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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

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)

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

Fibrinolysis V

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

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:

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

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

Hypercoagulability

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

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

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
Q

Thrombophilia

A

Clotting

Multiple DVTS (genetics) expect to see in extremities.

S/S:
warm, pain (blood accumulation problem);
cool (arterial problem)

26
Q

Acquired increased clotting

A

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
Q

Inherited bleeding disorders:

A

👉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
Q

Acquired bleeding: Disseminated Intravascular Coagulation (DIC)

A

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
Q

Anti-thrombolytic drugs

A
  • *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
Q

Antithrombic therapy

A

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
Q

Platelet aggregation inhibitor

A

Plavix (clopidogrel)- similar to anti-thrombolytics (ASA).

  • Specific inhibitor of ADP-induced platelet aggregation.
  • Doesn’t let platelets stick together
32
Q

Functions of blood

A
  • 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
Q

Hemoglobin

A

-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
Q

Erythropoiesis

A

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
Q

Why would a man receiving chemo for cancer develop anemia?

A

Erythropoiesis

From Myelosuppression
(Stem cell may not make RBC).

Cancer causes suppression of stem cells.

Chemo effects DNA synthesis and replication

36
Q

Why would a man with renal failure develop anemia?

A

Erythropoiesis

No erythropoietin -also in chronic kidney disease, sudden onset kidney problems

37
Q

Required dietary factors for RBCs

A
  • 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
Q

RBC Destruction

A
  • 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
Q

Hemoglobin is broken down:

A

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
Q

S/S anemia

A

-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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