Exam 7 (Musculoskeletal and Immunology) Flashcards
1
Q
Immunology
A
Study of rxns of host’s immune system when foreign substance introduced (immune response)
2
Q
Antigens
A
Foreign substance that causes immune response
3
Q
Epitope
A
Part of antigen body recognizes and antibodies attach.
4
Q
Immunity
A
Resistance to infection
5
Q
Immunization
A
Exposure to antigens which are foreign
6
Q
Passive immunity
A
Natural
Breast milk, placenta Ab transport
Or artificial
Ab in form of injection (gamma globulin)
7
Q
Innate immunity
A
Not specific
No memory
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
9
Q
Humoral immunity
A
Antibody mediated
Major defense for bacterial infection
Uses B Cells (plasma)
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
11
Q
Immunoglobulin structure
A
2 heavy chain
2 light chain
Held together by noncovalent forces.
Disulfide bridges between chains
12
Q
IgM
A
First immunoglobulin made in acute infection
On naive B cells
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
14
Q
Opsonization
A
Marking cells for destruction
15
Q
Fc fragment
A
Opsonization
Complement fixation
16
Q
Fab fragment
A
Binds to antigen
17
Q
C terminus
A
End of Fc portion
18
Q
N terminus
A
End of Fab portion
19
Q
Isotype
A
Unique amino acid sequence common to all immunoglobulin of a given class
20
Q
Allotype
A
Slight generic variation of Ig sequences in membrers of species
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
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
23
Q
IgE
A
Appears later in responses
Monomer
Bound to mast cells (not in serum)
Allergic/inflammatory responses
24
Q
BCR
A
B cell receptor
Immunoglobulin or antibody
Surface bound or secreted
25
TCR
T cell receptor
Alpha and beta chains or gama and delta chains
ONLY surface bound
26
Pro-B cells
Undergo gene rearrangement for antibody heavy chain production.
Then mu heavy chains produced in cell cytoplasm
27
Pre-B cells
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
28
Immature B cells
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
29
Mature B cells
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
30
Plasma cells
Most fully differentiated lymphocyte
Main function is antibody production
Located in germinal centers and in bone marrow
31
T-cell development stages
Prothymocyte
Double-negative thymocyte
Double-positive thymocyte
Mature T cell
32
B-cell development stages
Pro-B cell
Pre-B cell
Immature B cell
Mature B cell
33
When does T cell development begin
pro-thymocytes committed to becoming T cells travel to thymus.
Mature from traveling from outer cortex into inner madulla of thymus
34
Double negative thymocytes
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
35
Double-positive thymocytes
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
36
36
Negative selectoin
Occurs in corticomedullary junction
Cells exposed to self peptides bound to MHC molecules.
Those that are activated undergo apoptosis.
Unactivated goes into peripheral blood
37
CD4+ T cells
2/3 of T cells
Helper T cells
Recognize antigen with MHC II
38
CD8+ T cells
1/3 of T cells
Cytotoxic T cells
Recognize MHC I
39
How long do resting T cells live
Several years in lymphoid organ
40
Mechanical barriers
Epithelium
Directional air/fluid flow
Mucus
Cilia
41
Chemical barrier
Enzymes
pH
Fatty acids/Microcidal molecules
42
Biological barriers
Commensal microbes (normal flora)
43
Granulocytes
Most common WBCs
Neutrophils
Eosinophils
Basophils
Monocytes
Cytoplasmic granulocytes.
Can do surface adhesion to find intracellular opening.
Diapedesis
44
Diapedesis
Granulocytes ability to enter cell gaps
45
Eosinophil
Granulocyte
Releases proteins, cytokines, chemokines to trigger inflammatory response.
Used in parasitic infections and allergic reactions
46
Basophil
Least common granulocyte
Induce and regulate hypersensitivity reactions.
Resemble mast cells
Release histamine in response to IgE.
Attracted to prostaglandin D2 from mast cell
47
Mast cell
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
48
Monocyte
Granulocyte
Baby macrophage
Phagocytosis
Multinucleated
Kupffer cells in liver
Microglia
49
Macrophage
Phagocytosis
Tumor activity
Kill intracellular parasites
Secretes cell mediators
APC
Pathogen recognition receptors
Toll like receptors
50
Dendritic cells
Most potent phagocytotic cells
APC
Pathogen recognition receptors
Toll like receptors
51
Natural killer cells
Large granulated circulating
Innate immunity
Targets cells missing MHC I to induce apoptosis
52
Primary lymphoid organs
Where lymphocytes are made
Thymus (T-cells)
Bone marrow (B-cells)
53
Secondary lymphoid organs
Spleen
Lymph nodes
Tonsils
Apendix
Peyer's patches
Mucosal associated lymphoid tissue (MALT)
54
Where is antigen dependent lymphocyte reproduction
Secondary lymphiod tissue
55
Where is antigen independent lymphocyte reproduction
Primary lymphoid tissue
56
Spleen
Largest secondary lymphoid organ
Upper left abdominal quadrant
Filters old cells, damaged cells, and foreign antigens from blood.
57
Lymph
Colorless fluid
Enters thin-walled vessels from interstitial spaces between tissue cells
Filtered by lymph nodes
58
Lymphadenopathy
Enlargement of lymph node.
Antigen contact is made.
Lyymphocyte traffic stopped to immobilized antigen.
Increased number of lymphocytes recirculated
59
Classical complement pathway
Triggered by immune response
Antibodies needed
60
Mannose binding lectin complement pathway
Lectin binds to mannose groups of bacteria
61
Alternative complement pathway
From viruses, bacteria, tumor, fungus
62
Main factor of complement pathway
Cell lysis
63
What do proteins made during complement pathway do
Opsonization
Chemotaxis
Cell lysis
Activate B cells
Discard debris from apoptosis
64
Cytokines
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
65
Interleukin 1
Cytokine
Produced by macrophages
Stimualtes bone marrow to make more neutrophils
66
Interleukin-6
Cytokine
Endogenous pyrogen (causes fever)
Acts on liver to make acute phase reactants (APR)
67
Interleukin-8
Cytokine
Recruits neutrophils to site of infection
68
Tumor necrosis factor alpha
Cytokine
Endogenous pyrogen (causes fever)
Recruits neutrophils to site of infection
69
Acute phase reactants (APRs)
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
70
APR examples
C-reactive protein
Haptoglobin
Fibrinogen
and more
71
C reactive protein
APR
Most widely used indicator of acute inflammation because of rapid rise and decline.
Increased levels are significant risk factor for MI and stroke
72
Serum amyloid A
APR
Causes adhesion and chemotaxis of lymphs and phagocytic cells.
Contributes cleaning of inflammation
Increased levels show risk of atherosclerosis
73
Mannose binding protein
APR
Recognizes and binds to mannose and other sugars found on bacteria, viruses, yeasts, and parasites
Promotes phagocytosis.
Activates complement
74
Fibrinogen
APR
Promotes coagulation at site of injury
Acts as precursory to fibrin in coagulation cascade
Bridges platelets to assist in adhesion
75
Alpha-2 antitrypsin
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
76
Ceruplasmin
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)
77
Calor
Heat in inflammation
78
Rubor
Redness, erythema in inflammation from increased blood flow (hyperemia).
Mediated by prostacyclin and nitric oxide
79
Tumor
Edema or swelling in inflammation.
Vascular permeability causes movement of fluid and protein into tisssue
80
Dolor
Pain in inflammation
81
Nitric oxide
Major componenent of vasodilation in inflammation
82
Serous
Few cells
83
Serosanguineous
Red cells
84
Fibrinous
Containing fibrin
85
Purulent
Having white cells (pus)
86
Prostaglandins
Released from mast cells
Neuronal stimulation causes pain
87
Platelet activating factor
Released from mast cells
Potent platelet aggregator
Vasodilator
88
Platelets
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
89
Prostanoids
Prostaglandins and thromboxane A2
Made by COX
90
Nitric oxide
Made by L-Argininie through action of NO synthetases.
nNOS in neuronal
eNOS in endothelial
iNOS in inducible
Used in inflammation
91
Stages of tissue repair
Hemostatic
Inflammation
Proliferative
Angiogenesis
Reepithelization
Remodeling
92
Hemostatic phase of tissue repair
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.
93
Inflammatory phase of tissue repair
Neutrophils appear and udnergo apoptosis and macrophages clear.
Contributes to scab formation.
94
Proliferative phase of tissue repair
Formation of granulation tissue.
Replaces provisional matrix.
Angiogenesis starts
95
Angiogenesis phase fo tissue repair
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
96
Re-epithelialization phase
Continued formation of granulation creates surface with re-epithelialized tissue at wound edges.
Continues to move toward center
97
Type-1 allergic reaction
Immediate response
Production of IgE
Onset within 15-30 mins
Systemic reactions against peanut or bee venom antigens can cause anaphylaxes.
Allergic asthma
98
Type II allergic reaction
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
99
Type III allergic reaction
Immune complex medicated reactions
Mediated by antibody formed during immune response.
When not cleared it will setlle in tissues.
100
Type IV allergic reaction
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
101
Antibody mediated autoimmune disease
Majority of autoimmune diseases
IgG1 and IgG3 cause most of them by inducing complement-dependent damage attack on tissues.
IgG4 causes pemphigus.
102
What gender has most of the autoimmune diseases
Females (90%)
Estrogen thought to effect B-Cells
This thought supported by SLE appearance in preg
103
Secondary immunodeficiencies
More common than primary (genetic)
Resulted from factors that affected host with intrinsically normal immune system (drugs, disease, environment)
Most common is malnutrition
104
Organic component of bone
Collagen for flexibility
Ground substance made of glycoproteins, proteoglycans, and glycosaminoglycans fills around collagen and hydroxyapatite crystals
105
Inorganic component of bone
Hyoxyapatite made of calcium phosphate and and calcium carbonate.
Hardness and strength.
106
Axial skeleton
Skull
Vertebral column
Rib cage
Protects vital organs
107
Appendicular skeleton
Arms
Legs
Pelvis
Shoulder
Movement, blood cell production, mineral storage
108
Cortical/compact bone
Outer layer.
Thick, dense
Protection and strength.
Bone cells in lacunae
Nutrition from Haversian canals
80% of bone in the body
109
Trabecular/spongy bone
INside cortical bone
Metabolic unction
THin, porous.
Bone marrow
Composed of spicules sor plate.
20% of bone in body
110
Haversian cannals.
Contain blood vessels and nerve fibers.
111
Lamellae
Around haversian canals
112
Parathyroid hormone
Accelerates bone resporption
113
Osteoblast
Synthesize bone.
Come from osteoprogenitor cells
114
Osteocytes
Inactivated osteoblasts trapped in the bone they formed
115
Osteoclasts
Break down bone (resorption)
From monocyte cell line.
Multinucleated
116
Bone fracture repair order
Fracture hematoma forms
Fibrocartilaginous (soft) callus forms
Hard (bony callus forms
Bone is remodeled
117
Bone turnover
Balance of activity of osteoblast and osteoclasts
118
Why does bone resorption occur.
To release calcium and other ions into blood.
Remove old bone pieves to allow newer, better bone to form.
119
How does resorption occur
THrough secretion of acid and proteolytic enzymes that digest bone
120
How does bone formation happen
Osteoblasts secrete osteoid ten mineralize matrix
121
Long bones
Shaft with enlarged ends
Mostly compact bone with spongy at the end.
122
Flat bones
Thin, flattened, curved
Two layers of compact bone sandwich spongy bone in the middle (layer of diploë
123
Short bones
Cube shape
Mostly spongy with outer compact layer.
124
Sesamoud bones
Within tendons.
Type of short bone,
Patella
125
Irregular bone
Mainly spongy with outer compact layer.
Vertebrae
126
Diaphysis
Shaft of long bone.
Medullary cavity filled with bone marrow.
Outer walls are dense, hard compact bone
Covered by periosteum
127
Periostium
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
Epiphysis
Wider section at end of long bone.
Thin layer of compact bone surrounding spongy bone.
Covered by articular cartilage.
Meets diaphysis at metphysis.
129
Metaphysis
Meeting point of epiphysis and diaphysis.
Contains epiphyseal plate during growth.
After growth becomes epiphyseal line
130
Endosteum
Connective tissue.
Lines in bone
Growth, repair, remodel
131
Sarcoplasmic reticulum
ER of skeletal muscle fibers.
Stores, releases, retrieves Calcium
132
Sarcolemma
Plasma membrane of muscle fibers
133
Sarcoplasm
Cytoplasm of muscle fibers
134
Myofibrils
Structures of proteins in muscle fibers
135
Sarcomeres
Smalest functional part of skeletal muscle
136
Fascicle
Bundle of muscle fibers
137
Perimysium
Surround fascicles
138
Endomysium
Enclose muscl fiber
139
Epimysium
Surrounds whole muscle
140
Actin
Thin fillaments
Pulled by myosin
141
Myosin
Thick fillaments
Pull actin
142
Z line/disc
End of each sarcomere
Actin filaments attach to it
143
A band
Darker
Thick Myosin fillaments
144
I bands
Lighter
Thin actin
145
M line
Myosin filaments anchor to it
146
H band
Area adjacent to M line where myosin filaments are not superimposed by actin.
147
Muscle contraction
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
Isotonic contraction
Muscle contracts and changes length
Concentric - shortening
Eccentric - lengthining
149
Isometric contraction
Muscle contracts but does not change length.
Stabilizes posture and holds body upright
150
Components of connective tissue
Cells
Fibers
Ground substance
Ground substance + fibers = extracellular matrix
151
Cartilage
Flexible connective tissue.
Specialized cells (chondroblasts)
Elastic, hyaline, fibrocartilage
152
Perichodrium
Around cartilage
Highly vascularized to provide nutrients to cartilage
153
Chondrocytes
Cartilage cells.
Mature chondroblast
154
Chondroblasts
Undergo mitosis and secrete extracellular matrix components maturing as non-dividing chondrocytes
155
Elastic cartilage
More elastic than hyaline
Maintains shape while allowing flexibility.
External ear, epiglotis
156
Hyaline cartilage
Most abundant in body.
Transparent or glassy matrix.
Supports and shock absorption.
Embryonic skeleton, costal cartilages of ribs, nose, trachea, larynx
157
Fibrocartilage
Hyaline cartilage and dense regular connective tissue blended.
Compressible, resists tension.
Intervertebral discs, knee meniscus
158
Interstitial growth of cartilage
Growth from within
Lengthening of bones
Chondroblasts lay down more matrix inside existing cartilage
Childhood growth.
159
Apositional growth of cartilage
Growth from outside.
Increases width.
New surface layers added
160
What does injury, pain, or invasion cause
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
Prostanoids formed by COX 1
Prostaglandin GI2 (PGI2)
Thromboxane A2 (TXA2)
162
Prostaglandin GI2 (PGI2)
Made from COX 1
Provides gastric protection
163
Thromboxane A2 (TXA2)
Made from COX 1
Role in platelet aggregation
164
Prostaglandin E2 (PGE2)
Made form COX 2
Inflammation, pain, fever
165
Inhibition of COX 2 effect
Stops inflammation, pain, fever
(antiinflammatory, analgesic, antipyretic)
166
Aspirin
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
Aspirin Method of action
Irreversibly binds to COX-1 in platelets
Arachidonic acid can't bind to convert into TXA2.
Reduce vasoconstriction.
168
Aspirin precautions
Avoid in pts under 19 yrs old bc of Reye's syndrome.
Large doses toxic in children.
Hold 1-2 weeks before surgery.
169
Celecoxib
NSAID
Inhibits COX 2 ONLY
Decreased GI risk
Increased platelet aggregation.
Increases CV risk by 1/3
170
What non-aspirin NSAID works best
All work equally as good
171
Ketorolac
NSAID
Used for acute, severe pain.
Oral, IM, or IV
Can't be used more than 5 days
172
Diclofenac
NSAID
Worst for CV risk
173
Naproxen
NSAID
Least CV risk
174
At what age do NSAIDs risks significantly increase
>75 yrs old
175
NSAID adverse effects
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
NSAIDs contraindications
GI bleed/bleeding disorder
Cardiovascular disease
Kidney disease
Avoid in pregnancy
Decrease effects of ACEi/ARBS
Decrease effect of diuretic
177
Acetaminophen (Tylenol)
NOT NSAID
"APAP"
Paracetamol internationally
Analgesic and antipyretic only
Little to no risk of bleed (no effects on platelets)
178
Acetaminophen (tylenol) method of action
Inhibits COX enzymes in CNS inhibiting prostanoid synthesis in CNS causing analgesic and antipyretic effects.
Inactivated in PNS so no antiinflammatory effect
179
When to use Acetaminophen (tylenol)
Patients with Gi risk.
Children
Oral, IV, or rectal
180
Adverse effects of acetaminophen (tylenol)
Hepatotoxicity.
Medication error risk with IV use.
Hepatotoxicity
181
Acetaminophen (tylenol) contraindications
Hepatic disease
Hepatitis
Malnutrition
Alcohol users (greater than or equal to 3 drinks per day)
Max dose of 4g per day
182
Spasticity
Increases muscle tone due to increased excitability of muscle stretch reflex
183
Spasm
Involuntary muscle contractions.
Jerks, twitches, cramps
184
Skeletal muscle relactants
Antispasticity and antispasmodic.
Drowziness and dizziness.
Increased risk of respiratory depression.
185
Baclofen
Antispasticity
Similar structure to GABA
Binds to GABA receptors to inhibit excitatory muscles\
(helps GABA do its job)
186
Carisoprodol
Antispasmodic
Controlled because potential for physical dependence.
Acts on CNS.
Effects GABA receptors
Can have withdrawal
187
Cyclobenzaprine
Antispasmodic
CNS depression of brain stem.
Caution for patients with cardiac arrhythmias or conduction disturbances
188
Cyclobenzaprine contraindications
Acute narrow angle glaucoma
Older age
Moderate to severe hepatic impairment.
189
Metaxalone
Antispasmodic
CNS depression
Don't use with severe renal or hepatic impairment
190
Methocarbamol
Antispasmodic
CNS depression
191
Tizanidine
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
Dantrolene
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
Path of blood
L ventricle
Areteries and arterioles
Capillaries where it mingles with interstitial fluid.
Veins
194
Drains of lymphatic system
Thoracic duct and Right lymphatic duct
195
What all causes blood to move forward
Heart pumping
Diastolic recoil of arterial wall
Venous compression from skeletal muscle
Negative pressure in thorax during inspiration.
196
What resists blood flow
Diameter of vessels (mainly arterioles)
Viscosity of blood
197
Components of blood
55% is plasma (3L).
45% is celllular elements (2L
198
Plasma
Protein rich fluid where cellular elements are suspended
199
Make up of plasma
92% water
7% proteins
1% solutes
200
Albumin
Most abundant protein in plasma.
Regulates osmotic pressure (keeps water in the vessels)
201
Hematopoesis
Blood formation in bone marrow, spleen, and liver.
Amount made in each location is greatest to lowest in that order
202
How many cells made per day in hematopoesis
100 billion
75% are WBC
25% RBC
Lots more RBC in circulation bc live long time
203
Lifespan of red blood cell
120 days
204
Hematopoietic stem cell (HSC)
Start hematopoesis.
Self renewing
Can differentiate into ANY type of blood cell
205
Myeloid cell line
Grannulocytes
Erythrocytes
Monocytes
Platelets
206
Lymphoid cell line
B cells
T cells
Natural killer cells
207
Erythropoiesis
Production of RBC (erythrocytes)
Stimulated by erythropoietin (EPO) from kidney when O2 sat low
Tells BM to make more RBC
208
Erythropoiesis sequence
EPO --> HSC --> erythroblast --> nucleus and organelles removed --> reticulocyte
209
Reticulocyte
Immature RBC.
Larger
Still contains some organelle remnants.
210
Important nutrients for erythropoiesis
Iron to make hemoglobin.
B12/Folate for DNA synthesis.
B6
Copper
Zinc
AA
211
What hormones cause erythropoiesis
Erythropoiesis
Testosterone
NOT iron
212
Leukopoiesis
Production of WBC (leukocytes)
213
Where are T cells first made
Bone marrow
214
Where are natural killer cells first made
Bone marrow
215
Lymphoid line sequence of production
HSC --> Common lymphoid progenitor --> Lymphocytes and NK cells
216
Thrombopoiesis
Platelet production
HSC --> megakaryocytes --> fragment into platelets
Always being stimulated
217
Thrombopoietin (TPO)
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
What shape is mature RBC
Biconcave
219
What percent of RBC replaced each day
1%
220
Primary function of RBC
Transport O2 from lungs to tissue.
Transport CO2 from tissue to lungs
221
Hemoglobin
Red O2 carrying pigment in RBC
4 subunits.
Heme has iron
Globin is polypeptide.
Porphyrins absorb light
222
Most common hemoglobin make up
Hgb A1.
2 alpha and 2 beta chains
223
Hgb A2
2 alpha and 2 delta chains
224
Hgb F
Fetal hemoglobin
2 alpha and 2 gamma chains
225
Where does oxygen bind to on hemoglobin
On the iron molecule
226
What iron do we use
Fe2+
227
Functional hypoxia
Caused by methemoglobin.
Fe3+ used rather than Fe2+
228
Why is carbon monoxide toxicity usual
CO has higher affinity for hemoglobin than O2
229
G6PD
Deficiency causes spherocytosis
230
MCV
Mean corpuscular volume
Average volume of single RBC in femtoliters
80-100 fL
231
What all is actually measured in lab
RBC
Hgb
WBC
PLT
MCV
232
RBC x 3
Hgb
233
Hgb x 3
HCT
234
Neutrophils
First line of defense against pathogens
Lifespan is 8 hours
235
Platelets
Smallest formed element of blood
Fragments of Megakaryocytes
Used in coagulation
236
Steps of platelet function
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
Thrombocytosis
Too many platelets
238
Thrombocytopenia
Not enough platelets
239
What triggers intrinsic clotting pathway
Collagen
240
What triggers extrinsic clotting pathway
Tissue factor exposed in injured tissue
241
Where do the clotting pathways merge to become the common pathway
Factor X
242
Intrinsic clotting pathway
Collagen --> XII --> XI --> VIII --> X --> prothrombin (II) to thrombin --> fibrinogen (I) to fibrin
Slower and more complicated
243
Extrinsic clotting patwhay
Injury --> III (tissue factor) --> VII --> X --> prothrombin (II) to thrombin --> fibrinogen (I) to fibrin
Happens much faster
244
Common clotting pathway
X --> Prothrombin (II) to thrombin --> Fibrinogen (I) to fibrin.
XIII stabilizes the clot.
244
Vitamin K dependent factors
II
VII
IX
X
Proteins C and S
245
Plasminogen
Converts into plasmin and degrades clot that will then be eaten up by macrophages
246
Fibrinolysis
Clot formed --> platelets contract ---> Exposes plasminogen --> allows plasminogen activator to bind transforming plasminogin to plasmin --> breaks clot to be eaten by macrophages
247
Universal blood DONOR
O negative
248
Universal recipient
AB positive
249
Most common RH antigen
D
250
Stress response
Results from physiologic or psychological stimulus that disrupts homeostasis.
Includes anesthesia
251
What factors determine patients response to surgical stress
Basic fitness
Nature of injurious process
Severity of surgery
Duration of surgery
VIirulence of microorganisms involved (infection)
252
Factos influincing physiologic response to surgery
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
Three physiologic components of surgical stress response
Sympathetic
Endocrine
Immunologic
254
Sympathetic response to surgery stress
Increased catecholamines.
Causing Increase HR, contractility, vasoconstriction.
Causes increase renin, decrease blood flow, increase sodium resorption.
INcreasees glucagon
255
Endocrin response to surgery stress
Increase cortisol
Increase ADH
Increased catabolism causing weight loss
256
Immunologic response to surgery stress
Cytokines and acute phase protein release
Fever
D-dimer elevation
Inflammatory cascade
257
Pancreas reaction to surgery stress
Catabolic state
Increased glucagon
Decreased insulin
258
What does an elevated WBC count mean
Inflammation is present
NOT necessarily infection
259
What does D Dimer show
D dimer comes from breakdown of clot
260
Body water distribution
67% intracellular
33% extracellular
261
Major cation in plasma
Sodium
262
Major cation in extracellular fluid
Potassium
263
Major anion of intracellular fluid
Phosphorus
Sulfate
264
Major anion of extracellular fluid
bicarb
Chloride
265
Where are baroreceptors
Aortic arch and carotid sinuses
266
Most common perioperative fluid imbalance
Hypovolemia
267
Third space
Not in cell, not in vasculature.
AKA transcellular space
268
Fluid loss stage
Intravascular blood loss into third space causing hypovolemia, decreased cardiac output, hypotension, tachycardia.
Increasing fluid volume of interstitial space causing edema
269
Fluid absorption phase
Can cause Hypervolemia
HTN
Edema
Urine output increases
270
Hypovolemia lab findings
Elevated BUN/Cr levels
Elevated hematocrit
Metabolic acidosis/alkalosis
Low urinary Na
High urinary Cl
Urine osmolality raised
271
Examples of isotonic fluids
Lactated ringers
Normal saline
Normal saline can increase risk of hyperchloremic metabolic acidosis
272
5% dextrose
Given with isotonic and hypotonic fluids.
Maintainstonicity and prevents catabolism ketosis and hypoglycemia
273
Hyponatremia causes
High output NG tubes
Emesis
ENteric fistulas
274
Hyponatremia signs/symptoms
CNS cellular water intoxication causing increase in ICP
Headache, confusion, altered deep tendon reflexes, seizures, coma, HTN, bradycardia, N/V, anorexia
275
Hypernatremia
Hyperosmolality CNS effects.
Reslessness, lethargy, delirium, irritability, seizures, coma
276
Most common electrolyte disturbance that cases perioperative arrhythmias
Potassium
277
Peaked T waves
Hyperkalemia
278
Hypomagnesium
Usually comes with hypokalemia.
Give Mg first then give K.
Hyperactive reflexes
Tremors
Tetany
279
Hypocalcemia
Chvostek's sign
Trousseau's sign
280
What patient at highest risk for delirium
Cardiopulmonary bypass surgery
281
If patient had stroke in past three months and is in AFib
Delay surgery for at least 3 months
282
Postoperative MI
Twice as deadly as pt with regulary myocardial infarction
283
Atelectasis
Collapse of lung tissue with volume loss
284
Pulmonary problems after surgery
Atelectasis
Pneumonia
Respiratory failure
285
What separates epidermis and dermis
Basement membrane
286
Nonglabrous
Hair areas
287
Glabrous
Hairless areas
288
Epidermal layers superficial to deep
Corneum
Lucidum
Granulosum
Spinosum
Basale
289
Stratum Corneum
Most superficial layer of epidermis.
15-20 layers of keratinized cells
Sheds constantly.
30 days to replace all cells
290
Stratum Lucidum
Keratinocytes pushing up to stratum
Translucent layer
Only on palms and soles for thickness
291
Stratum granulosum
Keratinocytes from spinosum pushed up and move toward corneum.
Lipid rich for water loss
292
Stratum spinosum
Thickest layer
Living keratin form tonofibrils to phaogocytose melanocytes and release melanin and hold water.
Langerhans cells, melanocytes
293
Stratum Basale
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
Keratinocytes
Most abundant cells in epidermis.
Flat squamous cells
Secrete keratin
Provide mechanical strength and protection
295
What regulates melanocytes
Melanocortin receptors and ACTH
296
Langerhans cells
Dendritic cells that are first line of immune response in skin
297
Merkel cells
Sense light touch.
In stratum basale
298
