Immune & Sepsis Flashcards
(10 cards)
What are myeloid cells?
Myeloid cells are differentiated leukocytes, part of the innate immune response:
- Neutrophils: most plentiful, phagocytose pathogens and release cytotoxins: TNFa, arachidonic acid.
- Eosinophils: larger, can target parasites. Featured in the histamine release in asthmatic reactions.
- Basophils & Mast cells release large amounts of histamine, TNF-a, and prostoglandins in allergic responses.
- Macrophages are monocytes that have left the blood into tissues. They appear later on in the immune response, present antigen, and initiate procoagulant activity through IL-1 and TNF-a.
What are lymphoid cells?
Part of the adaptive immune response, produced in bone marrow:
- Natural killer cells release cytotoxic granules when the see infected or cancer cells, causing apoptosis.
- B-cells directly bind to an antigen and secrete antibodies that mark pathogens for destruction. They mature in the lymph nodes and spleen.
- T cells secrete cytokines and can see antigens on the major histocompatability complex (MHC). They are specifically cytotoxic, and mature in the thymus.
How do cytokines work?
These are the “hormones”, or chemical messangers of the immune system.
- Interleukens help immune cells find injury/infected site - inflammatory
- TNF increases vascular permeability, induces fever - inflammatory
- Interferons prevent viral replication
- Colony stimulating factor differentiates stem cells
- Transforming growth factor slows down the immune response when danger has subsided
Which patients are most at risk of infections?
- Pts with immunodeficiencies such as HIV
- Pharmacological treatment i.e. steroids, transplant medications, chemotherapy
- Advanced liver disease: impairs immune component supply
- Diabetes: increases viral/bacterial load in high sugar environments
- Very young or very old: immune system is underdeveloped OR aging thymus, liver, etc.
Which steroid can be given in anaphylaxis, and why?
Methylprednisolone is given to reduce severity of late-stage or biphasic reactions.
Dose is 125mg IV
What is the qSOFA score?
Not a diagnostic tool; however, serves as a “red flag” for sepsis warranting further investigation and treatment. 2/3 of the following critera to qualify:
- GCS <15
- RR less than or equal to 22/min
- SBP less than or equal to 100 mmHg
What lab value derangements might you see in a septic patient?
Increased
Bilirubin
Creatinine
Lactate
BGl
Decreased
Coagulation
Treatment ABC’s for sepsis
Antibiotics: start broad spectrum early, obtain cultures (find the source!)
Breathing: support ventilation as needed, maximize V/Q with positioning and fluid resusc as needed.
Cardiac output: support with preload, vasopressors and inotropes to maintain a MAP >65 and normalizing lactate.
Decrease demand: sedation, analgesia and temperature control.
Pathophysiology ABCC’s of sepsis
Arachidonic acid is a cell-derived (leukotrines) mediator causing vasodilation, increased permeability and pain. May also cause bronchospasm.
Bradykinin are plasma derived potent vasodilators. They further stimulate arachidonic acid pathways by stimulating mast cells. They are triggered by activation of Factor XII (Hageman factor stimulates intrinsic coagulation pathway).
Coagulation cytokines stimulate plasminogen activator inhibitor, preventing clot breakdown and promoting the formation of micro-emboli.
Complement system forms membrate attack complexes that intensify the inflammatory process, cell adhesion and damages endothelium - ultimately leading to cell death.
Systemic complications in septic shock
- Cardiac: dysfunction from release of myocardial depressant cytokines. Ventricular failure follows and microvascular thrombosis. Peripheral vasodilation = relative hypovolemia.
- CNS: hypoperfusion leads to SNS dysfunction, respiratory depression, thermoregulatory failure and coma.
- Hematologic: decreased blood product production, thrombocytopenia and DIC.
- Pulmonary: increased vascular permeability and microemboli lead to a-c thickening, pulmonary hypertension and V/Q mismatch - eventually ARDS
- Renal: dysfunction from vasoconstriction and hypoperfusion leads to AKI
- GI: hypoperfusion disrupts mucosal barrier, furthering release of pro-inflammatory substances.
