Mon Test Week 5 Day 1 Immuno-Deficiencies Flashcards
What is the difference between a primary and secondary immunodeficiency?
Primary is genetic and secondary is acquired from environmental, drug induced, disease induced or other change later in life.
Secondary can resolve depending on what caused it.
If there are problems with the complement system what is a person susceptible to?
Encapsulated bacteria
If there are problems with the phagocytes what is a person susceptible to?
Bacteria, fungi, and molds
If there are problems with B-cells what is a person susceptible to?
Bacteria
If there are problems with T Cells what is a person susceptible to?
Viruses, Fungi and Bacteria
What is the early Classical Pathway comprised of?
C1-C4
More deets
- C1q, C1r, C1s
- C4
- C3 leads into late aka last step of early pathway
What is the late Classical Pathway comprised of?
C5-C9 which make up the MAC or Membrane Attack Complex that inserts into an invaders membrane and lyses it
Early classical pathway defect lead to infections with what bacteria? What kind of symptoms/infections?
Sepsis, pneumonia and meningitis from encapsulated bacteria such as:
S. pneumoniae
H. influenzae
Neisseria meningitidis
Also Lupus and glomerulonephritis
What disease can be triggered by early complement defects that may lead to a loss of self tolerance? What is the treatment?
Systemic Lupus Erythematosus and glomerulonephritis from it.
An autoimmune disease with lots of symptoms all over the body
Treat symptoms with anti-inflammatories and steroids
Late pathway complement defects increase susceptibility by ~8000 to what bacteria?what’s special about this bacteria
Neisseria- Neisseria meningitidis, Neisseria gonorrhoeae
Neisseria usually infects teens
Their membrane is resistant to phagocytosis thus MAC lysis is super important.
They make H-binding protein that degrades C3 and wont let MAC happen
What is Bradykinin and what activates it?
A neurotransmitter peptide that when binds is active causing vascular permeability during inflammatory responses allowing for “leaky” vessels leading to swelling and pain.
It is activated by Kallikrein —>HMWK—> Active free bradykinin which binds to cause leaky vessels
C1-INH blocks this activation pathway 2 places before Kallikrein and after.
NO C1-INH and there is lots of edema/swelling and everything that goes along with that calor, rubor and sensitive nerve endings causing dolor
Is Angioedema from a C1- INH deficiency acquired or hereditary?
Both
Symptoms of Angioedema from a C1- INH deficiency?
Triggers?
Treatment?
Symptoms-
Rapid swelling in various tissues- can block airways (not caused by histamine)
Triggered by Trauma, anxiety, surgery, stress
Treatment - Androgenic hormones, C1 esterase inhibitor (Berinert),
Anxiety control during the operating phases
Does not respond well to epinephrine, antihistamines, or glucocorticoids
What is neutropenia and is it congenital or acquired? Why does it happen?
Low neutrophil count lacking first responders
Either but acquired is most common due to drugs , chemo or autoimmune
What bacteria are people susceptible too with neutropenia? Specific bacteria what does it infect?
Opportunistic bacteria attack the mouth, respiratory, gi tract and skin since they lack first responders.
E-Coli, pseudomonas and Gram neg rods
