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NUR 325 Intro Pathophysio > Wk 6: Coagulation/ DVT/ VTE/ Stress/ Steroids > Flashcards

Wk 6: Coagulation/ DVT/ VTE/ Stress/ Steroids Flashcards

1
Q

what is in blood

A

45% RBC
55% plasma

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2
Q

what makes up the formed elements of blood?

A

platelets
leukocytes
erythrocytes

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3
Q

what makes up plasma ?

A

7% protein
92% water
1% other solutions

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4
Q

what is the main plasma protein found in blood?

A

albumin (57%)

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5
Q

where are a majority of plasma proteins made?

A

the liver

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6
Q

what is the most plentiful clotting factor in plasma?

A

fibrinogen

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7
Q

what is serum?

A

it is plasma minus the clotting factor

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8
Q

erythrocytes

A

red blood cells with hemoglobin
-responsible for tissue oxygenation

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9
Q

leukocytes

A

WBC
responsible for bodies defense

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10
Q

neutrophils

A

WBC
active in early inflammation
acute bacterial infections
role in phagocytosis

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11
Q

eosinophils

A

WBC
allergic reactions and parasites

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12
Q

basophils

A

hypersensitivity, allergic reactions

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13
Q

monocytes

A

WBC for phagocytosis

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14
Q

lymphocytes

A

T/B cells for immunity
WBC

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15
Q

Natural killer cells

A

WBC
primary defense for viruses and tumors

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16
Q

platelets are responsible for

A

hemostasis, normal coagulation and the release of growth factors

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17
Q

are platelets true cells?

A

no
they have NO nucleus
they are cytoplasmic fragments for clotting

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18
Q

what is a cytoplasmic granule?

A

it is something that is released from platelets that has adhesive proteins to aid in coagulation and growth factors

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19
Q

what is a normal platelet count?

A

150,000-4000,000

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20
Q

when would a patient be considered thrombocytopenic ?

A

with a platelet count equal to or below 100,000

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21
Q

Why would we be concerned if a patient had thrombocytopenia ?

A

they are at high risk for bleeding

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22
Q

where are additional platelets stored, other than the blood

A

the spleen

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23
Q

what is the function of platelets ?

A

-they circulate through body unactivated (smooth platelet)
-activated when blood vessel is damaged
-they go to area of injury
-platelet adhesion (dendredic form)
-changes platelet shape and chemistry
-stick to one another
-activation of clotting system

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24
Q

what does a clotting cascade consist of?

A

it is a group of proteins that come together when they are activated, to form a blood clot

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25
Q

what activates the clotting cascade?

A

tissue injury (or infection)

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26
Q

what are the components of a blood clot?

A

fibrin strands and platelets
(with platelets as the primary activator)

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27
Q

what is hemostasis

A

the stopping of bleeding by clotting blood

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28
Q

is thrombin more active in the intrinsic or extrinsic pathway of the clotting cascade ?

A

intrinsic

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29
Q

what are the two chemicals that can stop the coagulation cascade?

A

1) anti-thrombin III (AT III): circulating inhibitor of thrombin (stops clotting process)

2) tissue factor pathway inhibitor (TFPI): inhibits factor Xa (ten a)

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30
Q

how does a clot naturally get removed from the body?

A

fibrinolysis : a breakdown that is carried out by the fibrinolytic system
-tPA: turns plasminogen into plasma, which breaks down fibrin clot
- plasmin does the same

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31
Q

why would someone be in coagulation therapy?

A

prevention of clots
break up an existing clot
increase circulation/ perfusion
decrease pain
prevent further tissue damage

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32
Q

heparin MOA

A

inhibit factor 11a (thrombin) and factor X a

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33
Q

warfarin MOA

A

inhibit vitamin K-dependent clotting factors (II, VII, IX, X)

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34
Q

apixaban MOA

A

inhibit factor Xa

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35
Q

aspirin MOA

A

anti platelet

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36
Q

clopidogrel and ticagelor MOA

A

ADP inhibitor anti platelet

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37
Q

what is the difference between an anticoagulant and an anti-platelet?

A

anticoag stops formation of clotting factor, PREVENTS clots

anti platelet stops platelet aggregation (stickiness) and prevent platelet plug formation

38
Q

which is better for preventing a heart attack or stroke? anticoagulant or anti-platelet?

A

anti-platelet

39
Q

what is a low molecular weight heparin?

A

enoxaparin

40
Q

what is the difference between heparin and enoxaparin?

A

enoxaparin only inactivates factor Xa, not thrombin

41
Q

what route do you use for heparin?

A

IV or SQ

42
Q

Heparin Induced thrombocytopenia (HIT)

A

low platelet count
increased development of clots
d/t heparin antibody development
it is like an allergic reaction

43
Q

If a patient is thought to have developed HIT then what are some nursing considerations?

A

monitor platelet counts
stop heparin if <100,000
use non heparin anticoagulant meds instead

44
Q

what lab values do you need to monitor with warfarin?

A

PT
INR

45
Q

what is a normal INR value and what is a therapeutic INR value

A

normal patient: ~1
Pt on warfarin: 2-3.5 ( monitor monthly)

46
Q

why should you avoid alcohol use if you are on warfarin?

A

alcohol thins your blood, so if you are an alcoholic and on a blood thinning medication it can cause numerous complications and worse bleeds

47
Q

what are some lifestyle recommendations for a patient that is on warfarin?

A

live like you are on bleeding precautions
-medical alert bracelet
-soft bristle toothbrush
-electric toothbrush
-electric razor
-avoid foods with high vitamin K (GREENS)

48
Q

thrombus

A

blood clot attached to vessel wall

49
Q

thromboembolus

A

blood clot not attached to vessel wall anymore

50
Q

are thrombus’ more common in arteries or veins? why?

A

veins (near valves)
d/t flow and pressure

51
Q

DVT

A

clot in lower extremity venous circulation

52
Q

triad of virchow

A

venous stasis
venous endothelial damage
hypercoagulable states

53
Q

what patients are at a high risk for clotting?

A

ortho surgery pt
spinal cord injuries
immobility, frequent travelers
OB/GYN pt (birth control, pregnancy)
clotting disorders
obese
smoker
CA/chemo
HF
IBS/chrons/ ulcerative colitis
H/o or FHx of DVT
age >60
varicose veins

54
Q

what causes the localized pain and erythema related to a DVT?

A

inappropriate platelet aggregation and the growth of the thrombus

55
Q

why would a leg swell up when there is a DVT?

A

the thrombus can cause a significant obstruction to venous blood flow, causing pressure to build up and present as edema

56
Q

pulmonary embolism ( PE)

A

clot lodged in pulmonary system
-prevents gas exchange

57
Q

chronic thomboembolic pulmonary hypertension

A

caused by repeated clots in the lungs which leads to increased pressure in the lung circulation
-common Sx: SOB
-rare

58
Q

post thrombotic syndrome

A

pain, aches, fatigue, swelling sensation, cramps, tingling, paresthesias, spider veins, cyanosis, increased pigmentation, venous ulcerations
-h/o multiple VTEs or untreated VTES

59
Q

phlegmesia cerula dolens

A

“painful blue inflammation”
-rare
-clots are in major leg veins and they become occluded.
-sudden onset of severe swelling, pain, cyanosis,
-if not treated quickly -> gangrene -> amputation

60
Q

Treatment for DVT/VTE

A

-anticoagulation therapy
-prevention of risk factors is crucial
-IVC filters
-embolectomy

61
Q

in general, what is stress?

A

alterations in our environment
-internal or external causes
-mental, physical or chemical factor that causes tension in body/mind
-stressor: force causing stress

62
Q

homeostasis

A

state of being
all systems within the body are around an ideal set point
-balance is achieved
-where body works best

63
Q

allostasis

A

body’s attempt to get BACK to homeostasis
-set points may need to be altered d/t certain situations

Ex: increased RR with vigorous exercise

64
Q

eustress

A

positive form of stress
-accomplishment, motivate, improve performance

65
Q

distress

A

negative reaction to stress
-outside of coping abilities
-can decrease performance

66
Q

coping mechanisms

A

ways which stress is managed or adapted to

67
Q

what influences our responses to stress ?

A

genetics
culture
prior experiences/ environment
pre-existing health status
allostatic state
ability to manage stress

68
Q

general adaptive syndrome and its three processes

A

body’s natural response to stressors
1. alarm
2. resistance
3. exhaustion (occasionally)

69
Q

alarm stage of general adaptive syndrome

A

initial state of arousal
initial defense mechanism
“fight or flight”
-CHS hormone
-SNS activated
-HPA axis

70
Q

norepinephrine

A

primary constrictor of smooth muscles in blood vessels
-regulates blood flow through tissues and its distribution to organ
-maintains BP by constricting smooth muscle in vessels
-dilates pupils
-decreases gastric secretion
-pancreas insulin secretion

71
Q

epinephrine

A

-enhances heart contractility / output
-dilates airways for better oxygenation
-stimulates liver for glycogenolysis
-inhibits insulin secretion from the pancreas

72
Q

what is our primary glucocorticoid?

A

cortisol
increased cardiac output and BP
inhibits reproductive hormones
increases amino acid levels
atrophy of lymph tissue
limits WBC response

73
Q

what is the primary mineralocorticoid?

A

aldosterone
absorbs Na+, more fluid on board

74
Q

when catecholamines and glucocorticoids work together, what does it aid in?

A

development of memory
this teaches brain how to respond to stress in the future

75
Q

resistance stage of general adaptive syndrome

A

counteracts the effects of continued stress
-coping and managing response
-counteract stress, lots of energy used
-limited time
-stress removed = relaxation => PNS takeover
OR stress continues and body runs out of supplied to counteract stress

76
Q

exhaustion stage of general adaptive syndrome

A

stressor is not relieved
body can no longer achieve homeostasis
depleted energy
inability to adapt
-can be in response to chronic stress as well
-neg. impact on physical/mental health
-immunosuppression
-excessive catecholamine

77
Q

allostatic load

A

occurs with chronic stress
-long term dysregulation

78
Q

allostatic overload

A

exhaustion
stress induced Dz or disorder

79
Q

symptoms of allostatic overload

A

hair loss, tension, mouth sores, asthma, palpations, tics, digestive disorders, irritable bladder, acne, irregular periods, impotence, sleep disturbance

80
Q

what are some symptoms that can occur d/t sleep deprivation ?

A

irritability and moodiness
apathy
impaired memory
poor judgement
hallucinations

81
Q

diseases linked to stress

A

CAD, HTN, stroke, tension HA, rheumatoid arthritis, autoimmune Dz, IBS, ulcers, sexual disorders, T2 DM

82
Q

what happens when there is an over production of stress hormones?

A

it can affect memory
major depressive disorders
immunosuppression

83
Q

what is the primary hormones related to stress?

A

cortisol

84
Q

cortisol is active in the metabolism of what?

A

CHO
gluocose

85
Q

cortisol

A

role in protein metabolism
fat redistribution
buildup of fat in face and trunk (lipogenesis)

86
Q

does exhaustion cause bleeding ulcers?

A

no
used to think it did

87
Q

what are steroids used for?

A

as a replacement
anti-inflammatory
immunosuppression
work well on allergies
asthma, COPD exacerbation, chronic inflammatory bowel disease, rheumatic disorders, post-transplant

88
Q

what is an important teaching point for patients who take steroids?

A

you must increase your dose during times of stress

89
Q

steroid replacement: glucocorticoids dosing

A

alternate-day therapy
multiple ways this steroid can be given

90
Q

steroid replacement: mineralocorticoids dosing

A

once a day
not used as frequently

NUR 325 Intro Pathophysio (7 decks)

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