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physiology II > exam 3 > Flashcards

exam 3 Flashcards

1
Q

glucose is reabsorbed using

A

sodium glucose transporters - 2dary active transport

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2
Q

the low affinity SGLT is located in the

A

pars convoluta

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3
Q

the high affinity SGLT is located in the

A

pars recta

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4
Q

where does excess glucose go

A

urine (saturation)

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5
Q

what level of glucose in the plasma will cause glucosuria by increased filtration and decreased reabsorption

A

> 10-15 mmol/L

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6
Q

what is osmotic diuresis

A

water follows glucose in the tubular lumen - more urine is produced

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7
Q

which are the long loops of henle that extend into the inner medulla

A

yuxtamedullary nephrons

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8
Q

long loop nephrons are important for

A

urine concentration

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9
Q

at the apical membrane of the thin descending limb, what is being reabsorbed

A

water via aquaporins

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10
Q

how does the thin descending limb concentrate the tubular fluid

A

no ions are reabsorbed - NaCl remains in the tubular lumen

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11
Q

the ascending limbs are impermeable to

A

water

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12
Q

effect of NaCl being reabsorbed in the ascending limbs without water following

A

tubular fluid in mTAL becomes diluted
renal medulla becomes more concentrated

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13
Q

fx of mTAL

A

dilute tubular fluid
maintain medullary hypertonicity

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14
Q

transporter at apical membrane of mTAL for reabsorption of Na, K, Cl

A

NKCC

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15
Q

in the mTAL, how do Ca, Mg, and Na get reabsorbed

A

paracellular diffusion

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16
Q

how does a diuretic like furosemide work

A

inhibits NKCC - stops reabsorption of Na, Na remains in the lumen and water follows

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17
Q

in the DCT, Ca is reabsorbed via

A

transcellular channels

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18
Q

at the apical membrane in the DCT, Na and Cl are co-transported via

A

NCC

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19
Q

NCC is inhibited by

A

thiazide diuretics

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20
Q

what is reabsorbed in the late DCT and cortical collecting ducts

A

water via ADH dependent aquaporins

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21
Q

how does ADH levels affect water reabsorption in the late DCT and cortical CD

A

high ADH = high water permeability and reabsorption

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22
Q

what is reabsorbed in the inner medullary collecting ducts

A

urea

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23
Q

transport systems at the apical membrane of the CD’s principal cells

A

ENaC - NaCl
ROMK - K

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24
Q

fx of CD’s intercalated cell type A

A

secrete H
reabsorb HCO3
relevant in acidosis

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25
Q

fx of CD’s intercalated cell type B

A

reabsorb H
eliminate HCO3
relevant in alkalosis

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26
Q

main reabsorption site for water

A

PCT

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27
Q

most Na is absorbed in the

A

PCT

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28
Q

effect of angiotensin II on Na

A

inc reabsorption in PT, TAL and DCT

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29
Q

effect of aldosterone on Na

A

stimulates ENaC reabsorption in CD

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30
Q

what metabolic abnormality stimulates aldosterone release

A

hyperkalemia

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31
Q

effect of ADH on Na

A

stimulates NKCC reabsorption in TAL

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32
Q

local inhibitors of Na reabsorption

A

NO
Endothelin-1

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33
Q

systemic inhibitor of aldosterone and renin to inc Na excretion

A

ANP

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34
Q

basolateral Na reabsorption in the PCT via

A

NaK ATPase
Na HCO3 symport

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35
Q

basolateral Na reabsorption in the ascending limbs of Henle’s loop via

A

NaK ATPase

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36
Q

basolateral Na reabsorption in the DCT and CT via

A

NaK ATPase
Na Ca exchanger

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37
Q

fx of calcitonin

A

promotes Ca to bone for bone mineralization

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38
Q

low [Ca] in plasma stimulates

A

inc secretion of PTH
inc calcitriol via the kidneys

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39
Q

effect of vitamin D hormone calcitriol

A

stimulates Ca reabsorption by Ca channels in the intestine

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40
Q

where is 65% of Ca reabsorbed

A

PT

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41
Q

regulation of phosphate reabsorption in the kidney is mediated by

A

PTH

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42
Q

PTH inhibits apical phosphate transporters in the PT which has what effect

A

inc renal excretion of P - dec phosphate

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43
Q

why do hypocalcemic animals usually become hypophosphatemic as well

A

PTH is released during hypocalcemia

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44
Q

reabsorption of Ca in the PCT via

A

paracellular and solvent drag

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45
Q

reabsorption of phosphate in the PCT via

A

Na, PO4 symport

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46
Q

reabsorption of Ca in henle’s loop via

A

paracellular

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47
Q

reabsorption of phosphate in henle’s loop via

A

active and transcellular

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48
Q

apical reabsorption of Ca in DCT and CD via

A

Ca channels

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49
Q

basolateral reabsorption of Ca in DCT and CD via

A

Ca pump
Na, Ca exchanger

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50
Q

places of water reabsorption

A

PT
thin descending limbs of Henle’s loop
CD

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51
Q

which part of the kidney has the highest osmolality

A

medulla

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52
Q

where and how is filtered urea reabsorbed

A

inner medullary collecting ducts
carrier mediated facilitated transport

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53
Q

water in the interstitium is reabsorbed by

A

vasa recta

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54
Q

effect of ADH absence on CD’s water permeability

A

becomes impermeable - diluted urine

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55
Q

water deficit will activate osmoreceptors in the ___ to stimulate ADH secretion

A

hypothalamus

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56
Q

stretch sensitive cells of the bladder communicate with

A

spinal cord to CNS

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57
Q

SNS innervation on the bladder by

A

hypogastric n
NE on B3 receptors

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58
Q

SNS effect on bladder

A

relaxed detrusor m
contracted inner urethral sphincter
inhibition of micturition

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59
Q

PSNS innervation on the bladder by

A

pelvic n
Ach on M3 receptors

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60
Q

PSNS effect on bladder

A

contracted detrusor m
relaxed inner urethral sphincter
activation of micturition

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61
Q

somatic NS innervation on the bladder by

A

pudendal n
Ach on N receptors

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62
Q

somatic NS effect on bladder

A

contraction of external urethral sphincter
continence

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63
Q

cloacal content with urine is transported to the intestine via

A

antiperistaltic contractions

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64
Q

type of nephrons in birds that lack a loop of henle

A

reptillian type

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65
Q

in birds, the amount of blood entering the renal portal system is regulated by

A

renal portal valve - autonomic
sympathetic closed
parasympathetic open

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66
Q

in birds, N is excreted as

A

uric acid

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67
Q

some species of birds have ___ that empty their fluid into the nasal cavity

A

salt glands

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68
Q

water that is trapped in a specific organ and has a physiological purpose

A

transcellular water

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69
Q

principal ions in ECF

A

Na
Cl
HCO3

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70
Q

principal ions in ICF

A

K
Mg
phosphate

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71
Q

effect of ECF osmolality inc

A

hypertonic to ICF
water moves from cell to ECF

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72
Q

effect of ECF osmolality dec

A

hypotonic to ICF
water moves from ECF into cell

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73
Q

hormones that regulate fluid imbalances

A

ADH
aldosterone
ANP

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74
Q

as osmolarity inc, ADH release ____

A

increases

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75
Q

effects of ADH

A

stimulates water reabsorption - urine concentration
stimulates thirst center to inc intake

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76
Q

aldosterone is secreted by

A

adrenal cortex

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77
Q

role of aldosterone

A

determining rate of Na absorption in the kidneys

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78
Q

T or F: aldosterone secretion is influenced by Na concentration in plasma

A

F

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79
Q

what situations cause release of aldosterone

A

activation of RAAS
inc K ECF levels

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80
Q

ANP is released by

A

cardiac muscle cells

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81
Q

how does ANP reduce blood volume and BP
1. inc water loss
2. reducing thirst
3. blocking release of ADH
4. ____

A

stimulate peripheral vasodilation

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82
Q

causes of intracellular edema
1. depression of metabolic systems of cells
2. reduced nutrition of cells - ischemia
3. inflammation - inc vasc. permability
4. _____

A

hyponatremia

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83
Q

causes of extracellular edema
1. abnormal leakage of fluid from plasma
2. inc capillary pressure
3. dec plasma proteins
4. inc capillary permeability
5. _____

A

blockage of lymph return

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84
Q

carbonic anhydrase diuretics block

A

Na and HCO3 reabsorption

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85
Q

loop diurectics block

A

NKCC in TAL

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86
Q

thiazide diuretics block

A

Na Cl symport in DT

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87
Q

aldosterone antagonists diuretics block

A

ENaC - Na channel

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88
Q

amiloride diuretics block

A

Na channel directly in CD

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89
Q

how do loop diuretics keep the GFR

A

high - favors high diuresis

90
Q

effect of diuretics

A

dec NaCl reabsorption
dec H2O reabsorption
dec ECF volume

91
Q

secondary effects of loop diuretics

A

negatively impact reabsorption of Ca and Mg in TAL

92
Q

secondary effects of loop and thiazide diuretics

A

inc K excretion in CD - hypokalemia

93
Q

K sparing diuretics

A

aldosterone antagonists
amilorides

94
Q

disease caused by a lack of ADH synthesis in the hypothalamus and release from posterior pituitary gland

A

diabetes insipidus centralis

95
Q

disease when ADH is produced but cannot act in the kidney

A

diabetes insipidus renalis

96
Q

what type of solution causes a cell to swell

A

hypotonic

97
Q

effect of hypertonic dehydration

A

inc osmolality in ECF
water leaves cells

98
Q

effect of isotonic dehydration

A

hypovolemia

99
Q

effect of hypotonic dehydration

A

dec osmolality in ECF
water gets into cells - swells

100
Q

effect of hypertonic overhydration - gain of electrolytes exceeds gain of water

A

inc osmolality of ECF

101
Q

effect of isotonic overhydration

A

hypervolemia

102
Q

effect of hypotonic overhydration - water intoxication - gain of water, no gain of electrolytes

A

dec ECF osmolality

103
Q

where is the thirst center located

A

hypothalamus

104
Q

thirst center is stimulated by
1. dec blood volume
2. dec BP
3. high angiotensin II levels
4. dry mouth
5. ___

A

high plasma osmolarity

105
Q

normal physiological pH

A

approx. 7.4

106
Q

normal body production of ___ can acidify the pH

A

CO2
metabolism of proteins
keto acids - fats
lactic acid - incomplete oxidation of glucose

107
Q

3 systems that help maintain the acid base balance

A

buffers
respiratory system
kidney

108
Q

which system reacts to small changes in pH, is fast acting and reversibly binds/releases H

A

buffers

109
Q

which system reacts to large changes in pH, is slow acting and eliminates/retains H

A

kidney

110
Q

what are the 3 buffers

A

bicarbonate
sodium
ammonia

111
Q

the extent to which a weak acid dissociates and the resultant concentrations of H, base and un-dissociated acid

A

Ka

112
Q

what does a higher Ka mean

A

the chemical can easily release H and make more acidic

113
Q

the pH at which there are equal amounts of the weak acid and its conjugate base

A

pKa

114
Q

what does a high pKa indicate

A

stronger ability to hold H; higher pH

115
Q

requirements for an effective buffer

A

pKa within +/- 1 pH unit of the solution
sufficiently plentiful

116
Q

optimal pKa for the body

A

6.4-8.4

117
Q

a ratio of ___ HCO3:H2CO3 is required for effective buffering

A

20:1

118
Q

the carboxyl group of a protein buffer (donates or binds) H

A

donates

119
Q

the amino group of a protein buffer (donates or binds) H

A

binds

120
Q

how does the lung adjust body pH

A

regulation of respiratory rate

121
Q

limitation of the respiratory system as a pH regulator is ___

A

the body produces fixed acids, metabolic acids or nonvolatile acids which cannot be eliminated by respiration

122
Q

urinary solutes that are filtered in base forms at the glomeruli and bind secreted protons in the tubule fluid

A

titratable acids

123
Q

most important acid secreted by the kidney which is generated in the PT and is not filtered at the glomeruli as a base form

A

ammonium

124
Q

T or F: plasma bicarbonate is freely filtered, meaning all of the filtered HCO3 is reabsorbed

A

T

125
Q

____ is essential for acid secretion

A

renal portal system

126
Q

how are urinary titratable acids generated

A

renal secretes H ions that bind to filtered buffers

127
Q

which regions of the nephron largely reabsorb HCO3 and secrete H, but do not significantly change the pH of the tubular fluid

A

PT and TAL

128
Q

which hormones regulate H excretion and HCO3 reabsorption at the PT and TAL

A

angiotensin II
glucocorticoid
PTH

129
Q

which part of the nephron excretes urine with a pH different from plasma due to the intercalated cells

A

CD

130
Q

which intercalated cell of the CD has a large apical surface and extensive membrane folds

A

type A

131
Q

intercalated type A cells secrete

A

acid

132
Q

H ATPase is stimulated by

A

angiotensin II
aldosterone
endothelin

133
Q

acid secretion by type A cells is regulated by

A

H ATPase and KAE1

134
Q

effect of acidosis on type A cells

A

inc acid secretion

135
Q

intercalated type B cells secrete

A

HCO3

136
Q

base secretion by type B cells is stimulated by

A

dietary restriction of NaCl or Cl
aldosterone analogs
angiotensin II

137
Q

ammonium (inc or dec) when acid secretion is upregulated

A

increases

138
Q

effect of ammonium being reabsorbed in the TAL

A

inc ammonium concentration in the medullary interstitium

139
Q

where are ammonium ions excreted

A

CD

140
Q

in which species are basal urinary ammonia excretion rates low and do not inc ammonia secretion during acidosis

A

rabbits

141
Q

excess accumulation of CO2

A

respiratory acidosis

142
Q

excess elimination of CO2

A

respiratory alkalosis

143
Q

excess accumulation of fixed acids or elimination of buffer bases

A

metabolic acidosis

144
Q

excess elimination of fixed acids or accumulation of buffer bases

A

metabolic alkalosis

145
Q

causes of respiratory acidosis include:
1. damage of resp. control centers
2. resp. pump injury
3. _____

A

severe resp. dz that obstructs airways or stiffens the lungs

146
Q

respiratory acidosis: compensatory changes by bicarb and non-bicarb buffers

A

inc HCO3

147
Q

respiratory acidosis: compensatory changes by kidney

A

inc H and NH3 secretion
eliminate H in the urine
generate new HCO3

148
Q

treatment of respiratory acidosis

A

restore alveolar ventilation

149
Q

causes of respiratory alkalosis include:
1. stimulation of chemoreceptors by hypoxemia
2. over use of a ventilator
3. ____

A

stimulation of intrapulmonary receptors by lung injury

150
Q

resp. alkalosis: compensatory changes by bicarb and non-bicarb buffers

A

dec HCO3

151
Q

resp. alkalosis: compensatory changes by kidney

A

inc elimination of HCO3 by dec secretion of H and NH3

152
Q

treatment of respiratory alkalosis

A

stop alveolar hyperventilation

153
Q

causes of metabolic acidosis include:
1. inc in H production
2. failure of H elimination by kidney
3. ___

A

loss of buffer base - diarrhea

154
Q

metabolic acidosis: compensatory respiratory changes

A

dec PCO2 by inc resp. rate

155
Q

treatment of metabolic acidosis

A

IV fluid that contains buffers
restoration of depleted base by kidney

156
Q

causes of metabolic alkalosis include loss of H by:
1. vomiting
2. right sided displaced abomasum
3. ____

A

hypokalemia - inc H secretion

157
Q

metabolic alkalosis: compensatory respiratory changes

A

inc PCO2 by dec resp. rate

158
Q

treatment of metabolic alkalosis

A

IV fluids w saline, K, HCl
cure the dz that caused it

159
Q

what are the characteristics of hormones

A

amplification - sm. amt. = sig. effect
slow action

160
Q

where are protein hormones synthesized

A

rough ER

161
Q

where are protein hormones stored

A

secretory vesicles

162
Q

what are steroid hormones synthesized from

A

cholesterol

163
Q

where is cholesterol synthesized

A

liver

164
Q

how is cholesterol stored within the cell

A

in a lipid droplet in ester form

165
Q

T or F: steroid hormones are stored

A

F - immediately secreted

166
Q

how are protein hormones transported in the plasma; why

A

in dissolved form - hydrophilic

167
Q

how are steroid hormones transported in the plasma; why

A

with binding proteins - hydrophobic

168
Q

how must hormones be in order to penetrate a target cell and elicit biological activity

A

free or unbound

169
Q

how are steroids metabolized

A

reduced then conjugated with sulfates and glucuronides

170
Q

T or F: steroids are excreted in the urine

A

T

171
Q

where does steroid metabolism occur

A

mainly liver

172
Q

how are protein hormones metabolized

A

reduction of disulfide bonds
cleaved by peptidases

173
Q

where is the receptor located for hydrophobic steroid hormones

A

cytoplasm or nucleus of target cells

174
Q

where is the receptor located for hydrophilic protein and peptide hormones

A

plasma membrane of target cell

175
Q

what are the 3 characteristics of hormone receptor interactions

A

specific
high affinity
reversible

176
Q

what can occur because of reversible binding between a hormone and its receptor

A

termination of hormone action by dissociation

177
Q

what is another way that hormone action can be terminated

A

degraded or recycled by endocytosis

178
Q

hydrophilic hormones require a

A

second messenger

179
Q

2nd messengers for hydrophilic hormones include

A

cAMP
IP3
DAG
Ca

180
Q

how is hormone production regulated

A

feedback regulation
circadian rhythms

181
Q

before ovulation, is LH (positively or negatively) feedback regulated

A

positive

182
Q

after ovulation is LH (positively or negatively) feedback regulated

A

negative

183
Q

what are the 6 major hormones secreted by the anterior pituitary gland and regulated by the hypothalamus

A

FSH
LH
TSH
GH
PRL (prolactin)
ACTH (adrenocorticotropic hormone)

184
Q

of the 6 ant. pit. hormones, which are glycoproteins

A

FSH
LH
TSH

185
Q

of the 6 ant. pit. hormones, which are somatomammotropins

A

GH
PRL

186
Q

of the 6 ant. pit. hormones, which is proopiomelanocortin

A

ACTH

187
Q

which hormone released by the hypothalamus regulates FSH and LH

A

gonadotropin-releasing hormone (GnRH)

188
Q

FSH and LH target organs

A

testes and ovaries

189
Q

TSH target organ

A

thyroid

190
Q

hypothalamic hormones that regulate TSH

A

thyrotropin releasing hormone (+)
dopamine (-)

191
Q

growth hormone target organ

A

liver

192
Q

hypothalamic hormones that regulate GH

A

growth hormone releasing hormone (+)
growth hormone inhibiting hormone (somatostatin) (-)

193
Q

prolactin target organ

A

mammary glands

194
Q

hypothalamic hormones that regulate PRL

A

prolactin releasing factor (+)
dopamine (-)

195
Q

ACTH target organ

A

adrenal glands

196
Q

hypothalamic hormone that regulates ACTH

A

corticotropin releasing hormone

197
Q

pituitary dwarfism is an autosomal recessive disorder that can occur in

A

german shepherds

198
Q

acromegaly (hypersomatotropism) can occur in older cats due to

A

pituitary adenoma or hyperplasia

199
Q

major hormones produced in the hypothalamus and released in the posterior pituitary gland

A

vasopressin - ADH
oxytocin

200
Q

how is vasopressin synthesized

A

in cell bodies w/in the hypothalamus
carried by axon flow to the posterior lobe

201
Q

stimuli for vasopressin secretion

A

dec blood volume
inc blood osmolality

202
Q

fx and location of vasopressin receptor 2

A

kidney
retain water

203
Q

fx and location of vasopressin receptor 1

A

blood vessels
vasoconstriction

204
Q

stimuli for oxytocin secretion

A

stretch of cervix in late pregnancy
sucking at nipple

205
Q

fx of oxtocin

A

contraction of sm. m.
myoepithelial cell contraction and milk ejection

206
Q

hormones produced by the thyroid gland

A

T3, T4
calcitonin

207
Q

fx of T3/T4

A

inc metabolic rate

208
Q

what 2 molecules are important for synthesis of thyroid hormone

A

iodine
tyrosine

209
Q

thyroid hormone synthesis is regulated by

A

hypothalamus (TRH)
anterior pituitary hormone (TSH)

210
Q

T3 and T4 are (lipid soluble or lipid insoluble)

A

lipid soluble

211
Q

T3 and T4 are transported in blood with

A

plasma proteins

212
Q

T4 is transformed into T3 in the tissues (liver, kidney, muscle) by what enzyme

A

5’-monodeiodenase

213
Q

which plasma protein is specific for T4/T3, high affinity, low capacity, and is in all domestic animals except cats

A

thyroxine binding protein

214
Q

which plasma protein is specific for T4/T3 and has intermediate capacity between TBG and albumin

A

thyroxine binding prealbumin

215
Q

the 3 mechanisms of thyroid metabolism are deiodination, formation of hormone conjugates and modification of the alanine moiety of the thyronine - which is the main mechanism

A

deiodination

216
Q

where does the formation of hormone conjugates occur

A

liver
kidney

217
Q

how do T3 and T4 execute their functions on a cell

A

bind intracellular receptors

218
Q

low thyroid hormone, common in dogs

A

hypothyroidism

219
Q

pathological findings of hypothyroidism
1. anemia
2. hypercholesterolemia
3. hypernatremia
4. ____

A

inc serum creatine phosphokinase

220
Q

pathological findings of hyperthyroidism
1. inc BUN - catabolism of muscle
2. inc GFR
3. inc ALT and AST (liver hypermetabolism)
4. dec cholesterol
5. ____

A

inc circulating catecholamine

physiology II (4 decks)

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