Final Exam - new material Flashcards
1
Q
what is the normal plasma pH
A
7.4
2
Q
what does the pH need to be for the person to be in acidosis
A
pH < 7.38
less than
3
Q
what does the pH need to be for the person to be in alkalosis
A
pH > 7.42
greater than
4
Q
what is the pH in the alkaline range
A
anything greater than 7
5
Q
what do disturbances in pH homeostasis cause
A
disruption of protein shape
disturbance of K+ levels
effects on excitable tissues
6
Q
what is the main problem that causes pH disturbances
A
excess H+
7
Q
what is the largest source of excess H+
A
metabolic production of CO2 (from respiratory system)
8
Q
what is the CO2/H+ equilibrium reaction
A
CO2 + H2O –> H+ + HCO3-
9
Q
what is a buffer system
A
mixture of two compounds that can remove or produce free H+ as needed
10
Q
what is the fastest response to pH disturbance
A
buffer system
(BUT doesnt remove anything from the body)
11
Q
what is the most important extracellular buffer
A
bicarbonate
12
Q
what is the bicarbonate buffering reaction
A
CO2 + H2O –><– H+ + HCO3-
carbonic anhydrase (CA)
13
Q
what are the main determinants of plasma pH
A
concentrations of CO2 and bicarbonate
14
Q
what organ is bicarbonate regulated by
A
kidneys
15
Q
what organ is CO2 regulated by
A
lungs
16
Q
what is the most important intracellular buffer
A
proteins
17
Q
what is an example of a protein buffer
A
hemoglobin
H+ + Hb –><– HbH
(absorbs H+ when Co2 is converted to bicarbonate)
18
Q
what is the urine and intracellular buffer
A
phosphate
19
Q
what is the urine buffer
A
ammonia
20
Q
what type of homeostatic pH compensation is slow? fast?
A
slow: renal
fast: respiratory
21
Q
what type of pH problems can respiratory compensation fix
A
metabolic
22
Q
how does the respiratory system regulate H+ concentration
A
by controlling rate of CO2 removal
CO2 + H2O –><– H+ + HCO3-
23
Q
what happens to the respiratory equilibrium equation when the body gets rid of CO2
A
shifts left
24
Q
what happens to the respiratory equilibrium equation when the body retains CO2
A
shifts right
25
what is the most powerful pH regulator
renal compensation
26
how does the renal system regulate pH
secrete/absorb H+
secrete/absorb HCO3-
27
what happens to the urine when the renal system secretes H+
the urine is acidic
28
what type of cells play a key role in renal pH compensation
intercalated cells in distal nephron
29
what are the two types of intercalated cells
type A
type B
30
when are type A intercalated cells active
when in acidosis (too acidic)
31
what do type A intercalated cells do
secrete H+ into filtrate
absorbs HCO3- into blood
32
how do type A intercalated cells secrete H+ into the filtrate? what does it often lead to?
uses a H+/K+ exchanger
acidosis often leads to hyperkalemia (high K+ in blood) (when H+ is secreted, the body pulls K+ into the blood via the exchanger)
33
when are type B intercalated cells active
when in alkalosis (too basic)
34
what do type B intercalated cells do
absorb H+ into blood
secrete HCO3- into filtrate
35
how do type B intercalated cells absorb H+ into the blood? what does it often lead to?
uses H+/K+ exchanger
alkalosis often leads to hypokalemia (low K+ in blood)
(when H+ is absorbed into the blood, body secretes K+ via the exchanger)
36
what is the underlying cause of respiratory acidosis or alkalosis
a change in PCO2
37
what is any other pH disturbance (other than respiratory) referred to as
metabolic
38
what is respiratory acidosis due to
hypoventilation
39
what happens to the equilibrium equation (CO2 + H2O --> H+ + HCO3-) due to respiratory acidosis
high PCO2 causes high H+ and slightly high HCO3-
40
if the respiratory system is the problem (like in respiratory acidosis) where does the compensation come from
all compensation is renal; secretes H+ and reabsorbs HCO3-
41
what happens to bicarbonate concentration with renal compensation in respiratory acidosis
high bicarbonate which restores the correct [HCO3-]/[CO2]
42
what is metabolic acidosis due to
addition of acids OR removal of HCO3-
43
what happens to the equilibrium equation (CO2 + H2O --> H+ + HCO3-) due to metabolic acidosis
high H+ causes high initial PCO2 and low HCO3-
44
what two ways does the body compensate for metabolic acidosis
compensation by lungs
renal compensation
45
how do the lungs compensate for metabolic acidosis
hyperventilation to lower PCO2 and restore correct [HCO3-]/[CO2]
46
how does renal compensation compensate for metabolic acidosis
secretes H+ and reabsorbs HCO3-
47
what is respiratory alkalosis due to
hyperventilation
48
what happens to the equilibrium equation (CO2 + H2O --> H+ + HCO3-) due to respiratory alkalosis
low PCO2 causes low H+ and slightly low HCO3-
49
if the respiratory system is the problem (like in respiratory alkalosis) where is all of the compensation coming from
renal compensation; absorbs H+ and secretes HCO3-
50
what happens to the bicarbonate concentration with renal compensation due to respiratory alkalosis
low HCO3- restores correct [HCO3-]/[CO2]
51
what is metabolic alkalosis due to
removal or acids OR addition of HCO3-
52
what happens to the equilibrium equation (CO2 + H2O --> H+ + HCO3-) due to metabolic alkalosis
low H+ leads to low initial PCO2 and high HCO3-
53
what two ways does the body compensate for metabolic alkalosis
compensation by lungs
renal compensation
54
how do the lungs compensate for metabolic alkalosis
hypoventilation --> high PCO2 which restores the correct [HCO3-]/[CO2]
55
how does renal compensation work when compensating for metabolic alkalosis
absorbs H+
secrete HCO3-
56
what are the two competing behavioral states for control of food intake
appetite (hunger)
satiety (lack of hunger)
57
what are the two hypothalamic control centers for control of food intake
feeding center: tonically active
satiety center: inhibits feeding center
58
what is neuropeptide Y (NPY)
neurotransmitter in brain responsible for increased food intake (hunger)
59
what is ghrelin
hormone secreted by stomach when empty to increase food intake
60
what is leptin
hormone secreted by adipocytes when fat stores increase to decrease food intake
61
what are CCK and GLP-1
hormones secreted by duodenum (small intestine) in response to fats and carbs in chyme to decrease food intake
62
what is happening in the GI tract during the fed/absorptive state
absorbing nutrients in GI tract
63
are the pathways in the fed/absorptive state mostly anabolic or catabolic
anabolic (building larger molecules)
64
what is the main energy source in the fed state
glycolysis (glucose-->pyruvate)
65
what happens to amino acids during the fed state
protein synthesis
66
what happens to glucose in the liver and muscle in the fed state
glyconeogenesis (glucose --> glycogen) (building up larger molecules)
67
what happens to lipids in adipocytes in the fed state
lipogenesis (fat synthesis)
68
what do glycerol and fatty acids play a role in (in fed state)
lipogenesis
69
what do converted excess carbohydrates and AAs play a role in (in fed state)
lipogenesis
70
what is happening in the GI tract during the fasted/postabsorptive state)
no absorption occurring in GI tract
71
are the pathways in the fasted state mostly anabolic or catabolic
catabolic (breakdown)
72
what is glycolysis a required energy source for in the fasted state
CNS and red blood cells
73
what is being maintained in the fasted state
blood glucose
74
what happens in the liver during the fasted state
glycogenolysis (breaking down glycogen --> glucose) and glucose release
75
how is glucose being produced in the fasted state
gluconeogenesis produces glucose from glycerol (from adipocytes) and pyruvate, lactate, and AA (from skeletal muscle)
76
how does skeletal muscle obtain glucose during the fasted state
from its own glycogens stores
77
do fats or glycogen have a higher energy content
fats have higher energy content but are slower to metabolize
78
what do fats (triglycerides (TGs)) provide
major energy source
79
what is lipolysis
TG --> glycerol + free fatty acid (FFA)
80
what does beta oxidation of fatty acids produce
acyl units
81
what happens to the acyl units that are produced via beta oxidation
they enter the krebs cycle (CAC) as acetyl CoA
82
what is glycerol from lipolysis used for
glycolysis
83
what happens to the body proteins with extended fasting
body proteins are used heavily as a source of AA
84
what does the brain use for energy in extended fasting
ketone bodies that are produced from FFA in liver
85
what ratio regulates metabolism
insulin-to-glucagon ratio
86
what kind of relationship do insulin and glucagon have
inverse relationship
87
is insulin or glucagon dominant in the fed state
insulin
88
what causes pancreatic beta cells to secrete insulin
high blood glucose and AA levels
89
what happens when pancreatic beta cells secrete insulin
increased: glucose uptake, glycolysis, glycogenesis (packaging glucose), lipogenesis, protein synthesis
90
what is the overall result of increased insulin secretion
decreased blood glucose
91
what kind of glucose uptake is insulin-dependent
glucose uptake by adipose tissue and resting skeletal muscle
92
how does glucose get in/out of the cell
by transporters being inserted in the membrane
93
what happens to glucose entry in adipose tissue and resting skeletal muscle in the fasted state
no insulin --> no GLUT4 transporters in membrane --> no glucose entry
94
what happens to glucose entry in adipose tissue and resting skeletal muscle in the fed state
insulin binds to receptor --> GLUT4 transporters inserted in membrane --> glucose allowed to enter cell
95
what does insulin indirectly alter glucose transport in
hepatocytes (liver)
96
what are always present in hepatocyte membrane
GLUT2 transporters
97
what happens to glucose transport in hepatocytes in the fasted state
glycogenolysis --> high glucose inside of cell --> glucose diffuses out of the cell
98
what happens to glucose transport in hepatocytes in the fed state
insulin activated glucokinase in cell --> phosphorylated glucose to G6P --> keeps glucose low inside of cell --> glucose diffuses into cell
99
what are three other factors that influence insulin secretion
carbohydrates in gut
distention of gut
sympathetic input
100
how do carbohydrates in gut affect insulin secretion
increased incretions (GIP, GLP-1 (peptides)) lead to increased insulin
101
how does distention of the gut affect insulin secretion
increased parasympathetic input leads to increased insulin
102
how does sympathetic input affect insulin secretion
it decreased insulin secretion because when stressed, hyperglycemia is good
103
what is dominant in the fasted state
glucagon
104
what kind of cells release glucagon
pancreatic alpha cells
105
what kind of cells release insulin
pancreatic beta cells
106
why is glucagon secreted
low blood glucose --> alpha cells secrete glucagaon
107
what is the target cell of glucagon
liver
108
what two things does the release of glucagon result in? what is the overall effect?
increased glycogenolysis
increased gluconeogenesis
overall: increased blood glucose
109
what are two other hormones that help increase blood glucose
cortisol and norepinephrine
110
what does it mean to say that humans are homeothermic
they regulate internal temperature within a narrow range (37 C or 98.6 F)
111
what happens when temperature is too high
hyperthermia
denatures enzymes
112
what happens when temperature is too low
hypothermia
chemical reactions too slow
113
what is the equation for heat loss
external heat input + internal heat production = heat loss
114
what are the four mechanisms of heat exchange
radiation (gain or loss)
conduction (gain or loss)
convection (gain or loss)
evaporative heat loss
115
what is radiation as a heat exchange mechanism
warm surfaces emit and absorb electromagnetic waves that travel through space
116
what is conduction as a heat exchange mechanism
heat transmission by contact that is transferred by thermal molecular motion
117
what is convection as a heat exchange mechanism
heat transmission by bulk flow of air or water
118
what is evaporative heat loss as a heat exchange mechanism
from skin to respiratory tract
119
what two types of heat production are not physiologically regulated
normal metabolism
voluntary muscle contractions
120
how can normal metabolism produce heat
~25% of nutrient energy is captured as cellular work and the rest is wasted as heat (can be used to maintain body temp)
121
what are voluntary muscle contractions used for
behavioral thermoregulation
122
what are the two kinds of physiologically regulated heat production
shivering thermogenesis
non-shivering thermogenesis
123
what is shivering thermogenesis
involuntary tremors in skeletal muscles
124
what is non shivering thermogenesis
mitochondrial uncoupling: energy from e transport chain is released as heat instead of ATP
125
where does non shivering thermogenesis occur
in brown adipose tissue where there is a higher density of mitochondria
-important in newborns
126
what two sensors are used for thermoregulation
central thermoreceptors (hypothalamus)
peripheral thermoreceptors (skin)
127
what is the integrator in thermoregulation
hypothalamus
128
what is the thermoneutral zone in thermoregulation
range of environmental temperatures in which thermoregulation requires only vascular adjustments
129
what are the two responses to decreased temperatures
sympathetic adrenergic neurons
somatic motor neurons
130
what do sympathetic adrenergic neurons do in response to decreased temperature
cutaneous vasoconstriction --> decreased convective flow from interior to skin --> decreased skin temperature --> decreased heat loss at skin
possibly non shivering thermogenesis in infants
131
what do somatic motor neurons do in response to decreased temperature
shivering thermogenesis
132
what are the two responses to increased temperatures
active cutaneous vasodilation
sweat glands secrete sweat-hyposmotic to blood
133
what is the process of active cutaneous vasodilation when temperatures increase
increased heat loss at skin due to sympathetic cholinergic neurons
NOT due to withdraw of adrenergic input
NOT a result of ACh
134
what is the process of sweat glands secreting sweat when temperatures increase
sympathetic cholinergic neurons --> ACh --> muscarinic receptor
135
why does sweat secretion increase metabolic rate above thermoneutral zone
it is energetically expensive
evaporative cooling = net heat loss
136
where do alterations to the setpoint occur
in hypothalamus
137
what causes an increased setpoint
fever due to pyrogens from immune cells
138
what causes a decreased set point
hot flashes
139
what is the function of the digestive system
move materials from external to internal environment
140
what regulates the digestive system
enteric nervous system (ENS) - brain of the gut
141
what makes up the enteric nervous system
neurons and sensory receptors in GI wall that control motility and secretion
142
what are the two different digestive reflexes
short reflex
long reflex
143
where does the short digestive reflex originate and integrate
originates within the ENS and is integrated there WITHOUT input from the CNS
144
where is the long digestive reflex integrated? where is the input/output coming from
integrated in the CNS
sensory input from ENS (or PNS)
autonomic output to ENS
145
what non-neural component is included in reflex pathways
GI peptides: hormones and paracrine signals secreted by gut wall
146
what are the three groups of absorbable units
carbohydrates, proteins, lipids
147
where is amylase produced by
saliva and pancreas
148
what does amylase do
digest polysaccharides to disaccharides
149
where are disaccharides located
on membrane of brush border cells of small intestine
150
what digests disaccharides into monosaccharides
enzymes located on the brush border of the small intestine
151
how do glucose and galactose first enter the membrane (apical entry)
sodium glucose linked transporter (secondary active transport)
152
how do glucose and galactose exit the membrane (basolateral exit)
GLUT2 transporter (facilitated diffusion)
153
how does fructose enter the membrane (apical entry)
GLUT5 transporter (facilitated diffusion)
154
how does fructose exit the membrane (basolateral exit)
GLUT2 transporter (facilitated diffusion)
155
how are most enzymes for protein digestion secreted
in inactive form
156
what do endopeptidases/proteases do
break peptide bonds in interior of protein/peptide
157
what are three examples of endopeptidases/proteases
pepsin
trypsin
chymotrypsin
158
where is pepsin located
in stomach
159
when are endopeptidases/proteases activated
once they are in the lumen
160
where are trypsin and chymotrypsin located
in small intestine (come from the pancreas)
161
what do exopeptidases do
remove AA at end
162
what are two examples of exopeptidases
carboxypeptidase
aminopeptidase
163
where does carboxypeptidase remove from
removes from carboxy-terminal end
164
where does aminopeptidase remove from
removes from amino-terminal end
165
how are free AA absorbed
most by cotransport with Na+
166
how are di and tripeptides absorbed
cotransport with H+
167
where are most di and tri peptides digested
inside the cell to free AA
168
how are some larger (small) peptides (~3AA) absorbed
by transcytosis
(gets endocytosed, then exocytosed)
169
what are most lipids
triglycerides (fats)
170
are lipids water soluble
no
171
where are bile salts secreted and stored
secreted by liver
stored in gallbladder
172
what do bile salts do
emulsify fats (break into smaller droplets) to increase surface area for enzymatic digestion
- speeds up digestion
173
where does lipase come from
pancreas
174
what does lipase do
digests triglycerides into monoglyceride and 2 free fatty acids (FFA)
175
where does colipase come from
pancreas
176
what is colipase
protein cofactor that displaces part of the bile salt coating to give lipase access to fats inside
177
what are the 3 enzymes (lipases) that help digest lipids
bile salts
lipase
colipase
178
what do products of lipid digestion assemble with and into after digested
assemble with bile salts and phospholipids into a micelle
179
where do free fatty acids (FFA) and monoglycerides enter after digestion? how?
enter enterocytes (brush border cells) by simple diffusion
180
what happens to FFA and monoglycerides after the enter enterocytes
the smooth ER reassembles them into triglycerides
181
how is cholesterol absorbed
actively via carrier protein
182
what are triglycerides and cholesterol coated with to form chylomicrons
lipoprotein
183
where do triglycerides and cholesterol chylomicrons go after they are coated with lipoprotein
exocytosed to interstitial fluid
184
how do chylomicrons get into the blood
they cannot cross basement membrane of blood capillaries so they enter lacteals (small lymphatic vessels) instead
185
what are the three phases of digestion
cephalic phase
gastric phase
intestinal phase
186
what kind of response is the cephalic phase
feedforward response to anticipation of food
187
what kind of reflex happens in the cephalic phase
long reflex
188
what is the pathway in the cephalic phase that ends in physiological responses
sight, smell, taste, thought of food --> medulla oblongata --> parasympathetic NS
189
what are the parasympathetic responses from the pathway in the cephalic phase
increase salivary gland secretion
increased secretion and motility throughout most of digestive system (stomach, intestines, pancreas, liver)
190
what nerve / nervous system is used to get physiological results in the cephalic phase
vagus nerve and ENS
191
what happens in the gastric phase
increase in gastric secretion and motility stimulated by entry of chyme into the stomach
192
what kind of reflexes does the gastric phase involve
short reflexes in addition to hormones/paracrines
193
what causes physiological responses in the gastric phase
distention and presence of peptides/AA in lumen
194
what are the results of distention and presence of peptides/AA in lumen in the gastric phase
increased gastrin (hormone) secretion by G cells
increased HCl (acid) secretion by parietal cells
increased pepsinogen secretion by chief cells (activated to pepsin by acid)
195
what kind of feedback occurs when there is acid in the lumen
negative feedback
196
what does the negative feedback due to acid in the lumen cause
increased somatostatin (paracrine) from D cells
decreased secretion by G cells, parietal cells, and chief cells
197
what starts the intestinal phase
entry of chyme into duodenum
198
what kind of reflexes are involved in the intestinal phase
short reflexes
199
what happens when acid enters the duodenum (intestinal phase)
increased secretin (hormone) --> increased pancreatic bicarbonate secretion (neutralizes the acid)
200
what happens when fats and proteins enter the duodenum (intestinal phase)
increased CCK (hormone) --> increased pancreatic enzyme secretion and bile released from gallbladder (bile emulsifies fats)
201
what happens when carbohydrates enter the duodenum (intestinal phase)
increased incretins (GIP and GLP-1 (hormones)) --> increased insulin secretion (feedforward effect)
202
what are gastric motility and acid secretion by the stomach inhibited by (in intestinal phase)
ENS, secretin, CCK, incretins (GIP, GLP-1)
203
what will increase acid
gastrin (gastric phase)
204
what will decrease acid
somatostatin (gastric phase)
secretin (increases pancreatic bicarbonate secretion in intestinal phase)
secretin, CCK, incretins, ENS (decreases stomach HCl secretion in intestinal phase)
205
what does it mean to say that embryonic structures are bipotential
they can develop into either female or male form
206
what sex develops if there is no Y chromosome
develop as female
207
what gene is on the Y chromosome that makes the embryo develop as male
SRY gene
208
what does the SRY gene cause
testis develop and secrete:
- anti-mullerian hormone
- testosterone --> dihydrotestosterone (DHT) (converted in peripheral tissues)
209
how can sexual genotypes (XX or XY) differ from sexual phenotype
if signals or receptors for signals are missing
210
what does the hypothalamus secrete in the HPG axis
GnRH (gonadotropin releasing hormone)
211
what does the anterior pituitary secrete in the HPG axis
gonadotropins
- FSH (follicle stimulating hormone)
- LH ( luteinizing hormone)
212
what does LH stimulate in the HPG axis
sex steroid hormone secretion by gonads
213
what does FSH stimulate in the HPG axis
gametogenesis (gamete production)
(sex steroids also play role in this)
214
where do the sex steroids feedback (neg or pos) to
hypothalamus or anterior pituitary
215
what three groups of steroids do both sexes produce
androgens: T and DHT
estrogens: estradiol (E)
progestins: progesterone (P)
216
what enzyme do both ovaries and testes have? what does it do?
aromatase
- converts T to E
217
what do the testes (gonads) produce after LH and FSH are released by GnRH
sperm and hormones
218
what does LH do in male hormonal regulation
secretes testosterone from Leydig cells
219
what does FSH (and testosterone) do in male hormonal regulation
secretes paracrines from sertoli cells which increase spermatogenesis
220
what two things do sertoli cells secrete
paracrines to increase spermatogenesis
androgen binding protein (ABP) to keep T from diffusing away
221
what does testosterone do in male hormonal regulation
decrease GnRH, LH, and FSH
- engage in negative feedback
222
what are the two cycles in the menstrual cycle
ovarian cycle: changes in follicles of ovary
uterine cycle: changes in uterine lining
223
what are the three phases of the uterine cycle
1. menses
2. proliferative phase
3. secretory phase
224
what is the menses phase of the uterine cycle
1. menses: if pregnancy not achieved, shed endometrium - bleeding from uterus
225
what is the proliferative phase of the uterine cycle
2. proliferative phase: endometrium thickens in preparation for pregnancy
226
what is the secretory phase of the uterine cycle
3. secretory phase: endometrial secretions promote implantation
227
what are the three phases of the ovarian cycle
1. follicular phase
2. ovulation
3. luteal phase
228
what happens in the follicular phase of the ovarian cycle
development of follicle
- granulosa cells proliferate and secrete estrogen
- maturation of oocyte
229
what happens during ovulation of the ovarian cycle
mature follicle bursts, releasing the oocyte
230
what happens during the luteal phase of the ovarian cycle
ruptured follicle develops into corpus luteum
- secretes progesterone and some estrogen to prepare from pregnancy
231
what do the ovaries (gonads) produce in response to LH and FSH release from GnRH
estrogen and some progesterone
232
what does LH cause in female hormonal regulation
androgens secreted by thecal cells, which diffuses into granulosa cells
233
what happens after androgens diffuse into granulosa cells
aromatase converts it into estrogen
234
what does FSH cause in female hormonal regulation
granulosa cells produce estrogen which increases follicular development
235
what does the corpus luteum secrete after ovulation
progesterone and some estrogen
236
generally, what are the results of estrogen and progesterone
decreased GnRH, LH, FSH
(negative feedback)
237
what is caused by persistent high estrogen
switches to positive feedback --> ovulation
238
what is the ovarian cycle phase called in days 0-7
early follicular phase
239
what is the uterine cycle phase in days 0-7
menses (no pregnancy - shedding of endometrium)
240
what hormones are being released during days 0-7 and what do they cause
FSH and LH: follicular development and estrogen
estrogen: decreases GnRH, LH, FSH
241
what is the phase of the ovarian cycle during days 7-14
late follicular phase (follicle matures)
242
what is the phase of the uterine phase during days 7-14
proliferative phase
- estrogen causes the endometrium to grow in preparation for pregnancy
243
what hormones are being released during days 7-14 and what do they cause
increased estrogen
- estrogen changes from negative to positive feedback on LH
LH surge triggers ovulation
244
what day does ovulation occur
day 14
245
what happens during ovulation
follicle ruptures, releasing oocyte
thecal and granulosa cells start to become luteal cells
246
what phase of the ovarian cycle occurs during days 14-21
early luteal phase
- corpus luteum develops from follicle
247
what phase of the uterine cycle occurs during days 14-21
secretory phase
- endometrial secretions promote implantation of fertilized oocyte
248
what hormones are secreted during days 14-21
corpus luteum secretes P (and E)
249
what does P promote in days 14-21
decreases GnRH, LH, FSH (negative feedback)
increased endometrial development
250
what phase of the ovarian cycle occurs during days 21-28 if no pregnancy
late luteal phase
- corpus luteum degenerates and ceases hormone production
251
what phase of the uterine cycle occurs during days 21-28 if no pregnancy
secretory phase
252
what hormones are secreted during days 21-28 if no pregnancy
LACK of P from corpus luteum leads to death of endometrium --> menses (day 0)
FSH and LH secretion resume for next cycle
253
what happens 5-7 days later if fertilization occurs
fertilized egg implants in endometrium
254
what is secreted as the placenta develops
human chorionic gonadotropin (hCG)
255
what does hCG maintain
corpus luteum
256
what does the corpus luteum secrete that is critical to maintain a pregnancy
progesterone and estrogen
257
what later takes over progesterone production later in pregnancy
placenta
- corpus luteum degenerates
258
what are oral contraceptives made of
progesterone and estrogen
259
what does synthetic estrogen and progesterone lead to
decreased GnRH, LH, FSH --> prevents follicle maturation and ovulation
progesterone thickens cervical mucus --> barrier to sperm
260
what are the three functions of the immune system
protect body from pathogens
remove dead and damaged cells
remove "abnormal self" cells (cancerous)
261
what are leukocytes
white blood cells / immune cells
262
what are immunogens
anything that triggers an immune response
pathogens
allergens: cause allergic response
263
what are the differences between an overactive response. incorrect response, and lack of response
overactive: allergy
incorrect: autoimmune disease
lack: immunodeficiency
264
what are the different cell surface markers/molecular markers
self markers
non self markers
265
what are the two different self markers
major histocompatibility complex (MHC) - on nucleated cells
ABO and Rh blood types - on non nucleated cells (RBCs)
266
what is the non self marker
antigens - molecules that trigger immune response
(pathogen-associated molecular patterns (PAMPs))
267
what do antigens bind to
pattern recognition receptors (PRR) on leukocytes
268
what are the two antigens expressed on RBCs
A and B
269
what leads to an O blood type
A and B both absent
- is recessive
270
what are the 4 possible blood types
A B AB O
271
which antibodies are in blood plasma
antibodies to any antigen that is not on RBC
(anti-A, anti-B, both, or neither)
272
what happens if matching antigens and antibodies mix
blood agglutinates (clumps)
273
when considering blood transfusions, what do you need to know
what antibodies the recipient has
what antigens are on the donors RBCs
274
what are the three lines of defense against pathogens
barriers
innate immune response
adaptive immune response
275
what are examples of the barriers
skin
mucous membranes
276
are innate immune responses
specific/nonspecific
rapid/slow
nonspecific
rapid (hours)
277
what kind of cells are involved in adaptive immune response
B cells
T cells
(lymphocytes)
278
what does it mean to say that the adaptive immune response has specificity
recognize and react to one antigen only
279
what is immunological memory
for stronger and quicker response (acquired immunity) to subsequent exposures
280
what is the main function of the innate immune response
removes dead and damaged cells
281
how does the innate immune response remove dead and damaged cells
creates pores in targer cell membrane to kill it
phagocytosis
282
how are abnormal self (cancer cells) killed
innate immune response created pores in the target cell membrane and natural killer cells kill them
283
what are the three types of phagocytes
macrophages, neutrophils, dendritic cells
284
what can phagocytosis be assisted by
antibodies
285
how is the target ingested in phagocytosis
destroyed with lysosomal enzymes
286
what kind of immune response is inflammation and what is it
innate immune response
- nonspecific reaction of immune system to foreign invader
287
what do mast cells secrete in response to inflammation
histamine
288
what is the affect of histamine
vasodilation --> increased blood flow --> redness and heat
289
what does increased capillary permeability in response to inflammation cause
increased capillary permeability --> proteins enter interstitial fluid --> edema --> pain
290
what do macrophages attract
neutrophils
291
what is a cytokine
peptide signals among leukocytes
292
where are neutrophils found
circulate in blood until attracted to site of infection
293
how are T cells activated
antigen fragment is presented within MHC self marker by antigen presenting cells (APC)
294
what are the three types of antigen presenting cells
dendritic cells
macrophages
B cells
295
what do dendritic cells intiate
adaptive immune response
(most important APC)
296
what kind of cells are involved in the adaptive immune system
B cells
cytotoxic T cells
helper T cells
(all are lymphocytes)
297
what does each cell of the adaptive immune system have its surface
antigen receptors for a specific antigen
- all cells in a clone have same antigen receptor
298
what is clonal expansion
correct match between antigen and receptor activated cell to divide rapidly which produces effector cells and memory cells
299
what are the effector and memory cells of B cells
effector: plasma cells
memory: memory B cells
300
what is the primary immune response
initial slow response
- clonal expansion produces effector and memory cells
301
what is the secondary immune response
quicker stronger response due to memory cells making clonal expansion faster
- basis for vaccines
302
what do B cells provide
antibody-mediated (humoral) immunity to extracellular pathogens
303
what two things does activation of B cells require
binding to antigen
cytokines from helper T cell
304
what do plasma cells secrete and what do they do
plasms cells secrete antibodies that attach to a pathogen to tag it for phagocytosis
305
what do cytotoxic T cells provide
cell-mediated immunity to intracellular pathogens
306
what two things does activation of cytotoxic T cells require
binding to matching antigen on APC
cytokines from helper T cell
307
what do cytotoxic T cells attack
abnormal cells
308
what does the cytotoxic part of cytotoxic T cells mean
they create pores in target cells, like NK (natural killer cells) but are antigen-specific
309
what do helper T cells secrete
cytokines
310
what are cytokines crucial for
activating B cells and cytotoxic T cells
311
what does activation of helper T cells require
binding to matching antigen on APC
