Nycc Lab Di Wells Test 2

Front 1

3 components of clot formation

Back 1

a. Vasoconstriction
b. Platelet activation
c. Blood coagulation

Front 2

Hemostasis

Back 2

THe controlled activation of coagulation factors and platelets leading to CLOT formation, and subsequent CLOT LYSIS. It stops hemmorhage w/o excessive clotting = THROMBOSIS

Front 3

What are the 4 steps of primary hemostasis?

Back 3

1. Adhesion to collagen at site of vascular injury

2. Release of platelet contents

3. Aggregation of additional platelets

4. Provision of phospholipid surface

Front 4

purpura(um)

Back 4

bruise

Front 5

Petechia(um)

Back 5

bruises < 2 mm in diameter

Front 6

Ecchymosis

Back 6

bruises greater than 2 mm in diameter

Front 7

Primary hemostasis

Back 7

Carried out by platelets in 4 steps.
Formation of clot after vascular injury.

Front 8

Secondary hemostasis

Back 8

Series of complements that work together to form a clot.
1. INTRINSIC pathway -activated by trauma w/in vascular system itself (atheromatous plaque inside vessel, for example)
2. EXTRINSIC pathway - the baseball basher - external trauma
3. COMMON pathway

Front 9

Primary hemostasis =

Back 9

platelets

Front 10

Secondary hemostasis =

Back 10

coagulation cascade

Front 11

What happens to call in secondary hemostasis:

Back 11

Intrinsic + Extrinsic + Common pathways:
Disruption of endothelium exposes TISSUE FACTOR [THROMBOPLASTIN/FACTOR III], triggering the EXTRINSIC pathway by converting intrinsic factor 7 to 7a

Endothelium disruption also exposes COLLAGEN, activating the INTRINSIC pathway

Front 12

tissue factor

Back 12

triggers extrinsic pathway and platelets

Front 13

trigger

Back 13

activator

Front 14

First component of clot formation:

Back 14

VASOCONSTRICTION: smooth muscle action activated by TRAUMA. SMOOTH MUSCLES in walls of small arterial structures contract and STOP leakage.

Front 15

Second component of clot formation

Back 15

PLATELET ACTIVATION: leads to platelet aggregation [primary hemostasis]. Proper platelet activity - form clot as starting point for complete formal clot

Front 16

Your liver is a manufacturing plant. It makes the majority of the proteins that circulate in bloodstream. ___________ -dependent factors

Back 16

Vitamin K-dependent factors

During synthesis in liver, these factors are enzymatically modified by gamma-carboxylase, allowing for Ca+ binding, necessary for optimal enzyme activity. No good liver, no good factors = bruised and bleeding.

Front 17

No vitamin ___, no synthesis by liver. No good liver, no vitamin __.

Back 17

K
K

Front 18

Third step of blood coagulation

Back 18

secondary hemostasis
Extrinsic and Intrinsic factors - forms mature clot

Front 19

Coumadin

Back 19

inhibits vitamin K dependent gamma-carboxylation

Coumadin is Warfarin

Make certain pt not taking these meds or are managed before doing any deep tissue/myofascial work

Front 20

3 components to clot formation

Back 20

Vasocostriction
Platelet activation
Blood coagulation

Front 21

Primary hemostasis:
1. ADHESION to collagen at site of vascular injury

Back 21

Mediated by glycoprotein Ib on the platelet surface and von Willenbrand factor, released by endothelial cell

Front 22

Primary hemostasis:
2. RELEASE OF PLATELET contents

Back 22

Platelets release GRANULES

Synthesis of PROSTAGLANDIN THROMBOXANE A2 - promotes platelet aggregation! ~ a potent vasoconstrictor

Front 23

Primary hemostasis
3. AGGREGATION of additional PLATELETS

Back 23

Mediated by glycoprotein 2a/3b - integrin protein COMPLEX on platelet surface
Integrin molecules can then BOND FIBRINOGEN [bridging platelets together]

Front 24

Primary hemostasis
4. PROVISION of PHOSPHOLIPID surface

Back 24

Platelet phospholipid MEMBRANE is crucial for ORGANIZING and PROMOTING INTERACTIONS of clotting factors.
Platelets also help integrate the INTRINSIC pathway

Front 25

4 FACTOR GROUPS in 2nd hemostasis:

Back 25

1. ACTIVATORS
2. vitamin K- dependent factors
3. CO-factors
4. FIBRINOGEN

Front 26

Explain the 2nd hemostasis factor ACTIVATORS

Back 26

Tissue factor activates 7 - 7a (extrinsic)
Collagen activates the CONTACT phase proteins which activate factors 11 - 11a

Front 27

Explain factor group VITAMIN K DEPENDENT factors of 2nd hemostasis:

Back 27

Prothrombin is 12
During synthesis in LIVER, these factors are enzymatically modified by gamma-carboxylase, allowing for Ca+ binding = necessary for optimal ENZYME activity
Hepatocyte gamma-carboxylase requires Vitamin K as a COFACTOR
Coumadin (Warfarin) is for clotters. Coumadin INHIBITS vitamin K dependent gamma-carboxylase
Patient w/ advanced liver dz will be bruised and bleed easily b/c cannot construct proteins (fibrinogen to fibrin to make mature clot). Affects cascade and most extrinsic pathways.

Front 28

Explain COFACTORS as a factor group in 2nd hemostasis

Back 28

Required for optimal activity

*do not memorize factors (8,9,10)

Front 29

Explain FIBRINOGEN as a factor in 2nd hemostasis

Back 29

Conversion of fibrinogen to FIBRIN = allows polymerization of fibrin monomers to make a CLOT [gel-phase, stabilized by action of factor XIII]

Front 30

What substances INHIBIT clotting?

Back 30

TISSUE PLASMINOGEN ACTIVATOR ("Activase") TPA and components of the contact phase convert circulating plasminogen to PLASMIN

ANTITHROMBIN 3: naturally occuring coagulant. HEPARIN administered in hospital keeps clots from forming, going against other vitamin K dependent factors

PROTEIN C & PROTEIN S:
Leydin factor

Front 31

Lab results for Platelet disorders number 1 check first?

Back 31

PLATELET COUNT:
150,000 to 400,000/ul blood

**Less than 20,000/ul means SPONTANEOUS BLEEDING

Front 32

Platelet count may be adequate, but the ________ may be impaired.

Back 32

function

Front 33

#1 reason for nosebleed

Back 33

1. Kicking the nose!

2. Other trauma
3. Superdry mucous membrane

Front 34

Bleeding time

Back 34

nick in skin to see how long it takes to stop bleeding

Non-specific test
Repeat to clot in between 3-8 min

Front 35

Platelet function analyzer

Back 35

Platelet CLOSURE time:

mimics platelet clotting time
measures adhesion and aggregation time
INDEPENDENT of platelet numbers
****This test is REPLACING BLEEDING TIME TEST

Front 36

What factors give you a prolonged closure time, similar to long bleeding time?

Back 36

Platelet count below 100k
Hematocrit less than 30%
(see list)

Front 37

Platelet aggregometry

Back 37

Detects responsiveness of a platelet to different PLATELET ACTIVATORS to ***see if they are aggregating properly

(ie, collagen/exposed basement membrane, Ep, ristocetin, ADP, arachidonic acid) - ntq

Front 38

Platelet Aggregation ASSAYS

Back 38

storage pool deficiency test
Defects in T-A2
Von WIllenbrand's dz

Front 39

If we really want to know what is happening with platelets, we look

Back 39

into the marrow

Front 40

Coagulation system laboratory tests

FIRST TEST:

Back 40

1. PRO time = extrinsic pathway
{prothrombin time is 11-12 sec}. Tissue factor and Ca++ are added to plasma and time to form a fibrin clot is measured. EXTRINSIC pathway.

To find WHICH factor is the problem, mark each and assay them individually, ie Leiden factor V

Front 41

What organ can cause extrinsic pathway to crash?

Back 41

LIver

VItamin K because factor 7 havs shortest half-life of all the Vit K dependent factors and Prothrombin time is typically sued to monitor COUMADIN therapy

Front 42

Coagulation time lab tests

SECOND test

Back 42

APTT
Activated Partial Thromboplastin Time
(22-33 sec)
Evaluated INTRINSIC factors and COMMON pathway

Ca+ and activator added
Commonly used to assess affect of heparin - ntq

Front 43

Coagulation time lab tests

THIRD test

Back 43

THROMBIN time

Front 44

Coagulation time lab tests

Specific Factor and PRotein assays detect

Back 44

specific factor anomalies

Front 45

Coagulation time lab tests

FIbrin degredation products (FDP) or Fibrin Split products FSP

Back 45

d-dimer x assay

fibrinolysis and fibrinogenolysis

Front 46

Disorders of Platelets may result in

Back 46

spontaneous bleeding:
Petechiae, epitaxis, menorrhagia, intracranial brain bleed

Front 47

ITP

Back 47

antibodies against platelets = purpura

ITP = Idiopathic Thrombocytopenia Purpura

Front 48

ITP lab data

Back 48

Platelet count DECREASED
PT and APTT stay normal!
Bone marrow - normal to increased megakaryocytes
Anti-platelet antibodies = POSITIVE

Front 49

DIC

Back 49

Disseminated Intravascular Coagulation

sys activation of coagulation w/ widespread thrombosis consumes platelets and fibrinogen, resulting in hemorrhage
Occurs in traumatic tissue damage = esp. head injury, sepsis, tumor, lysis, shock

Front 50

Clotting in all organs then you've used up all your coagulation platelets so you bleed

Back 50

DIC = trauma!

Disseminated INtravascular Coagulation

Front 51

lab for DIC

Back 51

Prolongation of PT, APTT increased

Platelet count decreased

Fibrinogen low

FSP/FDP increased

Front 52

Von Villebrandn's dz

Back 52

congenital
deficiency in vW factor - a cofactor necessary for factor 7 activity and platelet adhesion/aggregation

Front 53

Blood glucose over _____ is required to confirm something is wrong.

Back 53

100

Front 54

Blood glucose test requires 2 tests that measure over 126
OR...
FBG over 126 accompanied by the _________

Back 54

polys:
polyuria
polydypsia
polyphagia

Front 55

Range b/w 100-126 fasting blood glucose

Back 55

IMPAIRED fasting glucose

Front 56

Two fasting blood glucose of ___________

OR _____________ is the diagnostic criteria for DIABETES.

Back 56

1. TWO tests over 126

2. one test over 126 w/ POLYS

Front 57

Glucose tolerance test is NOT used for plain old diabetes*** either type.

It IS used for?

Back 57

1. pregnancy (gestational diabetes) **

2. hypoglycemia **

3. Impaired glucose metabolism of some description

Front 58

You do not memorize the GTT procedure steps. It is a pain in the 'tookus'

Back 58

There should be a rise, a peak and then a reduction in your blood sugar.

Front 59

RISE
PEAK
FALL

Back 59

Blood sugar

Front 60

2 hour post-prandial test

Back 60

2-hr PP:

140-199 mg/Dl = IMPAIRED GLUCOSE TOLERANCE
(this is NOT impaired fasting glucose, which means your body has NOT eaten anything and cannot maintain sugar)

Front 61

Impaired glucose tolerance means you HAVE eaten and your body

Back 61

still CANNOT manage sugar properly

[Glu-cola]

Front 62

MACROSOMIA

Back 62

babies of diabetic moms

before C-section, injured both mother and child because infant is HUGE from sugar diet

Front 63

Hb HA1c

Back 63

Gycated (Glycosalated) Hemoglobin test:

Index of how much HEMOGLOBIN is attached (GLYCATED) to our GLUCOSE

Gives idea of managing glucose by how much Hgb is glycated. If UP, then NOT managing glucose well.

Front 64

regarding Hb A1c, above ___% IS diabetes.

Back 64

6.5%

Know fasting glucose range too

Front 65

Hb A1c EAG

Back 65

Estimated Average Glucose**

a math calc where take A1c and convert it to average daily values of glucose

Front 66

Complications of diabetes

Back 66

1. macro vascular = heart attacks and strokes
2. micro vascular = kidney and eye
3. neurologic = sensory neural (polyneuropathy/glove and stocking)

Front 67

Mononeuropathy Multiplex

Back 67

subcategory of diabetic complications:
One or more SINGLE MOTOR PALSIES

ie, ptosis and lateral strabismus when they wake up one day. Can wake up with radial nerve palsey and cranial nerve palsey = more than one nerve involved at the same time (multiplex)

Front 68

Brittle diabetic

Back 68

no matter what is done, the diabetes type I just cannot be controlled

Front 69

Autonomic complications

Back 69

3rd subcategory of diabetic complications

erectile dysfunction
heart rate
respiratory rate
bowels

Front 70

difference b/w vascular and neuropathic ulcer

Back 70

SENSORY poly neuropathy of glove and stocking distribution is NEUROPATHIC sensory death - injuries cannot be felt, skin friable. Found at PRESSURE spots.

VASCULAR ulcer = small vessel complications. TIPS OF TOES, ANKLES, DORSUM OF FEET thin areas

Front 71

diagnostic criteria of hypoglycemia

Back 71

glucose below 50
resolution of sx w/ glucose administration
sx:
WHIPPLE'S TRIAD= Low blood glucose, Headaches, confusion, sweating, weakness, shakiness, lightheadness, rapid pulse, hunger, nausea

Front 72

Type 1 lipid/lioprotein abnormality

Back 72

IV: HYPER-TRIGLYCERID-EMIA 4 =

*FAT layer PRESENT on sample, even when fasting

Front 73

Type IIa and IIb lipoprotein abnormality

Back 73

II: HAMBURGER & FRIES

**Most easily responds to diet and exercise

Front 74

Trigs are not an independent risk factor for ________ but are a risk for _____ disease.

Back 74

atherosclerosis
heart disease

Front 75

Type III, IV & V lipoprotein abnormality

Back 75

III, IV & V: COMBINATION OF INCREASED TRIGS & CHOLESTEROL

***Don't respond as well to diet and cholesterol

Front 76

Increased triglycerides are generally _____ significant than increased cholesterol.

Back 76

less

*Increased trigs are often not treated but an independent risk factor in women

Front 77

Increased triglycerides have an INVERSE correlation between trigs and ___________

Back 77

HDL

*An increase in trigs can lead to PANCREATITIS

Front 78

Which type of trig abnormality has a FAT LAYER on top of sample, even if they are fasting?

Back 78

IV: HYPERTRIGLYCERIDEMIA

Front 79

All types of triglyceride abnormalities (types 1-4) respond to

Back 79

somewhat to STATINS, DIET & EXERCISE

Front 80

Trigs and HDL have an ________ correlation

Back 80

inverse

Front 81

Most cases of increased triglycerides are due to

Back 81

DIET!!!

Front 82

Secondary increases of increased triglycerides are due to

Back 82

DRAM:
Diabetes Mellitus
Renal fail
Alcohol abuse

*first cause of inc. trigs = diet

Front 83

The reference values of TRIGLYCERIDES are based on _________risk.

Back 83

atherosclerosis

<200 mg/dl for cholesterol

LDL less than 130, less than 100 in peeps w/ identifiable risk factors
HDL above 40-45

Front 84

Cardiac test interpretation is based on the _______________ diagnostic criteria

Back 84

WHO AMI

Front 85

WHO AMI cardiac criteria:

Back 85

Must be 2 of 3:
1. History of prolonged characteristic chest pain
2. ECG changes
3. Typical pattern of serum cardiac enzyme rise, peak and return to reference range

Front 86

What are typical CARDIAC markers

Back 86

SERUM ENZYMES
& ISOENZYMES

Front 87

What is a DIAGNOSTIC WINDOW for cardiac marker

Back 87

each marker has its own characteristic initial rise, peak and return to normal