimen to yeild a fibrin clot once the intrinsic pathway is initiated.

405
Q

What will prolong the APTT/PT test?

A

deficiencies in any of the factors involved.

406
Q

The APTT/PT test is used to monitor what?

A

Patients on therapeutic heparin.

407
Q

Name the 3 most common causes of prolonged APTT?

A
  1. Congenital coagulation factor deficiencies- hemophilia A and B. 2. Acquired coagulation factor deficiencies- chronic liver disease. 3. Anticoagulant medication- heparin and coumarin.
408
Q

How will Coumarin work?

A

It is a vitamin K antagonist. No vitamin K no factors needed for coagulation (or atleaste less).

409
Q

What is INR?

A

International normalized ratio. Used to monitor patients on theraputic coumarin.

410
Q

Will hemophilia A and B be more extrinsic or intrinsic pathways?

A

Intrinsic.

411
Q

What is fibrinolysis?

A

Physiologically controlled degradation of the clot.

412
Q

How will birinolysis happen?

A

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
Q

What is left after a clot undergoes fibrinolysis?

A

Fibrin degradation products.

414
Q

What is DIC?

A

Disseminated intravascular coagulopathy. This is a type of disorder of the fibrinolysis system and these are very serious medical emergencies.

Clin Lab (3 decks)

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