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PAS 506 > Exam 7 (Musculoskeletal and Immunology) > Flashcards

Exam 7 (Musculoskeletal and Immunology) Flashcards

1
Q

Immunology

A

Study of rxns of host’s immune system when foreign substance introduced (immune response)

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2
Q

Antigens

A

Foreign substance that causes immune response

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3
Q

Epitope

A

Part of antigen body recognizes and antibodies attach.

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4
Q

Immunity

A

Resistance to infection

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5
Q

Immunization

A

Exposure to antigens which are foreign

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6
Q

Passive immunity

A

Natural
Breast milk, placenta Ab transport
Or artificial
Ab in form of injection (gamma globulin)

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7
Q

Innate immunity

A

Not specific
No memory

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8
Q

Active immunity

A

Occurs through process of making Ab in response to presence of antigen in system
Specific
Takes 1-2 weeks to start
Uses T and B cells

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9
Q

Humoral immunity

A

Antibody mediated
Major defense for bacterial infection
Uses B Cells (plasma)

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10
Q

Cellular Immunity

A

Cell mediated
Uses T cells
Cytotoxic T cells destroy cells with antigen that activated them by putting in perforins causing apoptosis

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11
Q

Immunoglobulin structure

A

2 heavy chain
2 light chain
Held together by noncovalent forces.
Disulfide bridges between chains

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12
Q

IgM

A

First immunoglobulin made in acute infection
On naive B cells

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13
Q

IgG

A

Made in chronic (long) exposure to antigen
4 subclasses
Secondary responses
Long life span
Monomer
Mostly secreted (into blood)
Good at opsonization and activating complement
Cross placenta to protect fetus

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14
Q

Opsonization

A

Marking cells for destruction

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15
Q

Fc fragment

A

Opsonization
Complement fixation

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16
Q

Fab fragment

A

Binds to antigen

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17
Q

C terminus

A

End of Fc portion

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18
Q

N terminus

A

End of Fab portion

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19
Q

Isotype

A

Unique amino acid sequence common to all immunoglobulin of a given class

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20
Q

Allotype

A

Slight generic variation of Ig sequences in membrers of species

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21
Q

IgD

A

Expressed on naïve B cells.
Synthesis ends with activation
Membrane bound (not much secreted) so we don’t test blood for it
Monomer

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22
Q

IgA

A

Appears later in responses
2 subclasses
Monomer (IgA1) or dimer (IgA2)
Dimer secreted through breastmilk, tears, saliva, mucous through specialized epithelial cells

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23
Q

IgE

A

Appears later in responses
Monomer
Bound to mast cells (not in serum)
Allergic/inflammatory responses

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24
Q

BCR

A

B cell receptor
Immunoglobulin or antibody
Surface bound or secreted

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25
Q

TCR

A

T cell receptor
Alpha and beta chains or gama and delta chains
ONLY surface bound

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26
Q

Pro-B cells

A

Undergo gene rearrangement for antibody heavy chain production.
Then mu heavy chains produced in cell cytoplasm

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27
Q

Pre-B cells

A

Mu heavy chains get surrogate light chains making a pre-B cell receptor,
only cells with this receptor survive past this point
Lasts two days
Several divisions
Gene rearrangemen occurs for light chain production

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28
Q

Immature B cells

A

Complete IgM molecules on cell surface.
No more M chains in cytoplasm
Committed to produce specific antibody
Cells that make antibodies to self-antigen undergo apoptosis

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29
Q

Mature B cells

A

Express IgD and IgM of same specificity expressed on surface.
IgD is cell marker
IgM is more functional
Live only a few days if unstimulated
Stimulated cells undergo another phase to form specific memory or plasma cells

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30
Q

Plasma cells

A

Most fully differentiated lymphocyte
Main function is antibody production
Located in germinal centers and in bone marrow

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31
Q

T-cell development stages

A

Prothymocyte
Double-negative thymocyte
Double-positive thymocyte
Mature T cell

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32
Q

B-cell development stages

A

Pro-B cell
Pre-B cell
Immature B cell
Mature B cell

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33
Q

When does T cell development begin

A

pro-thymocytes committed to becoming T cells travel to thymus.
Mature from traveling from outer cortex into inner madulla of thymus

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34
Q

Double negative thymocytes

A

Negative for CD4 and CD8
Gene rearrangement of TCR heavy chain
Appearance of functional beta chain causes it to become positive for CD4 and CD8

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35
Q

Double-positive thymocytes

A

T-cells positive for both CD4 and CD8
Gene rearrangement occurs and once TCR complete positive selection takes place.
Cells that can’t recognize MCH undergo apotosis.
If bind to MHC I become CD8
If bind to MHC II become CD4

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36
Q
A
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36
Q

Negative selectoin

A

Occurs in corticomedullary junction
Cells exposed to self peptides bound to MHC molecules.
Those that are activated undergo apoptosis.
Unactivated goes into peripheral blood

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37
Q

CD4+ T cells

A

2/3 of T cells
Helper T cells
Recognize antigen with MHC II

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38
Q

CD8+ T cells

A

1/3 of T cells
Cytotoxic T cells
Recognize MHC I

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39
Q

How long do resting T cells live

A

Several years in lymphoid organ

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40
Q

Mechanical barriers

A

Epithelium
Directional air/fluid flow
Mucus
Cilia

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41
Q

Chemical barrier

A

Enzymes
pH
Fatty acids/Microcidal molecules

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42
Q

Biological barriers

A

Commensal microbes (normal flora)

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43
Q

Granulocytes

A

Most common WBCs
Neutrophils
Eosinophils
Basophils
Monocytes
Cytoplasmic granulocytes.
Can do surface adhesion to find intracellular opening.
Diapedesis

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44
Q

Diapedesis

A

Granulocytes ability to enter cell gaps

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45
Q

Eosinophil

A

Granulocyte
Releases proteins, cytokines, chemokines to trigger inflammatory response.
Used in parasitic infections and allergic reactions

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46
Q

Basophil

A

Least common granulocyte
Induce and regulate hypersensitivity reactions.
Resemble mast cells
Release histamine in response to IgE.
Attracted to prostaglandin D2 from mast cell

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47
Q

Mast cell

A

Granulated.
Proteoglycan, histamine, proteases in granulocytes.
nflammatory intiiated by IgE and igG and TNF-alpha in response to bacteria.
Respond in seconds to minutes.
Leukotrienes, prostaglandins, platelet activating factors produced after degranulation

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48
Q

Monocyte

A

Granulocyte
Baby macrophage
Phagocytosis
Multinucleated
Kupffer cells in liver
Microglia

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49
Q

Macrophage

A

Phagocytosis
Tumor activity
Kill intracellular parasites
Secretes cell mediators
APC
Pathogen recognition receptors
Toll like receptors

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50
Q

Dendritic cells

A

Most potent phagocytotic cells
APC
Pathogen recognition receptors
Toll like receptors

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51
Q

Natural killer cells

A

Large granulated circulating
Innate immunity
Targets cells missing MHC I to induce apoptosis

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52
Q

Primary lymphoid organs

A

Where lymphocytes are made
Thymus (T-cells)
Bone marrow (B-cells)

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53
Q

Secondary lymphoid organs

A

Spleen
Lymph nodes
Tonsils
Apendix
Peyer’s patches
Mucosal associated lymphoid tissue (MALT)

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54
Q

Where is antigen dependent lymphocyte reproduction

A

Secondary lymphiod tissue

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55
Q

Where is antigen independent lymphocyte reproduction

A

Primary lymphoid tissue

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56
Q

Spleen

A

Largest secondary lymphoid organ
Upper left abdominal quadrant
Filters old cells, damaged cells, and foreign antigens from blood.

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57
Q

Lymph

A

Colorless fluid
Enters thin-walled vessels from interstitial spaces between tissue cells
Filtered by lymph nodes

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58
Q

Lymphadenopathy

A

Enlargement of lymph node.
Antigen contact is made.
Lyymphocyte traffic stopped to immobilized antigen.
Increased number of lymphocytes recirculated

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59
Q

Classical complement pathway

A

Triggered by immune response
Antibodies needed

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60
Q

Mannose binding lectin complement pathway

A

Lectin binds to mannose groups of bacteria

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61
Q

Alternative complement pathway

A

From viruses, bacteria, tumor, fungus

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62
Q

Main factor of complement pathway

A

Cell lysis

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63
Q

What do proteins made during complement pathway do

A

Opsonization
Chemotaxis
Cell lysis
Activate B cells
Discard debris from apoptosis

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64
Q

Cytokines

A

Chemical messengers made by stimulated cells.
Affect activity of other cells
Local mediators of immune response
Bind to specific protein receptors on target cells.
Some are growth factors

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65
Q

Interleukin 1

A

Cytokine
Produced by macrophages
Stimualtes bone marrow to make more neutrophils

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66
Q

Interleukin-6

A

Cytokine
Endogenous pyrogen (causes fever)
Acts on liver to make acute phase reactants (APR)

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67
Q

Interleukin-8

A

Cytokine
Recruits neutrophils to site of infection

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68
Q

Tumor necrosis factor alpha

A

Cytokine
Endogenous pyrogen (causes fever)
Recruits neutrophils to site of infection

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69
Q

Acute phase reactants (APRs)

A

Proteins made by liver and found in serum.
Quickly increases by at least 25% due to infection or trauma.
Liver increases production in response to cytokines from monocytes and macrophages

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70
Q

APR examples

A

C-reactive protein
Haptoglobin
Fibrinogen
and more

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71
Q

C reactive protein

A

APR
Most widely used indicator of acute inflammation because of rapid rise and decline.
Increased levels are significant risk factor for MI and stroke

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72
Q

Serum amyloid A

A

APR
Causes adhesion and chemotaxis of lymphs and phagocytic cells.
Contributes cleaning of inflammation
Increased levels show risk of atherosclerosis

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73
Q

Mannose binding protein

A

APR
Recognizes and binds to mannose and other sugars found on bacteria, viruses, yeasts, and parasites
Promotes phagocytosis.
Activates complement

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74
Q

Fibrinogen

A

APR
Promotes coagulation at site of injury
Acts as precursory to fibrin in coagulation cascade
Bridges platelets to assist in adhesion

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75
Q

Alpha-2 antitrypsin

A

APR
Acts to clean up effects of neutrophil invasion during inflammatory response.
Protease inhibitor.
Protects elastin in lungs from elastase released from granules in neutrophils.
Deficiency causes emphysema

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76
Q

Ceruplasmin

A

APR
Principal copper-transporting protein in human plasma.
Scavenger of superoxide radicals made by phagocytes.
Deficiency causes Wilson’s disease (Kayser Fleisher rings in eyes)

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77
Q

Calor

A

Heat in inflammation

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78
Q

Rubor

A

Redness, erythema in inflammation from increased blood flow (hyperemia).
Mediated by prostacyclin and nitric oxide

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79
Q

Tumor

A

Edema or swelling in inflammation.
Vascular permeability causes movement of fluid and protein into tisssue

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80
Q

Dolor

A

Pain in inflammation

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81
Q

Nitric oxide

A

Major componenent of vasodilation in inflammation

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82
Q

Serous

A

Few cells

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83
Q

Serosanguineous

A

Red cells

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84
Q

Fibrinous

A

Containing fibrin

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85
Q

Purulent

A

Having white cells (pus)

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86
Q

Prostaglandins

A

Released from mast cells
Neuronal stimulation causes pain

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87
Q

Platelet activating factor

A

Released from mast cells
Potent platelet aggregator
Vasodilator

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88
Q

Platelets

A

Derived from megakaryocytes of bone marrow.
Stor serotonin in dense granules used to mediate aggregation and recruitment of neutrophils.
Induce vasoconstriction but in cerebral arterioles causes vasodilation.
Aggregated by TXa2

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89
Q

Prostanoids

A

Prostaglandins and thromboxane A2
Made by COX

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90
Q

Nitric oxide

A

Made by L-Argininie through action of NO synthetases.
nNOS in neuronal
eNOS in endothelial
iNOS in inducible
Used in inflammation

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91
Q

Stages of tissue repair

A

Hemostatic
Inflammation
Proliferative
Angiogenesis
Reepithelization
Remodeling

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92
Q

Hemostatic phase of tissue repair

A

Fibrin and fibronectin provide beginning matrix that acts as initial substrate for inward micration of Mø then fibroblasts, keratinocytes, and endothelial cells.
THrombin causes release proinlfammatory cytokines.
Plateletts in provisional matrix are rich source of chemotatic factors and cytokines.

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93
Q

Inflammatory phase of tissue repair

A

Neutrophils appear and udnergo apoptosis and macrophages clear.
Contributes to scab formation.

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94
Q

Proliferative phase of tissue repair

A

Formation of granulation tissue.
Replaces provisional matrix.
Angiogenesis starts

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95
Q

Angiogenesis phase fo tissue repair

A

Production of new capillaries from other vessels activated by TNF alpha and VEGF secretion from M2 macrophages.
Activated by low oxygen, high lactate, low tissue pH
New capillaries remain leaky for healing

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96
Q

Re-epithelialization phase

A

Continued formation of granulation creates surface with re-epithelialized tissue at wound edges.
Continues to move toward center

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97
Q

Type-1 allergic reaction

A

Immediate response
Production of IgE
Onset within 15-30 mins
Systemic reactions against peanut or bee venom antigens can cause anaphylaxes.
Allergic asthma

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98
Q

Type II allergic reaction

A

Antibody mediated cytotoxic
IgG IgM Complement
NKC, Eosinophils, neutrophils, macrophages
Onset in 5-8 hours.
Immunization to erythrocyte antigens during pregnancy (mom is Rh - baby is Rh +) Mom makes antibodies against Rh and kills baby

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99
Q

Type III allergic reaction

A

Immune complex medicated reactions
Mediated by antibody formed during immune response.
When not cleared it will setlle in tissues.

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100
Q

Type IV allergic reaction

A

Delayed hypersensitivity reaction
T-cell mediated
T helper cells secrete cytokines which activate macrphages and cytotoxic T clels.
Onset is 2-3 days.
Poison ivy.
TB Skin test

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101
Q

Antibody mediated autoimmune disease

A

Majority of autoimmune diseases
IgG1 and IgG3 cause most of them by inducing complement-dependent damage attack on tissues.
IgG4 causes pemphigus.

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102
Q

What gender has most of the autoimmune diseases

A

Females (90%)
Estrogen thought to effect B-Cells
This thought supported by SLE appearance in preg

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103
Q

Secondary immunodeficiencies

A

More common than primary (genetic)
Resulted from factors that affected host with intrinsically normal immune system (drugs, disease, environment)
Most common is malnutrition

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104
Q

Organic component of bone

A

Collagen for flexibility
Ground substance made of glycoproteins, proteoglycans, and glycosaminoglycans fills around collagen and hydroxyapatite crystals

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105
Q

Inorganic component of bone

A

Hyoxyapatite made of calcium phosphate and and calcium carbonate.
Hardness and strength.

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106
Q

Axial skeleton

A

Skull
Vertebral column
Rib cage
Protects vital organs

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107
Q

Appendicular skeleton

A

Arms
Legs
Pelvis
Shoulder
Movement, blood cell production, mineral storage

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108
Q

Cortical/compact bone

A

Outer layer.
Thick, dense
Protection and strength.
Bone cells in lacunae
Nutrition from Haversian canals
80% of bone in the body

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109
Q

Trabecular/spongy bone

A

INside cortical bone
Metabolic unction
THin, porous.
Bone marrow
Composed of spicules sor plate.
20% of bone in body

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110
Q

Haversian cannals.

A

Contain blood vessels and nerve fibers.

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111
Q

Lamellae

A

Around haversian canals

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112
Q

Parathyroid hormone

A

Accelerates bone resporption

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113
Q

Osteoblast

A

Synthesize bone.
Come from osteoprogenitor cells

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114
Q

Osteocytes

A

Inactivated osteoblasts trapped in the bone they formed

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115
Q

Osteoclasts

A

Break down bone (resorption)
From monocyte cell line.
Multinucleated

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116
Q

Bone fracture repair order

A

Fracture hematoma forms
Fibrocartilaginous (soft) callus forms
Hard (bony callus forms
Bone is remodeled

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117
Q

Bone turnover

A

Balance of activity of osteoblast and osteoclasts

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118
Q

Why does bone resorption occur.

A

To release calcium and other ions into blood.
Remove old bone pieves to allow newer, better bone to form.

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119
Q

How does resorption occur

A

THrough secretion of acid and proteolytic enzymes that digest bone

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120
Q

How does bone formation happen

A

Osteoblasts secrete osteoid ten mineralize matrix

121
Q

Long bones

A

Shaft with enlarged ends
Mostly compact bone with spongy at the end.

122
Q

Flat bones

A

Thin, flattened, curved
Two layers of compact bone sandwich spongy bone in the middle (layer of diploë

123
Q

Short bones

A

Cube shape
Mostly spongy with outer compact layer.

124
Q

Sesamoud bones

A

Within tendons.
Type of short bone,
Patella

125
Q

Irregular bone

A

Mainly spongy with outer compact layer.
Vertebrae

126
Q

Diaphysis

A

Shaft of long bone.
Medullary cavity filled with bone marrow.
Outer walls are dense, hard compact bone
Covered by periosteum

127
Q

Periostium

A

Fibrous connective tissue membrane over bone.
Growth, repair, remodelAttaches to tendons and ligaments.
Doesn’t cover site where epiphyses meet other bones in joint formation.

128
Q

Epiphysis

A

Wider section at end of long bone.
Thin layer of compact bone surrounding spongy bone.
Covered by articular cartilage.
Meets diaphysis at metphysis.

129
Q

Metaphysis

A

Meeting point of epiphysis and diaphysis.
Contains epiphyseal plate during growth.
After growth becomes epiphyseal line

130
Q

Endosteum

A

Connective tissue.
Lines in bone
Growth, repair, remodel

131
Q

Sarcoplasmic reticulum

A

ER of skeletal muscle fibers.
Stores, releases, retrieves Calcium

132
Q

Sarcolemma

A

Plasma membrane of muscle fibers

133
Q

Sarcoplasm

A

Cytoplasm of muscle fibers

134
Q

Myofibrils

A

Structures of proteins in muscle fibers

135
Q

Sarcomeres

A

Smalest functional part of skeletal muscle

136
Q

Fascicle

A

Bundle of muscle fibers

137
Q

Perimysium

A

Surround fascicles

138
Q

Endomysium

A

Enclose muscl fiber

139
Q

Epimysium

A

Surrounds whole muscle

140
Q

Actin

A

Thin fillaments
Pulled by myosin

141
Q

Myosin

A

Thick fillaments
Pull actin

142
Q

Z line/disc

A

End of each sarcomere
Actin filaments attach to it

143
Q

A band

A

Darker
Thick Myosin fillaments

144
Q

I bands

A

Lighter
Thin actin

145
Q

M line

A

Myosin filaments anchor to it

146
Q

H band

A

Area adjacent to M line where myosin filaments are not superimposed by actin.

147
Q

Muscle contraction

A

Electrical signal from brain from motor neuron to muscle cell.
ACh released.
ACh causes Ca release from sarcoplasmic reticulum
Ca binds to troponin bound to tropomyosin
Tropomyosin moves unblocking actin filament.
Myosin heads bind to actin filament.
Muscle contracts.

148
Q

Isotonic contraction

A

Muscle contracts and changes length
Concentric - shortening
Eccentric - lengthining

149
Q

Isometric contraction

A

Muscle contracts but does not change length.
Stabilizes posture and holds body upright

150
Q

Components of connective tissue

A

Cells
Fibers
Ground substance
Ground substance + fibers = extracellular matrix

151
Q

Cartilage

A

Flexible connective tissue.
Specialized cells (chondroblasts)
Elastic, hyaline, fibrocartilage

152
Q

Perichodrium

A

Around cartilage
Highly vascularized to provide nutrients to cartilage

153
Q

Chondrocytes

A

Cartilage cells.
Mature chondroblast

154
Q

Chondroblasts

A

Undergo mitosis and secrete extracellular matrix components maturing as non-dividing chondrocytes

155
Q

Elastic cartilage

A

More elastic than hyaline
Maintains shape while allowing flexibility.
External ear, epiglotis

156
Q

Hyaline cartilage

A

Most abundant in body.
Transparent or glassy matrix.
Supports and shock absorption.
Embryonic skeleton, costal cartilages of ribs, nose, trachea, larynx

157
Q

Fibrocartilage

A

Hyaline cartilage and dense regular connective tissue blended.
Compressible, resists tension.
Intervertebral discs, knee meniscus

158
Q

Interstitial growth of cartilage

A

Growth from within
Lengthening of bones
Chondroblasts lay down more matrix inside existing cartilage
Childhood growth.

159
Q

Apositional growth of cartilage

A

Growth from outside.
Increases width.
New surface layers added

160
Q

What does injury, pain, or invasion cause

A

Release of cytokines and COX-2 enzymes
Cytokines activate phospholipase A2
Phospholipase A 2 stimulates release of arachidonic acid.
COX enymes convert arachidonic acid into prostanoids.

161
Q

Prostanoids formed by COX 1

A

Prostaglandin GI2 (PGI2)
Thromboxane A2 (TXA2)

162
Q

Prostaglandin GI2 (PGI2)

A

Made from COX 1
Provides gastric protection

163
Q

Thromboxane A2 (TXA2)

A

Made from COX 1
Role in platelet aggregation

164
Q

Prostaglandin E2 (PGE2)

A

Made form COX 2
Inflammation, pain, fever

165
Q

Inhibition of COX 2 effect

A

Stops inflammation, pain, fever
(antiinflammatory, analgesic, antipyretic)

166
Q

Aspirin

A

NSAID
abbreviated “ASA” (acetylsalicylcic acid)
Mainly inhibits COX-1
Some analgesic and antipyretic effects
Anti-platelet
NO anti-inflammatory activity
Lower doses to prevent cardiovascular events.
Can be chewable for emergencies

167
Q

Aspirin Method of action

A

Irreversibly binds to COX-1 in platelets
Arachidonic acid can’t bind to convert into TXA2.
Reduce vasoconstriction.

168
Q

Aspirin precautions

A

Avoid in pts under 19 yrs old bc of Reye’s syndrome.
Large doses toxic in children.
Hold 1-2 weeks before surgery.

169
Q

Celecoxib

A

NSAID
Inhibits COX 2 ONLY
Decreased GI risk
Increased platelet aggregation.
Increases CV risk by 1/3

170
Q

What non-aspirin NSAID works best

A

All work equally as good

171
Q

Ketorolac

A

NSAID
Used for acute, severe pain.
Oral, IM, or IV
Can’t be used more than 5 days

172
Q

Diclofenac

A

NSAID
Worst for CV risk

173
Q

Naproxen

A

NSAID
Least CV risk

174
Q

At what age do NSAIDs risks significantly increase

A

> 75 yrs old

175
Q

NSAID adverse effects

A

Increased risk of bleed
Decrease of prostaglandin synthess causes Renal effects of increased Na and water retension causing increased BP.
HTN
Stroke
MI
Death
Asthma exacerbation
HA
Tinnitus
Dizziness
Hypersensitivity

176
Q

NSAIDs contraindications

A

GI bleed/bleeding disorder
Cardiovascular disease
Kidney disease
Avoid in pregnancy
Decrease effects of ACEi/ARBS
Decrease effect of diuretic

177
Q

Acetaminophen (Tylenol)

A

NOT NSAID
“APAP”
Paracetamol internationally
Analgesic and antipyretic only
Little to no risk of bleed (no effects on platelets)

178
Q

Acetaminophen (tylenol) method of action

A

Inhibits COX enzymes in CNS inhibiting prostanoid synthesis in CNS causing analgesic and antipyretic effects.
Inactivated in PNS so no antiinflammatory effect

179
Q

When to use Acetaminophen (tylenol)

A

Patients with Gi risk.
Children
Oral, IV, or rectal

180
Q

Adverse effects of acetaminophen (tylenol)

A

Hepatotoxicity.
Medication error risk with IV use.
Hepatotoxicity

181
Q

Acetaminophen (tylenol) contraindications

A

Hepatic disease
Hepatitis
Malnutrition
Alcohol users (greater than or equal to 3 drinks per day)
Max dose of 4g per day

182
Q

Spasticity

A

Increases muscle tone due to increased excitability of muscle stretch reflex

183
Q

Spasm

A

Involuntary muscle contractions.
Jerks, twitches, cramps

184
Q

Skeletal muscle relactants

A

Antispasticity and antispasmodic.
Drowziness and dizziness.
Increased risk of respiratory depression.

185
Q

Baclofen

A

Antispasticity
Similar structure to GABA
Binds to GABA receptors to inhibit excitatory muscles\
(helps GABA do its job)

186
Q

Carisoprodol

A

Antispasmodic
Controlled because potential for physical dependence.
Acts on CNS.
Effects GABA receptors
Can have withdrawal

187
Q

Cyclobenzaprine

A

Antispasmodic
CNS depression of brain stem.
Caution for patients with cardiac arrhythmias or conduction disturbances

188
Q

Cyclobenzaprine contraindications

A

Acute narrow angle glaucoma
Older age
Moderate to severe hepatic impairment.

189
Q

Metaxalone

A

Antispasmodic
CNS depression
Don’t use with severe renal or hepatic impairment

190
Q

Methocarbamol

A

Antispasmodic
CNS depression

191
Q

Tizanidine

A

Antispasticity and asntispasmodic
Binds to alpha2 reveptor on presynaptic neuron to inhibit releases of glutamate causing reduction of postsynaptic activation of upper motor neurion.
Don’t use in hepatic or renal impairment.

192
Q

Dantrolene

A

Direct acting (not centrally acting).
Binds to calcium channel in sarcoplasmic reticlum preventing release of Ca.
Used for malignant hyperthermia.
Causes muscle weekeness, sedation, occasionally hepatitis.

193
Q

Path of blood

A

L ventricle
Areteries and arterioles
Capillaries where it mingles with interstitial fluid.
Veins

194
Q

Drains of lymphatic system

A

Thoracic duct and Right lymphatic duct

195
Q

What all causes blood to move forward

A

Heart pumping
Diastolic recoil of arterial wall
Venous compression from skeletal muscle
Negative pressure in thorax during inspiration.

196
Q

What resists blood flow

A

Diameter of vessels (mainly arterioles)
Viscosity of blood

197
Q

Components of blood

A

55% is plasma (3L).
45% is celllular elements (2L

198
Q

Plasma

A

Protein rich fluid where cellular elements are suspended

199
Q

Make up of plasma

A

92% water
7% proteins
1% solutes

200
Q

Albumin

A

Most abundant protein in plasma.
Regulates osmotic pressure (keeps water in the vessels)

201
Q

Hematopoesis

A

Blood formation in bone marrow, spleen, and liver.
Amount made in each location is greatest to lowest in that order

202
Q

How many cells made per day in hematopoesis

A

100 billion
75% are WBC
25% RBC
Lots more RBC in circulation bc live long time

203
Q

Lifespan of red blood cell

A

120 days

204
Q

Hematopoietic stem cell (HSC)

A

Start hematopoesis.
Self renewing
Can differentiate into ANY type of blood cell

205
Q

Myeloid cell line

A

Grannulocytes
Erythrocytes
Monocytes
Platelets

206
Q

Lymphoid cell line

A

B cells
T cells
Natural killer cells

207
Q

Erythropoiesis

A

Production of RBC (erythrocytes)
Stimulated by erythropoietin (EPO) from kidney when O2 sat low
Tells BM to make more RBC

208
Q

Erythropoiesis sequence

A

EPO –> HSC –> erythroblast –> nucleus and organelles removed –> reticulocyte

209
Q

Reticulocyte

A

Immature RBC.
Larger
Still contains some organelle remnants.

210
Q

Important nutrients for erythropoiesis

A

Iron to make hemoglobin.
B12/Folate for DNA synthesis.
B6
Copper
Zinc
AA

211
Q

What hormones cause erythropoiesis

A

Erythropoiesis
Testosterone
NOT iron

212
Q

Leukopoiesis

A

Production of WBC (leukocytes)

213
Q

Where are T cells first made

A

Bone marrow

214
Q

Where are natural killer cells first made

A

Bone marrow

215
Q

Lymphoid line sequence of production

A

HSC –> Common lymphoid progenitor –> Lymphocytes and NK cells

216
Q

Thrombopoiesis

A

Platelet production
HSC –> megakaryocytes –> fragment into platelets
Always being stimulated

217
Q

Thrombopoietin (TPO)

A

Produced in liver, kidney, muscle, marrow
Stimulates thrombopoiesis
Release in marrow stimulated by platelet derived growth factor (PDGF) and fibroblast derived growth factor (FGF).
Constantly released from liver

218
Q

What shape is mature RBC

A

Biconcave

219
Q

What percent of RBC replaced each day

A

1%

220
Q

Primary function of RBC

A

Transport O2 from lungs to tissue.
Transport CO2 from tissue to lungs

221
Q

Hemoglobin

A

Red O2 carrying pigment in RBC
4 subunits.
Heme has iron
Globin is polypeptide.
Porphyrins absorb light

222
Q

Most common hemoglobin make up

A

Hgb A1.
2 alpha and 2 beta chains

223
Q

Hgb A2

A

2 alpha and 2 delta chains

224
Q

Hgb F

A

Fetal hemoglobin
2 alpha and 2 gamma chains

225
Q

Where does oxygen bind to on hemoglobin

A

On the iron molecule

226
Q

What iron do we use

A

Fe2+

227
Q

Functional hypoxia

A

Caused by methemoglobin.
Fe3+ used rather than Fe2+

228
Q

Why is carbon monoxide toxicity usual

A

CO has higher affinity for hemoglobin than O2

229
Q

G6PD

A

Deficiency causes spherocytosis

230
Q

MCV

A

Mean corpuscular volume
Average volume of single RBC in femtoliters
80-100 fL

231
Q

What all is actually measured in lab

A

RBC
Hgb
WBC
PLT
MCV

232
Q

RBC x 3

A

Hgb

233
Q

Hgb x 3

A

HCT

234
Q

Neutrophils

A

First line of defense against pathogens
Lifespan is 8 hours

235
Q

Platelets

A

Smallest formed element of blood
Fragments of Megakaryocytes
Used in coagulation

236
Q

Steps of platelet function

A
  1. Adhesion to wound
  2. Activation of stuff to call in more platelets and other stuff
  3. Aggregation - complete plug formation stopping blood loss
237
Q

Thrombocytosis

A

Too many platelets

238
Q

Thrombocytopenia

A

Not enough platelets

239
Q

What triggers intrinsic clotting pathway

A

Collagen

240
Q

What triggers extrinsic clotting pathway

A

Tissue factor exposed in injured tissue

241
Q

Where do the clotting pathways merge to become the common pathway

A

Factor X

242
Q

Intrinsic clotting pathway

A

Collagen –> XII –> XI –> VIII –> X –> prothrombin (II) to thrombin –> fibrinogen (I) to fibrin
Slower and more complicated

243
Q

Extrinsic clotting patwhay

A

Injury –> III (tissue factor) –> VII –> X –> prothrombin (II) to thrombin –> fibrinogen (I) to fibrin
Happens much faster

244
Q

Common clotting pathway

A

X –> Prothrombin (II) to thrombin –> Fibrinogen (I) to fibrin.
XIII stabilizes the clot.

244
Q

Vitamin K dependent factors

A

II
VII
IX
X
Proteins C and S

245
Q

Plasminogen

A

Converts into plasmin and degrades clot that will then be eaten up by macrophages

246
Q

Fibrinolysis

A

Clot formed –> platelets contract —> Exposes plasminogen –> allows plasminogen activator to bind transforming plasminogin to plasmin –> breaks clot to be eaten by macrophages

247
Q

Universal blood DONOR

A

O negative

248
Q

Universal recipient

A

AB positive

249
Q

Most common RH antigen

A

D

250
Q

Stress response

A

Results from physiologic or psychological stimulus that disrupts homeostasis.
Includes anesthesia

251
Q

What factors determine patients response to surgical stress

A

Basic fitness
Nature of injurious process
Severity of surgery
Duration of surgery
VIirulence of microorganisms involved (infection)

252
Q

Factos influincing physiologic response to surgery

A

Tissue trauma
Bleeding causing hypoxia
Excess IV fluids causing edema
Inflammation or infection
Pain
Psychological stress
Excess heat loss from open cavity
Starvation from being NPO before surgery

253
Q

Three physiologic components of surgical stress response

A

Sympathetic
Endocrine
Immunologic

254
Q

Sympathetic response to surgery stress

A

Increased catecholamines.
Causing Increase HR, contractility, vasoconstriction.
Causes increase renin, decrease blood flow, increase sodium resorption.
INcreasees glucagon

255
Q

Endocrin response to surgery stress

A

Increase cortisol
Increase ADH
Increased catabolism causing weight loss

256
Q

Immunologic response to surgery stress

A

Cytokines and acute phase protein release
Fever
D-dimer elevation
Inflammatory cascade

257
Q

Pancreas reaction to surgery stress

A

Catabolic state
Increased glucagon
Decreased insulin

258
Q

What does an elevated WBC count mean

A

Inflammation is present
NOT necessarily infection

259
Q

What does D Dimer show

A

D dimer comes from breakdown of clot

260
Q

Body water distribution

A

67% intracellular
33% extracellular

261
Q

Major cation in plasma

A

Sodium

262
Q

Major cation in extracellular fluid

A

Potassium

263
Q

Major anion of intracellular fluid

A

Phosphorus
Sulfate

264
Q

Major anion of extracellular fluid

A

bicarb
Chloride

265
Q

Where are baroreceptors

A

Aortic arch and carotid sinuses

266
Q

Most common perioperative fluid imbalance

A

Hypovolemia

267
Q

Third space

A

Not in cell, not in vasculature.
AKA transcellular space

268
Q

Fluid loss stage

A

Intravascular blood loss into third space causing hypovolemia, decreased cardiac output, hypotension, tachycardia.
Increasing fluid volume of interstitial space causing edema

269
Q

Fluid absorption phase

A

Can cause Hypervolemia
HTN
Edema
Urine output increases

270
Q

Hypovolemia lab findings

A

Elevated BUN/Cr levels
Elevated hematocrit
Metabolic acidosis/alkalosis
Low urinary Na
High urinary Cl
Urine osmolality raised

271
Q

Examples of isotonic fluids

A

Lactated ringers
Normal saline
Normal saline can increase risk of hyperchloremic metabolic acidosis

272
Q

5% dextrose

A

Given with isotonic and hypotonic fluids.
Maintainstonicity and prevents catabolism ketosis and hypoglycemia

273
Q

Hyponatremia causes

A

High output NG tubes
Emesis
ENteric fistulas

274
Q

Hyponatremia signs/symptoms

A

CNS cellular water intoxication causing increase in ICP
Headache, confusion, altered deep tendon reflexes, seizures, coma, HTN, bradycardia, N/V, anorexia

275
Q

Hypernatremia

A

Hyperosmolality CNS effects.
Reslessness, lethargy, delirium, irritability, seizures, coma

276
Q

Most common electrolyte disturbance that cases perioperative arrhythmias

A

Potassium

277
Q

Peaked T waves

A

Hyperkalemia

278
Q

Hypomagnesium

A

Usually comes with hypokalemia.
Give Mg first then give K.
Hyperactive reflexes
Tremors
Tetany

279
Q

Hypocalcemia

A

Chvostek’s sign
Trousseau’s sign

280
Q

What patient at highest risk for delirium

A

Cardiopulmonary bypass surgery

281
Q

If patient had stroke in past three months and is in AFib

A

Delay surgery for at least 3 months

282
Q

Postoperative MI

A

Twice as deadly as pt with regulary myocardial infarction

283
Q

Atelectasis

A

Collapse of lung tissue with volume loss

284
Q

Pulmonary problems after surgery

A

Atelectasis
Pneumonia
Respiratory failure

285
Q

What separates epidermis and dermis

A

Basement membrane

286
Q

Nonglabrous

A

Hair areas

287
Q

Glabrous

A

Hairless areas

288
Q

Epidermal layers superficial to deep

A

Corneum
Lucidum
Granulosum
Spinosum
Basale

289
Q

Stratum Corneum

A

Most superficial layer of epidermis.
15-20 layers of keratinized cells
Sheds constantly.
30 days to replace all cells

290
Q

Stratum Lucidum

A

Keratinocytes pushing up to stratum
Translucent layer
Only on palms and soles for thickness

291
Q

Stratum granulosum

A

Keratinocytes from spinosum pushed up and move toward corneum.
Lipid rich for water loss

292
Q

Stratum spinosum

A

Thickest layer
Living keratin form tonofibrils to phaogocytose melanocytes and release melanin and hold water.
Langerhans cells, melanocytes

293
Q

Stratum Basale

A

Deepest Epidermis layer
Cuboid cels attached to dermis by basement membrane
Constantly make epidermal keratinocytes from stem cells in basal layer and hair follicles of dermis.
Contains merkel cells and melanocytes

294
Q

Keratinocytes

A

Most abundant cells in epidermis.
Flat squamous cells
Secrete keratin
Provide mechanical strength and protection

295
Q

What regulates melanocytes

A

Melanocortin receptors and ACTH

296
Q

Langerhans cells

A

Dendritic cells that are first line of immune response in skin

297
Q

Merkel cells

A

Sense light touch.
In stratum basale

298
Q
A

PAS 506 (9 decks)

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