infection/inflammation/sepsis/septic shock Flashcards
lymphocytes
B cells and T cells
cells that mediate antibody immunity
B cells
- they are activated by an antigen
cells that mediate cell immunity
T cells
- activated by foreign markers and antigens
inflammation process step 1
innate and non specific
inflammation process step 2
mediators released from cells and complement system and cytokines activate along with nitrtic oxide
vascular stage
vasodilation along with increased permeability
cellular stage
WBC migrate into tissues toward the stimuli
signaling stage
pro inflammatory mediators attract more WBC
inflammation process step 3
increased interstitial volume causes pressure to be put on nociceptors which leads to pain
WBC most present in a bacterial infection
neutrophils
WBC most present in a viral infection
lymphocytes
blood composition
45% cells
55% plasma
based on suspected bacteria and started ASAP
- used in sepsis and septic shock
empiric treatment
penicillins, cephalosporins, bacitracin, vancomycin, carbapenems
cell wall synthesis inhibitors
erythromycin, tetracyclines, streptomycin
protein synthesis inhibitors
sulfanilamide
metabolite synthesis inhibitors
quinolones, rifampin
inhibitors of nucleic acid synthesis
using substances to enhance immunity and bodys response
immunotherapy
antibodies that are donor acquired (biologics)
give immediate immunity boost that provide short term protection
immune globulins
IVIG
- given IV route
immune globulin
immune mediators (synthetic drug) that stimulate the immune system
cytokines (interferons or interleukins)
Intron A
- given IV route
- used in hepatitis B
cytokine
immunizations
administered antigen that triggers synthesis of B cell antibodies
fetus immunity
IgG transferred during pregnancy via placenta
IgA transferred via breastmilk and protect the GI
innate immunity
non specific and born with
acquired immunity
antigen specific responses
adaptive immunity
established due to exposure/immunizations and is long term
septicemia/bacteremia
pathogen is in bloodstream and can lead to sepsis
infection continuum
infection –> systemic response –> sepsis –> acidosis –> septic shock
infection that causes an extreme inflammatory response and organ hypoperfusion
sepsis
presence of ongoing hypotension and acidosis due to anaerobic metabolism
septic shock
results of septic shock
renal failure, DIC, metabolic acidosis, hyperglycemia
3 types of shock
septic, anaphylactic, neurogenic
septic shock cause
response to pathogen
anaphylactic shock cause
response to allergen
neurogenic shock cause
response to injury
distributive shock
the umbrealla term for shock causing systemic inflammation and causes loss of blood vessel tone and increased permeability
LR in shock and sepsis
used due to lactate conversion to sodium bicarbonate
- mitigate metabolic acidosis
renal failure treatment
catecholamines (dobutamine) and IV fluids
intracellular dysregulation causes
hypoxia –> anaerobic metabolism –> lactic acid
lung dysregulation cause and effect
low O2 and high CO2 leading to metabolic acidosis
renal dysregulation
decreased clearance of acidic contents and causes acidosis
lactic acidosis
a type of metabolic acidosis
- elevated serum lactate due to tissue hypoxia
Kussmaul breathing, decreased BP, hyperkalemia, decreased renal pH
signs and symptoms of metabolic acidosis
metabolic acidosis treatment
O2, electrolytes, sodium bicarbonate , insulin
GI ischemia due to metabolic acidosis
occurs due to SNS activated vasoconstriction
GI ischemia treatment
NG, PPI, antiemetics
hyperglycemia due to metabolic acidosis
tissue hypoxia causes decreased cell metabolism and glucose transport to cells along with pro inflammatory mediators decreasing insulin efficacy
DIC due to metabolic acidosis
decreased perfusion to the liver
decreased plasmin for clot lysis and coagulation factor formation
- starts as widespread and then depletes
widespread DIC treatment
anticoagulants (heparin)
systemic DIC treatment
blood products (whole blood, platelets, vitamin K)
