FINAL Flashcards

1
Q

What are defensins?

A

“defense” peptides. Attracted to the phospholipids of pathogen and forms pores that disrupt intracellular compartment and kills pathogen

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2
Q

Steps recognition, recruitment, removal, and repair

A
  • 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
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3
Q

Know the resident macrophages

A

o Microglial Cells (CNS)
o Dust Cells (AKA alveolar macrophages in the lungs)
o Langerhans (skin)
o Kupffer cells (liver)

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4
Q

DAMPS and PAMPS

A
  • DAMPS: receptors on damaged cells

- PAMPS: on pathogens with things like peptidoglycan, lipoproteins, etc.

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5
Q

Cytokine and Chemokine

A
  • Cytokine: cell signaling; generates immune responses

- Chemokines: attracts leukocytes

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6
Q

Histamine and serotonin

A

Both cause vasodilation and come from mast cells

-Histamine causes inflammation

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7
Q

Anticholinergics

A

Effect first line defense: decreased saliva and decrease stomach acid

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8
Q

How do changes in BCOP and ICOP contribute to edema?

A

decrease in BCOP and increase in ICOP = accumulation of fluid

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9
Q

“Arachidonic Acid Metabolites”

A

prostaglandins and leukotrienes-> eicosanoids-> inflammation

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10
Q

Complement System

A
  1. Classical
  2. Lectin
  3. Alternative
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11
Q

MALT->Mucosa Associated Lymphoid Tissue

A

initiates immune responses to specific antigens encountered along all mucosal surfaces

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12
Q

Haptens

A

molecules are too small and have to be paired with something else-> penicillin

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13
Q

Types of Hypersensitivity

A
  1. Type I: Allergies and anaphylaxis
  2. Type II: Antibody-> specific to one type of organ (myasthenia gravis) (graves disease)
  3. Type III: Immune complex-> antibody and antigen bind activating complement pathways (rheumatoid arthritis)
  4. Type IV: Delayed-> cell mediated (contact dermatitis)
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14
Q

Colony stimulating factor (CSF)

A

stimulates the production of blood cells

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15
Q

Neutropenia

A

abnormally few neutrophils

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16
Q

Benign ethnic neutropenia

A

seen in people with african decent-> duffy mutation

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17
Q

Kostmann Syndrome

A

causes the lack of neutrophils-> neutrophils die alot-> ear, skin, respiratory infections

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18
Q

Felty syndrome

A

“super rheumatoid disease”-> rheumatoid arthritis as well as neutropenia and splenomegaly

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19
Q

Infectious Mononucleosis

A
  • EBV/HHV-4

- CMV/HHV-5

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20
Q

4 types of leukemia

A
  1. acute lymphocytic leukemia (ALL)-> adolescents
  2. acute myeloid leukemia (AML)-> adults
  3. chronic lymphocytic leukemia (CLL) -> adults & most common, NK cells
  4. chronic myeloid leukemia (CML)-> mostly adults
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21
Q

Philadelphia chromosome

A
  • chromosome 9 and 22 switch portions

- CML

22
Q

Leukemia

A

begins in bone marrow

23
Q

Hodgkin lymphoma and non-Hodgkin lymphoma

A
  • NHL: more common and life threatening; humoral

- HL: more predictable; cell mediated

24
Q

What are Reed-Sternberg cells?

A
  • Large leukocytes found in the superficial cortex of lymph nodes
  • Hodgkin lymphoma
25
What is multiple myeloma and what causes it
cancer that originates in the plasma cells
26
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
27
Symptoms of multiple myeloma
bone pain, frequent infections, constipation, loss of appetite
28
Naturally occurring anticoagulants
antithrombin III, tissue factor pathway inhibitor (TFPI), Prostacyclin, Nitric Oxide (NO), and ADPase
29
tPA
converts plasminogen into plasmin | removes clots
30
coumadin and warfarin and heparin
- Coumadin or Warfarin: inhibits clotting factors (vit K) | - Heparin: increase antithrombin III
31
Vitamin K
Needed for clotting factor VII (extrinsic)
32
PT and INR (extrinsinc)
- PT: test to see how fast you clot | - INR: how it is measured, (your INR/ regular INR)
33
aPTT
measures intrinsic pathway
34
Hemophilia
A: deficiency in factor VIII B: deficiency in factor IX
35
Factor V deficiency vs Factor V Leiden
Deficiency: not enough factor V Leiden: Protein C cannot be broken down
36
Von Willebrand Disease
Type 1: deficiency-> treatment DDVAP-> 3 to 5 times vWF | Type 2: not a deficiency but vWF is not functional
37
DIC -> Disseminated intravascular coagulation
abnormal activation of clotting factors throughout the body (infections, cancers)
38
Thrombocytosis vs Thrombocytopenia
- High platelet count | - Low platelet count
39
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
40
Iron
- Iron 2: active form | - Ferric Iron: iron 3
41
Hematocrit
packed red blood cells.
42
Mean corpuscular volume or MCV
measures size of red blood cells
43
Mean corpuscular hemoglobin concentration or MCHC
concentration of hemoglobin in red blood cells-> pale RBC's
44
two forms of dietary iron
1. first is heme iron or iron that is found in the porphyrin ring of the heme molecule 2. non-heme iron or ferric iron (Fe3+) and is less readily absorbed than heme iron
45
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
46
Megaloblastic anemia
vitamin B-12(cobalamin)(binds to intrinsic factor) deficiency or a folic acid deficiency
47
What is polycythemia?
abnormally high total red blood cell count with a hematocrit greater than 50%
48
Lipids
- Chylomicron: plasma lipoproteins - VLDL, LDL, IDL: very low or low density lipoprotein - HDL: high density lipoprotein
49
Difference between Preeclampsia and Eclampsia
Pre: sudden spike in blood pressure Eclamp: more severe and can include seizures or coma
50
Rheumatoid heart disease
Because of molecular mimicry