Week 10 Hematology and Sepsis Flashcards
AUTOIMMUNE THROMBOCYTOPENIC PURPURA
platelet production is normal
autoimmune against platelets
AUTOIMMUNE THROMBOCYTOPENIC PURPURA manifestations
1st seen on skin (bruises)
Anemia
Intracranial bleeding
THROMBOTIC THROMBOCYTOPENIC PURPURA
inappropriate clotting
clots don’t form in trauma but form in the blood
Fatal in 3 months without immunosuppressants
Hemophilia
deficiency in clotting factors
do not bleed more often, they just bleed for longer
Hemophilia labs
prolonged PTT
normal PT
hemophilia tx
infusions of clotting factor VIII
Heparin induced thrombocytopenia (HIT)
immune reaction that increases platelet activity
HIT symptoms
1 thrombocytopenia
DVT
PE
HIT risk factors
IV heparin
Female
Heparin use over 1 week
When to use Packed red blood cells (PRBCs)
Anemia; hemoglobin <6g/dL, 6-10g/dL, depending on symptoms
When to use washed RBCs (WBC-poor PRBCs)
Hematopoietic stem cell transplant patients
When to use pooled plateletes
Thrombocytopenia, platelet count <50,000
use single donor if hx of allergic reaction
When to use FFP
Deficiency in plasma coagulation factors, Prothrombin or partial thromboplastin time 1.5 times normal
When to use cryoprecipitate
Hemophilia VIII or von Willebrand’s disease, Fibrinogen levels <100mg/dL
When to use WBCs
Sepsis, neutropenic infection not responding to antibiotic therapy
MAP
mean arterial pressure
related to tissue and organ perfusion
Cardiovascular Manifestations of shock
Decreased CO, BP, central venous pressure, cap refill, peripheral pulses
Increased HR
Thready pulse, Narrowed pulse pressure, Postural hypotension, Flat neck and hand veins in dependent positions
Respiratory Manifestations of shock
Increased RR, Shallow respirations, Increased PaCO2, Decreased PaO2, Cyanosis
Early Neuromuscular Manifestations of shock
Anxiety, Restlessness, Increased thirst
Late Neuromuscular Manifestations of shock
Decreased CNS activity (lethargy to coma), Generalized weakness, Diminished/absent deep tendon reflexes, Sluggish pupillary response
Kidney Manifestations of shock
Decreased urine output, Increased specific gravity, Sugar and acetone present in urine
Integumentary Manifestations of shock
Cool/cold, Pale/mottled/ cyanotic, Moist, clammy, Mouth dry; paste-like coating present
Gastrointestinal Manifestations of shock
Decreased motility, Diminished or absent bowel sounds, N/V, Constipation
Initial (early) stage of hypovolemic shock
MAP < by 10mmHg
Compensatory mechanisms of > HR and vascular constriction are effective in maintaining oxygenation
Nonprogressive (compensatory) stage of hypovolemic shock
MAP < 10-15
Kidneys are involved to increase blood volume
Acidosis and hyperkalemia occur
Progressive (intermediate) stage of hypovolemic shock
compensitory mechanisms not effective, organs develop hypoxia
Must correct within 1 hour of onset to save life
Refractory (irreversible) stage of hypovolemic shock
vital organs have overwhelming damage
Multiple organ dysfunction syndrome (MODS)
cell damage caused by release of toxic metabolites and enzymes
Small clots form and block oxygenation to organs
Changes in BP with vasoconstriction compensation in hypovolemic shock
Diastolic (bottom) increases and systolic (top) stays the same causing narrow pulse pressure
Decreased urine output
early indicator of shock
First manifestation of central nervous system changes
increased thirst
pH in hypovolemic shock
Decreased: insufficient oxygenation causing anaerobic metabolism and acidosis
PaO2 in hypovolemic shock
Decreased: anaerobic metabolism
PaCO2 in hypovolemic shock
Increased: anaerobic metabolism
Lactic acid in hypovolemic shock
Normal-3-7
Increased: anaerobic metabolism with buildup of metabolites
H&H in hypovolemic shock
Increased: fluid shift/dehydration Decreased: hemorrhage
K+ in hypovolemic shock
Increased: dehydration, acidosis
Priority problems for patients with hypovolemic shock
- Hypoxia (from hypovolemia)
- Hypoperfusion (from fluid volume loss, Hypotension)
- Anxiety
- Confusion (from decreased cerebral perfusion)
When is plasma used in hypovolemic shock?
to restore osmotic pressure when H&H is normal
Adverse effects of inflammatory responses in sepsis/ systemic inflammatory response syndrome (SIRS)
widespread vasodilation and blood pooling, mild hypotension, low UO, increased RR, decreased CO
SIRS criteria
2 must be present plus 1 clinical manifestation to confirm sepsis
temp >100.4
HR >90
RR >20 or PaCO2 12,000 or <4,000
Clinical manifestations of sepsis
Must has at least 1 plus 2 SIRS criteria for sepsis dx
Hypotension, UO < intake, < cap refill, hyperglycemia (>120), Change in mental status, > creatinine
Disseminated intravascular coagulation (DIC)
microthrombi formation in hypoxia.
Anaerobic metabolism causes glucose release
HR increases and Pt may look better d/t > CO but is actually worse
Clinical manifestations in severe sepsis
low O2, rapid RR, </no UO, change in cognition
mortality rate is high
Septic shock
multiple organ failure and bleeding, capillary leak, death is likely, sx are like hypovolemic shock
Hallmark symptoms of sepsis
Left Shift: increased serum lactate, normal or low WBC, and decreasing segmented neutrophil with rising band neutrophils
Cardiac changes in early sepsis
Cardiac output and blood pressure are lower
Cardiac changes in late sepsis
CO, HR and BP are higher
Respiratory changes in early sepsis
Rate increases in an attempt to compensate
Respiratory changes in late sepsis
tissue hypoxia and metabolic acidosis depth and rate of respiration to increases
