Lecture 6 Flashcards
(96 cards)
1
Q
Prenatal period
A
Inherited antibodies (Abs) via placenta (passive)
2
Q
Infancy
A
1st 6 months inherited immunity
very susceptible before 6 months
12-20 months form abs
3
Q
Whooping cough
A
contagious respiratory disease, #1 passed form adults to child
4
Q
Breast feeding
A
additional antibodies from mom
5
Q
Childhood & Adolescence
A
Allergies
6
Q
Constituents
A
WBC
Plasma
Platelets
RBC
7
Q
Formed elements
A
Red component (serum) WBC & RBC
8
Q
WBC
A
Neutrophils Lymphocytes Monocytes Eosinophils Basophils
9
Q
Plasma
A
measures glucose, insulin, hormones
water/protein/other solutes
10
Q
Erythrocytes
A
transport hemoglobin
helps with clotting
has oxygen molecule & hemoglobin
11
Q
Hemoglobin A1c
A
glucose affects integrity of RBC, indication is chronic hyperglycemia
12
Q
RBC Mass
A
balance between production and destruction
120 days, track blood marker (A1c)
13
Q
RBC is produced in…
A
bone marrow sternum pelvis vertebrae ribs
14
Q
RBC is regulated by…
A
erythropoietin (EPO)
15
Q
EPO is produced by…
A
kidneys
16
Q
RBC production increases within…
A
24 hours
17
Q
EPO lifespan…
A
4-12 days
18
Q
RBC is increased in…
A
5 days
19
Q
Factors that decrease oxygenation
A
Low blood volume Anemia Low hemoglobin Poor blood flow Pulmonary disease
20
Q
Hematocrit
A
% volume of blood that is red cells
Men: 45%
Women: 40%
21
Q
Hemoglobin
A
34 gm/100 ml red cells
15-16 (male) gm Hb/100 ml blood
13-14 (female) gm Hb/100 ml blood
22
Q
Oxygen carrying capacity
A
gm Hg/100 ml blood * 1.34 O2/gm Hb
21 ml: men
19 ml: women
23
Q
Where are RBC ingested?
A
spleen
24
Q
What breaks down bilirubin?
A
Liver, if liver can’t break down the skin will turn yellowish, Jaundice
25
Iron is released from blood to...
Transferrin, to make more
26
Jaundice in infants due to...
baby's physic system being hyperactive, producing excessive RBC
hemoglobin needs to gets excreted
circulatory system is playing catch up with the body
27
Anemia
deficiency of Hb
28
Polycythemia
increase RBC production
increase viscosity
increased cardiac work
29
Blood leukocytes (WBC)
1) directly destroying invader = phagocytosis
| 2) forming drones (antibodies/Abs), cell mediated system
30
Leukocytes
```
Granulocytes
- Neutrophils
- Eosinophils
- Basophils
Monocytes
Lymphocytes
- B, Ab mediated
- T, Cell mediated
```
31
Platelets
own category, not RBC or WBC
| helps with clotting
32
Granulocytes
```
65%
- Neutrophils
- Eosinophils
- Basophils
Formed in bone marrow
```
33
Monocytes
5%
tissue macrophages
formed in bone marrow
34
Lymphocytes
30%
| formed in lymph tissue
35
Eosinophils
2%
active against parasites, skin diseases, chronic infections
phagocytic & immunomodulatory
decrease inflammation
36
Basophils
0.5%
similar to mast cells (heparin, histamine)
Release primarily histamine (allergic rxns)
Release due to binding of IgE (immunoglobin/antibodies)
37
Innate immunity
1) Phagocytosis of bacteria
2) Destruction of swallowed organism by acid secretions
3) Resistance of skin to invasion
* Attach and destroy
38
Phagocytosis
fastest way we can defend against foreign invader
| Neutrophils & Macrophages - strongest
39
Monocytes
macrophages upon tissue entry
40
Phagocytosis process
Diapedesis
Ameboid motion
Chemotaxis
Phagocytosis
41
Diapedesis
diffusing out
42
Ameboid motion
snail-like movement, no active ATP, just slithers their way, due to cellular structure
43
Chemotaxis
release of chemical from WBC to kill invader
44
Phagocytosis
Actual WBC that engulfs invader
cellular ingestion of foreign agent
fast, non specific
45
Phagocytosis depends on...
selectiveness of surface material
presence of protective coat
assistance from abs
digestion by intracellular enzymes
46
Neutrophils
phagosome (vesicle) via psuedopodia (bacteria)
47
Macrophages
larger particles, longer life span
48
Inflammation
Tissue damage
1) Chemicals (histamine, prostaglandins, kinins, leukotrienes) targets to an area
2) Blood clot forms, localize area
3) Abscess to start to form (yellow), indication of dead WBC, healing occurred
49
4 steps of inflammation
1) Tissue damage
2) Vasodilation and increased permeability of BV (brings in WBC to start repair and attack area, rid the harm)
3) Phagocyte migration and phagocytosis
4) Tissue repair
50
Cell-Mediated Response
1) Tissue macrophages - 1st line of defense (few mins)
2) Neutrophil invasion, neutrophilia, severe infection has taken place (few hours)
3) Macrophage proliferation, several hours to increase size (several hours to increase size)
4) Stimulation of granulocytes and monocyte production (3-4 days)
51
Cell mediated response to Inflammation: Neutrophils
circulatory system brings in neutrophils through different steps to target specific areas
*specific receptors on endothelial cells
52
Leukemia
Cancer of the blood cells;abnormal cells produced in the bone marrow
Increase number of WBC
53
Types of Leukemia: Categorize by origin and pathology
1) Lymphocytic (lymphoid cells)
2) Myelogenous (bone marrow)
3) Acute > undifferentiated cells, faster, more lethal
4) Chronic
54
Blood cancer causes body manifestation
```
weight loss
fever
frequent infections
easy SOB
muscular weakness
pain or tender bones/joints
fatigue
loss of appetite
swelling
enlargement of spleen/liver
night sweats
easy bleeding/bruising
purplish patches/spots
```
55
Adaptive Acquired Immunity
Humoral mediated: B cell
Cell mediated: T cell
Initiated by antigens = specific/distinct proteins contain on a foreign compound
56
Humoral mediated: B cell
circulating Abs
attack an invader
B cell clones form plasma cells
produce abs, secreted from lymph into blood
formation of memory cells, faster response the second time
57
Cell mediated: T cell
formation of activated
T lymphocytes
proliferate, form new T/memory cells
58
Lymphoid tissues
```
tissues that produce, store, or process lymphocytes
bone marrow
lymph nodes
spleen
thymus
tonsils
adenoids
appendixx
Peyer's patches (GALT)
```
59
Abs (Immunoglobins- Igs)
variable portion: binds to antigen
| constant portion
60
Mechanism of Ab Action
Direct to attack on invader, binding, neutralization, lysis
| Activation of complement system
61
Mechanism of Ab Action: Activation of complement system
Antibody bind to antigen, stimulates a reaction in compliment system, series of reactions that will cause infected/host cell to die
62
How is B differ from T?
T only respond to antigens only when bound to MHC proteins on antigen-presenting cells (APC) in lymphoid tissue
specifically target an invader so we don't attack ourselves
63
T-Cell mediated
APCs: macrophages, B-cells, dendritic cells
MHC proteins: bind fragments of antigen
I: antigens to cytotoxis T cells "killer"
II: antigens to helper T cells
64
Types of T-cells: Helper T cells (CD4)
Releases:
Lymphokines - promotes to activate, mini defender against antigen
Interleukins (IL): clinical measure of inflammation
Supressor T cells: suppress excessive cytotoxic T cell function
65
Types of T-cells: Cytotoxic T cells
Direct-attack cells
Killer cells
Perforins
(main mechanism, kills directly)
66
Immunizations
prevent from infection
helps patients form antibodies
expose to a strain to build abs
67
Hemostasis, prevention of blood loss
1) Severed vessel
2) Platelets agglutinate
3) Fibrin appears
4) Fibrin clot forms
5) Clot retraction occurs
68
Mechanism of Blood Coagulation
Prothrombin activator formation
Conversion of prothrombin into thrombin
Conversion of fibrinogen to fibrin
69
3 pathways for coagulation
intrinsic, skin abrasion (surface)
extrinsic, kidney damage (tissue)
common underlying between the two
source depends on location*
fibrinogen to fibrin for clot to occur
70
Coagulation defects:
1) Vitamin C deficiency
2) Hepatic failure
3) Vitamin K deficiency
71
Vitamin C deficiency
lack of stable collagen (fibrin) (elderly, alcoholics)
72
Hepatic failure
almost all clotting factors are made in the liver
73
Vitamin K deficiency
required for II (prothrombin), VII, IX, X
74
Innate Immunity: Aging
thinning of skin
losing acidity of GI tract, shallower breathing, less-acidic urine, less-elastic bladder
decrease phagocytic function
cytotoxicity impaired
75
Acquired Immunity: Aging
Thymic involution shrinks
T/B cells defects
decline Ab production
decrease Ab affinity (binding to antigen)
* decrease of vaccination efficacy
* increase autoimmune activity
76
Rheumatoid Arthritis
wrists and mcp joints of hands swollen/tender
chronic inflammatory disorder
affects small joints in hands and feet
lining of the joints, painful swelling resulting in bone erosion and joint deformity
attacks synovial tissue and joints
77
C-reactive protein
marker for inflammation
78
Rheumatoid Factor
auto-antibody that is produced in individuals that have RA, there are antibodies that are attacking the body
79
IMID
immune mediated inflammatory disease
80
OA
cartilage
early morning pain 20 min
wear and tear
affects one area
81
RA
```
synovial membrane
MCP joints
symmetrical
early morning pain >45 min
immune system attacking body
throughout the body
```
82
RA: Disease Initiation
```
Genetic susceptibility
30% of genetic risk
MHC binds amino acid residues
Triggers epidemological findings
- smoking
- periodontal disease
Propagation of RF Abs (when paired these are present)
```
83
Progression to RA
Environmental
Epigenetic (outside DNA)
Susceptibility (inside DNA)
84
Post transcriptional -> Protein Citrulination
we don't make the correct one and can't be used for the right thing
develop it's own antibody (ACPA) and gets rid
85
ACPA
attacks citrulinated proteins (these aren't normal)
86
Conditions that can exacerbate systemic
```
Vascular disease
Osteoporosis
Metabolic syndrome
Cognitive dysfunction and depression
Disability and functional decline
Socioeconomic status
Stress
```
87
RA: Pathogenesis
1) Endothelial activation
2) Macrophage activation
3) B-cell activated
*Producing antibodies and it's activating our WBC to an extent that the bone, synovium and cartilage to erode and destruct the joint
88
RA: Pathogenesis, severity
Early - pain, tenderness
Establish - boney erosion, fibrotic pannus formation
*dependent on intervention
Can prevent but can't reverse
89
RA: Clinical Manifestations
```
Swelling in joints
Red and puffy hands
Joint pain
Back pain
Tightening of skin
Skin rashes
Weight loss
```
90
RA: Long term complications
Affects other body symptoms
Spread and affect
If patient already has other comorbidities, exacerbation...
91
Rank-L
protein that breaks down bone, insulin resistance
92
How can we help those with RA?
diet
disease
exercise
93
Commonly prescribed...
Glucocorticoids
| Conventional DMARDs
94
RA: Treatment
Trial and error
| Play with diff drugs and therapy
95
How is RA dx?
blood test
x-rays
symptoms not aligned with OA
96
What is RA confused with?
fibromyalgia
Crohn's
complicated to dx...
