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87 Cards in this Set
- Front
- Back
3 components of clot formation
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a. Vasoconstriction
b. Platelet activation c. Blood coagulation |
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Hemostasis
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THe controlled activation of coagulation factors and platelets leading to CLOT formation, and subsequent CLOT LYSIS. It stops hemmorhage w/o excessive clotting = THROMBOSIS
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What are the 4 steps of primary hemostasis?
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1. Adhesion to collagen at site of vascular injury
2. Release of platelet contents 3. Aggregation of additional platelets 4. Provision of phospholipid surface |
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purpura(um)
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bruise
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Petechia(um)
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bruises < 2 mm in diameter
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Ecchymosis
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bruises greater than 2 mm in diameter
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Primary hemostasis
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Carried out by platelets in 4 steps.
Formation of clot after vascular injury. |
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Secondary hemostasis
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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 |
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Primary hemostasis =
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platelets
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Secondary hemostasis =
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coagulation cascade
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What happens to call in secondary hemostasis:
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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 |
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tissue factor
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triggers extrinsic pathway and platelets
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trigger
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activator
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First component of clot formation:
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VASOCONSTRICTION: smooth muscle action activated by TRAUMA. SMOOTH MUSCLES in walls of small arterial structures contract and STOP leakage.
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Second component of clot formation
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PLATELET ACTIVATION: leads to platelet aggregation [primary hemostasis]. Proper platelet activity - form clot as starting point for complete formal clot
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Your liver is a manufacturing plant. It makes the majority of the proteins that circulate in bloodstream. ___________ -dependent factors
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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. |
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No vitamin ___, no synthesis by liver. No good liver, no vitamin __.
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K
K |
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Third step of blood coagulation
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secondary hemostasis
Extrinsic and Intrinsic factors - forms mature clot |
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Coumadin
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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 |
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3 components to clot formation
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Vasocostriction
Platelet activation Blood coagulation |
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Primary hemostasis:
1. ADHESION to collagen at site of vascular injury |
Mediated by glycoprotein Ib on the platelet surface and von Willenbrand factor, released by endothelial cell
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Primary hemostasis:
2. RELEASE OF PLATELET contents |
Platelets release GRANULES
Synthesis of PROSTAGLANDIN THROMBOXANE A2 - promotes platelet aggregation! ~ a potent vasoconstrictor |
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Primary hemostasis
3. AGGREGATION of additional PLATELETS |
Mediated by glycoprotein 2a/3b - integrin protein COMPLEX on platelet surface
Integrin molecules can then BOND FIBRINOGEN [bridging platelets together] |
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Primary hemostasis
4. PROVISION of PHOSPHOLIPID surface |
Platelet phospholipid MEMBRANE is crucial for ORGANIZING and PROMOTING INTERACTIONS of clotting factors.
Platelets also help integrate the INTRINSIC pathway |
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4 FACTOR GROUPS in 2nd hemostasis:
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1. ACTIVATORS
2. vitamin K- dependent factors 3. CO-factors 4. FIBRINOGEN |
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Explain the 2nd hemostasis factor ACTIVATORS
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Tissue factor activates 7 - 7a (extrinsic)
Collagen activates the CONTACT phase proteins which activate factors 11 - 11a |
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Explain factor group VITAMIN K DEPENDENT factors of 2nd hemostasis:
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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. |
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Explain COFACTORS as a factor group in 2nd hemostasis
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Required for optimal activity
*do not memorize factors (8,9,10) |
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Explain FIBRINOGEN as a factor in 2nd hemostasis
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Conversion of fibrinogen to FIBRIN = allows polymerization of fibrin monomers to make a CLOT [gel-phase, stabilized by action of factor XIII]
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What substances INHIBIT clotting?
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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 |
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Lab results for Platelet disorders number 1 check first?
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PLATELET COUNT:
150,000 to 400,000/ul blood **Less than 20,000/ul means SPONTANEOUS BLEEDING |
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Platelet count may be adequate, but the ________ may be impaired.
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function
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#1 reason for nosebleed
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1. Kicking the nose!
2. Other trauma 3. Superdry mucous membrane |
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Bleeding time
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nick in skin to see how long it takes to stop bleeding
Non-specific test Repeat to clot in between 3-8 min |
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Platelet function analyzer
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Platelet CLOSURE time:
mimics platelet clotting time measures adhesion and aggregation time INDEPENDENT of platelet numbers ****This test is REPLACING BLEEDING TIME TEST |
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What factors give you a prolonged closure time, similar to long bleeding time?
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Platelet count below 100k
Hematocrit less than 30% (see list) |
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Platelet aggregometry
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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 |
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Platelet Aggregation ASSAYS
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storage pool deficiency test
Defects in T-A2 Von WIllenbrand's dz |
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If we really want to know what is happening with platelets, we look
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into the marrow
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Coagulation system laboratory tests
FIRST TEST: |
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 |
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What organ can cause extrinsic pathway to crash?
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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 |
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Coagulation time lab tests
SECOND test |
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 |
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Coagulation time lab tests
THIRD test |
THROMBIN time
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Coagulation time lab tests
Specific Factor and PRotein assays detect |
specific factor anomalies
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Coagulation time lab tests
FIbrin degredation products (FDP) or Fibrin Split products FSP |
d-dimer x assay
fibrinolysis and fibrinogenolysis |
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Disorders of Platelets may result in
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spontaneous bleeding:
Petechiae, epitaxis, menorrhagia, intracranial brain bleed |
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ITP
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antibodies against platelets = purpura
ITP = Idiopathic Thrombocytopenia Purpura |
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ITP lab data
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Platelet count DECREASED
PT and APTT stay normal! Bone marrow - normal to increased megakaryocytes Anti-platelet antibodies = POSITIVE |
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DIC
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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 |
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Clotting in all organs then you've used up all your coagulation platelets so you bleed
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DIC = trauma!
Disseminated INtravascular Coagulation |
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lab for DIC
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Prolongation of PT, APTT increased
Platelet count decreased Fibrinogen low FSP/FDP increased |
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Von Villebrandn's dz
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congenital
deficiency in vW factor - a cofactor necessary for factor 7 activity and platelet adhesion/aggregation |
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Blood glucose over _____ is required to confirm something is wrong.
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100
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Blood glucose test requires 2 tests that measure over 126
OR... FBG over 126 accompanied by the _________ |
polys:
polyuria polydypsia polyphagia |
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Range b/w 100-126 fasting blood glucose
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IMPAIRED fasting glucose
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Two fasting blood glucose of ___________
OR _____________ is the diagnostic criteria for DIABETES. |
1. TWO tests over 126
2. one test over 126 w/ POLYS |
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Glucose tolerance test is NOT used for plain old diabetes*** either type.
It IS used for? |
1. pregnancy (gestational diabetes) **
2. hypoglycemia ** 3. Impaired glucose metabolism of some description |
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You do not memorize the GTT procedure steps. It is a pain in the 'tookus'
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There should be a rise, a peak and then a reduction in your blood sugar.
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RISE
PEAK FALL |
Blood sugar
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2 hour post-prandial test
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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) |
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Impaired glucose tolerance means you HAVE eaten and your body
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still CANNOT manage sugar properly
[Glu-cola] |
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MACROSOMIA
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babies of diabetic moms
before C-section, injured both mother and child because infant is HUGE from sugar diet |
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Hb HA1c
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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. |
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regarding Hb A1c, above ___% IS diabetes.
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6.5%
Know fasting glucose range too |
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Hb A1c EAG
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Estimated Average Glucose**
a math calc where take A1c and convert it to average daily values of glucose |
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Complications of diabetes
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1. macro vascular = heart attacks and strokes
2. micro vascular = kidney and eye 3. neurologic = sensory neural (polyneuropathy/glove and stocking) |
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Mononeuropathy Multiplex
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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) |
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Brittle diabetic
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no matter what is done, the diabetes type I just cannot be controlled
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Autonomic complications
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3rd subcategory of diabetic complications
erectile dysfunction heart rate respiratory rate bowels |
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difference b/w vascular and neuropathic ulcer
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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 |
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diagnostic criteria of hypoglycemia
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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 |
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Type 1 lipid/lioprotein abnormality
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IV: HYPER-TRIGLYCERID-EMIA 4 =
*FAT layer PRESENT on sample, even when fasting |
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Type IIa and IIb lipoprotein abnormality
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II: HAMBURGER & FRIES
**Most easily responds to diet and exercise |
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Trigs are not an independent risk factor for ________ but are a risk for _____ disease.
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atherosclerosis
heart disease |
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Type III, IV & V lipoprotein abnormality
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III, IV & V: COMBINATION OF INCREASED TRIGS & CHOLESTEROL
***Don't respond as well to diet and cholesterol |
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Increased triglycerides are generally _____ significant than increased cholesterol.
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less
*Increased trigs are often not treated but an independent risk factor in women |
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Increased triglycerides have an INVERSE correlation between trigs and ___________
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HDL
*An increase in trigs can lead to PANCREATITIS |
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Which type of trig abnormality has a FAT LAYER on top of sample, even if they are fasting?
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IV: HYPERTRIGLYCERIDEMIA
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All types of triglyceride abnormalities (types 1-4) respond to
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somewhat to STATINS, DIET & EXERCISE
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Trigs and HDL have an ________ correlation
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inverse
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Most cases of increased triglycerides are due to
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DIET!!!
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Secondary increases of increased triglycerides are due to
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DRAM:
Diabetes Mellitus Renal fail Alcohol abuse *first cause of inc. trigs = diet |
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The reference values of TRIGLYCERIDES are based on _________risk.
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atherosclerosis
<200 mg/dl for cholesterol LDL less than 130, less than 100 in peeps w/ identifiable risk factors HDL above 40-45 |
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Cardiac test interpretation is based on the _______________ diagnostic criteria
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WHO AMI
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WHO AMI cardiac criteria:
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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 |
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What are typical CARDIAC markers
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SERUM ENZYMES
& ISOENZYMES |
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What is a DIAGNOSTIC WINDOW for cardiac marker
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each marker has its own characteristic initial rise, peak and return to normal
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