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GBA Physiology > Endocrine Physiology - Theoretical Questions (no Repro.) > Flashcards

Endocrine Physiology - Theoretical Questions (no Repro.) Flashcards

1
Q

What are the Hormones released by the PVN? to where? What are they Related to or Releasing?

A

CRH and TRH to Adenohypophysis Basophil cells for POMC and TSH.
Oxytocin to neurohypophysis - Suckling, Birth, Ejaculation.

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2
Q

What is the Hormone released by the SON? to where? What regulates its release?

A

ADH to neurohypophysis.

Blood volume↓, Osmolarity↑, Pain↑, Ethanol↓, AT-II↑

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3
Q

TRH - What elevates its release?

A

Pregnancy and Low temperature

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4
Q

CRH - What elevates its release?

A

Fever, stress and Hypoglycemia

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5
Q

What gets released from the Preoptic Nucleus? to where?

A

GnRH to the Adenohypophysis Basophil cells

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6
Q

What gets released from the Arcuate Nucleus? to where?

A

GHRH and PIH to Adenohypophysis Acidophil cells

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7
Q

What are the passages for Hormones or Hormone releasing factors in the Hypothalamo-Hypophyseal axis?

A

1) PVN+SON to Hypothalamo-Hypophyseal tract to Neurohypophysis Herring bodies for Peptide storage.
2) PVN, Preoptic and Arcuate to Hypophyseal Portal arteries to Acidophils and Basophils of Adenohypophysis.

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8
Q

What are the Hormones of the GH/PRL family? which cells secrete them?

A

Growth Hormone - Somatotroph cell
Prolactin - Lactotroph cells
Human chorionic Somatotropin and (p)GH - Placenta

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9
Q

What are the Hormones of the Glycoprotein family? which cells secrete them?

A

Thyroid Stimulating Hormone - Thyrotropic Cells
Follicle Stimulating Hormone - Gonadotropic Cells
Lutenizing Hormone - Gonadotropic Cells
Human Chorionic Gonadotropin - Placenta

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10
Q

What are the products coming from the Cleavage of Proopiomelanocortin? which cells secrete them?

A

Beta-Endorphin, melanocyte-stimulating Hormone and Adrenocorticotropic Hormone. POMC originates from Corticotropic Cells.

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11
Q

Hormone 4 important parts of definition:

A

1) Secreted by Glands (ADH and Oxytocin are exception)
2) Carried in blood
3) Distant receptor
4) Small amount creates a large effect (10^-6 - 10^-12)

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12
Q

What is the effect of Somatostatin on GH and TSH?

A

It has a Gi receptor of the Thyrotroph and Somatotroph cells. Leads to inhibition of their release.

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13
Q

What is the effect of Dopamine on the Release of PRL?

What are the general factors Stimulating its release?

A

It inhibits it by Gi (D2R) mechanism. Dopamin in this regard is called PIH.
VIP, TRH and Baby Suckling all cause release.

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14
Q

What are the factors causing GH NOT to be released?

How?

A

1) Somatostatin from PVN inhibits Somatotroph release
2) IGF-1 a - Negative Feedback to Somatotroph cell(GH)
3) IGF-1 a - Negative Feedback to Arcuate Nucleus(GHRH)
4) IGF-1 a - Negative Feedback to PVN to release SST

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15
Q

What other Hormone causes release of GH? (other than GHRH)

A

Ghrelin produced in stomach (hunger) causes Gq activation of GH.

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16
Q

What are the non-Hormonal Factors are causing release of GH?

A

1) Hypoglycemia
2) Fasting, Extreme exercise, Stress
3) Alpha-2 Adrenergic Stimulation (Gi but activates)
4) Basic AA
5) Sleep

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17
Q

Mechanism of GH activity:

A

Associated Tyrosine Kinase Receptor:

JAK2-(P) - STAT5-(P) - expression of Somatomedins

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18
Q

What are the direct effects of GH? (Acute)

A

1) Glucagon↑ - [Glucose]↑
2) Lipolysis↑ - [FFA]↑
3) Muscle AA Uptake↑ - Protein Synthesis↑
4) Somatomedin production - IGF-1↑

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19
Q

What are the Indirect effects of GH? (Chronic = IGF-1↑)

A

1) Bone length growth
2) Chondrocyte Differentiation
3) Collagen Synthesis
4) Organ growth

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20
Q

What prevents desensitization of GH receptors?

What is the mechanism?

A

Pulsatile secretion of GH - every 2 hours

Circadian secretion - Largest 1hr after sleep

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21
Q

What are the consequences of overproduction of GH in Childhood?

A

Gigantism

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22
Q

What are the consequences of overproduction of GH in Adults?

A

Acromegaly

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23
Q

What are the consequences of deficiency of GH in Childhood?

A

Pituitary Dwarfism

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24
Q

What are examples for Positive feedback?

A

1) During Ovulation Estradiol from ovary causes Increase in GnRH allowing more FSH .
2) Thrombin activating factors V, VIII, XI leading to Prothrombinase formation.

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25
Q

What are basic definitions of Primary, Secondary and Tertiary Hormone Disorders?

A

Primary - Originates in Hypothalamus
Secondary- Originates in Hypophysis
Tertiary - Originates in the Gland

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26
Q

What are the layers of the adrenal cortex?

Which hormones are produced in each level?

A

Outer) Z. Glomerulosa - Mineralocorticoids - Aldosterone
Middle) Z. Fasciculata - Glucocorticoids - Cortisol
Inner) Z. Reticularis- Androgens- DHEAS and Androstenedione.

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27
Q

What is the rate limiting step of the synthesis of Steroid hormones? Catalyzed by? What is required for it?

A

1) Cholesterol to Pregnenolone.
2) CYP11A1 (SCC) in the mitochondria.
3) ACTH activates StAR protein for entrance of Cholesterol to mitochondria.

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28
Q

What causes the release of Steroid hormones from storage?

A

Cholesterol is the Stored form (Lipid droplets) that is activated by entering the Mitochondria and allowing for conversion to Steroids which are released as formed by Simple diffusion to blood (Hydrophobic).

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29
Q

What are the CYP numbers for the formation of Aldosterone?

A

(SCC - 3HSD )- 21 - 11

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30
Q

What are the CYP numbers for the formation of Cortisol?

A

(SCC) - 17- (3HSD) - 21 - 11

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31
Q

What are the CYP numbers for the formation of DHEA?

A

SCC - 17- 17 (Lyase)

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32
Q

What is the other site of formation pathway of Steroids? (with than the mitochondria)

A

SER

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33
Q

What are the activators of the formation of Aldosterone?How?

-Inhibitor?

A

1) ACTH - Gs
2) AT-II - AT1R Gq
3) [K+]↑ - T type VGCC depole.
- Inhibitor: ANP - Gi

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34
Q

What happens to the DHEAS in the Gonads?

A

Gets converted to Estrogen by Aromatase

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35
Q

What are the forms for Cortisol in blood?

What is the Amount range?

A
  • 90% Bound to CBG
  • 7% Bound to Albumin
  • 3% Free
    Around the mM scale. ([Cortisol] > [Aldosterone])
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36
Q

What are the forms for Aldosterone in blood?

What is the Amount range?

A
  • 60% Bound to CBG and Albumin
  • 40% free
    Around the nM scale. ([Cortisol] > [Aldosterone])
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37
Q

What are the corticosteroid receptors? What is the basis for the overlap in the actions of Cortisol and Aldosterone?

A 
Type I (MR) - Equal affinity to Cortisol and Aldosterone  
Type II (GR) - Affinity only to Cortisol
([Cortisol] > [Aldosterone])
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38
Q

How is the mineralocorticoid effect of Cortisol is prevented in the Kidney and Intestines? Where is the opposite effect happening and how?

A

11beta-HSD2 - Converts Cortisol to the Inactive Cortisone.

In the Liver, Adipose and Brain the 11beta-HSD1 does the opposite and converts it back to Cortisol.

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39
Q

4 Major effects of Aldosterone:
Acting on Principle cells, Alpha intercalated cells of DCT,
Exocrine glands and Colon Epithelium.

A

1) Na/K ATPase↑ - Activity and Induction
2) Na Reabsorption ↑ - ENaC Induction
3) K/H Exchanger- Excretion of K↑
4) Increase in ROMK - Excretion of K↑

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40
Q

What are all the mechanisms of the upregulation of Aldosterone do? How? (Cellular Events)

A

Calcium signal - Directly from Gq or from PKA (Gs)

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41
Q

Cortisol Metabolic effects:

A

Carbohydrates - Gluconeogensis↑, GLUT
Proteins - Reduces synthesis in Muscle therefore AA↑but Protein synthesis in liver↑
Lipids - Lipolysis↑

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42
Q

Cortisol CNS and Immune effects:

A

CNS: Memory - Acute=Positive, Chronic = Negative

Immune : Suppressing and Anti-Inflammatory (Increasing the resolution of targets)

43
Q

Cortisol Stomach and Kidney effects:

A

Stomach - HCl↑

Kidney - GFR↑, Water Permeability of Collecting Duct↓

44
Q

Cortisol Sympathetic NS effects:

A

Permissive Effects - Alpha-1 and Beta-1↑

Adrenal Medulla - NE conversion to Epi ↑

45
Q

Cortisol Connective tissue and Bone effects:

A

CT -Collagen Synthesis ↑(Stria) +Fibroblast Proliferation↑

Bone - RANKL Expression ↑ - Osteoclast↑ - [Ca]↑

46
Q

Cortisol Fetal, Growth and Pregnancy effects:

A

Adenohypophysis - GH release↑
Liver - IGF-1↓
Fetal development - CNS, Lungs surfactant and more..
Therefore delivery of baby is initiated by a baby GC.

47
Q

Positive indirect regulators of Cortisol secretion: How?

ACTH is the only direct one

A

Stress - CRH release
Circadian Rhythm - CRH release (Mostly in Morning)
ADH (V1R) - ACTH Release

48
Q

Negative indirect regulators of Cortisol secretion: How?

ACTH is the only direct one

A

Cortisol - Negative Feedback for ACTH and CRH

Also effects of Cortisol on the body relieve stress and therefore remove stress.

49
Q

What is the cause of Cushing syndrome?
What is the cause of Cushing Disease?
Name a symptom that differentiates them?

A

Cushing syndrome - Cortisol or Synthetic Steroids↑

Cushing Disease - ACTH↑, Pigmentation (POMC) differentiates between them.

50
Q

What is the cause of Adrenogenital syndrome?

How is it differentiated from CYP11 deficiency ?

A

CYP21 Deficiency - Low GC and MC - leads to ACTH↑ and therefore DHEA↑
CYP11 Deficiency causes DOC↑ and therefore MAP↑

51
Q

Addison Disease? What is elevated?

A

Adrenal cortex Insufficiency

ACTH↑ - No negative feedback

52
Q

Cons Disease:

A

Hyperaldosteronism

Na↑ and MAP↑

53
Q

What is the Problem in Using Corticosteroids as a treatment for the long term?

A

Negative feedback mechanism causes the eventual Atrophy of Z. Fasciculata and Inability for Natural secretion of Cortisol later in life.

54
Q

What is the negative feedback mechanism specific for Aldosterone effects?

A

Aldosterone Escape:
Aldosterone↑ - Na↑ - TBW↑ - ANP↑ - ENaC↓
(Also K↓ - Aldosterone↑)

55
Q

Thyroid Glands General Features:

Position, Requirements, Functional Unit and Synthesis pathway positions

A

1) Palpable - Enlargement in case of goiter
2) Iodine requirement: 150ml/Day (Stores 7mg)
3) Functional unit: Follicle Surrounded by Thyrocytes
4) First step of Synthesis Iodination is in Follicle (ECM) the rest are Intracellular

56
Q

Thyroid Synthesis pathway :

Iodination

A

Iodide + Tyr + H2O = I-Tyr + H2O

Catalyzed by Thyroperoxidase and Duox2 (Both Membrane bound).

57
Q

Thyroid Synthesis pathway :

Coupling

A

Aromatic rings are transferred on to each other forming:
T4 = DIT on DIT, Less Active
T3 = MIT on DIT (2 I in, 1 I out) More active!
Reverse T3 = DIT on MIT, Non active.

58
Q

Thyroid Synthesis pathway :

Coupling - Where? By who?

A

In the Thyroid Follicle Lumen, the DIT and MIT are coupled while on Thyroglobulin and the reaction is catalyzed by TPO.

59
Q

What is the Thyroid to Serum ratio of Iodine?

A

30~

60
Q

What are the unique transporters on each side of the thyroepitherliel cell?

A

Apical side : Pendrin (Cl/I exchanger)

BL side: NIS (I/Na Symporter)

61
Q

How is the Thyroglobulin protein go to the thyroepitherliel cell?

A

MEGALIN - Receptor Mediated endocytosis

62
Q

Inhibitors of T3 and T4 production:

A

1) Iodine↑↑↑
2) Thiocyanate (SCN-) - Competes with Iodine (Glycoside)
3) Perchlorate (ClO4-) Competes with Iodine
4) Propylthiouracil - Inhibition of TPO

63
Q

How are the T3 and T4 travelling in blood?

(4 forms) difference between T4 and T3 is important.

A

Free: T3 = 0.2% and T4 = 0.02%
Thyroxine Binding Globulin (TBG) = 80%
Thyroxine Binding Pre-Albumin(TBPA)=15%
Albumin bound = 5%

64
Q

What is the mechanism of action for T3?

A

Thyroid receptor binding - Dimerization with RXR - Binds TRE at DNA and causes gene transcription

65
Q

What is the enzyme responsible for the conversion of T4 to T3?

A

5’ Idoinase

66
Q

Types of 5’ Idoinase?

A

Type 1) In liver, kidney and skeletal M.-Releases to Blood
Type 2)CNS - Keeps product in cell
Type 3) Inactivation by turning it to Reverse T3

67
Q

Effects of T3/T4?

8 things - generally increase BMR

A

1) Na/K ATPase↑
2) UCP1↑
3) CO↑ and TPR↓ (O2 consumption↑)
4) RR↑ and EPO↑ (Mitochondrial respiration↑)
5) GLUT↑ GNG↑ Glycogen+Lipo+ Proteolysis↑
6) Permissive effect for Beta 1 and 3 receptors
7) CNS development - Myelination, Synapse
8) Linear growth - Chondrocytes↑ (with GH and IGF-1)

68
Q

What is the first hormone checked for Newborns?

What is its action?

A

TSH - for CNS development and general growth

T3↑: Through NIS↑, MEGALIN ↑, DUOX2 ↑ and TPO ↑

69
Q

What is the cause of Goiter?

A

Decreased Iodine consumption (Rural high areas) leads to no T3 production halting of Negative feedback to TSH that causes enlargement of Thyroid gland (Cells+Size↑)

70
Q

What are the positive regulators of T3/T4 synthesis?

What are the Negative regulators of T3/T4 synthesis?

A

Food consumption↑ and Low temperature will cause release of TRH.
T3 and T4 will cause Negative feedback to TSH and TRH.

71
Q

Hypothyroidism (Cretinism in children): High TSH

A

1) Low BMR
2) Fatigue
3) Cold Sensitivity
4) Weight Gain
5) Bradycardia
6) Depression
7) Myxoedema (Deposits on Skin)

72
Q

Hyperthyroidism : Low TSH

A

1) High BMR
2) Increased Appetite
3) Hyperactivity
4) Sensitive to Heat
5) Weight Loss
6) Tremor and Muscle fatigue
7) Anxiety

73
Q

Grave’s diseases:

A

TSH like Antibodies activate the TSH-receptor.

Gs and Ca signal regular effect produced more and more - T3↑↑↑ and Goiter

74
Q

Synthesis stages of Insulin:

A

Pre-Pro-Insulin - Pro-Insulin - C Peptide + Insulin

75
Q

Main Function of Insulin:

A

Elimination of transport nutrients from blood

76
Q

What causes the release of Insulin from Beta cells?

A

ATP sensitive potassium channels.

Close when there’s ATP, Cause depolarization and Calcium signal for Release of Insulin Vesicles

77
Q

What are the activators of Insulin secretion? mechanism?

Beside Glucose and Amino acids(Arg, Lys, Leu)

A

1) GLP and GIP (Incretins)-Gs
2) Ach(Vagus) - Gq (M1)
3) Epinephrine - Beta2(Gs)
4) Glucagon and Cortisol - Indirectly by elevating Glucose

78
Q

What are the Inhibitors of Insulin secretion? mechanism?

A

1) Hypoglycemia
2) FFA
3) Somatostatin
4) Leptin
5) NE - Adrenergic Alfa2

79
Q

ATP sensitive potassium channels:

Pharmacological manipulation?

A

Sulphonylureas - Close them, DM treatment - Insulin ↑

Diazoxide - Open them, Hyperinsulinism treatment - Insulin ↓

80
Q

What are Incretins?

A

GIP and GLP
Hormones released when there is Oral glucose intake!
Insulin↑

81
Q

Langerhans Islets - Connection between the cells

A
  • Gap junctions
  • blood vessels
  • Same innervation
82
Q

Regulation relationship between Insulin and SST?

A

Both inhibit each other

83
Q

Regulation relationship between Glucagon and SST?

A

Glucagon releases SST

SST inhibits release of Glucagon

84
Q

Regulation relationship between Glucagon and Insulin ?

A

Glucagon releases Insulin

Insulin inhibits release of Glucagon

85
Q

What are the cascades led by Insulin in targets cells? how?

A

Tyrosine Kinase receptor:
IRS-grb-MAPK-Mitogenesis
IRS-PI3K-PIP3-PDK-PKB: GLUT4,Glycolysis,Glycogenesis

86
Q

cellular effects of Insulin - what is Activated?

A 
GLUT4 Translocation
Protein synthesis
Lipogenesis
Gluconeogenesis
Glycolysis
87
Q

cellular effects of Insulin - what is Inactivated?

A

Gluconeogensis
Proteolysis
Lipolysis

88
Q

Symptoms of someone with DM?

A

Glucosuria, Ketone Bodies, Glycated Hb

89
Q

What are the symptoms of Hyperinsulinism?

A

Hypokalemia

90
Q

What is the Difference between Type 1 and Type 2 DM?

A

DM1 - Loss of 60% of Beta-cells due to Autoimmune disease.

DM2 - Insulin resistance (Peripheral)

91
Q

What are the factors elevating and lowering the insulin resistance?

A

Resistin, TNF-Alpha, IL6 all cause elevation in Insulin resistance.
Adiponectin causes reduction of Insulin resistancc

92
Q

What is the action of TZD?

A

Activates PPAR-gamma that causes Lowering of Resistin and Adiponectin elevation.

93
Q

High amount of visceral fat yields?

A

Leptin, Resistin, TNF,IL6

94
Q

Low amount of triglycerides yields?

A

Adiponectin

95
Q

What are the functional cells of the Adrenal medulla? How are they activated? How they are looked at systematically because of that?

A

Nicotinic Ach receptor activates them causing them to release NE(20%) and Epi(80%) to blood stream. Therefore they are considered a ganglion of Sympathetic NS.

96
Q

Epinephrine Synthesis enzymes?

Which one is found in the the Chromaffin cells? which hormone activates it?

A

1) Tyrosine Hydroxylase
2) DOPA Decarboxylase
3) Dopamine Hydroxylase
4) PMNT, Activated by cortisol, Found only in Chromaffin

97
Q

What is unique about beta receptors of Adrenergic sys?

A

Higher affinity to Epinephrine

They cause Bronchodilation and Hepatic Vasodilation

98
Q

What is the most common degredation product of Epinephrine?

A

VMA

99
Q

What are the stress signals from the environment activating? (3 Pathways)

A

Limbic System - NE neurons - Arousal/Aggression

Hypothalamus - CRH- ACTH- Cortisol - Blocks Growth and Sexual Activity

Hypothalamus - Sympathetic - Epinephrine - Energy and Cardiovascular

100
Q

Mechanism Protecting from Hypoglycemia:

A

1) Glucagon
2) Cortisol
3) Catecholamines
4) Growth Hormone
5) T3/T4 (not affected by glucose concentration)

101
Q

Early Starvation (up to 24h):

A 
Glucagon↑
Cortisol
Liver Glycogenolysis
Adipocyte - Lipolysis
Sk. Musc - Glycolysis
102
Q

Intermediate Starvation (24h to 72h):

A 
Glucagon↑↑
Cortisol, Adrenaline and GH
Liver Gluconeogensis
Adipocyte - Lipolysis
Sk. Musc - Glycolysis + Proteolysis
103
Q

Long Starvation (above 72h):

A

Glucagon↑↑↑
Cortisol, Adrenaline, GH ( T3 lowers)
Kidney - Gluconeogensis
Liver - Ketogenesis

104
Q

What are the major metabolic differences regarding Exercise when compared to fasting?

A
  • Adrenaline is the activator on Skeletal muscles

- AMPK stimulates GLUT4 Translocation

GBA Physiology (12 decks)

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