Nycc Dr Wells Lab Diagnosis Exam 2

Front 1

pH range

Back 1

7.35 -7.45

Front 2

LEUKEMOID reaction

Back 2

WBC count over 50K/mm3 or a DIFFERENTIAL count with more than 5% IMMATURE cells

Front 3

Platelet count below this number means SPONTANEOUS BLEEDER

Back 3

below 20K

Front 4

UPPER LIMIT of plasma GLUCOSE

Back 4

100 mg/dl [low end varies by laboratory]

Front 5

RANGE of IMPAIRED FASTING GLUCOSE

Back 5

100-125 mg/dl [greater than 126 and with the POLYS = Diabetes Mellitus]

Front 6

Threshold before glucose SPILLS INTO URINE

Back 6

180 mg/dl

Front 7

When blood glucose EXCEEDS renal/kidney threshold (180), glucose is excreted where?

Back 7

URINE (glycosuria) and becomes a high urinary glucose ~> POLYURIA

Front 8

UPPER limit of total CHOLESTEROL (above this # is abnormal/undesirable)

Back 8

less than 200 mg/dl

Front 9

Upper limit of LDL cholesterol

Back 9

less than 130 mg/dl

Front 10

LOWER limit (“lower limit”because we want a lot of this) of HDL's

Back 10

Should be greater than 40 mg/dl *Your age! You can remember this – it's all good HDL's after 40

Front 11

Cardiac TROPONIN-I level and washout time

Back 11

TnI: 0-2 ng/ml Washout = 7 days

Front 12

Cardiac TROPONIN-T level and washout time

Back 12

TnT: 0 -3.1 ng/ml Washout = 14 days (2x as long as I take)

Front 13

Platelet REFERENCE RANGE (NORMAL)

Back 13

150K – 400K/ul of blood. This is a nice paycheck range. Just remember 150K is as low as you want to make while 400K would be ridiculously high.

Front 14

post traumatic/surgical bleeder platelet number

Back 14

20-50K of platelets. At this salary, you may have post-traumatic bleeding.

Front 15

spontaneous bleed platelet number (Let the right one in)

Back 15

less than 20K of platelets. If you make under 20K a year, no one can blame you for spontaneously bleeding from your eyeballs.

Front 16

Platelet count can be adequate but function may still be impaired. What to do?

Back 16

Bleeding time test

Front 17

BT

Back 17

Bleed Time = assesses platelet function (adhesion and aggregation). No one likes this test.

Front 18

BT procedure

Back 18

5mm long x 1mm wide slice through forearm made while BP cuff at 40mmHg on. Tissue damage stims platelet aggregation time. Ref range: 3-8 min.

Front 19

BT reference range for the ol' arm slice test

Back 19

3-8min

Front 20

PT

Back 20

PROTHROMBIN TIME: PT evaluates EXTRINSIC & COMMON factors

*Thank you for shopping at PETCO and buying Ca+TFat pills. Coume again!

Front 21

PROTHROMBIN TIME pathways

Back 21

EXTRINSIC & COMMON

Front 22

How does a PROTHROMBIN TIME isolate a defect in the EXTRINSIC pathway?

Back 22

Sample arr. To isolate extrinsic path and show evidence of clotting; abnormal = longer evidence of clot

Front 23

PROTHROMBIN TIME additions to patient PLASMA? (2)

Back 23

TISSUE FACTOR & CALCIUM, then the time to form a FIBRIN clot is measured

Front 24

Commonly used to monitor COUMADIN therapy (therapeutic use of which test and why?)

Back 24

PROTHROMBIN TIME, because Factor 7 [extrinsic] has the SHORTEST HALF LIFE OF ALL the vitamin K-dependent factors.

Front 25

APTT

Back 25

Activated Partial Thromboplastin Time evaluates INTRINSIC factors

A > P and TnT use Ca+ and Charge? phase to ignite!

Front 26

Evaluates INTRINSIC factors

Back 26

APTT = Activated Partial Thromboplastin Time

Front 27

Which INTRINSIC & COMMON factors does APTT evaluate?

Back 27

Intrinsic 8.9.11 and Common 2/5/10

Front 28

In Prothrombin Time test, Ca++ and Tissue Factor are added. What is added to APTT test?

Back 28

Ca++ and CONTACT PHASE activator added to plasma, then time taken to form fibrin clot reported

Front 29

AT in the APTT

Back 29

Activated Thromboplastin 3 = does NOT inhibit INTRINSIC factor 7 so is used to evaluated HEPARIN (crab likes to fish; will not bother line of another fisherman)

Front 30

Prothrombin Time test takes

Back 30

11-12 sec

Front 31

Activated Partial Thromboplastin Time takes

Back 31

22-33 sec (2x as long at Prothrombin Time)

Front 32

FIBRINOGEN test

Back 32

Fibrinogen levels determined by adding BOVINE THROMBIN then waiting to see how long clot takes. Compared on standardized curve of fibrinogen levels.

Front 33

What's the cow test?

Back 33

FIBRINOGEN (bovine thrombin added) 200-400 mg/dl

Front 34

TT

Back 34

Thrombin Time (9-15 sec)

Front 35

FIBRIN is CONVERTED to FIBRINOGEN by __________.

What is the TEST?

Back 35

THROMBIN

THROMBIN TIME [TT]

Prothrombin (coagulation factor II) is proteolytically cleaved to form thrombin in the first step of the coagulation cascade, which ultimately results in the stemming of blood loss. Thrombin in turn acts as a serine protease that converts soluble fibrinogen into insoluble strands of fibrin

Front 36

Used to screen for DYSfibrinogenemia

Back 36

THROMBIN TIME = abnormal forms of fibrinogen are picked up by the TT test

Front 37

What kinds of problems could cause DYSfibrinogenemia and require a TT test?

Back 37

congenital or hepatic disease could cause abnormal fibrinogen, requiring TT test

Front 38

ASSAY which determines a specific factor or protein abnormalities?

Back 38

SPECIFIC FACTOR ASSAY

Front 39

Are there specific factor assays for all hemostatic factors?

Back 39

yes! AT 3 (the crab that won't disturb the fishing line 7), Protein – C , Protein – S

Front 40

FDP/FSP

Back 40

Fibrin Degredation Products/Fibrin Split Products

Front 41

Fibrin is split by

Back 41

PLASMIN

Front 42

When fibrin is split by plasmin, a small # of ________ products are released.

Back 42

breakdown

Front 43

When are Fibrin Degredation Products/Fibrin Split Product tests used?

Back 43

FDP/FSP tests are used in diseases where THROMBOSIS occurs, like MI, inflammation, venous thrombosis, DIC and Pulmonary embolism

Front 44

DIC

Back 44

pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of diseases. DIC leads to the formation of small blood clots inside the blood vessels throughout the body.

Front 45

As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin (e.g. from sites where blood samples were taken), the gastrointestinal tract, the respiratory tract and surgical wounds

Back 45

Disseminated Intravascular Coagulation results (a disease where thrombosis occurs and so you test w/ a FDP(FSP) or D-dimer assay for a specific FDP. Either way, you detect fibrinolysis. The FDP detects both fibrinolysis and fibrinogenolysis.

Front 46

D-dimer assay

Back 46

D-Dimer assay is specific for FIBRINOLYSIS. Its presence means there is PLASMIN DEGREDATION of CROSSLINKED FIBRIN (ergo, there are fibrin degredation products running around.)

Front 47

the D-dimer assay is a very specific FDP test because it tests only for

Back 47

fibrinolysis.

Front 48

Unlike the D-dimer assay which only tests for fibrinolysis, the FDP (FSP) detects?

Back 48

Plasmin-cleaved fibrin OR fibrinogen, so it tests BOTH fibrinolysis AND fibrinogenolysis

Front 49

spontaneous bleeding, petechiae, nosebleeds (epistaxis), heavy menstrual periods (menorrhagia)

Back 49

What could a platelet disorder cause?

Front 50

What is major cause of MORBIDITY in patients w/ platelet disorders?

Back 50

INTRACRANIAL HEMORRHAGE

Front 51

Drug that can make your autoantibodies attack your own platelets?

Back 51

Heparin

Front 52

What is the name of the HEMOSTASIS disorder that is caused by Heparin?

Back 52

Idiopathic/Immune Thrombocytopenic Purpura (ITP) is drug-induced ACQUIRED and autoantibodies attack your own platelets so antiplatelet antibody lab test is positive.

Platelet count is decreased,

Bone marrow is normal or increased megakaryocytes.

APTT & PT normal.

Front 53

Why would your bone marrow show normal to increased megakaryocytes in ITP?

Back 53

Reticuloendothelial sys. Clears the antibody-coated platelets your own body attacked. Megakaryocytes make platelets; if you are destroying them, then megakaryocytes are having to work 3x as hard so must be more of them cranking out platelets.

Front 54

a bone marrow cell responsible for the production of blood thrombocytes (platelets), which are necessary for normal blood clotting

Back 54

megakaryocyte

Front 55

the condition of having an abnormally low platelet count (thrombocytopenia) of no known cause (idiopathic).[1] As most incidents of ITP appear to be related to the production of antibodies against platelets,

Back 55

Idiopathic/ Immune Thrombocytopenic PURPURA

Front 56

presentation of ITP?

Back 56

Visible symptoms of ITP include the spontaneous formation of bruises (purpura) and petechiae (tiny bruises), especially on the extremities, bleeding from the nostrils, bleeding at the gums, and menorrhagia (excessive menstrual bleeding), any of which may occur if the platelet count is below 20,000 per μ

Front 57

pathological activation of coagulation (blood clotting) mechanisms that happens in response to a variety of diseases. DIC leads to the formation of small blood clots inside the blood vessels throughout the body.[1] As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs

Back 57

DIC – Disseminated Intravascular Coagulation

Front 58

Say there's been an accident – a head trauma – and all the police platelets go to that one location so that there aren't any left to patrol.

Back 58

DIC – Disseminated Intravascular Coagulation. Systemic activation of COAGULATION w/ WIDESPREAD THROMBOSIS panic consumes all platelets (and fibrinogen), resulting in hemorrhage.

Front 59

Under homeostatic conditions, the body is maintained in a finely tuned balance of coagulation and fibrinolysis.

Back 59

The activation of the coagulation cascade yields thrombin that converts fibrinogen to fibrin; the stable fibrin clot being the final product of hemostasis

Front 60

The fibrinolytic system then functions to break down fibrinogen and fibrin.

Back 60

Activation of the fibrinolytic system generates plasmin (in the presence of thrombin), which is responsible for the lysis of fibrin clots.

Front 61

The breakdown of fibrinogen and fibrin results in polypeptides called fibrin degradation products (FDPs) or fibrin split products (FSPs)

Back 61

In a state of homeostasis, the presence of plasmin is critical, as it is the central proteolytic enzyme of coagulation and is also necessary for the breakdown of clots, or fibrinolysis.

Front 62

processes of __________ and __________ are dysregulated, and the result is widespread clotting with resultant bleeding.

Back 62

Coagulation and Fibrinolysis dysregulated: DIC – Disseminated Intravascular Coagulation

Front 63

Tissue Factor, not normally in contact w/ the blood, is released upon vascular damage. Why does DIC develop in cases of extensive trauma?

Back 63

TF binds with coagulation factors that then triggers the extrinsic pathway (via Factor VII) which subsequently triggers the intrinsic pathway (XII to XI to IX) of coagulation.

Front 64

Excess circulating thrombin results from the excess activation of the coagulation cascade. The excess thrombin cleaves fibrinogen, which ultimately leaves behind

Back 64

multiple fibrin clots in the circulation. These excess clots trap platelets to become larger clots, which leads to microvascular and macrovascular thrombosis. This lodging of clots in the microcirculation, in the large vessels, and in the organs is what leads to the ischemia, impaired organ perfusion, and end-organ damage that occurs with DIC.

Front 65

Lab results for DIC?

Back 65

PT and APTT are increased and Platelet count is, therefore, decreased because the TIMED tests are taking longer = there must be fewer platelets. Fibrinogen is low because they are being consumed so multiple clots are forming and the person starts to bleed like hell. FSP/FDP (or D-dimers) are increased = excess circulating thrombin assists in the conversion of plasminogen to plasmin, resulting in fibrinolysis. The breakdown of clots results in excess amounts of FDPs, which have powerful anticoagulant properties, contributing to hemorrhage. The excess plasmin also activates the complement and kinin systems. Activation of these systems leads to many of the clinical symptoms that patients experiencing DIC exhibit, such as shock, hypotension, and increased vascular permeability.

Front 66

The affected person is often acutely ill and shocked with widespread haemorrhage (common bleeding sites are mouth, nose and venepuncture sites), extensive bruising, renal failure and gangrene

Back 66

DIC – Disseminated Intravascular Coagulation

Front 67

Labs of DIC

Back 67

Severe cases with hemorrhage: The PT and APTT are usually very prolonged and the fibrinogen level markedly reduced. High levels of fibrin degradation products, including D-dimer, are found owing to the intense fibrinolytic activity stimulated by the presence of fibrin in the circulation. There is severe thrombocytopenia. The blood film may show fragmented red blood cells (schistocytes).

Front 68

Why do a FDP test for DIC? Why does DIC result in lower fibrinogen?

Back 68

DIC results in lower fibrinogen levels (as it has all been converted to fibrin), and this can be tested for in the hospital lab. A more specific test is for "fibrin split products" (FSPs) or "fibrin degradation products" (FDPs) which are produced when fibrin undergoes degradation when blood clots are dissolved by fibrinolysis.

Front 69

DIC means

Back 69

Death Is Coming 10-50% mortality rate from DIC

Front 70

Routine electrolytes: why are electrolytes present?

Back 70

to maintain electro-neutrality; the total concentration of cations MUST EQUAL the anions

Front 71

Functions of electrolytes 5

Ocean pacific Co. Human Resources

Back 71

1. OSMOTIC p & H2O
2. pH
3. HEART
4. REDOX
5. CO-FACTORs

Front 72

Chloride -

Back 72

Major extracellular ANION that maintains WATER BALANCE and OSMOTIC pressure with SODIUM

Front 73

Chloride SHIFT

Back 73

Cl- moves into cells in exchange for BICARBONATE to maintain electroneutrality

Front 74

Total CO2 [HCO-3] = BICARBONATE TOTAL

Back 74

HCO3- is the major component of total CO2 in the plasma = maintenance of ACID-BASE BALANCE

Front 75

What does bicarbonate/CO2 [HCO3-] do?

Back 75

maintains the ACID-BASE balance

Front 76

Name the extracellular anions and cations that are routine electrolytes

Back 76

Na+, Cl- and bicarbonate

Front 77

Name the intracellular anion

Back 77

K+

Front 78

Sodium

Back 78

Na+ : major extracellular cation that maintains WATER DISTRIBUTION & OSMOTIC PRESSURE IN PLASMA

Front 79

Potassium

Back 79

K+ = major INTRAcellular cation (watch for HEMOLYSIS!) important to METABOLISM and NEUROMUSCULAR fcn, particularly the HEART

Front 80

Most important electrolyte in cardiac function

Back 80

K+ = changes effect function; too much or too little K+ can be fatal

Front 81

K+ moves into the cells in response to _________?

Back 81

Increased INSULIN. Insulin therapy in DKA drives both K+ and glucose into the cell.

Front 82

Anion Gap

Back 82

Math estimate of the difference b/w the concentration of Unmeasured anions and cations in the SERUM. Used in d/dx of METABOLIC ACIDOSIS .

Front 83

What test is used to measure other ions besides unmeasured cations and anions in the serum? What ions are considered MEASURED in the serum?

Back 83

ANION GAP can detect: Ca++, Mg++, PO4-, SO4- (all of which are measurable, unlike the unmeasured Na+, Cl- and K+ which are unmeasured cations and anions)

Front 84

NORMAL anion gap result

Back 84

MORE ANIONS unmeasured. Varies in response to changes in concentration of serum PROTEINS, SULFATES & VARIOUS IONS

Front 85

measured cations

Back 85

Na+, Ca+, Mg+

Front 86

mmmmeasured anions

Back 86

Chloride/Bicarbonate/Phosphate

Cl-, HCO3-, PO3-

Front 87

predominate unmeasured anions

Back 87

sulfates and serum proteins (albumin)

Front 88

In normal health, there are more unmeasured _______ so the anion gap is usually ________

Back 88

anions, positive

Front 89

The presence of a HIGH anion gap

Back 89

search for conditions that lead to excess of anions

Front 90

A high anion gap indicates there is a loss of_______ WITHOUT an increase in ________

Back 90

loss of HCO3 without increase in Cl, meaning the CHLORIDE SHIFT ain't workin.

Electroneutrality is maintained by elevated levels of anions like lactate, PO4- and SO4-. These anions aren't part of the anion gap calculation, so if there is a high anion gap, search for a condition that could lead to an excess of one of these substances. Means electric neutrality has been lost because bicarbonate is not being exchanged for chloride.

Front 91

A high anion gap is often due to?

Back 91

LACTIC or KETOACIDOSIS (changes in the concentrations of lactate or acetate that ruined the electroneutrality of the serum and cause the chloride shift to not function)

Front 92

Normal values of unmeasured cations to unmeasured anions?

Back 92

Anion gap= 10-20

Front 93

C-peptide functions in the repair of

Back 93

MUSCULAR layer of the ARTERIES

Front 94

C-peptide not only repairs muscularis layer of arteries but helps what condition?

Back 94

C-peptide: DIABETES MELLITUS diabetic neuropathy prevention, plus improves heart blood flow

Front 95

major source of energy for most cells

Back 95

carbohydrates

Front 96

primary energy source for the human body

Back 96

GLUCOSE

Front 97

Where do we get glucose?

Back 97

body stores GLYCOGEN made from GLYCOGENESIS, synthesis from non-carbs GLUCONEOGENESIS, digestion of dietary carbs GLYCOLYSIS, breaking stored glycogen GLYCOGENOLYSIS

Front 98

Where does metabolism of dietary carbohydrates begin? How?

Back 98

mouth; SALIVARY AMYLASE hydrolyzes starch into maltose

Front 99

Converts intermediate products that weren't tackled by salivary amylase into maltose

Back 99

PANCREATIC amylase

Front 100

Where are maltose and ingested disaccharides (lactose and sucrose) hydrolyzed into monsaccharides?

Back 100

INTESTINAL MUCOSA = glucose, galactose, fructose

Front 101

From the intestinal mucosa, what happens to monosaccharides?

Back 101

Absorbed into bloodstream and transported to LIVER VIA PORTAL CIRCULATION

Front 102

Liver enzymes convert NONglucose monosaccharides into

Back 102

GLUCOSE

Front 103

3 possible pathways of glucose metabolism:

Back 103

1. Immediate production of ATP by complete conversion to CO2 and water GLYCOLYSIS, 2. Storage as glycogen (liver, muscle) or triglycerides (adipose tissue) GLYCOGNESIS, 3. Conversion to ketoacids, amino acids or protein GLYCOGENOLYSIS

Front 104

anaerobic conversion of glucose to pyruvate or lactate, used for energy production of ATP

Back 104

GLYCOLYSIS (breaking glucose then converting it to pyruvate for the TCA cycle to make ATP)

Front 105

glycogen formation from glucose, making stored glycogen in liver and muscle

Back 105

GLYCO-genesis (storage)

Front 106

breaking glycogen down to form glucose and releasing it for energy in muscles or to INCREASE blood glucose for the liver to maintain homeostasis

Back 106

GLYCOGEN-O-LYSIS (breaking stored energy from the muscles or liver = taking sugar out of the cupboard)

Front 107

making glucose out of NON carbs like proteins and lipids because the blood sugar has dropped to low. Most expensive. Cluck cluck.

Back 107

GLUCO-NEO-GENESIS (having to alchemy sugar out of non-sugar products = very expensive. King's ransom)

Front 108

Hormone that lowers blood sugar by prompting cells to uptake sugar in blood after a meal

Back 108

INSULIN

Front 109

Hormones that counteract insulin to make sure there is enough sugar circulating. They call for breakdown of stored sugar or making glucose out of non-carbs when blood sugar is too low:

Back 109

GLUCAGON (main one), IGF's, Growth hormone, cortisol, caecholamines, ACTH = all raise blood glucose levels

Front 110

Make insulin

Back 110

Pancreatic BETA-cells make insulin and store it as pro-insulin

Front 111

When blood glucose levels rise after a meal, pro-insulin is cleaved into _______and inactive ________

Back 111

Insulin & inactive C-peptide

Front 112

Insulin increases cell membrane _________ to glucose

Back 112

permeability; turns on glycogenesis (storage) and turns off gluconeogenesis (making love out of nothing at all)

Front 113

The pancreas of patients with type 1 diabetes is unable to produce ________, and therefore they will also have low levels of?

Back 113

insulin, C-peptide (the repairman of muscular layer of arteries and improver of heart circulation). Type II diabetics have normal levels of C-peptide, sometimes even higher than normal. This is the reward for being fat and not born with type I. Sucks.

Front 114

antagonist to insulin that is produced by adrenal Cortex

Back 114

Cortisol!

Cortisol from Cortex

Front 115

gold standard test for DM

Back 115

Fasting Blood Glucose
FBG

Front 116

Describe FBG test for DM

Back 116

100 mg/dl is top end of range
6-8 hour fast
detects disorders of CARBOHYDRATE metabolism,

mainly used to **diagnose DIABETES MELLITUS

Front 117

What is the criteria for diagnosis of DM using a Fasting Blood Glucose test?

Back 117

fasting specimen GREATER than >126 on 2 separate occasions

OR

one FBG GREATER than >126 accompanied by POLYS

Front 118

IMPAIRED FASTING GLUCOSE #

Back 118

100-125 mg/dl

remember it has to be equal to or over 126 to be diagnostic of diabetes mellitus

Front 119

GTT

Back 119

Glucose Tolerance Test

Glucose-LOADING test that measures BETA-cells ability to INCREASE INSULIN

Front 120

GTT (Glucose Tolerance test) can be used to detect DM but is not usually used that way. What is the PRIMARY use of the GTT?

Back 120

GESTATIONAL diabetes test GDM

Front 121

PROCEDURE for GTT

Back 121

~150g CARBOHYDRATE diet for 3 days prior to test
~10-16 hour fast PRIOR TO TEST
~75 g GLUCOSE orally

PLASMA COLLECTION TIMES:
1. FASTING (65-115 mg/dl)
2. 30 min (110-170 mg/dl)
3. 60 min (120-170 mg/dl)
4. 90 min (100-140 mg/dl)
5. 120 min (70-120 mg/dl)

Front 122

2 hr PP

Back 122

2 hours Post Prandial to Glucose Tolerance Test =

Glucose Loading test results are usually eval'd w/ the FBG gold standard to screen or monitor for Diabetes.

Front 123

2 hr PP GTT test

Back 123

2 hour post prandial glucose tolerance test:
75 mg glucose given
Collect plasma/serum 2 hours post-prandially (<120 mg/dl)

*IF after 2 hours, glucose is STILL 140-199 mg/dl, then IMPAIRED glucose tolerance

Front 124

PP

Back 124

Post Prandial
*simple glucose loading test

Front 125

1-hour PP GDM screen

Back 125

PREGNANCY only for Gestational Diabetes Mellitus
Simple glucose loading test at 24-28 weeks gestation

Patient given 50 g glucose and sample taken an hour later. If over 140 mg/dl, REQUIRES FULL 3 hr. GTT using 100 g load!

Front 126

INcreased glucose from the GDM test?

Back 126

over 140 after an hour means FETUS MACROSOMIA risk = could have developmental problems

Front 127

Glycosolated Hb aka:

Back 127

Hb HA1c

Front 128

Hb HA1c

aka: Hemoglobin HAve a LONG TIME

Back 128

Glycosolated Hb test:

Index of LONG TERM plasma glucose control over a 1-2 month period - indicates COMPLIANCY and EFFICACY of diabetes therapy

Front 129

Hb HA1c/Glycosolated Hb test mechanism

Back 129

LONG TERM glucose test:
AMINE groups react with glucose after protein synthesis = ALBUMIN & Hgb.
Protein concentration is directly related to PROTEIN LIFE SPAN and average chemical CONCENTRATION during test time months.
GLUCOSE-MODIFIED proteins are called GLYCATED.

Front 130

GLYCO-HEMOGLOBIN

Back 130

any Hb with glucose attached

Found during Hb HA1c/Glycosolated Hb test
Demonstrates long term plasma glucose control

Front 131

Formerly used only for monitoring and control of DM; now recommended by ADA for diagnosis of diabetes mellitus

Back 131

Hb HA1c/Glycosolated Hb test for 1-2 months

***** LONG TERM monitoring of plasma glucose

Front 132

Glycosolated Hb/Hb A1c percentage for diabetes

Back 132

6.5% is diabetes

5.7-6.4% is risk

Front 133

Total cholesterol levels should be under

Back 133

under 200 mg/dl

Front 134

During a TOTAL CHOLESTEROL test, why isn't fasting required?

Back 134

NO significant change after a meal; fasting not required but is preferred.

Values may vary from 6.5% daily
Reference values are based on ATHEROSCLEROSIS risk

Front 135

LDL cholesterol test

Back 135

should be under 130 mg/dl BUT with risk factors, should be under 100 mg/dl

Front 136

Major cause of CAD

Back 136

Coronary Artery Disease due to high LDL

Front 137

HDL cholesterol test

Back 137

OVER 45 mg/dl! WANT MORE!

High HDL = low risk for atherosclerosis

Front 138

LDL is a risk for _____

Back 138

CAD

Coronary Artery Disease

Front 139

Cholesterol tests are all based on ______________ risk.

Back 139

atherosclerosis

Front 140

PROTEIN ELECTROPHORESIS aka (2):

Back 140

Lipoprotein electrophoresis/ FREDRICKSON & LEVY classification by phenotype

Front 141

Protein electrophoresis classifies

Back 141

electrophoretic patterns of LIPOPROTEIN ABNORMALITIES seen w/ FAMILIAL or secondary lipid disorders

Front 142

Name 3 types of PROTEIN ELECTROPHORESIS:

Back 142

Type 1: HYPERTRIGLCYERIDEMIA = fat layer even on fasting. Can be managed.

Type 2: HAMBURGERS & FRENCH FRIES. Most easily controlled by diet and exercise.

Type 3, 4, 5: COMBINATIONS of Hypertryglyceridemia and Hamburger/Fries. HIGH TRIGLYCERIDES vs. cholesterol. Does NOT respond well to diet and exercise.

Front 143

Generally, an increase in this number doesn't mean as much as an increase in cholesterol:

Back 143

TRIGLYCERIDES

***however***it IS an independent risk factor in WOMEN! An inverse HDL to triglyceride ratio can precipitate PANCREATITIS

Front 144

An inverse HDL to ___________ ratio can precipitate PANCREATITIS

Back 144

TRIGLYCERIDES

Most due to diet, secondarily to BOOZE, diabetes mellitus and renal failure (a fat white guy that eats pizza w/ his beer every night)

Front 145

Total CK

Back 145

Creatine Kinase CPK

Front 146

Where is CK found?

Back 146

STRIATED mm (SKELETAL/CARDIAC)
&
BRAIN tissue

Front 147

CKM/B

Back 147

Creatine Kinase Muscle/Brain = GOLD STANDARD for early diagnosis of ACUTE MYOCARDIAL INFARCTION

Front 148

What test would you perform if you suspected ACUTE MYOCARDIAL INFARCTION [AMI]?

Back 148

CKM/B
Creatine Kinase Muscle/Brain test:

Diagnostic window 6-8 hrs RISE, then PEAK 24-36 hr, then returns to normal in 3-4 days

Front 149

When is the CKM/B no longer a good test for AMI?

Back 149

after 3-4 days when Creatine Kinase has returned to normal

Front 150

tHE PRIME FCNS OF THE COAGULATION MECHANISM ARE TO PROTECT THE INTEGRITY OF THE ______________ WHILE MAINTAINinG THE _____________ OF BLOOD.

Back 150

INTEGRITY OF THE BLOOD VESSELS WHILE MAINTAINING THE FLUID STATE OF BLOOD

Front 151

Hemostasis and coagulation tests are done for patients with

Back 151

bleeding disorders, vascular injury or trauma, or coagulopathies

Front 152

Normal response to vascular insult

Back 152

Reflex vasoconstriction

Once the first line defenses (skin and tissue) are breached.

Front 153

Platelets will adhere to the injured and exposed ___________ tissues.

Back 153

subendothelial

Front 154

removal of fibrin clot

Back 154

fibrinolysis

Front 155

Most common causes of hemmorhage

Back 155

thrombocytopenia (platelet deficiency) and other coagulation disorders, including liver disease, uremia, disseminated intravascular coagulation (DIC), and anticoagulant administration

Front 156

platelet deficiency

Back 156

THROMBOCYTOPENIA

Front 157

associated with delays in clot formation or premature clot lysis

Back 157

Bleeding tendencies

Front 158

associated with inappropriate clot activation or localization of the blood coagulation process

Back 158

Thrombosis

Front 159

Clotting disorders are divided into two classes:

Back 159

those caused by IMPAIRED COAGULATION and those caused by HYPERCOAGUABILITY

Front 160

Two general forms of HYPERcoagulability

Back 160

1. Hyperactivity of platelet system = ARTERIAL thrombosis

2. Accelerated activity of the clotting system = VENOUS thrombosis

Front 161

Platelet hyperactivity/coagulability =

Clotting acceleration =

Back 161

Platelet = artery

ClottINg = veIN

Front 162

Hypercoagulability

Back 162

UNNATURAL tendency towards THROMBOSIS

*the thrombus is an insoluble mass (fibrin or platelets) present in the blood stream or heart chambers

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an insoluble mass (fibrin or platelets) present in the blood stream or heart chambers

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Thrombus

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Diabetes mellitus is associated with hypercoagulability due to __________ abnormalities.

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platelet

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Arteriosclerosis is associated with hypercoagulability due to ___________ abnormalities.

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platelet

*remember: platelet = artery thrombosis and arteriosclerosis is about arteries and, therefore, about platelets

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Increased blood LIPIDS or CHOLESTEROL is associated w/ hypercoagulability due to __________ abnormalities.

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platelet

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INCREASED PLATELET levels are associated w/ hypercoagulability due to ___________ abnormalities.

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platelet

Many platelets would result in hyper coagulation in the arteries.
Platelets = arterial thrombosis

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SMOKING is associated w/ hypercoagulability due to _________ abnormalities.

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platelet

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What could cause arterial wall thrombosis?

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Platelet hyperactivity = arterial thrombosis...

Blood flow disturbances, Vessel wall changes, Increased platelet sensitivity to factors causing platelet adherence and aggregation.

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Some conditions that would result in CLOTTING system abnormalities/hyperactivity and therefore hypercoagulability states?

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CONGESTIVE HEART FAILURE
Immobility
Artificial surfaces (valves)
Damaged vasculature (surface wounds)
Oral contraceptives or estrogen
Preggers
Post-partum
Post surgery

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clotting system hypercoagulability disease states:

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malignancy
myeloproliferative (bone marrow) disorders
obesity
lupus disorders
genetics

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A balance normally exists between the factors that stimulate the formation of thrombin and forces acting to delay thrombin formation. The balance maintains circulating blood as a __________.

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FLUID!

if blood got too thick = clot
if blood got too watery = no clot
either way, imbalanced!
When injury occurs or blood is removed from a vessel, it upsets the balance and coagulation occurs!

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Factors are named in order of their discovery, not of their involvement. How many stages of clot formation?

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4:
Stage I phases 1 and 2
Stage II
Stage III
Stage IV

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Stage I phase 1 clot formation

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PLATELET activity; platelets themselves serve as source of thromboplastin.

*90% of all coagulation disorders are caused by Phase I defects!

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Stage I phase 2 coagulation/clotting

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Phase 2:
THROMBOPLASTIN; Factor III, an enzyme thought to be liberated by damaged cells, is formed by 6 different factors plus CALCIUM.

All 6 factors are involved in the formation of tissue thromboplastin [intrinsic prothrombin activiation]

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Stage II coagulation/clotting

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PROthrombin factor II is converted to THROMBIN in the presence of Ca++
then...
Thrombin converts fibrogenin to fibrin to make a clot.

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Stage III coagulation/clotting

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Thrombin interacts with fibrinogen (factor I) to form the clot framework.

At the end of this stage III, factor 13 stabilizes the clot.

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Stage IV coagulation/clotting

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Fibrinolytic system [antagonistic check-and-balance to clotting mechanism] is activated.

Removal of fibrin clot is through FIBRINOLYSIS. Plasminogen (again, think 'gen' as beginning) is converted to PLASMIN, which breaks clot into FIBRIN SPLIT PRODUCTS.

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Can be related to STASIS of blood flow, to coagulation alterations, or to increase in PROcoagulant factors or decrease in ANTIcoagulant factors

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VENOUS thrombosis

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most commonly recognized congenital vascular abnormality (vessel wall structural defect)

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Hereditary telangiectasia

*has normal lab studies so d/dx is from clinical presentation. Pts frequently report epistaxis and anemia sx.

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Factor I
Converted to fibrin along with platelets to form clot

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FIBRINOGEN

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Converted to thrombin (IIa), which splits fibrinogen into fibrin

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PROthrombin (prethrombin)

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Christmas factor IX

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activates X

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Hageman factor XII

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activates XI and prekallikrein

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von Willebrand's factor VIII-related antigen

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Stabilizes VIII
Mediates platelet ADHESION*

von Willenbrand's glue

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Fibronectin

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Fitzgerald factor
Mediates cell adhesion (*'nectin' is sticky like fruit pectin)

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Protein C is complexed with

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Protein S

*CS Lewis

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Plasminogen

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forms Plasmin, which LYSES the fibrin clot and inhibits other factors

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Tissue plasminogen

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activates plasminogen

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Acquired abnormality of vessel wall structure that is an allergic response to infection or drugs

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Henoch-Schhonlein purpura

Purpura can also be assoc. w/ steroid therapy and easy bruising in females (infectious purpura), or it can be the result of drug use.

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Thrombocytopenia

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caused by decreased production of platelets, increased use or destruction of platelets, or hypersplenism.

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Factors which cause thrombocytoPENIA

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bone marrow dz
autoimmune dz
DIC
bacterial or viral infection
chemo and radiation therapy
multiple transfusions
NSAIDS

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Thrombocytosis

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ELEVATED platelet count
*caused by hemorrhage
iron-deficiency anemia
inflammation
splenectomy

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Thrombocythemia is also called ____________

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THROMBOCYTOSIS (alias)

VERA MANY platelet count caused by granulocytic leukemia, polycythemia vera many or myeloid metaplasia (vera many myeloid cells)

*Often, it occurs in tandem with an inflammatory disease, as the principal stimulants of platelet production (e.g. thrombopoietin) are elevated in these clinical states as part of the acute phase reaction.

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An increased platelet count predisposes the patient to

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arterial thrombosis

Paradoxically, an elevated platelet count can also cause easy bleeding after dental surgery, GI bleeding, and epistaxis.

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When the platelet count is substantially decreased, bleeding can occur in the

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nose, GI tract, skin and gums

*places that usually get abrasive treatment but manage not to bleed normally

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deficiencies of factors VII and IX

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hemophilia A and B

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rare autosomal recessive trait that causes coagulation abnormality

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hemophilia C

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von Willebrand's dz is autosomal _________

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dominant

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DIC causes continuous production of _______, which, in turn, consumes the other clotting factors and results in uncontrolled _______

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THROMBIN
(thrombin converts fibrinogen into fibrin in order to make a clot).

bleeding

DIC leads to the formation of small blood clots inside the blood vessels throughout the body. As the small clots consume coagulation proteins and platelets, normal coagulation is disrupted and abnormal bleeding occurs from the skin

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Most coagulation factors are manufactured in the ____

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liver.
Consequently, in liver diz, the extent of coagulation abnormalities is directly proportional to the severity of the liver disease.

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Describe DIC

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uncontrolled formation and deposition of FIBRIN thrombi.

continuous generation of thrombin causes depletion (consumption) of the coagulation factors and results in uncontrolled bleeding.

Also, fibrinolysis is activated by DIC, further consuming clotting factors.

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Because DIC causes depletion of clotting factors and uncontrolled bleeding, what tests would be PROLONGED?

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Prothrombin Time [PT]

Activated Partial Thromboplastin
Time {APTT}

Bleeding Time (BT)

Thrombin Time [TT}

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Because DIC causes uncontrolled, continuous production of fibrin thrombi and continuous generation of thrombin causes depletion of clotting factors, Uncontrolled bleeding results. Fibrinolysis is also activated.
What counts are decreased?

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DIC gives you a CuP oF AT-III

Fibrinogen
Platelet count
Clotting factors
AntiThrombin (AT-III)

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Uncontrolled bleeding due to DIC activates fibrinolysis. What positive results?

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Fibrin split products
D-dimer

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Name some causes for DIC

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Brown recluse spider bites
Snake bites
Crushing trauma
Sepsis
Cancer malignancies
Obstetric emergencies
Cirrhosis
Sickle cell
Whoopsy! incompatible blood transfusion
Cold hemoglobinuria
Connective tissue dz (Ehlers-Danlos)

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Paradoxically, the treatment for uncontrolled bleeding of DIC is

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HEPARIN

Heparin blocks thrombin formation, which blocks consumption of other clotting factors and allows hemostasis to occur.

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reflects the data about the ability of platelets to function normally and the ability of the capillaries to constrict their walls

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BT
Bleeding Test

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determines the overall ability of the blood to clot

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PTT or APTT
Activated Partial Thromboplastin Time

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measures the function of SECOND stage clotting factors

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PT
Prothrombin Time

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Bleeding time is Prolonged when

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the level of platelets is decreased or when platelets are qualitatively abnormal (thrombocytopenia, DIC, renal failure, leukemia, von Willebrand's factor or fibrinogen decrease

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This test actually measures the time needed for plasma to clot when thrombin is added. Normally, a clot forms rapidly. If it does not, a Stage III deficiency is present.

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Thrombin Time [TT]

Stage III: thrombin interacts with fibrinogen to form the framework of the clot

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Test used to detect DIC and hypOfibrogenemia

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Thrombin Time

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Prolonged APTT occurs in

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All INTRINSIC pathway deficiencies: (hemophilia A & B)

Heparin therapy
Coumadin/warfarin therapy
Vitamin K deficiency
DIC
Liver dz
Fibrin Breakdown Products

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In deep vein thrombosis or acute myocardial infarction, Heparin is injected and monitored by _____ test.

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APTT

*Heparin is a direct anti-coagulant

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_____________= a protein produced by the liver for clotting of blood. Depends on adequate vitamin K intake and absorption.

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Prothrombin

The prothrombin in blood of liver disease patients is reduced b/c the liver usually makes prothrombin.

PT test measures Stage II EXTRINSIC clotting defects.

PT also evals disfibrogenemia and vitamin K deficiency.

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Why is a PT test used to test Coumadin therapy?

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Coumadin is an orally administered anticoagulant (Heparin is a direct/intravenously admin anticoagulant). Both of these drugs interfere w/ vitamin K related factors, which promote clotting.
Oral anticoagulants (coumadin) delay vitamin K formation and cause the PT to increase because there are fewer factors.

Front 218

3 states that increase Prothrombin Time

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vitamin K deficiency
coumadin/warfarin therapy
liver dz (alcoholic)

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Why are Fibrin Split Products/Fibrin Degredation Products associated w/ DIC?

Back 219

when fibrin is split by plasmin, split products (breakdown) occur.

Split products have anticoagulation properties. They inhibit clotting. Increased levels of FDP's occur with pathologies where clots form and lysis occurs, namely DIC.

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What test is even more specific for DIC than FDP test?

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D-dimer
*because D-dimers are produced only by the action of plasmin on crosslinked fibrin, not by the action of plasmin on unclotted fibrinogen

D-dimer is for DIC and subarachnoid hemorrhage

Front 221

Vitamin- K dependent protein that prevents thrombosis

*ie, if you are missing this protein, you cannot prevent clotting. IF you take an anti-clotting drug, you must have more of this protein.

Back 221

Protein C

*Protein Clotbuster

Front 222

Test used to determine specific amount of injury to myocardium and muscle

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Creatine Kinase (CK) or Creatine Phosphokinase (CPK)

Front 223

CPK can be divided into 3 isoenzymes:

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CK3/MM, CK1/BB, CK2/MB

Front 224

The CK isoenzyme that constitutes almost all the ciruclatory enzymes in healthy people is

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CK-MM

skeletal muscle = MM
Cardiac muscle = MM & MB
brain tissue = BB
Normal CK levels are virtually 100% CK-MM isoenzyme, so a slight increase in total CPK is reflected from elevated BB from CNS injury.
CPK isoenzyme studies help determine where the CPK came from: the heart (MB) or the skeletal muscle (MM).

Front 225

The CPK test is used in the diagnosis of ________ and as a reliable measure of skeletal and inflammatory muscle disease

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Acute Myocardial Infarction (AMI)

because it rises, peaks and disappears in r: 4-6 hours, then p: 12-24 hours, then f: 48 hours

Front 226

CK-MB, contained in cardiac muscle, are usually in a 1:1 ratio of CK-MB1 to CK-MB2. What is the diagnostic threshold ratio? What does it mean?

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5:1

In myocardial damage, MB2 exceeds Mb1 and ratio is altered from 1:1 to 5:1 = heart attack happened if measured in under 48 hours of occurrence.

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Increased CK levels occur during Acute myocardial infarction. Talk about LD?

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Lactate Dehydrogenase (LD) usually peaks 2 days after the onset of Acute Myocardial Infarction, when the LD1-LD2 inversion (FLIP!) is found.

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LD inversion

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LD2 is usually higher. When AMI occurs, LD1 becomes higher, hence the 'flip' or LD inversion signal as evidence that an AMI occurred

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Myoglobin

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oxygen binding protein found in striated mm that appears rapidly after mm INJURY

*sensitive marker for early diagnosis of AMI

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sensitivity

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the ability of a test to detect a disease when it is really there (rate of true positives in a population)

Results are true if they correctly identify the disease is present

Incorrect = false negative. WORST! The test missed the disease when it was actually there.

SENSITIVITY CAN GIVE YOU A FALSE SENSE OF SECURITY.

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specificity

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the test results are negative in patients who do not have the disease (trustworthy?)

False positives

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Sensitivity can give you a false sense of security.

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Worst case scenario of sensitivity test is a false negative.

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anemia likely lab results

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Is there anemia? H&H down

What morphology (form,type) is it? MCV, MCH, RDW

What is the cause? blood tests to specific anemia; CBC will tell you

Front 234

For anemias, review test 1 flashcards

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I don't feel like typing that again!

Front 235

When I say LEAD POISONING, you say

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BASOPHILIC STIPPLING

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process of WBC differentiation and proliferation

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LEUKOPOIESIS

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When immature cells are present in peripheral blood

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SHIFT TO THE LEFT

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INCREASE in the number of circulating WBC

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leukoCYTOSIS

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DECREASE in WBC

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leukoPENIA

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How to take a differential count?

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100's of cells are counted then expressed as a percent

If one is high, the rest will be low since you only count 100 - termed 'relatively low' based on 100 count ceiling.

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Absolute concentration should be used when evaluating a sample for a ________.

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DISEASE.

total WBC x % of cell type = number of that particular cell type

Gives absolute on high or low value so termed 'absolutely low' shows where elevation is or what problem is

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A decrease in the absolute number of circulating neutrophils

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neutroPENIA

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An increase in the absolute number of circulating neutrophils

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neutroPHILIA

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Leukemoid reaction is a WBC count over _________ K/mm3 or a differential count w/ more than _____% immature cells.

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over 50 K/mm3
or
more than 5%
=
LEUKEMOID reaction

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Inverted diff

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LYMPHOCYTES
greater than...pmn's

*usually due to VIRAL infections

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Increase in the absolute number of circulating lymphocytes

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lymphoCYTOSIS = viral infections

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DECREASE in number of lymphocytes

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LYMPH-O-PENIA due to PYOGENIC infections

PUS hijacks lymphocytes

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MonoCYTOSIS
vs
MonoPENIA

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CYTOSIS = increase

PENIA = decrease

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Eosinophilia

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increase in Eosinophils = allergE and wormE

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Eosinopenia

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decrease in Eosinophils due to inflammatory or stress conditions resulting in neutrophilia; corticosteroid use.

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Basophilia

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increase in Basophils =BOWEL IRON SINUS = BASE

May be associated w/ CML (leukemia) and other myeloproliferative disorders, ulcerative colitis, chronic sinusitis, Fe+ deficiency

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What does the immature leukocyte = LEUKEMOID REACTION = mean?

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More than 5% immature cells
BACTERIAL infection
BONE MARROW replacement by tumor
HEMOLYSIS and tissue destruction (burns, severe heart attacks)
CORTICOSTEROIDS

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What do immature forms of WBC mean?

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WBC precursors are STAB cells/BAND cells here to play while the fat lady sings = INFECTION

Metamyelocytes & myelocytes should be LESS THAN ZERO. If above, also a fat lady on crack comin' to sing your end.

Stab/Band cells, metamyelocytes and myelocytes are SUPPOSED TO STAY IN THE BONE MARROW. If you find them in blood, then it is a shift to the LEFT= BAD.

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Name the granulocytes:

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BEN
Basophils
Eosinophils
Neutrophils

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Neutrophils

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PMN's, granulocytes, 'seg':
~once PMN's enter tissue, they never return to circulation
~migrate to areas of infection or inflammation via chemotaxis
NeutroPENIA: myelodysplasia, acute leukemia's, Felty's, granulomatous dz, metastatic tumors, myelofibrosis, toxic chems, CA drugs, overwhelming infections, immune-mediated sx
NeutroPHILIA = acute bacterial/fungal/parasitic infections, non-infectious yet inflammatory conditions, tissue damage/necrosis, Solid tumors, metabolic dz, toxins and venom, steroids

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neutroPENIA quick

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leukemia
Felty's (RA variant)
Mets
myelo-anything

Front 257

neutroPHILIA quick

*What do you want to NEUTRALIZE w/ a crapload of neutrophils?

Back 257

bacterial fungal parasitic
venom

*snakes, spiders, bugs and 'shrooms

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Eosinophils

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attracted to wormE and allergE areas

Called en masse by MAST cells

contain MYELOperoxidase and Major B. Protein that kick parasitic ass

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BASOPHILS

B HE & HIS

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quick so you never see them
HYPERSENSITIVITY rx

release HISTAMINE & HEPARIN
(because they are granulocytes they release granules!) Bind IgE

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Name the A-granulocytes

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monocytes and lymphocytes

Front 261

monocytes moles = monomoles

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turn into MACROPHAGES that live in the tissue, never re-entering circulation. they are like moles; hate to swim, like to dig.

Phagocytic for trash and look alive during inflammation...VITAL ROLE in CELL MEDIATED and HUMORAL IMMUNITY.
APC - Antigen Presenting Cell - the mole takes the antigen of the invader and shows it to a T and B lymphocyte. Monocytes are the security guards of the tissue underworld.

Front 262

Monocytosis monomoles

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the moles are reacting to chronic illness like TB, SBE and syphilis so they INCREASE their numbers and try to swamp the sickness

Front 263

what kills monocyte moles off?

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HAIRY CELL leukemia is like a cat that eats monomoles

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Lymphocytes make up the _________ pool in the bone marrow.

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stem cell pool:
B lymphocytes mature in Bone marrow
T lymphs mature in Thymus

When they grow up, B and T move to peripheral lymphoid tissue outposts, but they can both move freely in circulation.

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T cells

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lymphocytes from the thymus that live in outpost lymphoid tissue

2 types:
1. Cytotoxic/suppressor cells: CD8 (murderous snowman) need antigen (hatchet) to kill. Has crazy-ass cousins called...
NATURAL KILLER CELLS don't need weapons/ exposure. They just kill with their bare hands.

2. T-Helper/inducers = CD4 assist in B cell antibodies and turn on T's (that is why they are called T-HELPER/inducers) - HELP B4 KILLING

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BETA cells are lymphocytes that become glorious

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PLASMA cells = produce ANTIBODIES

need T'helper/inducer cells

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Prothrombin is produced in the liver and is post-translationally modified in a vitamin K-dependent reaction that converts ten glutamic acids on prothrombin to gamma-carboxyglutamic acid (Gla). In the presence of calcium, the Gla residues promote the binding of prothrombin to phospholipid bilayers

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Deficiency of vitamin K or administration of the anticoagulant warfarin inhibits the production of gamma-carboxyglutamic acid residues, slowing the activation of the coagulation cascade.

Front 268

Beyond its key role in the dynamic process of thrombus formation, thrombin has a pronounced pro-inflammatory character, which may influence the onset and progression of _____________.

Back 268

atherosclerosis


Thrombin is a vasoconstrictor and also makes a subarachnoid hemorrhage much worse.

Front 269

thrombocytosis/themia

Back 269

presence of high platelet counts in the blood, and can be either primary (also termed essential and caused by a myeloproliferative disease) or reactive (also termed secondary). Although often symptomless (particularly when it is a secondary reaction), it can predispose to thrombosis in some patients.
*polycythemia vera many

Front 270

Often, it occurs in tandem with an inflammatory disease, as the principal stimulants of platelet production (e.g. thrombopoietin) are elevated in these clinical states as part of the acute phase reaction.

Back 270

THROMBOCYTOPENIA

Front 271

murderous snowman w/ a hatchet
crazy ass cousins

Help B4 killing

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T cell: CD8 needs antigen - cytotoxic/suppressor cells

natural killer T cell cousins don't need a weapon. Kill w/ bare hands.

Helper-T/inducers help B cells show T cells the antigen