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ENDOCRINE > ENDOCRINE- Physiology > Flashcards

ENDOCRINE- Physiology Flashcards

1
Q

How is Insulin synthesized?

A

Preproinsulin → cleavage of “presignal” → proinsulin (stored in secretory granules) → cleavege of proinsulin → exocytosis of insulin and C peptide equally

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2
Q

Where is Preproinsulin synthesized?

A

In RER

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3
Q

What is increased in Insulinomas?

A

Insulin and C peptide

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4
Q

What do exogenous insulins lack?

A

C peptide

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5
Q

Where is Insuline released from?

A

pancreatic β cells

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6
Q

Which is the mechanism of function of Insulin?

A

Binds insulin receptors, inducing glucose uptake (carrier mediated transport) in insulin dependent tissue and gene transcription

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7
Q

What kind of receptors are insulin receptors?

A

Tyrosine kinase activity

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8
Q

Which are anabolic effects of insulin?

A 
↑ Glucose transport in skeletal muscle and adipose tissue
↑ glycogen synthesis and storage
↑ triglyceride synthesis
↑ Na+ retention (kidneys)
↑ protein synthesis (muscles, proteins)
↑ cellular uptake of K+ and amino acids
↓ glucagon release
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9
Q

What is the purpose of insulin?

A

Move glucose into cells

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10
Q

Between Insulin and glucose, who crosses placenta?

A

Unlike glucose, insulin does not cross placenta

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11
Q

Insulin dependent glucose transporters

A

GLUT-4

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12
Q

Where are GLUT-4 found?

A

Adipose tissue

Skeletal muscle

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13
Q

Insulin independent transporters

A

GLUT-1
GLUT-5
GLUT- 2

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14
Q

Where are GLUT-1 found?

A

RBCs, brain, cornea

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15
Q

GLUT-5 is related to this simple ketonic monosaccharide

A

Fructose

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16
Q

Places where GLUT-5 is found

A

Spermatocytes, GI tract

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17
Q

Characteristic of GLUT-2

A

Bidirectional

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18
Q

Where are GLUT-2 found?

A

β islet cells, liver, kidney, small intestine

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19
Q

During starvation what does the brain uses for metabolism?

A

Ketone bodies

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20
Q

For the metabolism of RBCs what is used? can they use Ketone bodies?

A

RBCs always utilize glucose

They can’t use ketone bodies

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21
Q

Why RBC only utilize glucose?

A

Because they lack mitochondriafor aerobic metabolism

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22
Q

Who is the major regulator of Insulin release?

A

Glucose

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23
Q

Who cause ↑ insulin?

A

GH

β2 agonist

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24
Q

How does GH causes ↑ insulin release?

A

Causes insulin resistance → ↑ insulin release

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25
Q

How is Insulin exocytosis stimulated?

A

Glucose enters β cells → ↑ATP generated from glucose metabolism closes K+ channels and depolarizes β cell membrane →opens voltage gated Ca2+ channels, resulting in Ca2+ influx and stimualting insulin exocytosis

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26
Q

Made by α cells of pancreas

A

Glucagon

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27
Q

Functions of Glucagon

A

Catabolic effects of glucagon:
Glycogenolysis, gluconeogenesis
Lipolysis and cetone production

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28
Q

What stimulates the secretion of Glucagon?

A

Hypoglycemia

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29
Q

Who inhibits Glucagon?

A

Insulin
Hyperglicemia
Somatostatin

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30
Q

Which is the function of CRH?

A

↑ ACTH, MSH, β endorphin

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31
Q

Common condition of ↓ CRH

A

In chronic exogenous steroid use

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32
Q

Effect of Dopamine

A

↓ prolactin

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33
Q

Drugs that can cause galactorrhea? How do they act?

A

Antipsychotics- Dopamine antagonists

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34
Q

Who are increased with GnRH secretion?

A

FSH, LH

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35
Q

Who regulates GnRH?

A

Prolactin

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36
Q

Which situation can suppress Hipothalamic- pituitary axis?

A

Tonic GnRH

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37
Q

What leads to puberty, fertility

A

Pulsatile GnRH

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38
Q

Effect of Prolactin

A

↓ GnRH

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39
Q

Clinical effects of Pituitary prolactinoma

A

Amenorrhea

Osteoporosis

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40
Q

Function of Somatostatin

A

↓ GH, TSH

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41
Q

Which is the clinical use fro Somatostain?

A

Analogs used to treat acromegaly

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42
Q

Function of TRH

A

↑ TSH, prolactin

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43
Q

Where is Prolactin secreted?

A

Mainly by anterior pituitary

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44
Q

Function of Prolactin

A

Stimulates milk production in breast

Inhibits ovulation in females and spermatogenesis in males by inhibiting GnRH synthesis and release

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45
Q

Which clinical manifestation is associated with excessive amounts of prolactin?

A

↓ Libido

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46
Q

Who regulates Prolactin secretion?

A

Prolactin from anterior pituitary is tonically inhibited by dopamine from hypothalamus

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47
Q

Prolactin itself stimulates hypothalamus secretion of…

A

Dopamine, so at the end prolactin in turn inhibits its own secretion by ↑ Dopamine synthesis and secretion from hypothalamus

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48
Q

Which Dopamine product stimulates prolactin secretion?

A

TRH

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49
Q

Which drugs could be use to inhibit prolactin secretion?

A

Dopamine agonists

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50
Q

Dopamine agonist

A

Bromocriptine

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51
Q

Which is the clinicla use for Bromocriptine?

A

Treatment for Prolactinoma

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52
Q

Which drugs stimulate prolactin secretion

A

Dopamine antagonists

Estrogens

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53
Q

Who are Dopamine antagonists?

A

Antipsychotics

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54
Q

Estrogen related situation that stimulate prolactin secretion

A

OCPs

Pregnancy

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55
Q

Growth hormone

A

Somatotropin

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56
Q

Where is Somatotropin secreted?

A

Mainly by anterior pituitary

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57
Q

Function of Somatotropin

A

Stimulates linear growth and muscle mass

↑ insulin resistance

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58
Q

How does Somatotropin stimulates linear growth and muscle mass?

A

Through IGF-1/ somatomedin secretion

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59
Q

How is GH consider?

A

Diabetogenic

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60
Q

Who regulates the secretion of Somatotropin?

A

Released in pulses in response to GHRH

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61
Q

When is GH secretion increased?

A

During exercise and sleep

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62
Q

Who inhibits GH secretion?

A

By Glucose and somatostatin

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63
Q

Which are the possible outcomes of excess secretion of GH (eg. pitiuitary adenomas)?

A

Acromegaly (adults)

Gigantism (children)

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64
Q

Where is Antidiuretic hormone synthesized?

A

Hypothalamus (supraoptic nuclei)

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65
Q

Where is Antidiuretic hormone released?

A

Posterior pituitary

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66
Q

Antidiuretic hormone function

A

Regulates serum osmolarity and blood pressure

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67
Q

Which receptors regulate serum osmolarity?

A

V2 receptors

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68
Q

Which receptors regulate blood pressure stimulated by Antidiuretic hormone?

A

V1 receptors

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69
Q

Which is the primary function of ADH?

A

Serum osmolarity regulation

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70
Q

What is the effect of ADH?

A

↓ serum osmolarity

↑ urine osmolarity

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71
Q

How does ADH regulates Serum osmolarity?

A

Via regulation of aquaporin channel transcription in principal cells of renal collecting duct

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72
Q

When are ADH levels decreased?

A

↓ in central diabetes insipidus

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73
Q

In these situations ADH levels are normal or increased

A

In nephrogenic Diabetes insipidus

Primary polydipsia

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74
Q

What causes Nephrogenic Diabetes insipidus?

A

By mutation in V2 receptor

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75
Q

ADH analog

A

Desmopressin

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76
Q

Treatment for Central Diabetes Insipidus

A

Desmopressin (ADH analog)

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77
Q

Who are the regulators of ADH?

A

Osmoreceptors in hypothalamus (1º)

Hypovolemia (2º)

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78
Q

Who stimulates Cholesterol desmolase in the conversion from Cholesterol to Pregenolone?

A

ACTH

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79
Q

Which drug inhibits Cholesterol desmolase in the conversion from Cholesterol to Pregenolone?

A

Ketoconazole

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80
Q

The conversion from Corticosterone to Aldosterone, which enzime carries this process? and who positively stimulates it?

A 
Aldosterone synthase (enzyme)
Angiotensin II
81
Q

If 17 α hydroxylase is deficient, which are the results?

A

↑ Mineralocorticoids
↓ Cortisol
↓ Sex hormones

82
Q

Labs found in 17 α hydroxylase deficiency

A

Hypertension
Hypovolemia
↓ Dihydrotestosterone

83
Q

Presentation of 17 α hydroxylase deficiency

A

XY: pseudo hermaphroditism (ambiguous genitalia, undescend testis)
XX: lack secondary sexual development

84
Q

Name enzyme deficiency in Adrenal gland

A

17 α hydroxylase
21- hydroxylase
11 β hydroxylase

85
Q

If 21- hydroxylase is deficient, which are the effects?

A

↓ Mineralocorticoids
↓ Cortisol
↑ Sex hormones

86
Q

Which are the expected labs for 21- hydroxylase deficiency?

A

Hyperkalemia
Hypotension
↑ Renin activity
↑ 17-hydroxy- progesterone

87
Q

Which is the most common enzyme deficiency of Adrenal gland?

A

21- hydroxylase deficiency

88
Q

How is 21- hydroxylase deficiency presented during infancy?

A

Salt wasting

89
Q

How is 21- hydroxylase deficiency presented in childhood?

A

Precocious puberty

90
Q

How else is 21- hydroxylase deficiency presented?

A

XX: virilization

91
Q

Which is the effect of 11β hydroxylase?

A

↓ Aldosterone
↑ 11 deoxycorticosterone
↓ Cortisol
↑ Sex hormones

92
Q

What is affected in 11β hydroxylase deficiency?

A

Hypertension (low renin)

93
Q

Presentation of 11β hydroxylase deficiency

A

XX: virilization

94
Q

Which is the common characteristic of all congenital adrenal enzyme deficiencies?

A

By an enlargement of both adrenal glands

95
Q

Why there is enlargement of adrenal glands in congenital adrenal enzyme deficiencies?

A

Due to ↑ ACTH stimulation

96
Q

Why there is ↑ ACTH stimulation in congenital adrenal enzyme deficiencies?

A

Due to ↓ Cortisol in every adrenal enzyme deficiencies

97
Q

Source of Cortisol

A

Adrenal zona fasciculata

98
Q

Function of Cortisol

A 
BIG FIB
↑ Blood pressure
↑ Insulin resistance
↑ Gluconeogenesis, lypolisis, proteolysis
↓ Fibroblast activity
↓ Inflamatory and Immune responses
↓ Bone formation
99
Q

How does Cortisol increases blood pressure?

A

Upregulated α1 receptors on arterioles → ↑ sensitivity to norepinephrine and epinephrine

100
Q

How is Cortisol consider related to insulin?

A

Insulin resitance (diabetogenic)

101
Q

Which metabolic pathways are affected with Cortisol?

A

↑ Gluconeogenesis, lypolisis, proteolysis

102
Q

Why Cortisol causes striae?

A

↓ Fibroblast activity

103
Q

How does Cortisol causes ↓ Inflamatory and Immune responses?

A

Inhibits production of leukotrienes and prostaglandins
Inhibits leukocyte adhesion → Neutrophilia
Blocks histamine release from mast cells
Reduces eosinophils
Blocks IL-2 production

104
Q

How does Cortisol causes Decreased bone formation?

A

↓ Osteoblast activity

105
Q

How is cortisol trnasported in blood?

A

Bound to corticoesteroid binding globulin

106
Q

Why do you need to be very careful when administering cortisol?

A

Can cause reactivation of TB and candidiasis

107
Q

Why Cortisol can cause reactivation of TB and candidiasis?

A

Blocked IL-2 production

108
Q

Who stimulates ACTH release?

A

CRH (hypothalamus)

109
Q

Which is the effect of excess cortisol?

A

↓ CRH, ACTH, and cortisol secretion

110
Q

What does chronic stress induce in Adrenal Cortex?

A

Prolonged Cortisol secretion

111
Q

Source of PTH

A

Chief cells of parathyroid

112
Q

Which is PTH function?

A

↑ bone resorption of Ca2+ and PO4 3-
↑ Kidney reabsorption of Ca2+ in distal convoluted tubule
↓ reabsorption of PO4 3- in proximal convoluted tubule
↑ 1, 25 (OH)2 D3 production by stimulating kidney 1α hydroxylase

113
Q

Alternative name for 1, 25 (OH)2 D3

A

Calcitriol

114
Q

In resume what does PTH does?

A

↑ serum Ca2+
↓ serum (PO4 3-)
↑ urine (PO4 3-)

115
Q

Who is stimulated by PTH in order to produce Calcitriol?

A

Kidney 1α hydroxylase

116
Q

Where are Ca2+ and PO4 3- reabsorption points in kidneys?

A

In distal convoluted tubule

117
Q

Which other effect does PTH has related to Macrophages and NK?

A

↑ production of macrophage colony stimulating factor and RANK-L (receptor of activator of NF-κB ligand)

118
Q

What is the effect of RANK-L on osteoblasts?

A

RANK-L binds RANK on osteoblasts → Osteoclast stimulation and ↑ Ca2+

119
Q

When do we find PTH related peptide (PTHrP)?

A

Commonly increased in malignancy (eg paraneoplastic syndrome)

120
Q

What is the function of PTHrP?

A

Functions like PTH

121
Q

What stimulates regulate PTH?

A

↓ serum Ca2+ → ↑ PTH secretion
↓ serum Mg2+ → ↑ PTH secretion
↓↓ serum Mg2+ → ↓ PTH secretion

122
Q

Common causes of ↓ Mg2+

A

Diarrhea
Aminoglycosides
Diuretics
Alcohol abuse

123
Q

Which is the recombinant human PTH?

A

1-84

124
Q

Which calcium positiveli stimulated four parathyroid gland?

A

Low ionized calcium

125
Q

Name the three forms of Plasma Ca2+

A

Ionized
Bound to albumin
Bound to anions

126
Q

Which kind of Ca2+ can be presented in three forms?

A

Plasma Ca2+

127
Q

Which percentage of Ca2+ is ionized?

A

45%

128
Q

How much Ca2+ is bound to albumin?

A

40%

129
Q

Ca2+ bount to anions

A

15%

130
Q

What stimulate Increases the affinity of Albumin to bind Ca2+?

A

↑ in pH

131
Q

Why increased pH increases the affinity of albumin to bind Ca2+?

A

Albumin is negative charged

132
Q

Clinical manifestations of hypocalcemia

A

Cramps, pain, paresthesias, caspopedal spasm

133
Q

Alternative name for Vitamin D

A

Cholecalciferol

134
Q

How is D3 obtain?

A

From sun exposure in skin

135
Q

How is D2 obtain?

A

Ingested from plants

136
Q

Which Vitamin D is converted in the liver?

A

Both D2 and D3

137
Q

What is the product of Vitamin D2 and D3 after processed in liver?

A

25-OH

138
Q

Which organ metabolizes Vitamin D2 and D3 to become 25-OH?

A

Liver

139
Q

Which is the active form of 25-OH?

A

1, 25 (OH)2

140
Q

Where is 25-OH activated in order to become 1, 25 (OH)2?

A

Kidneys

141
Q

Which is the function of Cholecalciferol?

A

↑ absorption of dietary Ca2+ and PO4 3-

↑ bone resorption → ↑ Ca2+ and PO4 3-

142
Q

Which stimulates cause ↑ 1,25- (OH)2 production?

A

↑ PTH
↓ PO4 3-
↓ Ca2+

143
Q

Who inhibits 1,25 (OH)2 production?

A

1,25 (OH)2 feedback inhibits its own production

144
Q

Which disease is caused by Vitamin D deficiency in kids?

A

Rickets in kids

145
Q

Disease caused by Vitamin D deficiency in adults

A

Osteomalacia

146
Q

Which are the causes of Vitamin deficiency?

A

Malabsorption
↓ sunlight
poor diet
chronic kidney failure

147
Q

Inactive form of Vitamin D

A

24,25 (OH)2 D3

148
Q

What does PTH leads to?

A

↑ Ca2+ reabsorption and ↓ PO4 3- reabsorption in kidneys

149
Q

What does 1,25 (OH)2 leads to?

A

Absorption of both Ca2+ and PO4 3- in the gut

150
Q

Source of Calcitonin

A

Parafolicular cells (C cells) of thyroid

151
Q

Function of Calcitonin

A

↓ bone resorption of Ca2+

152
Q

Who regulates Calcitonin?

A

↑ serum Ca2+ causes calcitonin secretion

153
Q

Who opposes PTH actions?

A

Calcitonin

154
Q

Is calcitonin important in normal Ca2+ homeostasis?

A

No

155
Q

From which endocrine hormones is cAMP the signaling pathway?

A 
FLAT ChAMP
FSH
LH
ACTH
TSH
CRH
hCG
ADH (V2 receptor)
MSH
PTH
calcitonin, GHRH, glucagon
156
Q

cGMP is the signaling pathway from these endocrine hormones

A

ANP, NO (EDRF)

157
Q

IP3 is the signaling pathway from these endocrine hormones

A 
GOAT HAG
GnRH
Oxytocin
ADH (V1 receptor)
TRH
Histamine (H1 receptor)
Angiotensin II
Gastrin
158
Q

Who have Steroid receptor?

A 
VETTT CAP
Vitamin D
Estrogen
Testosterone
T3/T4
Cortisol
Aldosterone
Progesterone
159
Q

These endocrine hormones act in Intrinsic tyrosine kinase

A 
Insulin 
IGF-1
FGF
PDGF
EGF
160
Q

Which pathway is related to intrinsic tyrosine kinase?

A

MAP kinase pathway

161
Q

Receptor associated tyrosine kinase

A

Prolactin, Immunomodulators, GH

acidophiles, cytokines

162
Q

Who are immunomodulators?

A

cytokines, IL-2, IL-6, IL-8, IFN

163
Q

Which pathway is related to receptor associated tyrosune kinase?

A

JAK/STAT pathway

164
Q

How are steroid hormones consider?

A

Lipophilic

165
Q

If steroid hormones are lipophili, how do they circulate in the body?

A

Must circulate bound to specific binding globulins, which increase their solubility

166
Q

What happens if ↑ sex hormone binding globulin in men?

A

Lowers free testosterone→ fynecomastia

167
Q

What would be the result If ↓ sex hormone binding globulin in women?

A

Raises free testosterone → hirsutism

168
Q

Which situation increase sex hormone binding globulin?

A

OCPs

pregnancy

169
Q

Which estrogen levels remain unchanged in OCPs and pregnancy?

A

Free estrogen levels remain unchanged, the ones that change are the ones bind to sex hormone binding globulin

170
Q

What are the thyroid hormones?

A

Iodine containing hormones that control the bodys metabolic rate

171
Q

Where are Thyroid hormones formed?

A

Follicles of thyroid

172
Q

Where is most of T3 formed?

A

In target tissues

173
Q

Function of Thyroid hormones

A 
Bone growth 
CNS maturation
↑ β1 receptors in heart
↑ basal metabolic 
↑ glycigenolysis, gluconeogenesis, lipolysis
174
Q

For Bone growth which hormones have synergism?

A

GH and Thyroid hormones

175
Q

Which is the effect of ↑ β1 receptors in heart caused by thyroid hormones?

A

↑ Cardiac output, HR, Stroke volume, contractility

176
Q

Which channels are activated in order to increase basal Metabolic rate stimulated by Thyroid hormones?

A

Via ↑ Na+/K+-ATPase activity

177
Q

What is the effect of increase basal Metabolic rate Via ↑ Na+/K+-ATPase activity stimulated by Thyroid hormones?

A

↑ O2 consumption, Respiratory rate, body temperature

178
Q

How are thyroid hormones regulated?

A

TRH (hypothalamus) stimulates TSH (pituitary), which stimulates follicular cells

179
Q

How does the negative feedback for Thyroid hormones work?

A

Negative feedback by free T3, T4 to anterior pituitary ↓ sensitivity to TRH

180
Q

Who stimulate follicular cells?

A

Thyroid stimulating immunoglobulins (TSIs)

TSH

181
Q

What is the Wolf Chaikoff effect?

A

Excess iodine temporarily inhibits thyroid peroxidase → ↓ iodine organification → ↓T3/T4 production

182
Q

Excess iodine temporarily inhibits thyroid peroxidase → ↓ iodine organification → ↓T3/T4 production

A

Wolf Chaikoff effect

183
Q

T3 functions

A 
4 B's
Brain maturation
Bone growth
β adrenergic effects
Basal metabolic rate increased
184
Q

Which is the effect of Thyroxine binding globulin?

A

Binds most T3/T4 in blood

185
Q

Which Thyroid hormone is active?

A

Only free hormone

186
Q

When is Thyroxine binding globulin (TBG) decreased?

A

In hepatic failure

187
Q

During these situations Thyroxine binding globulin (TBG) increased

A

Pregnancy

OCP use

188
Q

Which hormone increases Thyroxine binding globulin (TBG)?

A

Estrogen

189
Q

Who is the major thyroid product?

A

T4

190
Q

Where is T4 converted to T3?

A

Peripheral tissue

191
Q

Which enzyme manage the conversion from T4 to T3?

A

5’ deiodinase

192
Q

Which Thyroid hormone binds receptors with greater affinity?

A

T3

193
Q

Which is the function of Peroxidase?

A

Is enzyme responsible for oxidation and organification of iodide as well as coupling of monoiodotyrosine (MIT) and diiodotyrosine (DIT)

194
Q

Who inhibits both peroxidase and 5’ deiodinase?

A

Propylthiouracil

195
Q

Which is the effect of Propylthiouracil?

A

Inhibits both peroxidase and 5’ deiodinase

196
Q

Which is the effect of Methimazole?

A

Inhibits peroxidase only

197
Q

Who inhibits peroxidase only?

A

Methimazole

198
Q

Anions that inhibit Follicular cell production of Thyroid hormones?

A

Perchlorate
Pertechnetate
thiocyanate

199
Q

Who are Antithyroid drugs?

A

Propylthiouracil

Methimazole

ENDOCRINE (4 decks)

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