Heme – 3Q

DIC/HIT
DIC – clot is problem; used up all
Intrinsic vs extrinsic
Intrinsic – endotheial injury; 12, 11, 9, 8
Extrinsic – tissue injury, tissue thrombopisstin, 7

5 10 calcium
prothrombin _ thrombin
fibrinogen 0 fibrin
plasmin – clot – FSP (anticoagulants)
lysed clot
obstretical emergency usually

labs
dec fibrinogen levels LOW used to make fibrin
inc PT PTT, fibrin split products, and d-dimers value

tx – heparin – stops clotting cascade (except during birth)

then FFP, cryopreciptate; get rid of triggering event/cause

heparin inhibits the conversion of prothrombin into thrombin

heparin inactivates circulating thrombin
heparin inhibits the conversion of fibrogen into fibrin

HIT – patients don’t have anti-thrombin III – causing blood to clot

Argatroban – a thrombin inhibitor which does not require anti-thrombin III is given
instead of heparin

ITP (idiopathic thrombocytopenic purpura

Antibodies form and destroy the body’s platelets resulting in thrombocytopenia
Causes
Bone marrow doesn’t produce enough platelets – leukemia, lymphoma, anemias,
bone marrow disorderes, chemotherapy, radiation therapy

Platelets become entrapped in enlarged spleen – cirrhosis with congestive

splenomegaly

Use or destruction of platelets increases – HIV infection, meds (Heparin, quinidine,

oral diabetic drugs), DIC, septicemia from gram negative bacteria

Plt less than 50000

Both Hb and hct decreased
Pallor, petachiae, purpura, ecchymoses and ozzing of blood from venipuncture sites;
Platelet consumption than platelet production (may no need for platelets)
Multisystem 8% 12Q
Shock (septic and anaphylactic)
Multiorgan dysfunction syndrome (MODS)
Multisystem trauma
Toxic ingestions

MODS failure of
Lungs (ARDS)
Kidneys (ATN)
Liver (liver failure)
Blood (DIC)
Brain (low CPP)
Heart (ischemia/injury)

Multisystem trauma
Stress, - EBB – occurs after injury initiated by tissue injury, acute blood loss, shock,
hypoxia, acidosis, pain, anxiety and fear; SNS release epi, norepi, cortisol, inc HR, BP,
venti, prolonged stimulation leads to severe vasoconstriction, impaired delivery of
oxygen and nutrients to tissue
Hypothalamic-pituitary-adrenal secretions such as cortisol, ADH
Renin-angiotension release – renin causes vasoconstriction and aldosterone release
psychological,
metabolic derangement –
edema – influx of fluid from intravascular space into intersititial area
increased cardic output
impaired oxygen transport due to vasoconstriction at tissue level
altered glucose metabolism – glucose level increases due to stress hormone release
altered protein and fat metabolism

A
M
P
L
E

Poision
Tylenol
Mucomyst
140mg/kg loading dose
70mg/kg every 4 hours for 17 doses
given activated charcoal if less than 4 hours since ingestion (wait 1 hr before giving
NAC if charcoal is given)
liver
I – nausea and vomiting
II – RUQ pain
III – liver function abnormalities
Aspirin – kidney destroy
Antidote
Lavage or induce emesis
Activated charcoal
Urinary aklalinization with sodium bicarb to excrete asa faster
Hemodialysis

Massive blood transfusion = low calcium level

TPN causes hypophosphatemia
Amphogen reduces hyperphosphatemia (phosphate binder)

What’s a VVI pacemaker? Chamber paced, sensed, mode

How do you drain left lower lung lobe? Trans
Upper – sit up, cup and clap
Left ventricular assist device – blood is diverted from the left atrium and returned to
the patient via ascending aorta
IABP augments cardiac output by 15%
Tousades de points tx = magnesium
MVA risk for fat embolism
Complication of PEEP is barotrauma (rupture of lung tissue)
Renal transplant acute rejection occurs within 1-2 weeks
A-line, dicrotic notch = closure of the aortic valve
ARDS – keep the patient dry (decreased fluids)
Acidosis –causes a rise in potassium level
MCL – helps differentiate ventricular arrhythmia (ectopy) from supraventricular
arrhythmias (aberrancy) or V1
RBBB – light mt, little problem
LBBB
PVC from LV – irritable cell; mostly going to positive sticky (big mt, big problem)
PVC from RV

up in V6 is good
down in V6 you’re dead

psych 4% 6Q -