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NUE 325: Pathopharm I > Coagulation Cascade > Flashcards

Coagulation Cascade Flashcards

1
Q

two main components of blood

A

plasma (55%) and formed elements (45%)

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2
Q

composition of plasma

A

proteins, water, other solutes
- 92% water
- electrolytes

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3
Q

composition of formed elements

A

platelets, WBC, RBC
- majority is RBC

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4
Q

plasma proteins

A
  • albumin and globulins (albumin 57%)
  • clotting proteins (fibrinogen most plentiful clotting factor)
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5
Q

function of albumin in blood

A

regulates how much water is in cellular vs vascular space
regulates oncotic pressure

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6
Q

serum

A

plasma without the clotting factors

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7
Q

erythrocyte

A

RBC, most abundant cell in the blood
- transports O2 to and from the lungs and tissue cells

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8
Q

leukocytes

A

WBC whose main role is defense

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9
Q

neutrophils

A

type of WBC who is the first responder to site of injury
- also plays a role in phagocytosis

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10
Q

eosinophils

A

WBC who plays a role in allergic rxn and parasitic infections

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11
Q

basophil

A

type of WBC who plays a smaller role in allergic rxn

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12
Q

monoyte/macrophages

A

type of WBC whose role is phagocytosis
- eats debris and waste

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13
Q

lymphocyte

A

types of WBC who is responsible for defending and remembering pathogens
- b and t immunity cells

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14
Q

natural killer cells

A

type of WBC whose is the primary defense against tumors and viruses

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15
Q

platelet

A

irregularly shaped, anuclear cell w cytoplasmic properties that are essential for clotting
- contain cytoplasmic granules that can release adhesive proteins, coagulation, and growth factors when they sense vessel injury

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16
Q

normal platelet count

A

150,000-400,000

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17
Q

thrombocytopenia

A

less than 100,000 platelets
high risk for bleeding bc you cant clot

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18
Q

where are additional platelets stored

A

spleen

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19
Q

platelets circulate in a [blank] state

A

unactivated

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20
Q

what happens to platelets when bv is damaged

A

1) inc platelet adhesion (become sticky/dendritic)
2) activation leads to platelet aggregation
3) platelet/platelet and platelet-vascular wall adhesion inc
4) activation of clotting system forming immobilizing meshwork

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21
Q

clotting cascade

A

group of proteins that will form blood clot when activated

22
Q

blood clot

A

meshwork of fibrin strands and platelets
- protein strands stabilize platelet plug and trap other cells

23
Q

primary activator of clotting cascade

A

platelet

24
Q

hemostasis

A

the stopping of blood flow
- clot plugs damage vessel to stop the bleeding

25
Q

fibrin is made up of

A

protein strands

26
Q

ways to stop the clot

A

anti thrombin and tissue factor pathway inhibitor

27
Q

antithrombin

A

inhibits thrombin to stop clotting process

28
Q

tissue factor pathway inhibitor

A

inhibits factor Xa

29
Q

natural removal of clot

A

breakdown carried out by fibrinlytic system
- tissue plasminogen activator turns plasminogen into plasmin
- plasmin degrades fibrin to breakdown clot

30
Q

coagulation therapy goals

A
  • prevent clot formation
  • break apart existing clots
  • can help inc circulation and perfusion
  • dec pain
  • prevent further tissue damage
31
Q

drugs that inhibit coag

A
  • heparin, low wt molecular heparin
  • warfarin
  • apixaban
  • aspirin
  • clopidogrel
32
Q

biggest concern for anti coags

A

bleeding
- internal or external
- know why pt is taking, and area of most risk for bleeding
- monitor h&h and vs

33
Q

what happens to vs if pt is bleeding

A

HR inc
RR inc
inc pallor
BP dec

34
Q

types of drugs used for clotting

A

anticoagulants
anti-platelet

35
Q

anticoagulants

A

inhibit the action or formation of clotting factors
PREVENT CLOTS

36
Q

anti platelet

A

prevent platelet plugs form forming by inhibiting platelet aggregation (dec sticky platelets)
- best for prevent stroke/heart attacks

37
Q

thrombus

A

blood clot that remains attached to bv
- most common in veins due to flow and pressure

38
Q

thromboembolism

A

detached blood clot

39
Q

deep vein thrombosis

A

thrombus occurring in the lower extremity
- typically veins and more specifically around valves

40
Q

triad of virchow

A

there are three factors that promote the formation of a clot
1) venous stasis
2) venous endothelial damage
3) hyper coagulation

41
Q

high risk of triad of virchow

A
  • ortho surgeries
  • spinal cord injuries
  • obstetric/gynecologic conditions
42
Q

venous stasis

A

slow flow of the venous system
- typical in older adults, dec mobility, heart failure

43
Q

venous endothelial damage

A

injury typically related to trauma, surgery or some types of IV meds

44
Q

hyper coagulable states

A

high clotting state
- caused by malignancy, pregnancy, oral contraceptives, genetics

45
Q

thrombus typically occur near

A

venous valves

46
Q

patho of DVT/VTE

A

inflammation around the thrombus promotes inappropriate platelet aggregation and thrombus grows
- cause pain and redness but also no symptoms

47
Q

thrombus can cause

A

significant obstruction to venous blood flow and can cause pressure buildup and cause edema of extremity

48
Q

risk of DVT/VTE

A
  • clotting disorders
  • immobility
  • injury/surgery
  • pregnancy
  • oral contraceptive/hormone replacement therapy
  • overwt/obese
  • smoking
  • cancer/chemo
  • heart failure
  • inflammatory bowel diseases
  • hx of DVT or fam hx
  • over age 60
  • varicose veins/spider veins
49
Q

serious complication of DVT/VTE

A
  • PE (prevents gas exchange in the lungs)
  • chronic thromboembolic pulmonary HTN (caused by repeated clots, inc pressure in lungs, rare)
  • post thrombotic syndrome (related to chronic te pulm HTN, pain, achy, fatigue, nerve issue, spider veins, inc pigmentation)
  • phlegmesia cerula dolens (rlly rare, clots in major veins causing total occlusion, deep pain, intense cyanosis, can lead to gangrene and amputation)
50
Q

treatment for DVT/VTE

A
  • anti coag
  • prevention of risk factors
  • IVC filters
  • embolectomy

NUE 325: Pathopharm I (23 decks)

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