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PT 509 Physiology > Lecture 6 > Flashcards

Lecture 6 Flashcards

1
Q

Prenatal period

A

Inherited antibodies (Abs) via placenta (passive)

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2
Q

Infancy

A

1st 6 months inherited immunity
very susceptible before 6 months

12-20 months form abs

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3
Q

Whooping cough

A

contagious respiratory disease, #1 passed form adults to child

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4
Q

Breast feeding

A

additional antibodies from mom

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5
Q

Childhood & Adolescence

A

Allergies

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6
Q

Constituents

A

WBC
Plasma
Platelets
RBC

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7
Q

Formed elements

A 
Red component (serum)
WBC & RBC
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8
Q

WBC

A 
Neutrophils
Lymphocytes
Monocytes
Eosinophils
Basophils
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9
Q

Plasma

A

measures glucose, insulin, hormones

water/protein/other solutes

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10
Q

Erythrocytes

A

transport hemoglobin
helps with clotting
has oxygen molecule & hemoglobin

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11
Q

Hemoglobin A1c

A

glucose affects integrity of RBC, indication is chronic hyperglycemia

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12
Q

RBC Mass

A

balance between production and destruction

120 days, track blood marker (A1c)

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13
Q

RBC is produced in…

A 
bone marrow
sternum
pelvis
vertebrae
ribs
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14
Q

RBC is regulated by…

A

erythropoietin (EPO)

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15
Q

EPO is produced by…

A

kidneys

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16
Q

RBC production increases within…

A

24 hours

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17
Q

EPO lifespan…

A

4-12 days

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18
Q

RBC is increased in…

A

5 days

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19
Q

Factors that decrease oxygenation

A 
Low blood volume
Anemia
Low hemoglobin
Poor blood flow
Pulmonary disease
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20
Q

Hematocrit

A

% volume of blood that is red cells
Men: 45%
Women: 40%

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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

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22
Q

Oxygen carrying capacity

A

gm Hg/100 ml blood * 1.34 O2/gm Hb
21 ml: men
19 ml: women

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23
Q

Where are RBC ingested?

A

spleen

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24
Q

What breaks down bilirubin?

A

Liver, if liver can’t break down the skin will turn yellowish, Jaundice

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25
Q

Iron is released from blood to…

A

Transferrin, to make more

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26
Q

Jaundice in infants due to…

A

baby’s physic system being hyperactive, producing excessive RBC
hemoglobin needs to gets excreted
circulatory system is playing catch up with the body

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27
Q

Anemia

A

deficiency of Hb

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28
Q

Polycythemia

A

increase RBC production
increase viscosity
increased cardiac work

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29
Q

Blood leukocytes (WBC)

A

1) directly destroying invader = phagocytosis

2) forming drones (antibodies/Abs), cell mediated system

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30
Q

Leukocytes

A 
Granulocytes
- Neutrophils
- Eosinophils
- Basophils
Monocytes
Lymphocytes
- B, Ab mediated
- T, Cell mediated
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31
Q

Platelets

A

own category, not RBC or WBC

helps with clotting

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32
Q

Granulocytes

A 
65%
- Neutrophils
- Eosinophils
- Basophils
Formed in bone marrow
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33
Q

Monocytes

A

5%
tissue macrophages
formed in bone marrow

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34
Q

Lymphocytes

A

30%

formed in lymph tissue

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35
Q

Eosinophils

A

2%
active against parasites, skin diseases, chronic infections
phagocytic & immunomodulatory
decrease inflammation

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36
Q

Basophils

A

0.5%
similar to mast cells (heparin, histamine)
Release primarily histamine (allergic rxns)
Release due to binding of IgE (immunoglobin/antibodies)

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37
Q

Innate immunity

A

1) Phagocytosis of bacteria
2) Destruction of swallowed organism by acid secretions
3) Resistance of skin to invasion
* Attach and destroy

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38
Q

Phagocytosis

A

fastest way we can defend against foreign invader

Neutrophils & Macrophages - strongest

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39
Q

Monocytes

A

macrophages upon tissue entry

40
Q

Phagocytosis process

A

Diapedesis
Ameboid motion
Chemotaxis
Phagocytosis

41
Q

Diapedesis

A

diffusing out

42
Q

Ameboid motion

A

snail-like movement, no active ATP, just slithers their way, due to cellular structure

43
Q

Chemotaxis

A

release of chemical from WBC to kill invader

44
Q

Phagocytosis

A

Actual WBC that engulfs invader
cellular ingestion of foreign agent
fast, non specific

45
Q

Phagocytosis depends on…

A

selectiveness of surface material
presence of protective coat
assistance from abs

digestion by intracellular enzymes

46
Q

Neutrophils

A

phagosome (vesicle) via psuedopodia (bacteria)

47
Q

Macrophages

A

larger particles, longer life span

48
Q

Inflammation

A

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
Q

4 steps of inflammation

A

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
Q

Cell-Mediated Response

A

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
Q

Cell mediated response to Inflammation: Neutrophils

A

circulatory system brings in neutrophils through different steps to target specific areas
*specific receptors on endothelial cells

52
Q

Leukemia

A

Cancer of the blood cells;abnormal cells produced in the bone marrow
Increase number of WBC

53
Q

Types of Leukemia: Categorize by origin and pathology

A

1) Lymphocytic (lymphoid cells)
2) Myelogenous (bone marrow)
3) Acute > undifferentiated cells, faster, more lethal
4) Chronic

54
Q

Blood cancer causes body manifestation

A 
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
Q

Adaptive Acquired Immunity

A

Humoral mediated: B cell
Cell mediated: T cell
Initiated by antigens = specific/distinct proteins contain on a foreign compound

56
Q

Humoral mediated: B cell

A

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
Q

Cell mediated: T cell

A

formation of activated
T lymphocytes
proliferate, form new T/memory cells

58
Q

Lymphoid tissues

A 
tissues that produce, store, or process lymphocytes
bone marrow
lymph nodes
spleen
thymus
tonsils
adenoids
appendixx
Peyer's patches (GALT)
59
Q

Abs (Immunoglobins- Igs)

A

variable portion: binds to antigen

constant portion

60
Q

Mechanism of Ab Action

A

Direct to attack on invader, binding, neutralization, lysis

Activation of complement system

61
Q

Mechanism of Ab Action: Activation of complement system

A

Antibody bind to antigen, stimulates a reaction in compliment system, series of reactions that will cause infected/host cell to die

62
Q

How is B differ from T?

A

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
Q

T-Cell mediated

A

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
Q

Types of T-cells: Helper T cells (CD4)

A

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
Q

Types of T-cells: Cytotoxic T cells

A

Direct-attack cells
Killer cells
Perforins

(main mechanism, kills directly)

66
Q

Immunizations

A

prevent from infection
helps patients form antibodies
expose to a strain to build abs

67
Q

Hemostasis, prevention of blood loss

A

1) Severed vessel
2) Platelets agglutinate
3) Fibrin appears
4) Fibrin clot forms
5) Clot retraction occurs

68
Q

Mechanism of Blood Coagulation

A

Prothrombin activator formation
Conversion of prothrombin into thrombin
Conversion of fibrinogen to fibrin

69
Q

3 pathways for coagulation

A

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
Q

Coagulation defects:

A

1) Vitamin C deficiency
2) Hepatic failure
3) Vitamin K deficiency

71
Q

Vitamin C deficiency

A

lack of stable collagen (fibrin) (elderly, alcoholics)

72
Q

Hepatic failure

A

almost all clotting factors are made in the liver

73
Q

Vitamin K deficiency

A

required for II (prothrombin), VII, IX, X

74
Q

Innate Immunity: Aging

A

thinning of skin
losing acidity of GI tract, shallower breathing, less-acidic urine, less-elastic bladder
decrease phagocytic function
cytotoxicity impaired

75
Q

Acquired Immunity: Aging

A

Thymic involution shrinks
T/B cells defects
decline Ab production
decrease Ab affinity (binding to antigen)

  • decrease of vaccination efficacy
  • increase autoimmune activity
76
Q

Rheumatoid Arthritis

A

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
Q

C-reactive protein

A

marker for inflammation

78
Q

Rheumatoid Factor

A

auto-antibody that is produced in individuals that have RA, there are antibodies that are attacking the body

79
Q

IMID

A

immune mediated inflammatory disease

80
Q

OA

A

cartilage
early morning pain 20 min
wear and tear
affects one area

81
Q

RA

A 
synovial membrane
MCP joints
symmetrical 
early morning pain >45 min
immune system attacking body
throughout the body
82
Q

RA: Disease Initiation

A 
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
Q

Progression to RA

A

Environmental
Epigenetic (outside DNA)
Susceptibility (inside DNA)

84
Q

Post transcriptional -> Protein Citrulination

A

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
Q

ACPA

A

attacks citrulinated proteins (these aren’t normal)

86
Q

Conditions that can exacerbate systemic

A 
Vascular disease
Osteoporosis
Metabolic syndrome
Cognitive dysfunction and depression
Disability and functional decline
Socioeconomic status
Stress
87
Q

RA: Pathogenesis

A

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
Q

RA: Pathogenesis, severity

A

Early - pain, tenderness
Establish - boney erosion, fibrotic pannus formation

*dependent on intervention
Can prevent but can’t reverse

89
Q

RA: Clinical Manifestations

A 
Swelling in joints
Red and puffy hands
Joint pain
Back pain
Tightening of skin
Skin rashes
Weight loss
90
Q

RA: Long term complications

A

Affects other body symptoms
Spread and affect
If patient already has other comorbidities, exacerbation…

91
Q

Rank-L

A

protein that breaks down bone, insulin resistance

92
Q

How can we help those with RA?

A

diet
disease
exercise

93
Q

Commonly prescribed…

A

Glucocorticoids

Conventional DMARDs

94
Q

RA: Treatment

A

Trial and error

Play with diff drugs and therapy

95
Q

How is RA dx?

A

blood test
x-rays
symptoms not aligned with OA

96
Q

What is RA confused with?

A

fibromyalgia
Crohn’s
complicated to dx…

PT 509 Physiology (9 decks)

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