FINAL Flashcards
What are defensins?
“defense” peptides. Attracted to the phospholipids of pathogen and forms pores that disrupt intracellular compartment and kills pathogen
Steps recognition, recruitment, removal, and repair
- Recognition: macrophages and mast cells recognize and release IL-1
- Recruitment: complement activated activating vasodilation and recruiting t cells
- Removal: phagocytosis on pathogens
- Repair: WBCs stimulate fibrin, collagen, and fibroblasts
Know the resident macrophages
o Microglial Cells (CNS)
o Dust Cells (AKA alveolar macrophages in the lungs)
o Langerhans (skin)
o Kupffer cells (liver)
DAMPS and PAMPS
- DAMPS: receptors on damaged cells
- PAMPS: on pathogens with things like peptidoglycan, lipoproteins, etc.
Cytokine and Chemokine
- Cytokine: cell signaling; generates immune responses
- Chemokines: attracts leukocytes
Histamine and serotonin
Both cause vasodilation and come from mast cells
-Histamine causes inflammation
Anticholinergics
Effect first line defense: decreased saliva and decrease stomach acid
How do changes in BCOP and ICOP contribute to edema?
decrease in BCOP and increase in ICOP = accumulation of fluid
“Arachidonic Acid Metabolites”
prostaglandins and leukotrienes-> eicosanoids-> inflammation
Complement System
- Classical
- Lectin
- Alternative
MALT->Mucosa Associated Lymphoid Tissue
initiates immune responses to specific antigens encountered along all mucosal surfaces
Haptens
molecules are too small and have to be paired with something else-> penicillin
Types of Hypersensitivity
- Type I: Allergies and anaphylaxis
- Type II: Antibody-> specific to one type of organ (myasthenia gravis) (graves disease)
- Type III: Immune complex-> antibody and antigen bind activating complement pathways (rheumatoid arthritis)
- Type IV: Delayed-> cell mediated (contact dermatitis)
Colony stimulating factor (CSF)
stimulates the production of blood cells
Neutropenia
abnormally few neutrophils
Benign ethnic neutropenia
seen in people with african decent-> duffy mutation
Kostmann Syndrome
causes the lack of neutrophils-> neutrophils die alot-> ear, skin, respiratory infections
Felty syndrome
“super rheumatoid disease”-> rheumatoid arthritis as well as neutropenia and splenomegaly
Infectious Mononucleosis
- EBV/HHV-4
- CMV/HHV-5
4 types of leukemia
- acute lymphocytic leukemia (ALL)-> adolescents
- acute myeloid leukemia (AML)-> adults
- chronic lymphocytic leukemia (CLL) -> adults & most common, NK cells
- chronic myeloid leukemia (CML)-> mostly adults
Philadelphia chromosome
- chromosome 9 and 22 switch portions
- CML
Leukemia
begins in bone marrow
Hodgkin lymphoma and non-Hodgkin lymphoma
- NHL: more common and life threatening; humoral
- HL: more predictable; cell mediated
What are Reed-Sternberg cells?
- Large leukocytes found in the superficial cortex of lymph nodes
- Hodgkin lymphoma
What is multiple myeloma and what causes it
cancer that originates in the plasma cells
What is an M-spike and Bence Jones proteins?
M-spike: number of gamma globulins found in the blood plasma
Bence Jones: small partially formed gamma globulins-> filtered in urine
Symptoms of multiple myeloma
bone pain, frequent infections, constipation, loss of appetite
Naturally occurring anticoagulants
antithrombin III, tissue factor pathway inhibitor (TFPI), Prostacyclin, Nitric Oxide (NO), and ADPase
tPA
converts plasminogen into plasmin
removes clots
coumadin and warfarin and heparin
- Coumadin or Warfarin: inhibits clotting factors (vit K)
- Heparin: increase antithrombin III
Vitamin K
Needed for clotting factor VII (extrinsic)
PT and INR (extrinsinc)
- PT: test to see how fast you clot
- INR: how it is measured, (your INR/ regular INR)
aPTT
measures intrinsic pathway
Hemophilia
A: deficiency in factor VIII
B: deficiency in factor IX
Factor V deficiency vs Factor V Leiden
Deficiency: not enough factor V
Leiden: Protein C cannot be broken down
Von Willebrand Disease
Type 1: deficiency-> treatment DDVAP-> 3 to 5 times vWF
Type 2: not a deficiency but vWF is not functional
DIC -> Disseminated intravascular coagulation
abnormal activation of clotting factors throughout the body (infections, cancers)
Thrombocytosis vs Thrombocytopenia
- High platelet count
- Low platelet count
ITP, HIT and HITT, TTP, HUS
- ITP: autoimmune disease that destroys thrombocytes
- HIT: antibodies against heparin (low platelets)
- HITT: thrombosis-> stroke
- TTP: platelets excessively activated
- HUS: helmet cells, excessive platelets
Iron
- Iron 2: active form
- Ferric Iron: iron 3
Hematocrit
packed red blood cells.
Mean corpuscular volume or MCV
measures size of red blood cells
Mean corpuscular hemoglobin concentration or MCHC
concentration of hemoglobin in red blood cells-> pale RBC’s
two forms of dietary iron
- first is heme iron or iron that is found in the porphyrin ring of the heme molecule
- non-heme iron or ferric iron (Fe3+) and is less readily absorbed than heme iron
Hepcidin, Transferrin and Ferritin
Hepcidin: prevent the absorption of iron into the blood
Transferrin: recycled and used to make RBCs
Ferritin: storage form of iron
Megaloblastic anemia
vitamin B-12(cobalamin)(binds to intrinsic factor) deficiency or a folic acid deficiency
What is polycythemia?
abnormally high total red blood cell count with a hematocrit greater than 50%
Lipids
- Chylomicron: plasma lipoproteins
- VLDL, LDL, IDL: very low or low density lipoprotein
- HDL: high density lipoprotein
Difference between Preeclampsia and Eclampsia
Pre: sudden spike in blood pressure
Eclamp: more severe and can include seizures or coma
Rheumatoid heart disease
Because of molecular mimicry
