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What is ITP?
- Auto-IMMUNE (ideopathic) Thrombocytopenia Purpura.
- Its an early destruction of platelets
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What s/s will you see in patients with ITP?
Petechiae, purpura, easy brusing, epistaxis, gingival bleeding and menorrhagia.
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Will the H & H be low or high with ITP?
why?
LOW due to bleeding
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Will the platelet count be low with ITP patients?
yes
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ITP...If a patient is severely bleeding and labs show platelet count of <30,000, how is it treated?
Platelet transfusion, intravenous immune globulin (IVIG) and high dose of glucorticoids (like Methlprednisolone)
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ITP...if platelet count is <20,000, with NO bleeding, what do we administer?
short term glucocorticoids
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regarding ITP...If platelet count is between 30,000 and 100,000, then what do we do?
Nothing right now, but will monitor closely. Also, they will be referred to a hematologist to try to determine cause.
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In a nutshell...what is TTP-HUS?
Clumps of platelets blocking small blood vessels and ends up damaging the kidneys, heart and brain.
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What will the labs look like for TTP-HUS patients?
What are the 2 significant lab findings that will be elevated? and why?
- Bilirubin increased because of , rapid breakdown of RBC's
- and
- Lactate level increase because this indicates hemolysis and ischemia
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What will the labs look like for TTP-HUS in regards to platelets and urinalysis?
- Low platelet count
- Urinalysis will show mild proteinuria and red cell casts.
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What are 2 medical treatment for TTP-HUS?
1. Plasma exchange because it will replace the platelets the patient currently has (which have the coating) and replace it with ones that do not.
2. Refractory-immunosuppressive agents like glucocorticoids.
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What are the nursing responsibilities with thrombocytopenia?
- Monitor for bleeding
- FFP/platelet transfusion (doesnt have to be the same blood type, very fragile and needs to be infused quickly)
- Patient education
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What is HIT?
What is a simple way to explain how this happens?
- Heparin induced thrombocytopenia.
- 1. Patient exposed to heparin in some way
- 2. PF4 protein on hep causes some people to be adverse to that and develop antibodies to it.
- 3. These platelets (HIT antibodies) then activates the platelet and makes the platelet release procoagulant, which...
- 4. causes lots of thrombi causing ischemia to the tissues/organs.
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What is the PRIORITY treatment of HIT?
OFF heparin sources AND put them on an alternate anticoagulant like argatroban or bivalrudin (which are direct thrombus inhibitor)
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What is the pathophysiology of DIC?
- Exposure to procogulants (tissue factor and cancer proagulant)
- increased fibrinogen formation in circulation.
- depletion of clotting factors
- end-organ damage
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In Acute DIC, what are some predisposed conditions?
- trauma/excessive surgery
- infections
- obstetric complications
- toxins
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In Chronic DIC, what are some prodisposing conditions?
- having cancer (tumor)
- shock
- pulmonary issues
- prosthetic devices
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With DIC, what is the piece that sets it apart from other hematologic disorders?
Systemic circulation of fribrin (clotting), therefore using up coagulation factors. INCREASE of fibrilolysis which means they end up clotting and bleeding, clotting and bleeding.
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Why does the condition of DIC often end with organ damage?
Because of the widespread clotting, oxygen rich blood isn't perfusing organs and they become ischemic and stop functioning.
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Does giving cryopercipitate replacing firbrinogen in DIC?
yes
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With DIC, why is the d-dimer and fibrin degradation level high?
It shows that you have clots and the body is trying to break them down.
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With DIC, why is serum fibrinogen low?
- Because its being used up in the body.
- Youll also find platelet count to be <100,000
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Which specific labs are significant ONLY to DIC?
- pt,ptt prolonged
- D-dimer increased
- fibrin degradation high
- serum fibrinogen low
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What is hypovolemic shock?
What is cardiogenic shock?
loss of volume in vascular space
pump failure...need to give positive ionotrope like dobutamine.
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What are the 3 types of distributive shock?
The distributive is that the volume isnt where its supposed to be.
- neurogenic (has massive vasodilation)
- anaphylactic
- septic (find underlying cause)
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What are some clinical manisfestations seen in a person with Sepsis?
- HYPOtension (<90 SBP)
- S/S specific to an infectious source
- Tachypnea....RR >20
- MAP <70
- FEVER
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In early stages of sepsis, what does the skin look like?
warm and flushed. when it progresses they become cyonotic and mottiling. Decreased cap refill
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What is the purpose of qSOFA?
measurement of calculating the risk of death
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What are the 3 warning signs included in a qSOFA assessment?
- alteration of mental status
- SBP <100
- RR >22
note: Inquire about current or previous infections?
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What is the laboratory finding that is an indicator the body is not perfusing well and possibly in septic shock?
LACTATE thats elevated. normal is between 0.5-1 mmol/L
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What are the components that make up the Surviving Sepsis Campaign treatment bundle?
(4 of them)
within 1 hour....
- 1. measure lactate level
- 2.Obtain blood cultures BEFORE giving antibiotics.
- 3.Administer 30mL/kg crystalloid for HYPOtension or lactate >4.
- 4. Apply vasopressors to maintain a MAP of >65. (like norephinephrine (levophed) which is FIRST choice)
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What are some collaborative intervention for sepsis/septic shock regarding to administration of antibiotics and corticosteroids?
- 1st-give antibiotics
- 2nd give corticosteroids if fluids and pressors dont resore hemodynamic stability
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What med can be given to help keep GI system moving?
administer metoclopramide (prokinetic agent) and early enteral feeding.
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Treat stress ulcers and Deep Vein Thrombosis prophetically.
YUP!
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What s/s do you see in the INITIAL stage?
- INCREASE in RR
- INCREASE HR
- Peripherially vasoconstriction (in an attempt to keep blood flow to the heart and organs)
- (this will cause DBP to increase slightly)
You DON'T see hypotension until later
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What are the cardinal signs of shock? (5)
- 1. Aneraboic metabolism
- 2. HYPOtension
- 3. cool clammy skin
- 4. abnormal LOC changes
- 5. Oliguria
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What are the s/s of the NON-PROGRESSIVE stage of shock?
- Cont with peripherally vasoconstriction
- decrease in urine output
- Increased thirst
- DBP cont to rise, causing narrowing pulse pressure.
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What are the s/s of the PROGRESSIVE stage of shock?
- Drop in MAP by 20 points
- O2 sats start to drop.
- Increase in anerobic metabolism aeb increase lactic acid, which will turn into metabolic acidosis.
- Youll also see a significant potassium increase (hyperkalemia)
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What are the s/s of the REFRACTORY (irreversible)stage of shock?
- Severe tissue hypoxia
- loss of consciousness
- cool, mottled skin
- unable to feel pulses
- O2 Sat <70%
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What would you monitor with shock?
- VS, especially BP.
- skin color/temp
- O2 Saturation
- urine output
- lactate levels
- ABG's
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What is the outcome of MODS?
possible lifelong organ problems/dysfunction
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What does SHOCK really mean?
The inability of the body to keep up with oxygen and perfusion needs.
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