Patho II Flashcards
1
Q
A
2
Q
diastole
A
cardiac muscle at rest
3
Q
systole
A
cardiac muscle during contraction
4
Q
Isovolumic ventricular contraction
A
first phase of ventricular contraction when AV valves are pushed closed by the pressure within ventricles; semi lunar valves; semi lunar valves remain closed
5
Q
ventricular ejection
A
pressure within ventricles increases forcing semilunar valves open; allows ejection of blood into pulmonary or aortic circit
6
Q
isovolumic ventricular relaxation
A
as blood ejection completes ventricles relax; blood falls back into semilunar valves to snap them closed
7
Q
S1
A
“lub” first heart sound closing of AV valves
8
Q
S2
A
“dub” second heart sound due to closure of semilunar valves
9
Q
SV =
A
EDV - ESV
10
Q
EF =
A
SV/EDV
11
Q
preload
A
degree of myocardial stretch before contraction begins
12
Q
afterload
A
ventricular force must overcome the resistance by blood filling the arterial system; the combined load of EDV and arterial resistance during ventricular contraction
13
Q
contractility
A
intrinsic ability of a cardiac muscle fiber to contract at any given fiber length
14
Q
normal SV
A
70
15
Q
normal EDV
A
135
16
Q
4 factors that determine venous return
A
1) skeletal muscle pump 2) respiratory pump 3) symp nervous system innervation of veins 4) Blood Volume
17
Q
how do diuretics affect blood volume, EDV, SV?
A
decrease
18
Q
SNS activity increase contractility
A
increase heart rate and contractility
19
Q
ionotroph effects ___ cells.
A
myocardial
20
Q
chronograph effects ___ cells.
A
SA nodal
21
Q
increased cAMP in cardiac myocytes results in (2 things)
A
increased VGCC & phospholamban
22
Q
phospholamban
A
removes inhibitory (think activates) effect on SR Ca+2 ATPase (SRCA); increases calcium delivery to SR more Ca+2 available to increase contractile force
23
Q
NE is a ____ iontroph, meaning ____
A
positive; increases contractibility & SV
24
Q
Verapamil is a ___ iontroph and a ___ chronotroph, meaning
A
negative, negative, decreases ability of heart to contract at any EDV
25
Milrinone is a ____ inhibitor, how does this affect contractility & why
blocks degradation of cAMP; increased cAMP = increase in VGCC and increase in phospholamban leading to a + ionotrophic effect
26
an increase in preload =
an increase in contractility (EDV) and increase in SV
27
an decrease in afterload =
decrease in EDV and increase in SV
28
vasodialators (ACE inhibitor)
decreases afterload to heard move down to curve
29
heart failure signs & symptoms
"shortness of breath", nausea, no tolerance to exercise, high BP, fluid in lungs, low EF,
30
2 strategies to treat heart failure
+ ionotroph (diuretics) & ACE inhibitors
31
how does a diuretic affect afterload curve
shifts up to the left, decreases EDV, increases SV, lowers BP; good treatment for hypertension
32
how do ACE inhibitors affect afterload
similar effect as diuretics; works by increase effects of M2 receptor on heart which will lower high BP
33
positive ionotroph (diuretics)
move patients to a higher ventricular function curve resulting in greater cardiac work for a given level of ventricular filing pressure
34
vasodilators (ACE inhibitors)
move patients to improved ventricular function curves while reducing cardiac filling pressures
35
diuretics
improve symptoms of congestive heart failure by moving patients to lower cardiac filling pressures along the same ventricular function curve.
36
Digoxin
selective inhibitor for Na/K ATPase; decrease Na+ reduces gradient for N+ exchanger; elevated Ca+2 in cytosol is pumped into SR by Ca+2 ATPase and is release upon Ca+ induced Ca+2 release (increases contractility)
37
3 layers of filtration of the glomerular capillary
1) endothelial cells (most leaky) 2) basal lamina 3) outer podocytes (least leaky)
38
glomerularnephritis
change in the basement membrane where glomerular cap loses its negative charge; allows different charges to escape through; get through an infection
39
goodpastures syndrome
autoimmune disorder; antibodies produced against basement membrane; loses negative charge; allows different charges to escape through
40
net filtration pressure
PH - pi - Pfluid
41
GFR =
kf [(PGC - PBS) - (piGC - piBS)
42
glomerular cap epithelium
fenstrated; large pores; negative charge; mesengial cells
43
basal lamina
negatively charged glycoproteins; coarse sieve
44
epithelium of Bowmans Cap
podocytes create filtration slits
45
PiGC
increases from aff to eff
46
as mesangial cells contract, KF ___ and relax, KF \_\_\_
decreases; increases
47
kidneys receive ___ of CO
20%
48
RBF =
RPF\* (1-Hct)
49
filtration barrier allows __ of plasma to enter bowmans space
20%
50
average GFR =
125 mL/min
51
if eff is contracted
RBF decreases Ph increases GFR increases
52
if aff is contracted
RBF decreases Ph decreases GFR decreases
53
movement of water is ___ and __ to solute transport
passive; secondary
54
solvent drag
passive movement of water along with Na, K, etc.
55
PCT
proximal conv tubule; initial segment of the nephron; 70% filtrate is reabsorbed; conc does not change; most transcellular
56
secretion
removal of toxic substances and drugs
57
Loop of Henle
concentrates urine
58
thick ascending limb
perm to ions; dilutes filtrate; has transporter on luminal side (1 K+, Na+, Cl-); dilutes filtrate
59
thin descending limb
highly perm to water; concentrates filtrate; water moves out and is picked up by vasa recta; 15% is reabsorbed;
60
countercurrent multiplier
peritubular capillaries reabsorb water so medulla interstitium conc is high due to loss of water; sends to vasa recta
61
vasa recta
capillaries that circulate around the loop of henle; associated with juxtamedullary nephrons
62
in the vasa recta; medulla absorbs ___ actively transported across the TAL
solutes
63
in the vasa recta; cortex reabsorbs ___ from the surrounding medullary space
water
64
The DCT is ___ than osmotic compared to the initial filtrate
less
65
The DCT is impermeable to
water
66
later DCT and collecting duct may become permeable to water in the presence of
ADH
67
urea
major waste product; controlled by ADH & Vasopressin
68
\_\_\_ is most permeable to urea
papillary duct
69
\_\_ is a good indicator of renal function
BUN; too high is bad flow; body is reabsorbing waste
70
biggest contributer to GFR
blood flow
71
most important factor in regulating GFR
PGC
72
myogenic response
arterial stretch for an extended period causes eventual constriction of afferent to prevent damage to vessels RBF still remains constant making GFR remain constant
73
tubuloglomerular feedback
based of delivery of filtrate to the DCT sensed by macula densa cells
74
macula densa cells
in jux app; sense less volume and comp of filtrate; signal aff t dilate decreasing resistance and increase GFR
75
tubuloglomerular feedback
adjustments occur through release of prostaglandins
76
RAAs
on of the most important regulator of blood volume and blood pressure
77
diseases involved with RAA system
hypertension, CHF, diabetes mellitus, atherosclerosis, hyperlipidemia
78
drugs that inhibit or prevent RAA are effective in
lowering BP & volume
79
RAA is activated in response to
SNS activation decrease of BP and volume NaCl concentration (regulated if body keeps Na or not)
80
Renal clearance
how drugs are eliminated in the body; the amount of drug excreted depends on filtration, reabsorption and secretion
81
excreted =
filtered - reabsorped + secreted
82
many drugs are removed from the body and excreted renally; in patients with decreased renal function you would need to
lower dose
83
inulin
100% filtered but is made outside the body renal clearance of inulin = GFR
84
Creatinine
99% filtered endogenous / made in the body easiest concentration to watch when assessing renal function normal production = breakdown meaning plasma concentration should remain steady; similar properties as inulin
85
CrCl
excretion rate \* vol _______________ plasma conc
86
normal CrCl is
180 ish
87
Cockcroft-Gault formula
CrCl = (140-age) (kg) ___________ (SCr) (72) \*multiply by .85 if its a female pt bc lower muscle mass
88
renal threshold
concentration of which a substance is dissolved in blood above which the kidneys will begin to remove it; urea = low glucose = high main reason for exceeding threshold = diabetes
89
long term complications with renal failure
cardiovascular issues / plaque formation eye disease nervous system caused by an overwork of removing excess glucose and urine
90
Acute Renal Failure
kidney is unable to excrete waste products and maintain acid base balance / diagnosed by CrCl levels
91
ppl at risk for acute renal failure
preexisting renal complications, age, hypertension, cardiac issues, diabetes
92
stage 1 of acute kidney disease is qualified when lab values
increase by .3 mg/dL or increase by 1.5-2x from baseline with urine output less than .5 ml/kg within 6 hours
93
3 causes of acute renal failure
prerenal azotemia postrenal obstruction intrinsic
94
prerenal azotemia
hemolytic issues including shock, hemorrhage, anything due to lack of blood volume
95
post renal obstruction
medication isn't soluble, medication does not dissolve, crystallization, etc
96
intrinsic
affects on actual anatomy (good pastures syn and glomerularnephritis)
97
ADH is released from
posterior pit
98
ADH is secreted in response to
decrease in plasma volume, less atrial stretch, increase of plasma osmolarity
99
diabetes insipidious
lack of ADH hypernatremia (too much loss of water) very dilute urine central vs nephrogenic
100
signs and symps of diabetes insipidious
polyuria, polydipsia, hypernatremia, high plasma osmolarity
101
central diabetes insipidous
lack of ADH treat with vesopressin
102
nephrogenic diabetes insipidious
ADH is nonfunctional (dont get vesopressin)
103
SIADH
symptoms of inappropriate ADH release; too much ADH leads to too much reabsorption, caused by tumors, pulmonary issues, TB, hypothyroidism, drugs
104
signs and symps of SIADH
hyponatremia (osmolarity is too low) neurological - lethargy, confusion, seizures, coma
105
regulation of K
most is in ICF; normal 3.5-5
106
3 things that body does to decrease k concentration
aldosterone (increases renal secretion) insulin (increases uptake into cells) epi (increases uptake into cells)
107
2 methods of aldosterone regulation
1) hyperkalemia (DIRECTLY) on nephron 2) hypotension (INDIRECTLY) increases Ang II which increases aldosterone also severe hyponatremia
108
what inhibits secretion of aldosterone
severe dehydration (no water there to absorb)
109
natriuretic peptides
decrease R decrease vol increase CO
110
Atrial NP
released in response to atria stretching
111
ANP
increase excretion of Na and water decrease RAA system decreased blood volume increased lipolysis
112
BNP
first isolated in the brain secreted from ventricles increased natauresis increased diuresis decreased vol
113
Nesiritide
given to heart failure patients to decrease R and increase functionality of heart; increasing CO
114
BNP levels are a good indicator
of congestive heart failure; high BNP = farther along stages
115
normal pH
7.38-7.42
116
normal Na and K concentrations
Na = 135-140 K = 3.5-5
117
life cannot exist outside what pH range
6.8-7.8
118
what happens when you are outside normal pH range
potassium disturbances acidosis/ alkylosis CNS depression affects respiration
119
sources of acids in the body
foods: fats and carbs met of cys and met = sulfuric acid met of lys, arg, his = hydrochloric acid met of glu, asp, citric acid = generation of bicarb dietary intake of phosphate
120
body handles large acid load by
buffering systems renal compensation respiratory compensation
121
buffering refers to the ability of a solution to resist
changes in pH
122
buffers are typically composed of
a WA and its CB
123
high buffering capacity = low buffering capacity =
alot needs to be added to see change not very much needs to be added to see change
124
main buffering system
bicarb
125
H2o + CO2 combines to form H2CO3
using carbonic anhydrase
126
H2CO3 rapidly hydrolyzes to form
H + bicarb
127
pH =
6.1 + log [HCO3] _________ .03 x PCO2
128
if plasma pH is lower than 7.4 =
acidosis
129
if bicarb is low and pH is low =
metabolic acidosis
130
if bicarb is low and pH is low and CO2 is low
metabolic acidosis was compensated renally
131
if CO2 is high and plasma pH is low
respiratory acidosis
132
if CO2 is high and plasma pH is low and bicarb is also high
renal compensation is occurring with respiratory acidosis
133
if plasma pH is higher than 7.4 =
alklosis
134
if plasma pH is high, and bicarb is high
metabolic alklosis
135
if plasma pH is high, and bicarb is high and Pco2 is also high
metabolic alklosis with respiratory compensation
136
if plasma pH is high and Pco2 is low
respiratory alklosis
137
if plasma pH is high and PCO2 is low and bicarb is also low
respiratory alklosis with renal compensation is occuring
138
bicarb enters the tubular fluid by
glomerular filtration
139
HCO3 gets transported into the
peritubular capillaries across the basolateral membrane
140
2 mechanisms used to reabsorb bicarb
1) Na+ and H antiporter (Na gets reabsorbed with HCO3-) 2) glutamine breaks into NH4 and H+ / Na+ and bicarb are reabsorbed into blood stream
141
in acidosis, pH is low and collecting duct cells can secrete H into filtrate which is done in exchange for K+ which means ppl with acidosis typically have
high K+ plasma concentration
142
in alkalosis, pH is high and collecting duct cells reabsorb H+ meaning the exchangers are releasing K into filtrate which means patients with alkalosis typically have
low K+ plasma concentration
143
normal kidneys function to
eliminate H+ and reabsorb HCO3-
144
diabetic keto-acidosis patients
have an addition of acid = metabolic acidosis
145
profuse vomiting
loss of HCl - metabolic alklosis
146
ingestion of antacids
gain of bicarb - metabolic alklosis
147
profuse diarrhea
loss of bicarb - metabolic acidosis
148
in compensating for acidosis, RR
increases / hyperventilation to get CO2 out
149
in compensating for alklosis, RR
decreases / keep in CO2 / leads to lack of O2 which causes muscle weakness
150
drugs treating pain, fear and anxiety
increase RR, get rid of too much CO2 leading to alklosis
151
drugs treating emphysema, edema, sedatives, alcohol
decrease RR, have build up of CO2 lead to acidosis
152
drugs treating emphysema, edema, sedatives, alcohol
decrease RR, have build up of CO2 lead to acidosis
153
drugs treating pain, fear and anxiety
increase RR, get rid of too much CO2 leading to alklosis
154
in compensating for alklosis, RR
decreases / keep in CO2 / leads to lack of O2 which causes muscle weakness
155
in compensating for acidosis, RR
increases / hyperventilation to get CO2 out
156
profuse diarrhea
loss of bicarb - metabolic acidosis
157
ingestion of antacids
gain of bicarb - metabolic alklosis
158
profuse vomiting
loss of HCl - metabolic alklosis
159
diabetic keto-acidosis patients
have an addition of acid = metabolic acidosis
160
normal kidneys function to
eliminate H+ and reabsorb HCO3-
161
in alkalosis, pH is high and collecting duct cells reabsorb H+ meaning the exchangers are releasing K into filtrate which means patients with alkalosis typically have
low K+ plasma concentration
162
in acidosis, pH is low and collecting duct cells can secrete H into filtrate which is done in exchange for K+ which means ppl with acidosis typically have
high K+ plasma concentration
163
2 mechanisms used to reabsorb bicarb
1) Na+ and H antiporter (Na gets reabsorbed with HCO3-) 2) glutamine breaks into NH4 and H+ / Na+ and bicarb are reabsorbed into blood stream
164
HCO3 gets transported into the
peritubular capillaries across the basolateral membrane
165
bicarb enters the tubular fluid by
glomerular filtration
166
if plasma pH is high and PCO2 is low and bicarb is also low
respiratory alklosis with renal compensation is occuring
167
if plasma pH is high and Pco2 is low
respiratory alklosis
168
if plasma pH is high, and bicarb is high and Pco2 is also high
metabolic alklosis with respiratory compensation
169
if plasma pH is high, and bicarb is high
metabolic alklosis
170
if plasma pH is higher than 7.4 =
alklosis
171
if CO2 is high and plasma pH is low and bicarb is also high
renal compensation is occurring with respiratory acidosis
172
if CO2 is high and plasma pH is low
respiratory acidosis
173
if bicarb is low and pH is low and CO2 is low
metabolic acidosis was compensated renally
174
if bicarb is low and pH is low =
metabolic acidosis
175
if plasma pH is lower than 7.4 =
acidosis
176
pH =
6.1 + log [HCO3] _________ .03 x PCO2
177
H2CO3 rapidly hydrolyzes to form
H + bicarb
178
H2o + CO2 combines to form H2CO3
using carbonic anhydrase
179
main buffering system
bicarb
180
high buffering capacity = low buffering capacity =
alot needs to be added to see change not very much needs to be added to see change
181
buffers are typically composed of
a WA and its CB
182
buffering refers to the ability of a solution to resist
changes in pH
183
body handles large acid load by
buffering systems renal compensation respiratory compensation
184
sources of acids in the body
foods: fats and carbs met of cys and met = sulfuric acid met of lys, arg, his = hydrochloric acid met of glu, asp, citric acid = generation of bicarb dietary intake of phosphate
185
what happens when you are outside normal pH range
potassium disturbances acidosis/ alkylosis CNS depression affects respiration
186
life cannot exist outside what pH range
6.8-7.8
187
normal Na and K concentrations
Na = 135-140 K = 3.5-5
188
normal pH
7.38-7.42
189
BNP levels are a good indicator
of congestive heart failure; high BNP = farther along stages
190
Nesiritide
given to heart failure patients to decrease R and increase functionality of heart; increasing CO
191
BNP
first isolated in the brain secreted from ventricles increased natauresis increased diuresis decreased vol
192
ANP
increase excretion of Na and water decrease RAA system decreased blood volume increased lipolysis
193
Atrial NP
released in response to atria stretching
194
natriuretic peptides
decrease R decrease vol increase CO
195
what inhibits secretion of aldosterone
severe dehydration (no water there to absorb)
196
2 methods of aldosterone regulation
1) hyperkalemia (DIRECTLY) on nephron 2) hypotension (INDIRECTLY) increases Ang II which increases aldosterone also severe hyponatremia
197
3 things that body does to decrease k concentration
aldosterone (increases renal secretion) insulin (increases uptake into cells) epi (increases uptake into cells)
198
regulation of K
most is in ICF; normal 3.5-5
199
signs and symps of SIADH
hyponatremia (osmolarity is too low) neurological - lethargy, confusion, seizures, coma
200
SIADH
symptoms of inappropriate ADH release; too much ADH leads to too much reabsorption, caused by tumors, pulmonary issues, TB, hypothyroidism, drugs
201
nephrogenic diabetes insipidious
ADH is nonfunctional (dont get vesopressin)
202
central diabetes insipidous
lack of ADH treat with vesopressin
203
signs and symps of diabetes insipidious
polyuria, polydipsia, hypernatremia, high plasma osmolarity
204
diabetes insipidious
lack of ADH hypernatremia (too much loss of water) very dilute urine central vs nephrogenic
205
ADH is secreted in response to
decrease in plasma volume, less atrial stretch, increase of plasma osmolarity
206
ADH is released from
posterior pit
207
intrinsic
affects on actual anatomy (good pastures syn and glomerularnephritis)
208
post renal obstruction
medication isn't soluble, medication does not dissolve, crystallization, etc
209
prerenal azotemia
hemolytic issues including shock, hemorrhage, anything due to lack of blood volume
210
3 causes of acute renal failure
prerenal azotemia postrenal obstruction intrinsic
211
stage 1 of acute kidney disease is qualified when lab values
increase by .3 mg/dL or increase by 1.5-2x from baseline with urine output less than .5 ml/kg within 6 hours
212
ppl at risk for acute renal failure
preexisting renal complications, age, hypertension, cardiac issues, diabetes
213
Acute Renal Failure
kidney is unable to excrete waste products and maintain acid base balance / diagnosed by CrCl levels
214
long term complications with renal failure
cardiovascular issues / plaque formation eye disease nervous system caused by an overwork of removing excess glucose and urine
215
renal threshold
concentration of which a substance is dissolved in blood above which the kidneys will begin to remove it; urea = low glucose = high main reason for exceeding threshold = diabetes
216
Cockcroft-Gault formula
CrCl = (140-age) (kg) ___________ (SCr) (72) \*multiply by .85 if its a female pt bc lower muscle mass
217
normal CrCl is
180 ish
218
CrCl
excretion rate \* vol _______________ plasma conc
219
Creatinine
99% filtered endogenous / made in the body easiest concentration to watch when assessing renal function normal production = breakdown meaning plasma concentration should remain steady; similar properties as inulin
220
inulin
100% filtered but is made outside the body renal clearance of inulin = GFR
221
many drugs are removed from the body and excreted renally; in patients with decreased renal function you would need to
lower dose
222
excreted =
filtered - reabsorped + secreted
223
Renal clearance
how drugs are eliminated in the body; the amount of drug excreted depends on filtration, reabsorption and secretion
224
RAA is activated in response to
SNS activation decrease of BP and volume NaCl concentration (regulated if body keeps Na or not)
225
drugs that inhibit or prevent RAA are effective in
lowering BP & volume
226
diseases involved with RAA system
hypertension, CHF, diabetes mellitus, atherosclerosis, hyperlipidemia
227
RAAs
on of the most important regulator of blood volume and blood pressure
228
tubuloglomerular feedback
adjustments occur through release of prostaglandins
229
macula densa cells
in jux app; sense less volume and comp of filtrate; signal aff t dilate decreasing resistance and increase GFR
230
tubuloglomerular feedback
based of delivery of filtrate to the DCT sensed by macula densa cells
231
myogenic response
arterial stretch for an extended period causes eventual constriction of afferent to prevent damage to vessels RBF still remains constant making GFR remain constant
232
most important factor in regulating GFR
PGC
233
biggest contributer to GFR
blood flow
234
\_\_ is a good indicator of renal function
BUN; too high is bad flow; body is reabsorbing waste
235
\_\_\_ is most permeable to urea
papillary duct
236
urea
major waste product; controlled by ADH & Vasopressin
237
later DCT and collecting duct may become permeable to water in the presence of
ADH
238
The DCT is impermeable to
water
239
The DCT is ___ than osmotic compared to the initial filtrate
less
240
in the vasa recta; cortex reabsorbs ___ from the surrounding medullary space
water
241
in the vasa recta; medulla absorbs ___ actively transported across the TAL
solutes
242
vasa recta
capillaries that circulate around the loop of henle; associated with juxtamedullary nephrons
243
countercurrent multiplier
peritubular capillaries reabsorb water so medulla interstitium conc is high due to loss of water; sends to vasa recta
244
thin descending limb
highly perm to water; concentrates filtrate; water moves out and is picked up by vasa recta; 15% is reabsorbed;
245
thick ascending limb
perm to ions; dilutes filtrate; has transporter on luminal side (1 K+, Na+, Cl-); dilutes filtrate
246
Loop of Henle
concentrates urine
247
secretion
removal of toxic substances and drugs
248
PCT
proximal conv tubule; initial segment of the nephron; 70% filtrate is reabsorbed; conc does not change; most transcellular
249
solvent drag
passive movement of water along with Na, K, etc.
250
movement of water is ___ and __ to solute transport
passive; secondary
251
if aff is contracted
RBF decreases Ph decreases GFR decreases
252
if eff is contracted
RBF decreases Ph increases GFR increases
253
average GFR =
125 mL/min
254
filtration barrier allows __ of plasma to enter bowmans space
20%
255
RBF =
RPF\* (1-Hct)
256
kidneys receive ___ of CO
20%
257
as mesangial cells contract, KF ___ and relax, KF \_\_\_
decreases; increases
258
PiGC
increases from aff to eff
259
epithelium of Bowmans Cap
podocytes create filtration slits
260
basal lamina
negatively charged glycoproteins; coarse sieve
261
glomerular cap epithelium
fenstrated; large pores; negative charge; mesengial cells
262
GFR =
kf [(PGC - PBS) - (piGC - piBS)
263
net filtration pressure
PH - pi - Pfluid
264
goodpastures syndrome
autoimmune disorder; antibodies produced against basement membrane; loses negative charge; allows different charges to escape through
265
glomerularnephritis
change in the basement membrane where glomerular cap loses its negative charge; allows different charges to escape through; get through an infection
266
3 layers of filtration of the glomerular capillary
1) endothelial cells (most leaky) 2) basal lamina 3) outer podocytes (least leaky)
267
vascular contraction leading to decrease blood flow to organs of digestion
alpha 1
268
dilation of pupils
alpha 1
269
mydriasis
alpha 1
270
increase BP by vasoconstriction of blood vessels
alpha 1
271
increase sweat by contraction of sweat glands
alpha 1
272
autoreceptors and heteroreceptors activing to turn off NE signaling
alpha 2
273
decrease secretions in digestive tract
alpha 2
274
increase HR by force of contraction
Beta 1
275
directly opposes M2
Beta 1
276
+ iontropic effect
Beta 1
277
kidney regulation of renin secretion; leads to an increase in BP
Beta 1
278
vascular beds
beta 2
279
vasodialation
beta 2
280
skeletal muscle, coronary and lung vessel
beta 2
281
bronchioles; dilation; relaxation
beta 2
282
increased glycogneeisis and glycogeslysis in liver
beta 2
283
increases plasma glucose
beta 2
284
directly opposes alpha 2
beta 2
285
adipose tissue increased lipolysis and thermogeneisis
beta 3
286
urinary bladder relaxation
beta 3
287
decreased HR
M2
288
hyperpolarization of SA node
M2
289
smooth mucle and gland contraction
M3
290
vasodilation
M3
291
increased secretions (SLUD)
M3
292
receptors where NE\>E
alpha 1 and alpha 2
293
receptors with NE or E
Beta 1 and Beta 3
294
receptor with only E
Beta 2
295
alpha 1 is Gs/Gq/Gi??
Gq
296
alpha 2 is Gs/Gq/Gi??
Gi
297
Beta 1 is Gs/Gq/Gi??
Gs
298
Beta 2 is Gs/Gq/Gi??
Gs
299
Beta 3 is Gs/Gq/Gi??
Gs
300
M2 is Gs/Gq/Gi??
Gi
301
M3 is Gs/Gq/Gi??
Gq
