Wk 6: Coagulation/ DVT/ VTE/ Stress/ Steroids Flashcards
(90 cards)
1
Q
what is in blood
A
45% RBC
55% plasma
2
Q
what makes up the formed elements of blood?
A
platelets
leukocytes
erythrocytes
3
Q
what makes up plasma ?
A
7% protein
92% water
1% other solutions
4
Q
what is the main plasma protein found in blood?
A
albumin (57%)
5
Q
where are a majority of plasma proteins made?
A
the liver
6
Q
what is the most plentiful clotting factor in plasma?
A
fibrinogen
7
Q
what is serum?
A
it is plasma minus the clotting factor
8
Q
erythrocytes
A
red blood cells with hemoglobin
-responsible for tissue oxygenation
9
Q
leukocytes
A
WBC
responsible for bodies defense
10
Q
neutrophils
A
WBC
active in early inflammation
acute bacterial infections
role in phagocytosis
11
Q
eosinophils
A
WBC
allergic reactions and parasites
12
Q
basophils
A
hypersensitivity, allergic reactions
13
Q
monocytes
A
WBC for phagocytosis
14
Q
lymphocytes
A
T/B cells for immunity
WBC
15
Q
Natural killer cells
A
WBC
primary defense for viruses and tumors
16
Q
platelets are responsible for
A
hemostasis, normal coagulation and the release of growth factors
17
Q
are platelets true cells?
A
no
they have NO nucleus
they are cytoplasmic fragments for clotting
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
19
Q
what is a normal platelet count?
A
150,000-4000,000
20
Q
when would a patient be considered thrombocytopenic ?
A
with a platelet count equal to or below 100,000
21
Q
Why would we be concerned if a patient had thrombocytopenia ?
A
they are at high risk for bleeding
22
Q
where are additional platelets stored, other than the blood
A
the spleen
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
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
25
what activates the clotting cascade?
tissue injury (or infection)
26
what are the components of a blood clot?
fibrin strands and platelets
(with platelets as the primary activator)
27
what is hemostasis
the stopping of bleeding by clotting blood
28
is thrombin more active in the intrinsic or extrinsic pathway of the clotting cascade ?
intrinsic
29
what are the two chemicals that can stop the coagulation cascade?
1) anti-thrombin III (AT III): circulating inhibitor of thrombin (stops clotting process)
2) tissue factor pathway inhibitor (TFPI): inhibits factor Xa (ten a)
30
how does a clot naturally get removed from the body?
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
31
why would someone be in coagulation therapy?
prevention of clots
break up an existing clot
increase circulation/ perfusion
decrease pain
prevent further tissue damage
32
heparin MOA
inhibit factor 11a (thrombin) and factor X a
33
warfarin MOA
inhibit vitamin K-dependent clotting factors (II, VII, IX, X)
34
apixaban MOA
inhibit factor Xa
35
aspirin MOA
anti platelet
36
clopidogrel and ticagelor MOA
ADP inhibitor anti platelet
37
what is the difference between an anticoagulant and an anti-platelet?
anticoag stops formation of clotting factor, PREVENTS clots
anti platelet stops platelet aggregation (stickiness) and prevent platelet plug formation
38
which is better for preventing a heart attack or stroke? anticoagulant or anti-platelet?
anti-platelet
39
what is a low molecular weight heparin?
enoxaparin
40
what is the difference between heparin and enoxaparin?
enoxaparin only inactivates factor Xa, not thrombin
41
what route do you use for heparin?
IV or SQ
42
Heparin Induced thrombocytopenia (HIT)
low platelet count
increased development of clots
d/t heparin antibody development
it is like an allergic reaction
43
If a patient is thought to have developed HIT then what are some nursing considerations?
monitor platelet counts
stop heparin if <100,000
use non heparin anticoagulant meds instead
44
what lab values do you need to monitor with warfarin?
PT
INR
45
what is a normal INR value and what is a therapeutic INR value
normal patient: ~1
Pt on warfarin: 2-3.5 ( monitor monthly)
46
why should you avoid alcohol use if you are on warfarin?
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
what are some lifestyle recommendations for a patient that is on warfarin?
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
thrombus
blood clot attached to vessel wall
49
thromboembolus
blood clot not attached to vessel wall anymore
50
are thrombus' more common in arteries or veins? why?
veins (near valves)
d/t flow and pressure
51
DVT
clot in lower extremity venous circulation
52
triad of virchow
venous stasis
venous endothelial damage
hypercoagulable states
53
what patients are at a high risk for clotting?
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
what causes the localized pain and erythema related to a DVT?
inappropriate platelet aggregation and the growth of the thrombus
55
why would a leg swell up when there is a DVT?
the thrombus can cause a significant obstruction to venous blood flow, causing pressure to build up and present as edema
56
pulmonary embolism ( PE)
clot lodged in pulmonary system
-prevents gas exchange
57
chronic thomboembolic pulmonary hypertension
caused by repeated clots in the lungs which leads to increased pressure in the lung circulation
-common Sx: SOB
-rare
58
post thrombotic syndrome
pain, aches, fatigue, swelling sensation, cramps, tingling, paresthesias, spider veins, cyanosis, increased pigmentation, venous ulcerations
-h/o multiple VTEs or untreated VTES
59
phlegmesia cerula dolens
"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
Treatment for DVT/VTE
-anticoagulation therapy
-prevention of risk factors is crucial
-IVC filters
-embolectomy
61
in general, what is stress?
alterations in our environment
-internal or external causes
-mental, physical or chemical factor that causes tension in body/mind
-stressor: force causing stress
62
homeostasis
state of being
all systems within the body are around an ideal set point
-balance is achieved
-where body works best
63
allostasis
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
eustress
positive form of stress
-accomplishment, motivate, improve performance
65
distress
negative reaction to stress
-outside of coping abilities
-can decrease performance
66
coping mechanisms
ways which stress is managed or adapted to
67
what influences our responses to stress ?
genetics
culture
prior experiences/ environment
pre-existing health status
allostatic state
ability to manage stress
68
general adaptive syndrome and its three processes
body's natural response to stressors
1. alarm
2. resistance
3. exhaustion (occasionally)
69
alarm stage of general adaptive syndrome
initial state of arousal
initial defense mechanism
"fight or flight"
-CHS hormone
-SNS activated
-HPA axis
70
norepinephrine
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
epinephrine
-enhances heart contractility / output
-dilates airways for better oxygenation
-stimulates liver for glycogenolysis
-inhibits insulin secretion from the pancreas
72
what is our primary glucocorticoid?
cortisol
increased cardiac output and BP
inhibits reproductive hormones
increases amino acid levels
atrophy of lymph tissue
limits WBC response
73
what is the primary mineralocorticoid?
aldosterone
absorbs Na+, more fluid on board
74
when catecholamines and glucocorticoids work together, what does it aid in?
development of memory
this teaches brain how to respond to stress in the future
75
resistance stage of general adaptive syndrome
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
exhaustion stage of general adaptive syndrome
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
allostatic load
occurs with chronic stress
-long term dysregulation
78
allostatic overload
exhaustion
stress induced Dz or disorder
79
symptoms of allostatic overload
hair loss, tension, mouth sores, asthma, palpations, tics, digestive disorders, irritable bladder, acne, irregular periods, impotence, sleep disturbance
80
what are some symptoms that can occur d/t sleep deprivation ?
irritability and moodiness
apathy
impaired memory
poor judgement
hallucinations
81
diseases linked to stress
CAD, HTN, stroke, tension HA, rheumatoid arthritis, autoimmune Dz, IBS, ulcers, sexual disorders, T2 DM
82
what happens when there is an over production of stress hormones?
it can affect memory
major depressive disorders
immunosuppression
83
what is the primary hormones related to stress?
cortisol
84
cortisol is active in the metabolism of what?
CHO
gluocose
85
cortisol
role in protein metabolism
fat redistribution
buildup of fat in face and trunk (lipogenesis)
86
does exhaustion cause bleeding ulcers?
no
used to think it did
87
what are steroids used for?
as a replacement
anti-inflammatory
immunosuppression
work well on allergies
asthma, COPD exacerbation, chronic inflammatory bowel disease, rheumatic disorders, post-transplant
88
what is an important teaching point for patients who take steroids?
you must increase your dose during times of stress
89
steroid replacement: glucocorticoids dosing
alternate-day therapy
multiple ways this steroid can be given
90
steroid replacement: mineralocorticoids dosing
once a day
not used as frequently
