Final Exam! Flashcards
1
Q
Comparison of Endocrine and Nervous System
A
are both control systems of the body. Both release ligands (chem. messengers) that attach to target cells. Unlike nervous system, endocrine uses hormones, is widespread, can target any cell, exhibits longer reaction times and longer-lasting effects.
2
Q
Steroids
A
lipid-soluble molecules synthesized from cholesterol
3
Q
biogenic amines (monoamines)
A
modified amino acids; are water soluble except for thyroid hormone. Includes catecholamines, TH, and melatonin
4
Q
proteins
A
most hormones are proteins, water-soluble chain of amino acids
5
Q
local hormones
A
signaling molecules that don’t circulate in blood
6
Q
eicosanoid
A
local hormone. Includes prostaglandins.
7
Q
How to water-soluble hormones enter cell
A
use membrane receptors. These hormones are polar and cannot diffuse through the membrane.
8
Q
Synergistic interaction
A
one hormone reinforces activity of another. ex: estrogen and progesterone effects of target cell.
9
Q
Permissive interactions
A
one hormone requires activity of another. ex: oxytocins milk ejection effect requires prolactin’s milk generating effect.
10
Q
Hypothalamo-hypophyseal portal system
A
system of blood vessels that connects hypothalamus to anterior pituitary. Contains a primary plexus (capillary network near hypothalamus), secondary plexus (capillary in ant. pit.) and hypophyseal portal vein that drains primary plexus and transport to secondary plexus.
11
Q
Posterior pituitary
A
storage and release sight for oxytocin and antidiuretic hormone which is released from synaptic knobs into blood when neurons fire impulses.
12
Q
antidiuretic hormone
A
functions to decrease urine production, stimulate thirst, and constrict blood vessels.
13
Q
oxytocin
A
functions in uterine contraction, milk ejection, and emotional bonding.
14
Q
Hormones of hypothalamus
A
releasing hormone: increase secretion of anterior pituitary hormones and includes thyrotropin RH, prolactin RH, gonadotropin RH, corticotropin RH and growth hormone RH.
Inhibiting hormones: decreases secretion of ant. pit. hormones.
15
Q
anterior pituitary hormones
A
TSH, PRL, adrenocorticotropic hormone, and gonadotropins.
16
Q
thyroid stimulating hormone (TSH)
A
release triggered by TRH from hypothalamus, causes release of TH from thyroid
17
Q
Prolactin (PRL)
A
release triggered by PRH, inhibited by PIH. causes milk production, and mammary gland growth in females.
18
Q
Adrenocorticotropic Hormone (ACTH)
A
release triggered by CRH from hypothalamus. Causes release of corticosteroids by adrenal cortex.
19
Q
Gonadotropins
A
FSH and LH, released by anterior pituitary.
20
Q
growth hormone
A
stimulates release of nutrients from storage (glycogenolysis, gluconeogenesis, lipolysis)
21
Q
glycogenolysis
A
breakdown of glycogen into glucose
22
Q
gluconeogenesis
A
conversion of nutrients to glucose
23
Q
glycogenesis
A
synthesis of glycogen
24
Q
lipolysis
A
breakdown of triglycerides
25
lipogenesis
formation of triglycerides
26
follicular cells of thyroid
synthesize thyroglobulin that produces and releases TH
27
parafollicular cells of thyroid
makes calcitonin to decrease blood calcium levels
28
thyroid hormone
increases metabolic rate and protein synthesis in targets, fosters ATP production
29
calcitonin
released when blood is high in calcium or stress from exercise. Stimulates kidneys to increase excretion of calcium in urine.
30
adrenal medulla
releases epinephrine and norepinephrine with sympathetic stimulation
31
adrenal cortex
synthesizes mineralocorticoids, glucocorticoids, and gonadocorticoids.
32
mineralocorticoids
hormones that regulate electrolyte levels. Made in zona glomerulosa (outer layer). Includes aldosterone which foster Na retention and K secretion
33
glucocorticoids
hormones that regulate bg; in zona fasciculata (middle layer). Includes cortisol which increases bg.
34
gonadocorticoids
sex hormones made in zona reticularis (inner layer). Includes androgens which are male sex hormones made by adrenals that is converted to estrogen in females. More androgens are released in testes.
35
Cortisol and corticosterone
increase nutrient level in blood to resist stress and repair injured tissues. Release is regulated by hypothalamic-pituitary-adrenal axis and neg. feedback.
36
Effects of cortisol
causes target cells to increase blood nutrient level. Liver cells increase glycogenolysis and gluconeogenesis while decreasing glycogenesis. Adipose cells increase lipolysis and decrease lipogenesis. Body cells break down proteins and cells decrease glucose uptake; sparing it for the brain.
37
Cushing syndrome
chronic exposure to excessive glucocorticoid hormones in people taking corticosteroids for therapy. Some cases when adrenal gland produces too much hormone.
38
pancreas
has endocrine and exocrine functions. Acinar cells generate exocrine secretion for digestion. Pancreatic islets contain endocrine cells: alpha cells secrete glucagon, beta cells secrete insulin.
39
Lower BG
beta cells detect rise in bg and secrete insulin. Insulin travels through blood and randomly leaves to encounter target cells and initiates 2nd messenger systems. hepatocytes remove glucose from blood to make glycogen and adipose increases lipogenesis. body cells increase nutrient uptake (amino acids, glucose)
40
pineal gland
secretes melatonin to regulate circadian rhythm.
41
parathyroid glands
contain chief (principal) cells that make parathyroid hormone. PTH increases blood calcium by taking it from bones and decrease its loss in urine; activates calcitriol.
42
functions of blood
transportation, protection, regulation of body temp, pH, and fluid balance.
43
blood: transportation
transports formed elements, dissolved molecules and ions. Carries o2 and co2, nutrients, hormones, heat, and waste
44
blood: protection
leukocytes, plasma proteins and more protect against pathogens, platelets and some plasma proteins protect against blood loss
45
regulation of body temp. by blood
blood absorbs heat from body cells and releases at skin blood vessels, can also vasoconstrict to conserve heat.
46
regulation of body pH by blood
blood absorbs acids and bases from body cells and contains buffers.
47
fluid balance
water is added to blood from GI tract and is lost through urine, respiration, and skin. fluid is exchanged between blood and interstitial fluid and blood contains plasma proteins and ions to help maintain osmotic balance
48
blood pH
slightly alkaline; between 7.35 and 7.45. Crucial for normal plasma protein shape (avoid denaturing)
49
Components of blood
buffy coat (1%), plasma (55%) and erythrocytes (44%)
50
Whole blood
plasma and formed elements; can be separated with a centrifuge
51
buffy coat
thin, gray-white, middle layer in centrifuge. Composed of leukocytes and platelets and 1% of sample
52
Plasma in centrifuge
straw-colored at top of tube, 55%
53
Hematocrit
percentage of volume and all formed elements. Clinical definition is percentage of only erythrocytes. 42-56% for males and 38-46% in females because testosterone causes more erythropoietin secretion by kidneys.
54
Plasma composition
92% water, 7% plasma proteins, 1% dissolved molecules and ions. It is an extracellular fluid that has a similar composition to interstitial fluid, just higher protein concentration.
55
plasma proteins
most are produced by liver and include albumins, globulins, fibrinogen, enzymes, other clotting proteins, and some hormones. They exert colloid osmotic pressure to prevent loss of fluid from blood
56
colloid osmotic pressure
helps prevent loss of fluid from blood as it moves through capillaries which maintains blood volume and pressure
57
Albumins
smallest and most abundant plasma protein (58%). Exert greatest colloid osmotic pressure
58
gamma-globulins
also called antibodies, type of globulin plasma protein that is part of body's defenses.
59
Hemopoiesis
production of formed elements occurring in red bone marrow of some bones.
1. hemoblast (stem cell)
2. Pluripotent, can differentiate into many types of cells and produce 2 lines:
3a. Myloid line: forms erythrocytes, all leukocytes except lymphocytes, and megakaryocytes
3b. Lymphoid line: forms only lymphocytes
60
colony-stimulating factors
stimulate hemopoeisis
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erythropoiesis
red blood cell production requiring iron, b vits, and amino acids.
62
Leukopoiesis
production of leukocytes, involves maturation of granulocytes, monocytes, and lymphocytes. granulocytes include neutrophils, basophils, and eosinophils. Monocytes are derived from myeloid stem cells. Lymphoblasts mature into b and t lymphocytes
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thrombopoiesis
platelet production. megakaryocyte is formed from myeloid stem cell and produces these platelets.
64
Hemoglobin
red protein that transports o2 and co2. considered oxygenated when fully loaded with o2. each hemoglobin has 4 globins. O2 bonds are fairly week for quick attachment in lungs and detachment in body tissues and the co2 binds weakly to the globin protein, not iron
65
erythrocyte destruction
erythrocytes lack organelles so they cant repair themselves. Maximum lifespan is 120 days and old erythrocytes are phagocytized in spleen or liver.
66
blood type
blood group depends on surface antigens projecting from erythrocyte membrane. Either A, AB, B or no surface antigens; this determines antibody status
67
Rh factor
determines if blood is positive or negative. Rh antibodies do not usually appear until an Rh negative person is exposed to Rh positive blood.
68
neutrophils
granulocyte; most numerous leukocyte in blood. Phagocytize pathogens and rise in chronic bacterial infections.
69
eosinophils
phagocytize antigen-antibody complexes or allergens; active in cases of parasitic worm infection
70
basophils
releases histamine to increase blood vessel diameter and heparin to inhibit blood clotting.
71
t-lymphocytes
manage immune response
72
b-lymphocytes
become plasma cells and produce antibodies
73
nk cells
attack abnormal and infected tissue cells
74
monocytes
phagocytize bacteria, viruses, debris
75
platelets
small, membrane enclosed cell fragments that help stop bleeding
76
Hemostasis
stoppage of bleeding; involves 3 overlapping phase.
1. vascular spasm: blood vessel constriction: lasts many minutes. platelets and endothelial cells release chemicals to further constrict.
2. platelet plug formation: normal blood vessels walls have prostacyclin which repels platelets, but when it is damaged a platelet plug forms and platelets aggregate
3. Coagulation: network of fibrin (from fibrinogen) forms a mesh to form a clot.
77
prostacyclin
an eicosanoid that causes endothelial cells and platelets to make cAMP which inhibits platelet activation in undamaged blood vessel.
78
sympathetic response to blood loss
if greater than 10% of blood is lost, sympathetic increases vasoconstriction, HR, and force of heart contraction and blood is redistributed to heart and brain. Effective in maintaining bp until 40% of blood is lost.
79
cardiac muscle myofilaments
arranged in sarcomeres; gives striated appearance
80
Sarcolemma of cardiac muscle
Sarcolemma is folded at connections between cells to increase structural stability of myocardium and facilitate communication between cells. cells are connected by these intercalated discs
81
gap juntions
electrically join cells (allow ion flow) to make each heart chamber a functional unit (functional syncytium)
82
cardiac muscle metabolism
high energy demand; is able to use different types of fuel molecules such as Fatty acids, glucose, lactic acid, amino acids, and ketone bodies
83
sinoatrial node
initiates heartbeat and is located high in posterior wall of right atrium
84
cardiac cell membrane proteins
Na/K pumps, Ca pumps, leak channels, slow voltage-gated Na channels, fast voltage-gated Ca channels and voltage-gated K channels
85
autorhythmicity
spontaneous firing of sa node.
86
action potential in SA node
1. reaching threshold: slow Na voltage-gated Na open and Na flows in. Membrane potential goes from -60 to -40 mV (threshold)
2. depolarization: fast Ca channels open and Ca flows in; -40 to just above 0 mV
3. Repolarization: calcium channels close and voltage K open so K flows out. RMP goes back to -60, where voltage Na open again.
87
vagal tone
parasympathetic activity by vagus nerve on SA node keeping the heart rate slower than 100bpm.
88
direction of action potential spread through heart
After starting at SA node the action potential spreads 1. Action potential is distributed through atria, reaches AV node • Excitation travels via gap junctions and the two atria contract together 2. Action potential is delayed at the AV node • AV nodal cells are slow because of small diameter and few gap junctions • Insulation of fibrous skeleton means AV node is bottleneck (only path) • Delay allows ventricles to fill before they contract 3. Action potential travels through AV bundle to Purkinje fibers • AV node → AV bundle → Bundle branches → Purkinje fibers 4. Action potential spreads through ventricles • Gap junctions allow impulse to spread through cardiac muscle fibers • Cells of the two ventricles contract nearly simultaneously
89
electrical events in cardiac muscle
1) Depolarization • Impulse from conduction system (or gap junctions) opens fast voltage-gated Na+ channels • Na+ enters cell changing membrane potential from −90 mV to +30 mV • Voltage-gated Na+ channels start to inactivate
2) Plateau • Depolarization opens voltage-gated K+ and slow voltage-gated Ca2+ channels
• K+ leaves cardiac muscle cell as Ca2+ enters
• Stimulates sarcoplasmic reticulum to release more Ca2+ • Membrane remains depolarized
3) Repolarization • Voltage-gated Ca2+
channels close while K+ channels remain open • Membrane potential goes back to −90 mV
90
why cant cardiac muscle exhibit tetany
have longer refractory period due to plateau phase. Heart must relax before it can be stimulated again
91
P wave
Reflects electrical changes of atrial depolarization originating in SA node
92
QRS complex
Electrical changes associated with ventricular depolarization • Atria also simultaneously repolarizing
93
T wave
• Electrical change associated with ventricular repolarization
94
PQ segment
Associated with atrial cells’ plateau (atria are contracting
95
ST segment
Associated with ventricular plateau (ventricles are contracting)
96
PR interval
Time from beginning of P wave to beginning of QRS deflection or from atrial depolarization to beginning of ventricular depolarization. Is the time to transmit action potential through entire conduction system
97
QT interval
Time from beginning of QRS to the end of T wave • Reflects the time of ventricular action potentials
98
Atrial contraction and ventricular filling
SA node starts atrial excitement, atria contract pushing remaining blood into ventricles to end diastolic volume
99
isovolumetric contraction
Purkinje fibers initiate ventricular excitation • Ventricles contract, pressure rises, and AV valves are pushed closed • Ventricular pressure is still less than arterial trunk pressure, so semilunar valves still closed
100
ventricular ejection
Ventricles continue to contract so that ventricular pressure rises above arterial pressure • Semilunar valves forced open as blood moves from ventricles to arterial trunks
101
stroke volume
amount of blood ejected by ventricle
102
end systolic volume
amount of blood remaining in ventricle after contraction finishes
103
ESV equation
end systolic volume= EDV-SV
104
cardiac output
amount of blood pumped by a single ventricle in one minute; measure effectiveness of CV system and increases in healthy individuals during exercise
105
cardiac output equation
CO = HR X SV
106
cardiac reserve
capacity to increase cardiac output past resting level. cardiac output can increase 4 fold in normal people. CO w/ exercise - CO at rest
107
chronotropic agents
change heart rate
108
positive chronotropic agents
increase HR by sympathetic nerve stimulation causing norepinephrine and epinephrine to bind to nodal cells to increase firing rate.
109
Negative chronotropic agents
decrease heartrate through parasympathetic axons releasing acetylcholine onto nodal cells making cells more negative.
110
atrial reflex
baroreceptors in atrial wall are stimulated by increased venous return to send signals to cardioacceleratory center to increase excitation of sympathetic axons to heart to increase HR so the heart doesn't over stretch.
111
venous return
volume of blood returned to the heart, directly related to stroke volume
112
preload
pressure stretching heart wall before contraction
113
frank-starling law
as EDV increases, greater heart stretch will result in more optimal overlap of thick and thin filaments so Heart contracts more forcefully when filled with more blood so SV increases
As EDV increases, so will SV
114
inotropic agents
change stroke volume by altering contractility (force of contraction)
115
afterload
Resistance in arteries to ejection of blood by ventricles. is the pressure that must be exceeded before blood is ejected
116
vesicular transport
endothelial cells use pinocytosis and endocytosis. Certain hormones and fatty acids transported by this method
117
bulk flow
fluids flow down pressure gradient. Movement of fluids and dissolved substances
118
filtration
fluid moves out of blood; occurs on arterial end of capillary
119
reabsorption
fluid moves back into blood; Occurs on venous end
120
Blood hydrostatic pressure
force exerted per unit of area by blood on vessel wall. promotes filtration from capillary
121
colloid osmotic pressure
the pull on water due to the presence of proteins (colloid). Blood colloid osmotic pressure (COPb) draws fluid into blood due to blood proteins
122
net filtration pressure
NFP is the difference between net hydrostatic pressure and net colloid osmotic pressure; that is: NFP = (HPb - HPif) - (COPb - COPif).
NFP changes along length of capillary; higher at arterial end than venous
123
lymphatic system
Picks up 15% of fluid not reabsorbed at venous capillary end and Filters fluid and returns it to venous circulation
124
local blood flow depends on
degree of tissue vascularity and myogenic response
125
degree of vascularization in different tissues
Metabolically active tissues have high vascularity • E.g., brain, skeletal muscle, heart, liver • Other structures have little vascularity or are avascular • Tendons, ligaments, epithelia, cartilage, cornea, lens of eye
126
angiogenesis
formation of new vessels to increase potential perfusion in response to aerobic training, weight gain, and gradual blockage.
127
regression blood vessels
return to previous state of blood vessels due to weight loss, becoming sedentary
128
myogenic response
smooth muscle in blood vessel wall keeps local flow relatively constant • If systemic blood pressure rises and more blood enters an arteriole, it will stretch • Smooth muscle of arteriole wall will respond by contracting • Contraction will return local flow to original levels
129
vasoactive chemicals
alter blood flow; includes vasodilators that relax precapillary sphincters and dilate arterioles to alter blood flow and vasoconstrictors to constrict and decrease blood flow to capillary beds.
130
histamine and bradykinin effects on arterioles
causes dilation and is released in response to trauma, allergy, infection, exercise. May also stimulate release of nitric oxide, another vasodilator.
131
total blood flow
amount of blood transported through vasculature per unit of time; equal to cardiac output. About 5.25 L/min at rest
132
mean arterial pressure
MAP is average arterial blood pressure across entire cardiac cycle. Since diastole lasts longer than systole, the mean is weighted to be closer to diastolic pressure. MAP less than 60 may indicate insufficient blood flow
MAP = diastolic pressure + 1/3 pulse pressure
ex: 120/ 80 bpm
MAP= 80 + 40/3 = 93
133
skeletal muscle pumps
assist venous return from limbs
134
respiratory pump
assists in venous return in thorax. Inspiration contracts diaphragm, increasing abdominal pressure so blood goes up into thorax. In expiration, thoracic pressure increases due to diaphragm relaxation, so blood is driven towards heart.
135
peripheral resistance
Resistance of blood in blood vessels. Affected by viscosity, vessel length, lumen size
136
viscosity
resistance of fluid to its flow. depends on percentage of particles in fluid which thickens blood. Blood has formed elements and proteins and so it is about 5 times more viscous than water
137
resistance
resistance can be increased by: increasing blood viscosity, increasing vessel length, or decreasing vessel lumen diameter
138
cardiac center
houses 2 nuclei, cardioacceleratory center and cardioinhibitory center.
139
sympathetic activation of blood vessels can cause
increased peripheral resistance due to constriction, larger circulating blood volume increasing bp, and redistribution of blood flow to heart and muscles.
140
aortic arch baroreceptors transmit signals to cardiovascular center via
vagus nerve (CN X)
141
carotid sinus baroreceptors transmit nerve signals to cardiovascular center via
glossopharyngeal nerve (CN IX)
142
baroreceptor reflexes for decrease in bp
baroreceptor firing decreases, activating cardioaccceleratory center to increase sympathetic pathways to increase CO. Activates vasomotor center to stimulate sympathetic pathways to increase vasoconstriction.
143
baroreceptor reflex for increase in bp
cardioacceleratory center sends less signals to sympathetic pathways and cardioinhibitory activates parasympathetic pathways to SA and AV nodes. Causes vasomotor center to send less signals along sympathetic pathways to blood vessels decreasing CO and resistance.
144
peripheral chemoreceptors
aortic and carotid body. both send input to cardiovascular system. aortic is in aortic arch and carotid are at a bifurcation of common carotid artery. High carbon dioxide, low pH, very low oxygen stimulate chemoreceptors and vasomotor center to Increase BP and shift blood to lungs, expire CO2 and raise pH
145
renin release in blood
released in response to low bp or sympathetic nervous system activity. renin converts angiotensinogen into angiotensin I
146
angiotensin II
raises blood pressure through vasoconstriction. also stimulates thirst center and works on kidneys to decrease urine formation and stimulates release of aldosterone and antidiuretic hormone.
147
aldosterone
decreases urine output by increasing absorption of sodium
148
atrial natriuretic peptide
increases urine output and stimulates vasodilation.
149
cytokines
small proteins that regulate immune activity. they are chemical messengers released from one cell that bind to receptors of target cell.
150
Innate immunity
present at birth and nonspecific. first line of defense is skin and mucosal membranes and second line of defense if neutrophils, macrophages, dendritic cells, eosinophils, basophils and nk cells.
151
adaptive immunity
acquired, specific immunity involving t and b lymphocytes, takes several days to become effective.
152
mucous membranes
line body openings and produce mucus and release antimicrobial substances like defensins, lysozymes, and IgA
153
Nonspecific Phagocytotic cells
neutrophils, macrophages, dendritic cells. Neutrophils and macrophages destroy engulfed particles and dendritic cells destroy particles are then present fragments to t- lymphocytes
154
cells that promote inflammation
basophils and mast cells. Basophils circulate in the blood while mast cells reside in connective tissue, mucosa, internal organs. They release granules containing chemotaxic chemicals (meaning they attract immune cells)
155
apoptosis initiating cells
NK cells and eosinophils. NK cells destroy virus and bacteria infected cells, tumor cells, and transplanted tissue by releasing cytotoxic chemicals. eosinophils attack multicellular parasites and phagocytize antigen-antibody complexes and participate in immune response to allergies
156
Interferons
a class of cytokines that nonspecifically impedes viral speed. They bind to neighboring cells and prevent their infection and trigger synthesis of enzymes that destroy viral nucleic acids. also stimulates NK cells and macrophages to destroy virus-infected cells.
157
complement system
group of over 30 plasma proteins that are activated by an enzyme cascade after pathogen entry. They complement antibodies by attaching to them. Especially potent against bacterial infections
158
Opsonization
complement protein binds to pathogen to enhance its likelihood of phagocytosis.
159
Inflammation
immediate response to ward of unwanted substances. Local, nonspecific, innate.
160
effects of inflammation
fluid moves from blood to injured area and gives tissue proteins and immune cells to promote healing. This fluid is later taken into lymphatic capillaries to be cleaned. Within 72 hours inflammation response slows as macrophages eat bacteria, damaged host cells, dying neutrophils. Tissue repair begins as fibroblasts form new connective tissue
161
cardinal signs of inflammation
(RUBOR, CALOR, TUMOR, DOLOR, FUNCTIO LAESA) • Redness from increased blood flow • Heat from increased blood flow and increased metabolic activity within the area • Swelling from increase in fluid loss from capillaries • Pain from stimulation of pain receptors • Due to compression (extra fluid) and chemical irritants (kinins, prostaglandins, microbial secretions) • Loss of function from pain and swelling in severe cases
162
pus
contains destroyed pathogens, dead leukocytes, macrophages, and cellular debris. Removed by lymphatic system or through skin.
163
branches of adaptive immunity
cell-mediated: involves t lymphocytes
| humoral: involves b lymphocytes, plasma cells, and antibodies
164
antigen
substance that binds to a t lymphocyte or antibody. This is how pathogens are detected
165
helper t-lymphocytes (CD4 cells)
assist in cell-mediated, humoral and innate immunity.
166
antigen presentation
cells display antigen on plasma membrane so T-cells can recognize it. Two categories of cells present antigens: nucleated body cells and antigen presenting cells
167
antigen presenting cells
present to both helper t and cytotoxic t cells
168
MHC (major histocompatibility complex)
group of transmembrane proteins that help display fragments.
169
MHC class 1 molecules
glycoproteins synthesized and modified by rough ER and inserted into cell membrane where they display fragments of proteins bound in rough ER
170
MHC class II molecules
glycoproteins that are loaded with fragments the antigen presenting cell destroyed and are then displayed
171
3 main life events in life of lymphocytes
formation: occurs in primary lymphatic structures (red marrow and thymus) and become able to recognize 1 specific antigen
activation: In secondary lymphatic structures they are exposed to antigen and become activated. Also replicate themselves.
effector response: T-lymphocytes migrate to site of infection • B-lymphocytes stay in secondary lymphatic structure (as plasma cells) • Synthesize and release large quantities of antibodies.
172
formation of t lymphocytes
T-lymphocytes originate in red bone marrow and migrate to thymus as pre-T-lymphocytes to complete maturation
173
naïve t cell
not yet exposed to antigens they recognize
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antigen challenge
first encounter between antigen and lymphocyte. Usually occurs in secondary lymphatic structures
175
activation of helper t
first signal: contact with MHC molecule of APC in secondary lymphatic structure
second signal: helper t-cells proliferate forming clones of helper t-cells. some are activated helper t's that produce IL-2 and others become memory helper t's
176
activation of cytotoxic t
first signal: direct contact between TCR of cytotoxic t-cell and peptide fragment with MHC I molecules
Second signal: IL-2 released from helper t's bind and stimulate cytotoxic t-lymph. Some become activated and others become memory
177
activation of b-lymphocytes
first signal: antigen binds to BCR, cross-linking 2 BCRs. Then stimulated b cell engulfs, processes and presents antigen to t cell.
second signal: activated helper t-cell releases IL-4, stimulating b cells to proliferate and differentiate into plasma cells and memory b cells.
178
Helper t-lymphocytes
releases IL-2 and other cytokines and regulates cells of adaptive and innate immunity
179
cytotoxic t-lymphocytes
destroy unhealthy cells by apoptosis
180
plasma cells
produce antibodies
181
effector response of helper T cells
After exposure to antigen (in secondary lymphatic structures), activated and memory helper T-cells migrate to infection site • Continually release cytokines to regulate other immune cells
182
effector response of cytotoxic t-cells
After exposure to antigen, activated and memory cytotoxic T-cells migrate to infection site • They destroy infected cells that display the antigen. After recognizing antigen, cytotoxic T-cell releases granules containing perforin and granzymes (cytotoxic chemicals) • Perforin forms channel in target cell membrane • Granzymes enter channel and induce death by apoptosis • Because this works against antigens associated with cells, the system is called cell-mediated immunity
183
effector response of b cells
Most activated B-lymphocytes become plasma cells. Plasma cells synthesize and release antibodies.The cells remain in the lymph nodes and they produce millions of antibodies in their 5 day lifespan
184
antibodies
immunoglobulin proteins produced against a particular antigen • Antibodies “tag” pathogens for destruction by immune cells
185
variable regions
Located at the ends of the antibody “arms” • Contain antigen-binding site (most antibodies have two sites
186
agglutination
antibody cross-links antigens of foreign cells causing clumping, especially effective against bacterial cells.
187
precipitation
antibody cross links antigens to form antigen-antibody complex that becomes insoluble and precipitates out of body fluids. Precipitated complexes engulfed and eliminated by phagocytes
188
Opsonization
Fc region of certain antibody classes makes it more likely target cell will be “seen” by phagocytic cell
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IgG
make up 75-85% of antibodies.
190
IgM
is found mostly in blood and normally has pentamer structure. Is most effective at agglutination and binding complement. Responsible for rejection of mismatched transfusions
191
IgA
is found in areas exposed to environment • Produced in mucus, saliva, tears, breastmilk
192
IgE
attracts eosinophils; usually formed in response to parasites and in allergic reactions
193
immunological memory
There is a lag time between first exposure and direct contact that leads to memory cell formation. However, with a subsequent antigen exposure, many memory cells make contact with antigen more quickly to produce a powerful secondary response
194
how long does antibody production take in primary response
1-2 weeks
195
active immunity
results from direct encounter with pathogen and/or its antigens. vaccine, exposure
196
passive immunity
Obtained from another individual • Can occur naturally via transfer of antibodies from mother to fetus (through placenta or milk) • Can occur artificially when serum transferred from one person to another (e.g., antibodies to snake venom) • Neither form of passive immunity produces memory cells
197
hypersensitivities
Abnormal and exaggerated response of immune system to antigen. Causes symptoms such as allergic asthma, hives, vomiting, watery eyes, vasodilation, anaphylactic shock
198
AIDS and HIV
AIDS (acquired immunodeficiency syndrome) is the result of human immunodeficiency virus (HIV) • Infects and destroys helper T-lymphocytes • Resides in body fluids of infected individuals. death usually due to opportunistic infections.
199
proabsorptive state
time between meals (after 4 hours) body relying on stores of nutrients. glucagon is major regulatory hormone during postabsorptive stage
200
metabolic rate
Measure of energy used in a given period of time
201
basal metabolic rate
metabolic rate at rest; measured by calorimeter or respirometer. Thyroid hormone increases BMR
202
respirometer
instrument measuring oxygen consumption. Indirect measure BMR (basal metabolic rate) Oxygen used to produce ATP, ATP utilized to produce heat
203
body surface and Basal metabolic rate
greater surface area of skin, more heat lost. The more heat he has lost, the more active body cells must be to maintain temp.
204
total metabolic rate
BMR + metabolism associated w/ physical activity.
205
temp control
mediated through hypothalamus. Behavior changes initiated in cortex in response to temperature (can meaningfully contribute to regulation) ex. jumping in pool when hot.
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Intracellular fluid
fluid within our cells; 2/3 of total body fluid. has more K, Mg, PO3 and negatively charged proteins
207
plasma part of whole
plasma is 1/2 of extracellular fluid which is 1/3 of total body fluid, so plasma is 1/9 of body fluid.
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extracellular fluid
fluid outside cells such as cerebrospinal fluid and synovial joint fluid. has 2 components: interstitial fluid and blood plasma. Both are similar and have high concentrations of Na+, Ca2+, Cl-, HCO3 –. Just more protein in blood
209
fluid intake
Addition of water to the body (2500 mL/day). Ingested (preformed) water is water absorbed from food and drink; around 2300 mL per day • Major way to increase body fluid
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sensible water loss
Measurable, Includes fluid lost through feces and urine
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insensible water loss
Not measurable, Fluid lost in expired air and from skin through sweat and cutaneous transpiration
212
obligatory water loss
loss of water that always happens (breathing, skin, feces, minimal urine)
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volume depletion
occurs when isotonic fluid loss is greater than isotonic fluid gain.
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hypotonic hydration
water gain or retention. Fluid moving from blood plasma into interstitial fluid and into cells • Possible swelling of cells (edema)
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electrolytes
• Dissociate in solution to form cations and anions • Ability of substances to conduct electrical current when dissolved • Each with unique function and osmotic functions
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sodium ion
99% in ECF and 1% in ICF
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potassium ion
98% in ICF, 2% in ECF. most potassium lost in urine.
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fixed acid
Wastes produced from metabolic processes • E.g., lactic acid from glycolysis • E.g., phosphoric acid from nucleic acid metabolism H2CO3 • E.g., ketoacids from metabolism of fat • Regulated by the kidney
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volatile acid
Carbonic acid produced when carbon dioxide combines with water • Occurs readily with the enzyme carbonic anhydrase Referred to as “volatile” because it is produced from an expired or “evaporated” gas
• Regulated by respiratory system
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respiratory alkalosis
caused by hyperventilation (anxiety, hypoxia)
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metabolic acidosis
from loss of HCO or gain of H. may be caused by Increased production of metabolic acids • E.g., ketoacidosis from diabetes, lactic acid from glycolysis, acetic acid from excessive alcohol intake • Decreased acid elimination due to renal dysfunction • Increased elimination of HCO3 – due to severe diarrhea
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metabolic alkalosis
loss of H or increase of HCO. caused by Vomiting (most common) • Increased loss of acids by kidneys with diuretic overuse • Large amounts of antacids
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gametogenesis
Process of forming human sex cells
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Meiosis
4 haploid daughter cells genetically different from parent cell, Includes crossing over
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what does the primary follicle secrete?
estrogen, to stimulate changes in uterine lining
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ovaries before birth
contain primordial germ cells called oogonia and are arrested in prophase 1 until puberty.
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Hypothalamus release of gonadotropin-releasing hormone stimulates...
release of follicle-stimulating hormone (FSH) and luteinizing hormone (LH) • Levels vary in cyclical pattern to produce monthly sequence of events called ovarian cycle
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follicular phase of ovarian cycle
Around 20 primordial follicles stimulated to mature into primary follicles by LH and FSH. Granulosa cells release inhibin • Helps inhibit further FSH production
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ovulation
second stage of ovarian cycle. Release of secondary oocyte from mature follicle • Occurs on day 14 of 28-day cycle • Usually only one ovary ovulates each month • Induced with peak in LH secretion
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luteal phase
last stage of ovarian cycle. causes menstruation
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regulation of the ovarian cycle in depth
1) Hypothalamus secretes GnRH • Stimulates anterior pituitary to secrete FSH and LH 2) FSH and LH target ovaries and stimulate follicular development • Cause maturation of follicles • Affect secretion of other hormones 3) Maturing ovarian follicles secrete inhibin and estrogen • Negative feedback effect on hypothalamus and anterior pituitary 4) Estrogen assists development of mature ovarian follicle 5) Mature follicle produces a larger amount of estrogen • Positive feedback loop initiated
6) Feedback loop results in an LH surge from anterior pituitary • Without surge, no ovulation 7) Corpus luteum forms from ovulated follicle 8) Corpus luteum secretes large amounts of progesterone, estrogen, and inhibin • Inhibits hypothalamus and anterior pituitary and builds uterine lining • Degenerates in 10 to 13 days (if not fertilized)
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Uterine cycle
Cyclical changes in endometrial lining • Influenced by estrogen and progesterone • 3 distinct phases of development • Menstrual phase, proliferative phase, secretory phase
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menstrual phase
first phase of uterine cycle, sloughing off of functional layer
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proliferative phase
days 6-14 of uterine cycle; Development of new functional layer of endometrium
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secretory phase
days 15-28 of uterine cycle.Increased progesterone secretion from corpus luteum • Results in increased vascularization and uterine gland development
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prolactin
Produced in anterior pituitary and responsible for milk production • With increase, mammary gland forms more and larger alveoli
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oxytocin
Produced by hypothalamus and released form posterior pituitary • Responsible for milk ejection
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seminiferous tubules
convoluted, long tubes in scrotum. up to 4 per lobule. Contains nondividing support cells (sustentacular cells) that nourish sperm and release inhibin when sperm count is high. also inhibits fsh secretion and regulates sperm production.
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blood-testis barrier
Protects developing sperm from material in blood • Protects sperm from body’s leukocytes • Formed from tight junctions between sustentacular cell
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spermatogenesis
Process of sperm development • Occurs within seminiferous tubule • Begins during puberty with significant levels of FSH and LH
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spermatogonia
Primordial germ cells from which all sperm develop • Diploid cells near base of seminiferous tubule • Surrounded by cytoplasm of sustentacular cell • Divide by mitosis into new spermatogonium and primary spermatocyte
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primary spermatocyte
Diploid cells that undergo meiosis
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secondary spermatocytes
Two cells produced by primary spermatocyte from meiosis I • Haploid cells, 23 chromosomes only • Relatively closer to seminiferous tubule lumen
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spermatid
Formed when secondary spermatocytes complete meiosis II • Haploid cell near seminiferous tubule lumen • Circular appearance
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spermiogenesis
final stage of spermatogenesis where spermatid becomes mature spermatozoa. Excess cytoplasm shed and nucleus elongates • Acrosome cap forms over nucleus • Digestive enzymes to help penetrate secondary oocyte. tail formed from microtubules in cell
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semen
Formed from seminal fluid and sperm
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epididymis
stores sperm until fully mature (can be motile)
