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Medical Physiology I > Block 7 Exam > Flashcards

Block 7 Exam Flashcards

1
Q

Negative Feedback

A

Goes back to earlier steps in the cascade to turn off hormone release

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2
Q

Positive feedback

A

Promoting a step later in the cascade pathway

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3
Q

Ligand

A

Any molecule that binds to a hormone receptor

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4
Q

Agonist

A

A hormone or synthetic ligand that activates hormone receptor function and signal transduction

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5
Q

Antagonist

A

A naturally occurring or synthetic ligand that prevents hormone receptor activation and signal transduction

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6
Q

EC50

A

Concentration of a hormone that attains half-maximal response

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7
Q

IC50

A

Concentration of an inhibitor at which the biological response is reduced by half

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8
Q

Kd

A

Concentration at which 50% of the binding sites are occupied by a hormone
Dissociation constant

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9
Q

High Kd

A

Low affinity

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10
Q

Low Kd

A

High affinity

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11
Q

Potency

A

Sensitivity

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12
Q

Efficacy

A

Responsiveness

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13
Q

Amino Acid-derived hormones

A 
Dopamine (DA)
Epinephrine
Norepinephrine
Serotonin (5-HT)
Thyroid hormone (T3/T4)
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14
Q

Steroid hormone

A 
Aldosterone
Cortisol
Estradiol (E2)
Progesterone
Testosterone
Vitamin D
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15
Q

Steroid hormone storage pools

A

none

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16
Q

Steroid hormone interaction w/ cell membrane

A

Diffusion through the membrane

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17
Q

Steroid hormone receptor location

A

cytoplasm or nucleus

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18
Q

Steroid hormone action

A

Regulation of gene transcription

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19
Q

Steroid hormone response time

A

Hours to days

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20
Q

Peptide and amine hormones storage pools

A

Secretory vesicles

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21
Q

Peptide and amine hormones interaction w/ cell membrane

A

binding to receptor on cell membrane

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22
Q

Peptide and amine hormones receptor location

A

Cell membrane

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23
Q

Peptide and amine hormones Action

A

Signal transduction cascades affecting a variety of cell processes

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24
Q

Peptide and amine hormones Response time

A

Seconds to minutes

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25
Q

PTH Receptor

A

G-alpha s

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26
Q

ANGII receptor

A

G-alpha i

Gi/Go

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27
Q

AVP, ANGII, TRH receptor

A

G-alpha i

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28
Q

ANP receptor

A

Guanylyl cyclase

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29
Q

Insulin, IGF-1, IGF-2, EGF, PDGF receptor

A

Tyrosine kinase

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30
Q

GH, erythropoietin, LF

A

Tyrosine kinase associated receptor (Jak/Stat)

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31
Q

Possible responses

A 
Transcription independent (immediate)
Transcription dependent (delayed)
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32
Q

Hormones that use GPCR

A

Hypothalamus-derived “releasing” peptides
Anterior pituitary-derived hormones
Posterior pituitary-derived vasopressin and oxytocin
Glucagon
PTH, Calcitonin, and Ca2+
Epinephrine from adrenal medulla

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33
Q

Second messenger molecules

A

Cyclic nucleotides
Lipids and lipid-derived breakdown products
Ca2+ ions

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34
Q

Glucocorticoid receptor

A

GR/GR

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35
Q

Mineralocorticoid receptor

A

MR/MR

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36
Q

Thyroid hormone receptor

A

TR/RXR

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37
Q

Retinoic acid receptor

A

RAR/RXR

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38
Q

Hormones that use binding proteins

A 
Thyroid hormone
Glucocorticoids
Estrogens
Androgens
Vitamin D
Growth Hormones
IGF1 and IGF2
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39
Q

No binding proteins

A 
Catecholamines
PTH
Calcitonin
Glucagon
Insulin
ADH
Renin
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40
Q

GHRH Target cell in anterior pituitary

A

Somatotroph

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41
Q

TRH Target cell in anterior pituitary

A

Thyrotroph

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42
Q

CRH Target cell in anterior pituitary

A

Corticotroph

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43
Q

GnRH Target cell in anterior pituitary

A

Gonadotroph and lactotroph

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44
Q

GHRH hormone released by anterior pituitary

A

GH

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45
Q

TRH hormone released by anterior pituitary

A

TSH

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46
Q

CRH hormone released by anterior pituitary

A

ACTH

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47
Q

GnRH hormone released by anterior pituitary

A

FSH
LH
PRL

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48
Q

Target of GH

A

Stimulates IGF-1 production

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49
Q

Target of TSH

A

Thyroid follicular cells, stimulated to make T3/T4

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50
Q

Target of ACTH

A

Fasiculata and reticularis cells of adrenal cortex, make corticosteroids

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51
Q

Target of FSH

A

Ovarian follicular cells, make estrogens and progestins

Sertoli cells, initiate spermatogenesis

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52
Q

Target of LH

A

Leydig cells, make testosterone

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53
Q

Target of PRL

A

Mammary glands, initiate and maintain milk production

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54
Q

AVP target

A

Collecting duct, increases water permeability

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55
Q

OT target

A

Uterus and breast

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56
Q

Autocrine

A

Cell stimulates self

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57
Q

Paracrine

A

Stimulates cell in close proximity

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58
Q

Juxtacrine

A

Stimulated cells immediately adjacent to the hormone-secreting cell

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59
Q

Endocine

A

Secretes hormone into the blood stream

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60
Q

Hierarchical control

A

Multiple control points

Brain involved

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61
Q

Simple feedback loop

A

No intervention from the brain

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62
Q

What are anterior pituitary hormones responsible for?

A

Reproduction
Growth
Energy metabolism
Stress

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63
Q

What are the posterior pituitary hormones responsible for?

A

Water balance

Uterine contraction

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64
Q

Zona glomerulosa

A

Aldosterone synthesis

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65
Q

Zona Fasciculata

A

Glucocorticoid production

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66
Q

Zona Reticularis

A

Androgen production

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67
Q

Glucocorticoid function

A

Metabolism of carbohydrates and proteins

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68
Q

Mineralocorticoid function

A

Water balance and ECF volume

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69
Q

What is the rate limiting enzyme of adrenal steroid biosynthesis

A

SCC

Side chain cleaving enzyme

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70
Q

Cortisol hormone type

A

Steroid

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71
Q

Cortisol hormone class

A

glucocorticoid

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72
Q

Cortisol precursor

A

Cholesterol

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73
Q

Where is cortisol secreted

A

Fasciculata

Reticularis (minor)

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74
Q

Physiological effects of cortisol

A 
Gluconeogenesis
Proteolysis
Lipolysis
Immunosuppression
Anti-inflammatory activity
CNS differentiation/mood
Differentiation of tissues
Diuretic
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75
Q

Cortisol inhibitors

A

RU-486

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76
Q

Aldosterone hormone type

A

Steroid

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77
Q

Aldosterone hormone class

A

Mineralocorticoid

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78
Q

Aldosterone precursor

A

Cholesterol

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79
Q

Where is Aldosterone secreted

A

Glomerulusa

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80
Q

Aldosterone physiological effects

A

NaCl reabsorption via ENaCs

K+ excretion

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81
Q

Aldosterone inhibitors

A

Spironolactone

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82
Q

DHEA/Androgens hormone type

A

Steroid

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83
Q

DHEA/Androgens Hormone class

A

Sex/Androgen

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84
Q

DHEA/Androgens precursor

A

Cholesterol

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85
Q

Where are DHEA/Androgens secreted

A

Reticularis

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86
Q

DHEA/Androgens physiological effects

A

Masculinization
Protein anabolism
Growth

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87
Q

11 Beta-HSD1 location

A

Liver
Adipocytes
Placenta

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88
Q

11 Beta-HSD1 forward reaction

A

Cortisone => Cortisol

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89
Q

11 Beta-HSD1 reverse reaction

A

Cortisol => Cortisone

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90
Q

11 Beta-HSD2 location

A

Kidney

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91
Q

11 Beta-HSD2 reaction

A

Cortisol => Cortisone ONLY!

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92
Q

When is cortisol secretion highest?

A

8 AM

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93
Q

CRH GPCR

A

G-alpha s => Ca2+ influx

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94
Q

ACTH GPCR

A

G-alpha s => Increased activity of P-450 and synthesis of several enzymes

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95
Q

Major stimulation of aldosterone regulation

A

High serum K+

ANGII

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96
Q

Minor stimulation of aldosterone regulation

A

ACTH

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97
Q

Cushing’s Disease

A

Pituitary adenoma

Too much ACTH production => Excess cortisol production => Decreased CRH production

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98
Q

Cushing’s syndrome

A

Excess cortisol

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99
Q

Addison’s disease

A

Primary adrenal insufficiency

Too little cortisol => Increased levels of ACTH and cortisol

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100
Q

Adrenal adenoma or carcinoma (Cushing’s syndrome)

A

Too much cortisol => Decreased CRH and ACTH

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101
Q

Ectopic CRH (Cushing’s syndrome)

A

Tumor producing CRH => High ACTH => High cortisol

Low endogenous CRH

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102
Q

Primary disease

A

Last gland in HPA axis

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103
Q

Secondary disease

A

Pituitary gland

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104
Q

Tertiary disease

A

Hypothalamus

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105
Q

Cortisol effect on blood sugar

A

Raises

Promotes expression of gluconeogenic enzymes

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106
Q

Primary Hyper aldosteronism

A

Conn’s syndrome
Adrenal carcinoma/hyperplasia
Lead to hypertension

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107
Q

Secondary hyperaldosteronism

A

Hypersecretion of aldosterone due to issue somewhere higher up in axis

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108
Q

What does hypersecretion of cortisol lead to

A

Hyperglycemia
Decreased inflammatory response
Muscle wasting
Increased abdominal adipose tissue

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109
Q

Pseudo-Cushing’s syndromes

A

Idiopathic

Obesity, depression, PCOS, diabetes, ALD

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110
Q

Hypersecretion of androgens can lead to:

A

Secondary male characteristics

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111
Q

Addison’s disease

Primary hypoaldosteronism

A

Insufficient adrenal cortex function

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112
Q

What can Addison’s disease lead to

A 
Hypotension
Weight loss
Muscle weakness
Fatigue
Hyperpigmentation (increased POMC/ACTH)
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113
Q

Secondary hypoaldosteronism

A

Hyporeninemic hypoaldosteronism

Pseudo hypoaldosteronism

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114
Q

Why is norepinephrine not essential for life?

A

Released elsewhere

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115
Q

What enzyme is needed to convert Epi to NE

A

PNMT

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116
Q

A1-AR sensitivity efficacy

A

Epinephrine = Norepinephrine = ISO

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117
Q

A1-AR sensitivity potency

A

Epinephrine = Norepinephrine > ISO

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118
Q

Beta1-AR sensitivity efficacy

A

ISO = Epinephrine = Norepinephrine

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119
Q

Beta1-AR sensitivity potency

A

ISO > Epinephrine = Norepinephrine

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120
Q

Beta2-AR sensitivity efficacy

A

ISO = Epinephrine = Norepinephrine

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121
Q

Beta2-AR sensitivity potency

A

ISO > Epinephrine > Norepinephrine

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122
Q

Catecholamine function

A

Increased myocardial excitability
Increased force and rate of contraction in the heart (beta-1)
Vasoconstriction (alpha-1)

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123
Q

What intermediate is epinephrine converted to

A

Metanephrine

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124
Q

What intermediate is norepinephrine converted to

A

Normetanephrine

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125
Q

What are metanephrine and normetanephrine converted to

A

VMA by MAO

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126
Q

Pheochromocytoma

A

Life-threatening

Tumor of the adrenal medulla

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127
Q

Symptoms associated with sympathetic hypersensitivity

A 
Tachycardia
Headache
Hypertension
Hyperglycemia
Gland enlargement
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128
Q

Environmental factors for obesity

A 
Diet type (low fat vs high fat)
Basal metabolism (UCP and neuropeptides)
Level of hormones, cytokines, adipokines
Quantity of sleep
Microbiota
Infectobesity
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129
Q

What do decreased leptin and adiponectin lead to

A

Increased food intake

Insulin resistance

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130
Q

UCP-1

A

Disrupts proton gradient

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131
Q

Regulation of Lipid Breakdown

A

Lipolysis is regulated by hormone sensitive lipase

Increase in cAMP activates lipase

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132
Q

Where is leptin produced

A

Adipocytes

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133
Q

Where is adiponectin produced

A

Adipocytes

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134
Q

Where is Ghrelin produced

A

Stomach

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135
Q

Where is CCK produced

A

Duodenum

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136
Q

What does leptin act on

A

Hypothalamus

Skeletal muscle

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137
Q

What does adiponectin act on

A

Systemic

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138
Q

What does Ghrelin act on

A

Hypothalamus

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139
Q

What does CCK act on

A

Stomach

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140
Q

Effect of leptin

A

Decrease food intake = feel full

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141
Q

Effect of adiponectin

A

Lowers blood glucose levels

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142
Q

Effect of Ghrelin

A

Promotes food intake

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143
Q

Effect of CCK

A

Decreases food intake

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144
Q

Effect of PYY

A

Decrease food intake

Results in weight loss

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145
Q

Effect of NPT neurons

A

Promotes food intake

Decrease in energy expenditure

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146
Q

Effect of POMC

A

Decreases food intake

Increases energy expenditure

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147
Q

What does PYY act on

A

Hypothalamus

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148
Q

What does NPY neurons act on

A

Hypothalamus

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149
Q

What does POMC act on

A

Hypothalamus

Brainstem

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150
Q

Where is PYY produced

A

Intestines

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151
Q

Where is NPY neurons produced

A

Hypothalamus

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152
Q

Where is POMC produced

A

Hypothalamus

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153
Q

Leptin and resistin

A

Induced by Feeding

Reduced by Fasting

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154
Q

Adiponectin

A

Positively correlated with insulin sensitivity

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155
Q

Plasma glucose fasting

A

60-80mg/dL

3.3-4.4 mM

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156
Q

Plasma glucose Fed

A

100-140 mg/dL

5.6-7.8 mM

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157
Q

What happens in the liver in a fasted state

A

Increase glycogenolysis
Increase Gluconeogenesis
Decrease Glycogen synthesis

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158
Q

What happens in the liver in a fed state

A

Decrease glycogenolysis
Decrease gluconeogenesis
Increase glycogen synthesis

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159
Q

What is released from pancreatic alpha cells

A

Glucagon

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160
Q

What is released from pancreatic beta cells

A

Insulin
Proinsulin
C-peptide
Amylin

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161
Q

What is released from pancreatic delta cells

A

Somatostatin

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162
Q

What is released from pancreatic F cells

A

Pancreatic polypeptide

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163
Q

How much insulin is taken up by the liver

A

50%

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164
Q

Positive modulators of insulin secretion

A 
ATP
Beta agonists (G-alpha-s)
Glucagon (G-alpha-s)
CCK (G-alpha-q)
ACh (G-alpha-q)
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165
Q

Negative modulators of insulin secretion

A

Somatostatin (G-alpha-i)
Galanin (G-alpha-i)
Alpha adrenergic agonists (G-alpha-i)
Exercise

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166
Q

Oral Glucose Tolerance Test

A

Incretins, stimulated by oral glucose, enhance insulin release

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167
Q

Liver GLUT transporter

A

GLUT2

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168
Q

Muscle and adipose tissue GLUT transporter

A

GLUT4

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169
Q

What is the major stimulator of glucagon secretion

A

Amino acids

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170
Q

Glucagon GPCR

A

G-alpha-s

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171
Q

Somatostatin

A

Suppresses insulin, glucagon, and other hormones

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172
Q

Type I diabetes

A

Decrease insulin, preserved glucagon
Ketoacids produced lead to metabolic acidosis
Immune-mediated selective destruction of beta cells

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173
Q

Type II Diabetes

A

Resistant to action of insulin

Beta cells don’t respond to increase in glucose

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174
Q

Thyroxine (T4)

A 
Less active 
More abundant (90%)
Half life = 8 days
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175
Q

Triiodothyronine (T3)

A 
More active
Less abundant (10%)
Half life = 24 hours
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176
Q

Thyroid gland follicle

A

Follicular epithelial cell + Follicular lumen (colloid)

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177
Q

Thyroglobulin

A

Glycoprotein sequestered by follicular cells

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178
Q

TRH GPCR

A

G-alpha-q

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179
Q

TSH GPCR

A

G-alpha s

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180
Q

TSH stimulates

A 
Iodide trapping
Iodide oxidation
Iodination
Conjugation
Endocytosis
Proteolysis
Secretion
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181
Q

Type 1 5’/3’ deiodinases

A

Kidney
Liver
Thyroid
Skeletal muscle

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182
Q

Type 2 5’/3’ deiodinases

A

Pituitary
CNS
Placenta

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183
Q

Intracellular actions TH

A

Increase Na/K ATPase activity
Stimulates mitochondria and respiratory enzymes
Increase O2 consumption
Increase metabolic rate
Increase B-adrenergic receptor responsiveness

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184
Q

Extracellular and whole body response of TH (mainly catabolic)

A 
Increase BMR
Increase cardiac output
Increase ventilation
Increase food intake
Increase gluconeogenesis/glycogenolysis
Proteolysis > Proteogenesis
Lipolysis > Lipogenesis
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185
Q

Hashimoto’s thyroiditis

A

Antibodies against follicular cells and TSH receptors

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186
Q

Cretinism

A

Hypothyroidism during infancy

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187
Q

Cretinism symptoms

A 
Mental retardation
Short stature
Delay in motor development
Coarse hair
Protuberant abdomen
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188
Q

Dwarfism

A

Develop hypothyroidism before fusion of growth plates

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189
Q

Grave’s Disease

A

Autoimmune disorder

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190
Q

Cold nodules

A

Non-functioning

More likely to be malignant

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191
Q

Hot nodules

A

Functional adenomas or carcinoma

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192
Q

Pendrin defect

A

Iodide can’t enter colloid, backflows into bloodstream

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193
Q

Propylthiouracil

A

Block deiodinases to assess T3 levels/sources

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194
Q

GHRH GPCR

A

G-alpha s

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195
Q

GH inhibitors

A

GH
IGF-1 (directly: inhibits somatotrophs)
IGF-1 (indirectly: inhibits GHRH release, stimulates somatostatin)
Somatostatin

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196
Q

Growth hormone and prolactin

A

Same affinity for PRL receptor

PRL has no affinity for GH receptor

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197
Q

GH acute effects

A

Increased lipolysis
Decreased glucose uptake
Increases gluconeogenesis
High doses => Insulin resistance

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198
Q

GH long term effects

A

Stimulate chondrocytes proliferation
Promotes longitudinal bone growth
Stimulates EC matrix formation
Promotes growth in almost every cell of the body

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199
Q

Stimulators of GH release

A 
Exercise
Stress
High protein meals
Fasting
Ghrelin
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200
Q

Ghrelin receptor

A

GH secretagogue receptor 1a (GHSR1a)

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201
Q

Inhibitors of GH release

A

Somatostatin
Obesity
Pregnancy
Hyperglycemia

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202
Q

Somatostatin receptor

A

SSTR

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203
Q

IGF-1

A

Mediates somatic long-term effects of GH

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204
Q

When is IGF-1 highest

A

~12 years of age

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205
Q

When is IGF-2 highest

A

During fetal life

206
Q

Other hormones that increase growth

A

Thyroid hormone
Sex steroids
Insulin

207
Q

Other hormones that decrease growth

A

Glucocorticoids
Lack of T3
IR defect

208
Q

Hormones that regulate body mass

A

Insulin
Glucocorticoid
Adiponectin
Leptin

209
Q

Hormones that regulate linear growth

A 
GH
IGF-1 and IGF-2
Insulin
TH
Glucocorticoids
Androgens
Estrogens
210
Q

Where in the brain do leptin and ghrelin act

A

Arcuate nucleus
Anorexigenic neuron
Orexigenic neuron

211
Q

Gigantism

A

Excess GH before puberty

212
Q

Acromegaly

A

Excess GH after puberty

Growth of bone width and vital organs

213
Q

GH deficiency

A

Pituitary dwarfism

Laron’s syndrome

214
Q

Where is PTH made and stored

A

Chief cells of parathyroids

215
Q

Stimulators of PTH

A

Low EC Ca

Low EC MG

216
Q

Inhibitors of PTH

A 
High EC Mg
High vitamin D
Prolonged low Mg
High plasma Ca
FG23
217
Q

PTH effects on kidney

A

Increases Ca reabsorption
Decreases phosphate reabsorption
Stimulates 1-alpha-hydroxlyase

218
Q

PTH effects on GI

A

Increase Ca reabsorption

Increase phosphate reabsorption

219
Q

Vitamin D effects

A

Stimulates Ca reabsorption
Stimulates phosphate reabsorption (NaPi)
Inhibits PTH gene expression
Inhibits self

220
Q

Vitamin D conversion in the skin

A

7-Dehydrocholesterol => Cholecalciferol (Vitamin D3)

221
Q

Vitamin D conversion in the liver

A

Cholecalciferol (Vitamin D3) => 25-Hydroxycholecalciferol (25-OHD3)

222
Q

Vitamin D conversion in the kidney

A

25-Hydroxycholecalciferol (25-OHD3) => 1,25-(OH)2D3

223
Q

Calcitonin stimulators

A

High EC [Ca2+]

224
Q

Calcitonin inhibitors

A

Low EC [Ca2+]

225
Q

Effects of calcitonin

A

Inhibits osteoclasts and osteocytic osteolysis

G-alpha s in osteoclasts

226
Q

Bone cells with PTH receptors

A

Osteoblasts only

227
Q

What does pulsatile bone release lead to?

A

Bone formation

228
Q

What does continuous PTH release lead to?

A

Bone resorption

229
Q

Vitamin D direct effect

A

Stimulates osteoblasts to release M-CSF to mature osteoblasts
Bone resorption

230
Q

Vitamin D indirect effect

A

Increased P and Ca2+ from kidney and GI promotes bone mineralization

231
Q

Osteocytic osteolysis

A

Transfer of Ca2+ from interior to bone surface

232
Q

Role of OPG

A

Bind RANK ligand so it can’t bind RANK

Inhibits osteoclast from doing its job

233
Q

What does RANK ligand do

A

Increases differentiation and activity of osteoclasts

234
Q

V-type proton pump

A

Acidifies lacuna, dissolves minerals, stimulates lysosomal enzymes

235
Q

Integrins

A

Bind vitronectin; seal

236
Q

Lysosomal enzymes

A

Hydrolyze matrix proteins

237
Q

Lacuna

A

Resorption space

238
Q

Puberty

A

Period of development of secondary sex characteristics

239
Q

LH role in males

A

Testosterone synthesis

240
Q

FSH role in males

A

Spermatogenesis

241
Q

Inhibins in males

A

Inhibit FSH release

242
Q

Estrogens in males

A

Inhibit FSH and GnRH release

243
Q

Testosterone in males

A

Inhibits LH and GnRH release

244
Q

Why can’t sertoli cells produce testosteron

A

Missing 17 alpha hydroxylase

245
Q

Why can’t leydig cells produce estradiol

A

Missing P450 aromatase

246
Q

Effects of testosterone

A

Differentiation of external and internal male genitalia
Spermiogenesis
Erythropoiesis

247
Q

Testosterone clinical assessment

A

Pubertal growth spurt
Deepening voice
Increased muscle mass, growth of skeletal muscle
Growth of hair

248
Q

What does FSH promote in males

A

Androgen Binding Proteins
P450 Aromatase
Growth factors
Inhibins

249
Q

Growth factors in males

A

Support sperm cells, spermatogenesis, and stimulate leydig cells

250
Q

Sperm volume in semen

251
Q

Seminal plasma volume in semen

252
Q

What supplies sperm its energy

253
Q

Male sex act sympathetic innervation

A

T1 to T12

L1 to L3

254
Q

Male sex act parasympathetic innervation

255
Q

Innervation responsible for erection

A

Parasympathetic

256
Q

Innervation responsible for emission

A

Sympathetic

257
Q

What causes ejaculation

A

Spinal cord reflex

258
Q

Ovary cortex

A

Developing follicles
Corpus lutea
Stroma

259
Q

Ovary medulla

A

Blood vessels and stromal elements

260
Q

Menarche

A

Beginning of menstrual cycles

261
Q

Thelarche

A

Breast development

262
Q

Adrenarche

A

Increase in adrenal androgen secretion that occurs around the age of 6-8 years

263
Q

LH receptors in women

A

Theca and granulosacells

264
Q

FSH receptors in women

A

Granulosa cells

265
Q

Luteal phase

A

Negative feedback by estrogen/progesterone

266
Q

Follicular phase

A

Positive feedback by estrogen/progesterone

267
Q

Why can’t theca cells produce estrogen

A

lack aromatase

268
Q

Why can’t granulosa cells produce androgens?

A

Lack 17 alpha hydroxylase

269
Q

Primordial follicles

A

Appear at 6 weeks in the fetus
Complete set @ 6 months after birth
Represents 95% of follicles

270
Q

What hormone is dominant during follicular phase

271
Q

Zona compacta and zona spongiosa

A

Functional layer of the endometrium

272
Q

Zona basalis

A

Layer left behind after menstruation

273
Q

Hormone levels during menopause

A

Ovarian steroid levels fall
Gonadotropin levels rise
High FSH, LH
Low estrogen, progesterone, inhibin

274
Q

Chromaffin cell

A

Modified postganglionic sympathetic neuron

Stimulated by pre-ganglionic acetylcholine

275
Q

What blocks L-type Ca2+ channels in chromaffin cell

A

Nifedipine

276
Q

What blocks N-type Ca2+ channels in chromaffin cell

A

Conotoxin GVIA

277
Q

What blocks P/Q-type Ca2+ channels in chromaffin cell

A

Agatoxin IVA

278
Q

P/Q type Ca2+ channgels

A

Elicits exocytosis by action potentials

279
Q

L-type Ca2+ channels

A

Increases stimulus-secretion efficacy as frequency increases

280
Q

Normal/Basal conditions Sympathetic tone

A

Low rate firing

281
Q

Normal/Basal conditions catecholamine release

282
Q

Normal/Basal conditions response

A

Maintain normal:

  • Blood pressure
  • Heart rate
  • Vascular tone
  • Enteric activity
  • Blood glucose level
283
Q

Sympatho-adrenal stress reflex sympathetic tone

A

Increased

Burst mode firing

284
Q

Sympatho-adrenal stress reflex catecholamine release

285
Q

Sympatho-adrenal stress reflex results

A

Increased:

  • Blood pressure
  • Cardiac output
  • Pulmonary ventilation
  • Blood flow to muscle
  • Glucagon secretion
286
Q

Stress Reflex

A

Heightened splanchnic firing
Nicotinic path desensitized
PACAP released from splanchnic nerve

287
Q

PAC1-R GPCR

A

G-alpha s

G-alpha q

288
Q

PACAP and ACh

A

PACAP release in ACh independent

289
Q

PKC role in PACAP signaling

A

Activates NCX
Stimulate T-type Ca channels
Gap junctions and allows for communication between cells

290
Q

What does PACAP elicited catecholamine secretion need

A 
Extracellular calcium
PLC activity
PKC activity
NCX activity (depolarization)
T-type Ca2+ channel activity
291
Q

Carbon Fiber Electrode

A

Measures actual catecholamine release as a function of time (electrochemistry)

292
Q

Patch Pipette

A

Measures current and capacitance

293
Q

Fast scanning Cyclic Voltammetry

A

Detects Norepinephrine and Epinephrine

294
Q

Electrical Methods used in determining mechanisms of secretion in chromaffin cells

A

Carbon Fiber electrode
Patch Pipette
Fast scanning cyclic voltammetry

295
Q

Fast scanning cyclic voltammetry

A

Found that chromaffin cells release epinephrine only if they contain PNMT

296
Q

PNMT

A

Converts norepinephrine to epinephrine

297
Q

Physiological functions of cortisol

A

Increase blood glucose to supply energy
Maintenance of cardiac contractility
Immunosuppressive/anti-inflammatory

298
Q

Regulation of cortisol levels

A

Diurnal variation in cortisol secretion

299
Q

Assessing Serum cortisol

A

Timing
Protein binding
Episodic secretion

300
Q

Basal secretory rate of cortisol

A

~9-12 mg per day

301
Q

Stress response cortisol release

A

Secretory rate increases up to ~10x normal

302
Q

Stimulation of Aldosterone production

A

Renin-Angiotension system
Hyperkalemia
ACTH

303
Q

Physiological effects of aldosterone

A

Increases Na/H2O reabsorption

Increases K/H secretion

304
Q

Target tissues of aldosterone

A 
Kidney
Sweat glands
Salivary glands
GI tract
Muscle
Bone
305
Q

Cushing’s Syndrome hormone levels

A

Elevated Cortisol
Suppressed ACTH
Suppressed CRH

306
Q

Cushing’s disease hormones

A

Elevated ACTH
Elevated Cortisol
Suppressed CRH

307
Q

Ectopic ACTH hormones

A

Elevated cortisol levels
Elevated ACTH
Suppressed CRH

308
Q

Dexamethasone test normal patient

A

Negative feedback decreases CRH, ACTH, and cortisol

309
Q

Dexamethasone

A

Corticosteroid that mimics cortisol

310
Q

Dexamethasone test adrenal tumor

A

No suppression of cortisol because the tumor itself is causing cortisol hyper-secretion

311
Q

Dexamethasone test cushing’s disease

A

No suppression of cortisol under low dose

Some suppression of cortisol at high dose

312
Q

Dexamethasone test ectopic ACTH

A

No suppression of cortisol because ACTH is produced from ectopic tumor

313
Q

Cushing’s Screening

A

24-hour urinary free cortisol
Very low dose dexamethasone
Salivary cortisol

314
Q

Cushing’s Diagnostic

A

Low and high dose dexamethasone tests
Measure plasma ACTH
Imaging to look for tumor

315
Q

Petrosal Sinus testing use

A

Ectopic ACTH vs Cushing’s disease

316
Q

Petrosal sinus testing interpretation

A

Petrosal/peripheral ACTH is >2:1 = Cushing’s disease

Petrosal/peripheral ACTH is <2:1 = Ectopic ACTH

317
Q

Primary adrenal insufficiency

A

Adrenal gland problem

318
Q

Secondary adrenal insufficiency

A

Pituitary problem

319
Q

Tertiary adrenal insufficiency

A

Hypothalamus problem

320
Q

Adrenal insufficiency results

A 
Decreased blood glucose
Decreased lipolysis
Decreased gluconeogenesis
Lack of energy
Muscular weakness
Inability to handle stress
321
Q

Primary adrenal insufficiency hormones

A

Low cortisol

High CRH and ACTH

322
Q

Primary Adrenal insufficiency causes

A 
Autoimmune
Infection
Cancer
Adrenal hemorrhage
Infiltrative disorders
Congenital adrenal hyperplasia
Drugs
323
Q

ACTH stimulation test

A

Tests between primary and secondary adrenal insufficiency

324
Q

ACTH stimulation test primary adrenal insufficiency

A

Low dose ACTH = no increase in cortisol

High dose ACTH = no increase in cortisol

325
Q

ACTH stimulation test Secondary adrenal insufficiency

A

Low dose ACTH = no increase in cortisol

High dose ACTH = Cortisol will increase

326
Q

Insulin tolerance test

A

Insulin induces hypoglycemia => Cortisol production increases => Glucose back to normal

327
Q

Metyrapone teste

A

Inhibits 11-beta hydroxylase => 11-deoxycortisol accumulates and cortisol decreases => converted to 17-OH corticosteroid by liver => Excreted in urine

328
Q

Primary hyperaldosteronism

A

Conn’s disease

329
Q

Conn’s disease cause

A

adrenal tumor

330
Q

Conn’s disease hormones

A

Low Renin
Low Ang II
High Aldosterone

331
Q

Conn’s disease effects

A

Increased NaCl reabsorption
Increased ECF volume
Increased K secretion
Metabolic alkalosis

332
Q

Secondary hyperaldosteronism causes

A 
Renal artery stenosis
Congestive heart failure
Renal salt wasting
Juxtaglomerular hyperplasia
Liver cirrhosis
333
Q

Secondary hyperaldosteronism hormones

A

Increased renin = RAAS activation

334
Q

Primary adrenal insufficiency

A

Adrenal gland problem

335
Q

Secondary adrenal insufficiency

A

RAAS problem

336
Q

Primary adrenal insufficiency example

A

Addison’s disease

337
Q

Addison’s disease hormones

A

Low aldosterone = RAAS activation

High ACTH

338
Q

Addison’s disease causes

A 
Autoimmune
Infection
Cancer
Adrenal hemorrhage
Infiltrative disorders
Congenital adrenal hyperplasia
339
Q

Pheochromocytoma symptoms

A

Sweating
Palpitations
Headache

340
Q

Pheochromocytoma

A

Excess secretion of catecholamines

341
Q

Metabolic Syndrome Diagnostic criteria

A

Central obesity: waist circumferency >102 cm or 40 inches (male), >88 cm or 35 inches (female)
Dyslipidemia: TG >1.7 mM, 150mg/dL
Dyslipidemia: HDL-C <40mg/dL (male), <50 mg/dL (female)
Blood pressure > 130/85 mmHg (or hypertension medication)
Fasting plasma glucose > 6.1 mM, 110 mg/dL
(Must have 3)

342
Q

Role of 11b-HSD1 in hepatocyte hypothesis

A

Decreased dietary magnesium induces metabolic changes in hepatocytes that favor obesity and promote the onset of metabolic syndrome and complications

343
Q

Mg deficiency findings

A

Decreased hepatic Mg and ATP
Decreased glucose uptake, and accumulation
Increased G6P content being used by H6PD
Increased NADPH production
Increased cortisol production from cortisone
Increased 11-beta-HSd1 expression
Increased intrahepatic triglyceride content and liver steatosis
Increased Nf-kB translocation
Increased TNF-alpha expression
Upregulation of gluconeogenic genes, cholesterol related genes, and FAs- related genes via PPAR-g/SREBP1c

344
Q

GLUT1

A

Resting uptake in most cells

345
Q

GLUT2

A

Liver
Beta islet cells
Kidney
Enterocytes

346
Q

GLUT3

347
Q

GLUT4

A

Muscle
Adipose tissue
Stimulated by phosphorylated AMPK

348
Q

GLUT5

349
Q

SGLT1

A

Enterocytes and S3

2:1 Na:glucose

350
Q

SGLT2

A

S1 and S2 in proximal tubule

1:1 Na:glucose

351
Q

What happens to urine/serum K, Ca, Pi, Mg during polyuria

A

Urine levels of each increase

Serum levels of each decrease

352
Q

Type 1 diabetes symptoms

A

Polyuria, nocturia
Polyphagia
Fatigue
Weight loss

353
Q

Type 1 diabetes

A

Destruction of beta cells

Little to no endogenous production of insulin

354
Q

Type 2 diabetes

A

Beta cells are capable of producing insulin but it’s either insufficient amount or resistance is present

355
Q

Type 1 diabetes onset

356
Q

Type 1 diabetes age of onset

A

Any age, mostly young

357
Q

Type 1 diabetes body type

A

Thin or normal

358
Q

Type 1 diabetes Ketoacidosis

359
Q

Type 1 diabetes autoantibodies

A

Usually present

360
Q

Type 1 diabetes endogenous insulin secretion

A

Low or absent

361
Q

Type 1 diabetes Identical twins

362
Q

Type 1 diabetes prevalence

A

Less common

363
Q

Type 2 diabetes onset

364
Q

Type 2 diabetes age of onset

A

Mostly in adults

365
Q

Type 2 diabetes body type

A

Often obese

366
Q

Type 2 diabetes ketoacidosis

367
Q

Type 2 diabetes Autoantibodies

368
Q

Type 2 diabetes endogenous insulin secretion

A

Normal, decreased, or increased

369
Q

Type 2 diabetes identical twins

370
Q

Type 2 diabetes Prevalence

A

90-95% of US diabetics

371
Q

Type 2 diabetes symptoms

A

Polyphagia
Fatigue
Nocturia

372
Q

Type 2 diabetes risk factors

A 
Familial disposition
Overweight 
>45 years of age
Physically active <3 times/week
Diet
History of gestational diabetes
Race/Ethnicity
373
Q

Type 1 diabetes risk factors

A

Familial disposition
Young age
Viral infections
Environment

374
Q

Normal BMI

375
Q

Overweight BMI

376
Q

Obese BMI

377
Q

Extremely obese BMI

378
Q

Normal HbA1C

379
Q

Pre-diabetic HbA1C

380
Q

Diabetic HbA1C

381
Q

Normal glucose range

A

65-100 mg?dL

3.5-5.5 mM

382
Q

Pre-diabetic fasting glucose

A

> 100 and <126

383
Q

Pre-diabetic post prandial blood glucose

A

> 140 and <200

384
Q

Diabetic Fasting blood glucose

385
Q

Diabetic coma glucose level

A

> 600 mg/dL

386
Q

Diabetic post-prandial or random blood glucose

387
Q

Amount of criteria needed

A

One with symptoms

Two without symptoms

388
Q

Ultra-short-acting insulin

A

Aspart (novolog)
Glulisine (apidra)
Lispro (Humalog)

389
Q

Intermediate-acting insulin

A

NPH

Used overnight, while fasting and between meals

390
Q

Long-acting insulin

A

Detemir (Levemir)
Glargine (Lantus)
Used overnight, while fasting, and between meals

391
Q

Treatment of Type 2 Diabetes

A

Sulfonyl-Urea
Metformin
Thiazolidinedione

392
Q

Rate ADOPT study drugs most to least

A

Sulfonylurea
Metformin
Thiazolidinedione

393
Q

Acute complications of diabetes

A

Hypoglycemia
Diabetic Ketoacidosis (T1DM)
Nonketotic hyperosmolar coma (T2DM)

394
Q

Key features of DKA

A 
Acetone/fruity breath
Kussmaul respirations
Dehydration
Altered LOC
Serum pH <7.3
Metabolic acidosis
395
Q

Key features of Nonketotic hyperosmolar coma

A 
Extreme dehydration
Confusion
Seizures
Hypotension
Tachycardia
Serum pH > 7.3
Urine osmolarity >320 mOsm/L
396
Q

Microvascular Chronic complications of diabetes

A

Retinopathy
Nephropathy
Neuropathy

397
Q

Macrovascular Chronic complications of diabetes

A

Coronary artery disease
Cerebrovascular disease
Peripheral vascular disease

398
Q

Nonvascular Chronic complications of diabetes

A

Gastroparesis
Dermopathy
Infections

399
Q

Pre-eclampsia

A

Hypertension and proteinuria with onset after week 20

Can have long-term sequelae affecting mother and fetus

400
Q

Eclampsia

A

Convulsions or coma unrelated to other cerebral conditions with signs and symptoms of pre-eclampsia
Can occur before or after birth

401
Q

Most common symptoms of pre-eclampsia

A 
Epigastric pain
CNS involvement
Nausea/vomiting
Reduced platelets, elevated livere enzymes
Pulmonary edema
402
Q

Fetal outcomes of pre-eclampsia

A 
Premature birth
Intrauterine growth retardation 
Placental abruption
Oligohydramnios
Non-reassuring fetal surveillance
403
Q

Pathophysiology of pre-eclampsia

A 
Abnormal trophoblast invasion
Poor spiral artery remodeling
Placental ischemia
Increased HIF1aa + placental oxidative stress
Increased inflammatory cytokines
Decreased anti-inflammatory cytokines
Increased sFLT1, decreased PLGF and VEGF
404
Q

Pre-eclampsia risk factors

A 
Nulliparity
Age >40 years
Family history of pre-eclampsia
Woman born small for gestational age
Obesity/gestational diabetes
Multi-fetal gestation
Pre-eclampsia in previous pregnancy
Poor outcome in previous pregnancy
Fetal growth restriction, placenta abruption, fetal death
Preexisting medical or genetic conditions
405
Q

Mild pre-eclampsia blood pressure criteria

A

Systolic >140 and diastolic >90

406
Q

Mild pre-eclampsia proteinuria criteria

A

300mg of proteinuria over 24 hours

407
Q

Severe pre-eclampsia blood pressure criteria

A

Systolic >160
OR
Diastolic >110

408
Q

Severe pre-eclampsia proteinuria criteria

A

> 5g in 24 hours

409
Q

HELLP Syndrome diagnosis

A

Hemolysis
Elevated liver enzymes
Severe anemia unrelated to blood loss
Low platelets

410
Q

Hemolysis criteria HELLP

A

Two of these:
Peripheral smear (schistocytes, burr cells)
Serum bilirubin (>1/2 mg/dL)
Low serum haptoglobin

411
Q

Elevated liver enzymes criteria HELLP

A

AST or ALT > twice upper level of normal

Lactate dehydrogenase > twice upper level of normal

412
Q

Low platelets criteria HELLP

A

<100,000/mm^3

413
Q

Erectile Dysfunction definition

A

Inability of a man to achieve or maintain an erection sufficient for his or his partner’s sexual needs

414
Q

ED epidemiology

A

Experienced by >40% of men
Atherosclerosis accounts for 50-60% of ED cases
35-50% of men with diabetes have ED

415
Q

Prevertebral nerve plexuses for male sex act

A

Celiac
2 mesenteric
2 hypogastric

416
Q

Ganglia of male sex act

A

Spermatic and pelvic

417
Q

Physical causes of ED

A 
Circulatory problems
Nerve/heart disorders
Diabetes
Medications
Smoking and alcohol use
Prostate surgery
Radiation
Colon cancer surgery
Neurological problems
418
Q

Psychological causes of ED

A

Stress
Depression
Performance Anxiety

419
Q

Diagnosis of ED

A 
Duplex ultrasound
Impulse to penile nerves to assess function
Nocturnal penile tumescence
Penile biothesiometry
Dynamic infusion cavernosometry
Corpus cavernosometry
Magnetic resonance angiograpahy
420
Q

Duplex ultrasound

A

Give prostaglandins => Should improve blood flow => stimulate erection

421
Q

Tumescence

A

Engorgement of blood in erectile tissues due to decreased sympathetic tone

422
Q

Nocturnal penile tumescence

A

If night time erections happen = psychological issue

If night time erections don’t happen = non-psychological issue

423
Q

Treatment options for ED

A

Lifestyle changes
Medications
Devices
Surgery

424
Q

Lifestyle changes ED

A 
Exercise
Balance dies
Reduce/quit smoking and alcohol
Lose weight
Reduce stress/anxiety
425
Q

Medications ED

A

Phosphodiesterase 5 inhibitors
Prostaglandins
Papaverine

426
Q

Phosphodiesterase 5 inhibitors ED

A

PDE5 promotes breakdown of cGMP in penile vascular smooth muscle
Inhibitors allow cGMP conentrations to remain high
Sustained erection

427
Q

Prostaglandins ED

A

Local injection

Transurethral cream

428
Q

Papaverine ED

A

Local injection

429
Q

Devices ED

A

Penis pump

430
Q

Surgery ED

A

Prosthesis

Penile implant

431
Q

Sildenafil brand names

A

Viagra

Revatio

432
Q

Vardenafil brand names

A

Levitra

Staxyn

433
Q

Taldalafil brand names

A

Cialis

Adcirca

434
Q

Viagra side effects

A 
Abnormal vision
Constant headache
Loss of hearing
Facial flushing
Nausea
Chest pain
Dizziness
Pain during urination
Nasal congestion
435
Q

Sildenafil half life

436
Q

Vardenafil half life

437
Q

Tadalafil half life

A

17.5 hours

438
Q

Endometriosis definition

A

Cells lining uterus appear and flourish outside of the uterine cavity, most commonly in the ovaries

439
Q

Risk factors of endometriosis

A

Genetics
Environment
Aging

440
Q

Why is endometriosis less common post-menopause?

A

Estrogen levels are lower post-menopause

441
Q

Pathophysiology theories for endometriosis

A

Oxidative stress

Metabolic changes in endometrial tissue

442
Q

Oxidative stress theory Endometriosis

A

8-iso-PGF2a and oxysterols promote oxidative stress

443
Q

Metabolic changes in endometrial tissue theory Endometriosis

A

Increased adherence to peritoneal cells
Dysregulation of matrix metalloproteinases
Changes in VEGF-A, sVEGFR-1/2, angiopoietin-2, and IL-4 promoting vascularization

444
Q

Theories on ectopic endometrial forrmation

A

Retrograde menstruation
Mullerianosis
Coelomic metaplasia
Transplantation

445
Q

Retrograde menstruation Endometriosis

A

Most common theory

Menstruation occurs in reverse direction

446
Q

Mullerianosis Endometriosis

A

Cells with potential to become endometrial tissue are misplaced during embyronic development and organogenesis

447
Q

Coelomic metaplasia Endometriosis

A

Coelomic epithelium is the common ancestor of endometrial and peritoneal cells

448
Q

Transplantation Endometriosis

A

Endometriosis caused by abdominal incisional scars

449
Q

Symptoms of Endometriosis

A

Pelvic pain
Infertility
Constipation
Chronic fatigue

450
Q

Pelvic pain Endometriosis

A

Dysmenorrhea
Dyspareunia
Dysuria

451
Q

Dysmenorrhea

A

Painful menstrual cycle

452
Q

Dyspareunia

A

Pain during sexual intercourse

453
Q

Dysuria

A

Pain during urination

454
Q

Endometriosis complications

A 
Infertility
Scarring
Adhesion
Pelvic cysts
Chocolate cyst of the ovary
Ruptured cyst
Abscess
Peritonitis
Bowel obstruction
455
Q

Endometriosis Diagnosis

A

Laparoscopic biopsy
Ultrasound
MRI

456
Q

Stage 1 Endometriosis

A

Minimal

Findings restricted to only superficial lesions and possibly a few filmy adhesions

457
Q

Stage 2 Endometriosis

A

Mild
Some deep lesions are present in the cul-de-sac
Plus Stage 1

458
Q

Stage 3 Endometriosis

A

Moderate
Presence of endometriomas on the ovary and more adhesions
Plus stage 1 and 2

459
Q

Stage 4 Endometriosis

A

Severe
Large endometriomas, extensive adhesions
Plus Stage 1, 2 and 3

460
Q

Endometriosis Treatment options

A

Hormonal modification
Other medications
Surgery

461
Q

Hormonal modification Endometriosis

A 
Continuous GnRH
Avoid xenoestrogens
Contraceptive patches
Aromatase inhibitors
Danazol
462
Q

Danazol

A

Suppressive steroid with androgen activity

463
Q

Other medications Endometriosis

A

NSAIDs or morphine

Pentoxifylline

464
Q

Pentoxifylline

A

PDE inhibitor to decrease cytokine production

465
Q

Surgery Endometriosis

A

Conservative
Semi-conservative
Neurectomy

466
Q

Conservative surgery Endometriosis

A

Cystectomy and adhesion resection

467
Q

Semi-conservative surgery Endometriosis

A

Less invasive

468
Q

Neurectomy surgery Endometriosis

A

More painful and serious cases

469
Q

Vaginal childbirth and Endometriosis

A

Decreases recurrence

470
Q

Caesarian section and Endometriosis

A

Increases recurrence

471
Q

Somatic cell

A

Any cell in the body except sperm and egg cells

472
Q

Sox9

A

Think males

473
Q

Wnt4

A

Think females

474
Q

What does SRY+ code for

A

TDF (testes determining factor)

475
Q

When does spermatogenesis arrest

A

Primordial germ cell

Just before mitosis

476
Q

When does oogenesis arrest

A 
Prophase I (4n) of Meiosis I
Metaphase II (2n) of Meiosis II
477
Q

Meiosis regulation

A

Retinoic acid => promotes meiosis in females

Degraded in males => prevent meiosis

478
Q

aneuploidy

A

Abnormal number of chromosomes

479
Q

Spermiogenesis

A

Process by which spermatids become mature sperm

480
Q

Spermiation

A

Heads of the spermatozoa are released from the Sertoli cell

481
Q

Primordial follicles

A

Primary oocytes with a single layer of pre-granulosa cells

Complete set is made by 6 months after birth

482
Q

What triggers ovulation

483
Q

What leads to resumption of meiosis I in females

484
Q

What leads to resumption of meiosis II

A

Fertilization

485
Q

Where does the nucleus come from during fertilization

A

Male and female contribute equally

486
Q

Where does the cytoplasm come from during fertilization

487
Q

What is the trigger for reproduction

488
Q

Site of fertilization

A

Fallopian tubes

489
Q

Cause of hCG release

A

Blastocyst cells release within a couple days after implantation has occured

490
Q

hCG role

A

Keeps corpus luteum alive

491
Q

Hatching

A

Degeneration of zona pellucida surrounding the blastocyst

Occurs 6-7 days after ovulation

492
Q

Apposition

A

Blastocyst nears the endometrial lining

493
Q

Adhesion

A

Blastocyst actually adheres to the endometrial lining

494
Q

Invasion

A

Formation of syncytiotrophoblasts which take over maternal blood supply

495
Q

Syncytiotrophoblast

A

Multi-nucleated cell of trophoblasts that have divided and fused

496
Q

Lacuna

A

Blood lakes of maternal blood for nutrients

497
Q

When does the placenta develop

A

14 days after fertilization

498
Q

Hemochorial placenta

A

Maternal blood bathes chorionic villi

499
Q

Molecular size to cross the placenta

500
Q

LH placental hormone

A

Chorionic Gonadotropin (CG) aka hCG

501
Q

GH and prolactin placental hormone

A

Placental lactogen (PL)

502
Q

ACTH placental hormone

A

ACTH-like protein

503
Q

PTH placental hormone

A

PTH-related protein

504
Q

GnRH, TRH, CRH, somatostatin placental hormone

A

Hypothalmic-like releasing hormones

505
Q

Phasic contraction of uterus for birth

A

Tonic clamping to prevent hemorrhage

506
Q

Progesterone in parturition

A

Quiescent, decreases uterine contraction

507
Q

Estrogen in parturition

A

Promote uterine contraction

Primes uterus for labor

508
Q

Prostaglandins & oxytocin in birth

A

Promote uterine contraction in labor

509
Q

PRL role in lactation

A

Milk production

510
Q

Oxytocin role in lactation

A

Milk ejection

511
Q

Why doesn’t lactation happen during pregnancy

A

Estrogen and progesterone are high and block PRL

Medical Physiology I (8 decks)

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