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Pathophysiology > EXAM #2: Chapters 8, 12, 13, 20, 21, 22 > Flashcards

EXAM #2: Chapters 8, 12, 13, 20, 21, 22 Flashcards

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1
Q

Thrombocytosis

A

Platelets

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2
Q

Hemostasis

A

Stopping blood flow

NORMAL: blood usually fluid, seals broken blood vessel’s (clot forms)

ABNORMAL: not clotting

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3
Q

Thrombus

A

Blood clot

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4
Q

lysis

A

Loosening, separation

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5
Q

thrombocytopenia

A

Blood clot deficiency

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6
Q

Thrombocytes (platelets)

A

NORMAL: 150,000-400,000

Stored in spleen
Lives 8 to 10 days
Disc shaped for clotting
Meds (NSAIDS) stick to life of platelets
Antiplatelets: don't stick very well

<150,000 = risk for bleeding

> 400,000 = clotting too much

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7
Q

Mediators of Hemostasis

A
  • Chemicals produced by platelets
  • Released after injury to start clotting
  • Help platelet stick
  • Stimulate wound healing
  • Help platelet stick to the vessel wall
  • Constrict blood vessels
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8
Q

Hemostasis phases

A

Phase 1/Primary:

  • Vasospasms and Constrictions = reduces blood flow, temporary fix
  • Endothelial injury
  • Vascular spasm/vasoconstriction of smooth muscle in vessel wall)
  • Decrease blood flow
  • Short-lived/localized

Phase2/Platelet:

  • Release of Vonwillebrand’s Factor (makes everybody stick together) by epithelial cells (lining of vessel walls) and platelets.
  • Platelets secreate ATP = Aggregations = (everybody sticks)
  • Aggregated platelets release thromboplastin (Factor III).
  • Platelet Plug (NOT a clot yet!)- platelets clumped together

Phase3/Coagulation: (2 ways)

  • Extrinsic pathway-injury outside the cell
  • Intrinsic pathway-injury inside the cell
  • Activates X Factor (common pathway):
  • *Prothrombin to Thrombin (without thrombin, can’t aggregate) then Fibrinogen to Fibrin.

*MUST HAVE X FACTOR TO MAKE CLOT!

  • **Prothrombin—>Thrombin—>
  • –> Fibrinogen—>Fibrin= CLOT***
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9
Q

Hemostasis 1st Phase

A

1st Phase/Primary:
*Vasospasms and Constrictions = reduces blood flow, temporary fix

  • Endothelial injury
  • Vascular spasm/vasoconstriction of smooth muscle in vessel wall)
  • Decrease blood flow
  • Short-lived/localized
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10
Q

Hemostasis 2nd Phase

A

2nd Phase/Platelet:
*Release of Vonwillebrand’s Factor (makes everybody stick together) by epithelial cells (lining of vessel walls) and platelets.

  • Platelets secreate ATP = Aggregations = (everybody sticks)
  • Aggregated platelets release thromboplastin (Factor III).
  • Platelet Plug (NOT a clot yet!)- platelets clumped together
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11
Q

Hemostasis 3rd Phase

A

Phase3/Coagulation: (2 ways)
*EXTRINSIC pathway-injury outside the cell

*INTRINSIC pathway-injury inside the cell

  • Activates X Factor (common pathway):
  • *Prothrombin to Thrombin (without thrombin, can’t aggregate) then Fibrinogen to Fibrin.

*MUST HAVE X FACTOR TO MAKE CLOT!

  • **Prothrombin—>Thrombin—>
  • –> Fibrinogen—>Fibrin= CLOT***
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12
Q

Extrinsic pathway

A

PT value
* Occurs in tissues (“extrinsic” to blood)

  • Clotting process for chemical shortcut
  • VERY RAPID-
    takes 10-15 seconds (Quick patch process measured by value of PT)
  • Production of thrombin is low and resulting clot is small
  • 2 ways to get a clot-
    A tissue problem or a vascular problem
  • Not Antithrombolytics (PT/PTT)
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13
Q

PT and PTT

A

(Extrinsic Pathway)

NOT ANTITHROMBOLYTICS

*PT: Warfarin (Coumadin) “Rat poison”
Takes twice as long to clot
don’t want client to clot too fast.
Measure with labs

  • PTT: Heparin
    Prolongs bleeding time
    Measure with labs
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14
Q

Intrinsic pathway-PTT

(Phase 3/Coagulation)

A

(Intrinsic pathway) Phase 3/Coagulation

  • Collagen in the blood vessel wall activates
  • Slower (five-10 minutes) but measured in seconds as a PTT lab value
  • Large amounts of Thrombin = Larger clot
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15
Q

PT and INR

A

Assessment of Extrinsic coagulation

  • Used to monitor clients taking certain meds as well as to help diagnose clotting disorders

*(evaluate oral anticoagulation therapy:
Warfarin (Coumadin) = PT/INR

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16
Q

PTT & aPTT

A
  • activated partial thromboplastin time
  • Assessment of intrinsic coagulation used to monitor Heparin
  • Lab values: NORMAL range 25-35 seconds
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17
Q

Common Pathway (Phase III)

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A
  • Factor X active- Prothrombin activator (without it cannot clot!!)
18
Q

Fibrinolysis V

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A
  • Occurs in response to Enzyme Plasmin (digest/degrades Fibrin)
  • T-PA Tissue plasminogen activator converts plasminogen to plasmin
  • Plasmin digest clot (synthetic T-PA used in strokes, sometimes heart attacks)
  • If injury was not completely healed then client at risk for bleeding
  • Do not give in surgery or brain bleed
  • No Foley catheter or IV after med
  • Thrombolytic-at risk for bleeding
19
Q

Factors that affect Coagulation

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A
  • Vit K deficiency (necessary for synthesis and regulation of components that make a clot, without it you will bleed; stored in liver).
  • Liver disease-causes hemostasis disorder = defects in Coagulation, Fibrinolysis, and Platelet number/function. (Liver cirrhosis = going to bleed)
  • Babies get Vit K shot at birth
  • Green, leafy veg has Vitamin K
20
Q

Platelet disorders:

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A

Thrombocytopenia: platelets <150,000

  • Causes: Hypersplenism, Autoimmune disorders, Hypothermia, Viral/Bacterial infections that cause DIC (disseminated intravascular coagulation)
  • check PT, PTT, platelets if client is bleeding

< 50,000-hemorrhage from minor trauma (IV stick)

<15,000-spontaneous bleeding (petechiae)

<10,000-severe bleeding (doctor wouldn’t let them in surgery; need platelet transfusion)

21
Q

Bleeding disorders

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A
  • Platelets (low or high) defect and platelet function
  • Coagulation factors
  • Vessel integrity (blood vessel defect) inherited or acquired
22
Q

Hypercoagulability

Study These Flashcards
A

Clotting too much

Inherited (diseases) or Acquired (over a lifetime)

  • Increase platelet function-Increased number, Endothelial injury (Von Willebrand’s too much), Increased Procoagulation factors or Decreased Anticoagulation factors
23
Q

Inherited: Hypercoagulation

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A

Associated with Venus thrombosis

Deficiency Protein C or S

Protein C and S work together to in activate Factor V (cause clot) and stop villa (causes clot) in order to stop the clot

So if there is not enough C or S clots are more probable

Protein C deficiency = DVT
Protein S deficiency = risk of arterial thrombosis

24
Q

Factor V Leiden (FVL) deficiency

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A

AKA Activated Protein C resistance = Clotting

Genetic mutation of Factor V which causes resistance to the action of protein C

(unable to stop the clot; C would normally stop clot from continuing)

25
Thrombophilia
Clotting Multiple DVTS (genetics) expect to see in extremities. S/S: warm, pain (blood accumulation problem); cool (arterial problem)
26
Acquired increased clotting
Most common acquired- smoking, disseminated CA, obesity, r/t polycythemia vera (too many RBC), sickle cell disease. Most common female acquired-oral contraceptives. At risk-give heparin so they won't clot as fat
27
Inherited bleeding disorders:
👉Von Willebrand disease- does not allow platelets to aggregate (come together to clock). Normal platelet count with prolonged bleeding. **Affects men/women (menstruation, circumcision). **Three variations. **Released from platelets and endothelial lining of vascular wall. **May 350,000 platelets PT, PTT, still bleeding 👉 Hemophilia- most common. X linked genetic disease.**Female cases rare. **Lack of clotting factors prevents stable clot. **Passed on by females, given to males. **Hemophilia A- >80% Hemophiliacs (a.k.a. classic, Factor VII or A) give factor A. **Hemophilia B- (a.k.a. Christmas disease-factor) give Factor B
28
Acquired bleeding: Disseminated Intravascular Coagulation (DIC)
Complex, acquired disorder: clotting and hemorrhage simultaneously occur. **Sepsis, CA, trauma, blood transfusion-very sick client. **Endothelial damage or tissue damage is primary initiator. **Results in clotting that leads to bleeding. **Widespread vascular clotting-micro clots everywhere. **First S/S: bleeding, used up vitamin K, etc. = can't clot anymore. *Petechiae. Hypotension, infarction everywhere. **TX: give platelets, vitamin K, platelet transfusion. * Greater than 90% death. * Key is to turn off the trigger (sepsis, etc.) * Will see profound bleeding-eyes, IV, nose, foley
29
Anti-thrombolytic drugs
* *Anticoagulants- - Heparin- Binds to AT. - Coumadin (warfarin)- drugs interfere with vitamin K action of the liver (oral) * * Antiplatelet drugs- ASA (aspirin) - Inhibits platelet plug formation. - Decreased platelet adherence and may increase bleeding - Clopidogrel (Plavix)- invention of platelet aggregation * * Thrombolytic drugs- - plasminogen activators are used to lyse thrombin in vivo
30
Antithrombic therapy
ASA (Aspirin). -Irreversible inhibition of platelet enzyme Cyclooxygenase, which is needed for proper platelet aggregation. - Reduces the "stickiness" of platelets. - Affects last for the lifetime of the platelets (7-10 days). - We don't form a clot-won't let platelets together. - NSAID drugs compete for cyclooxygenase may be used in conjunction with ASA
31
Platelet aggregation inhibitor
Plavix (clopidogrel)- similar to anti-thrombolytics (ASA). - Specific inhibitor of ADP-induced platelet aggregation. - Doesn't let platelets stick together
32
Functions of blood
- Transport medium for defense cells (WBC) and metabolic waste, distribution of nutrients, oxygen, hormones. - Goal of erythrocyte (RBC): carry 02 with help of hemoglobin. - Hemoglobin must have iron! - Approximately 65% of iron is form on hemoglobin. - 30% stored in liver as ferritin. - (1/3 reserve in case we need it)
33
Hemoglobin
-Complex proteins; composed of: Heme (iron and biliverdin portion) + Globin (amino acid portion). -2 alfalfa + 2 beta chains. -Carries 02 from lungs to tissues and CO2 from tissues and lungs. - Converts biliverdin to liver to feces. - Recycles iron and amino acids. - Jaundice- if we don't rid of biliverdin
34
Erythropoiesis
Erythrocyte production/simulation depends upon the erythropoietin (hormone made in kidneys in response to low O2 sats). Produced in kidneys-stimulated by hypoxia. Synthetic erythropoietin available (stem cells make RBC) Decreased erythropoiesis caused by kidney failure, chemo, meds. (Client with bad kidneys may not be producing good rbc = anemia)
35
Why would a man receiving chemo for cancer develop anemia?
Erythropoiesis From Myelosuppression (Stem cell may not make RBC). Cancer causes suppression of stem cells. Chemo effects DNA synthesis and replication
36
Why would a man with renal failure develop anemia?
Erythropoiesis No erythropoietin -also in chronic kidney disease, sudden onset kidney problems
37
Required dietary factors for RBCs
- Vit. B12 (cobalamin): required for DNA synthesis. More RBCs created intrinsic factor necessary for absorption B12 - Folic Acid (folate): required for DNA synthesis-prevents NTD (pregnancy-spina bifida defect) - Iron: required for hemoglobin synthesis - Vit. C: increases absorption of iron ** give iron and vitamin C together if client is anemic** What foods have iron and vitamin C?
38
RBC Destruction
- RBC last about 120 days (four months). - Destroyed in the spleen or liver (recycles grabs amino acid and iron) - Hemoglobin is broken down: - -Biliverdin, - -Iron, - -Goblin/Amino acid portion
39
Hemoglobin is broken down:
Hbg broken down into: - Biliverdin: converted to bilirubin and excreted in bile the gallbladder - Iron (heme element): is carried on transferrin to the liver where it is stored as ferritin or back to the bone marrow to be reused - Globin/Amino acid portion: is recycled
40
S/S anemia
-Hypoxia: fatigue, weakness, dyspraxia, pallor, tachycardia, more lactic acid, increased respiratory rate -Hypoxemia: cells don't thrive, no O2=lactic acid

Pathophysiology (2 decks)

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