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BHS 550 Endocrinology > Endocrinology Knowledge Gaps > Flashcards

Endocrinology Knowledge Gaps Flashcards

1
Q

True or False:
Vitamin D and it’s metabolites are also considered steroid hormones

A

True

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2
Q

True or False:

80% of steroid hormones are synthesized from dietary LDL cholesterol, while only 20% of steroid hormones come from the de-novo synthesis of cholesterol from acetate/(acetyl CoA)

A

True

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3
Q

What are the steps in steroid hormone synthesis?

A
  1. LDL circulating in the bloodstream is taken up into cells via receptor-mediated endocytosis.
  2. Lysosomal hydrolases release free cholesterol
  3. Free cholesterol is then converted to a steroid hormone precursor called pregnenolone.
  4. The precursor pregnenolone can then be converted into various steroid hormones (aldosterone, cortisol, testosterone, & estradiol)
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4
Q

What is the response time for steroid hormones?

A

Primarily, hours to days if binding to intracellular receptors. This is due to their effect being at the nuclear level, having to account for processing through transciptio, translation, etc.

Can also be quicker, in seconds to minutes, if it is binding to a membrane receptor (like protein and amino acid hormones).

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5
Q

What is the response time in peptide or amine hormones?

A

Seconds to minutes

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6
Q

What class of hormones require binding globulins (binding proteins) to travel through the blood to the target organ?

A

Steroid hormones:

  • cortisol
  • aldosterone
  • estrogen/estradiol
  • progesterone
  • testosterone
    • triiodothyronine (T3) & thyroxine (T4) (AA hormones, but act like steroids)
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7
Q

What are the primary modes of regulation of circulating hormones?

A
  1. Biosynthesis & precursor processing
  2. Hormone secretion
  3. Hormone transport
    4 .Hormone metabolism
  4. Feedback loops (mostly negative, some positive) Most important regulatory factor!
  5. Receptor regulation
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8
Q

What is an “ultra-short” feedback loop?

A

An “ultra-short” feedback loop is a regulatory mechanism where the regulatory product/metabolite), has regulatory effects on the same organ or tissue that the metabolite was produced or secreted by.

Also called an “autocrine” feedback mechanism/loop.

Distinction between long, short, and ultra-short feedback loops relates directly to the distance the metabolite travels to illicit its regulatory effects.

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9
Q

When serum calcium levels are low in the blood, PTH is released from the parathyroid gland, which will increase serum calcium levels by increasing osteoclast (bone breakdown) activity. The subsequent rise in serum calcium will be detected by the parathyroid gland and will then inhibit or stop further PTH secretion.

The regulatory mechanism of calcium on PTH secretion is an example of a what level feedback loop?

A

The regulatory action of calcium on PTH secretion is an example of a single level or simple feedback loop.

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10
Q

The stress response pathway of hormone secretion that results in secretion of cortisol, is an example of what level feedback control loop? Simple or Hierarchical?

A

The stress response is an example of a hierarchichal level of control.

Hierarchical level feedback loops have metabolites that can regulate its production pathway by forming feedback loops at multiple levels in the process.

The stress response is a tropic response which involves multiple levels of tropic hormone secretion to other endocrine organs before eventually secreting the final product, cortisol, to the target tissues.

Once enough cortisol has reached target tissues, it has the ability to then “feed back” into the stress response pathway it was stimulated by & regulate the secretion of the hormones at multiple levels, inhibiting further cortisol synthesis and secretion.

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11
Q

Explain receptor desensitization or adaptation.

A

Receptor adaptation or desensitization is a reversible regulatory mechanism that allows hormones to alter (either upregulate or downregulate) target cell responsiveness to itself or other hormones, by modulating receptor function.

Can be done in multiple ways:

Downregulation (decrease target cell responsiveness):
- receptor endocytosis & lysosomal destruction
- receptor phosphorylation (rendering it inactive)
- production of an inhibitor that blocks the signal transduction/second messenger signaling process
- decreasing the expression of another hormone’s receptor, thereby reducing that hormones effectiveness

Upregulation (increase target cell responsiveness):
- Increase number of receptors for itself or another hormone when that hormone’s levels are persistently low

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12
Q

What is the mechanism of G protein coupled to adenylyl cyclase (GPCR-AC)? Explain the steps from ligand binding to cellular response.

A

Ligand binds&raquo_space; exchanges GDP for GTP&raquo_space; α subunit/GTP bind to and activate AC&raquo_space; AC converts ATP to cAMP&raquo_space; cAMP binds to PKA repressor to activate it&raquo_space; Active PKA phosphorylates many enzymes and TFs = increased gene expression

  1. Ligand binds to GPCR-AC ligand binding site on the extracellular surface.
  2. Gsα subunit (G-proteins) exchanges GDP for GTP and dissociates from the rest of the G-protein
  3. GTP bound to the alpha subunit then binds to adenylyl cyclase (AC), which converts ATP to cyclic AMP (cAMP)
  4. Elevated intracellular cAMP levels then act on the inactive Protein Kinase A enzymes by binding to their repressors.
  5. Once cAMP binds to the PKA repressor, the repressors disassociate from PKA, and PKA becomes active.
  6. Active PKA (“promiscuous” protein kinases) will then go on to phosphorylate several enzymes and transcription factors to enhance gene expression.
  7. Phosphodiesterases (PDEs), a regulatory enzyme of secondary messengers cAMP & cGMP, will then act as a “break” on the signaling pathway by breaking down cAMP and terminating it’s activity once the initial signal has been received.
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13
Q

What is the mechanism of G protein coupled to phospholipase C (GPCR-PC)? Explain the steps from ligand binding to cellular response.

A

Ligand binds&raquo_space; Gα q subunit is activated&raquo_space; activation of Gα q activates connected and membrane bound phospholipase C (PLC)&raquo_space; PLC cleaves PIP2 into the two signaling molecules IP3 & DAG&raquo_space; IP3 induces intracellular calcium (Ca2+) release&raquo_space; DAG then binds to calcium to activate calcium-dependent kinase, Protein Kinase C (PKC)&raquo_space;PKC will phosphorylate many enzymes and transcription factors = increase in gene expression

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14
Q

What is the mechanism of G protein coupled to phospholipase A2 (GPCR-PLA2)? Explain the steps from ligand binding to cellular response.

A

Ligand binds&raquo_space; Gα q or Gα 11 subunit is activated & subsequently activates connected and membrane bound phospholipase A2 (PLA2)&raquo_space; PLA2 cleaves membrane phospholipids producing lypophospholipid & Arachidonic Acid&raquo_space; Arachindonic Acid can then be converted by many different enzymes into a variety of bioactive eicosanoids = increase in prostanglandins, prostacyclins, thromboxanes, & leukotrienes (all eicosanoids)

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15
Q

What is the mechanism of Guanylyl Cyclase Receptors (GC’s)? Explain the steps from ligand binding to cellular response.

A

Ligand binds&raquo_space; Guanylyl Cyclase being both the receptor & the acting enzyme itself, converts GTP to cyclic GMP (cGMP)&raquo_space; similar to cAMP, cGMP then activates various cGMP-dependent kinases, phosphotases, & ion channels

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16
Q

What is the mechanism of Receptor Tyrosine Kinases (RTK’s)? Explain the steps from ligand binding to cellular response.

A

Two Ligands bind to each TKR receptor&raquo_space; the coupled tyrosine kinase molecules dimerize&raquo_space; Tyrosine kinase autophosphorylates the tyrosine molecules within the receptor itself, convertingATP to ADP in the process, activating it&raquo_space; activated tyrosine kinase then binds to and activates relay proteins and other substrates within the cytosol&raquo_space; Activated relay proteins initiates cascade of other phosphorylation reactions within the cell

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17
Q

What is the mechanism of Tyrosine-Kinase Associated Receptors (TKARs)? Explain the steps from ligand binding to cellular response.

A

Single ligand binds&raquo_space;brings the two tyrosine kinase molecules each bound to Janus kinases (JAKs) together (dimerization)&raquo_space; dimerization activates JAKs which will phosphorylate STAT proteins&raquo_space; phosphorylation of two STAT proteins causes them to dimerize&raquo_space; Dimerized STAT can then enter the nucleus & regulate transcription = upregulation of gene expression

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18
Q

Name a hormone that binds to GPCR-AC?

A

Parathyroid Hormone (PTH) & Vasopressin/ADH

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19
Q

Name a hormone that binds to GPCR-PLC?

A

Vassopressin/Antidiuretic Hormone (ADH) & PTH

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20
Q

Name a hormone that binds to GPCR-PLA2?

A

Thyrotrophin Releasing Hormone (TRH)

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21
Q

Name a hormone that binds to Receptor Tyrosine Kinase?

A

Insulin

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22
Q

Name a hormone that binds to Guanylyl Cyclase Receptor?

A

Atrial Natriuretic Peptide (ANP)

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23
Q

Name a hormone that binds to Tyrosine Kinase- Associated Receptors (TKARs)?

A

Growth Hormone (GH)

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24
Q

What is the mechanism for intracellular steroid hormone receptors? Explain from ligand binding to cellular response.

A

Cytosolic or nuclear receptor is bound to repressor&raquo_space; steroid hormone binds intracellular receptor and repressor disassociates&raquo_space; receptor (oftena transciption factor itself) can then enter nucleus & cause changes in gene expression = up or downregulation of gene expression

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25
Q

How are hormone concentrations measured in biological fluids?

A

Immunoassays.

Immunoassays rely on the ability of specific antibodies to recognize specific hormones.

Hormone levels can be measured in plasma, serum, urine, or other biologic samples.

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26
Q

What hormone is produced and secreted by the supraoptic nuclei in the hypothalamus?

A

Antidiuretic Hormone/ADH/Arginine Vasopressin/AVP/Vasopressin

(All used interchangeably to refer to the same hormone, ADH)

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27
Q

What hormone is produced and secreted by the paraventricular nuclei in the hypothalamus?

A

Oxytocin

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28
Q

Which division of the pituitary gland developed from Rathke’s pouch of the oral ectoderm?

A

Anterior pituitary

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29
Q

Which neurosecretory cells of the hypothalamus pass through the infundibulum to the neurohypophesis?

A

Magnocellular Neurosecretory Cells

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30
Q

Which neurosecretory cells of the hypothalamus pass through the median eminence to the adenohypophysis?

A

Parvocellular Neursecretory Cells

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31
Q

What are the two hormones of the ovaries AND the corpus luteum?

A

Estradiol & Progesterone

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32
Q

What is the connecting stalk between the hypothalamus and the anterior pituitary called?

A

Median Eminence

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33
Q

What is the connecting stalk between the hypothalamus and the posterior pituitary called?

A

Infundibulum

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34
Q

What is the primary blood supply source of the anterior pituitary?

A

Superior Hypophyseal Artery

(A.S)
A - Anterior
S - Superior Hypophyseal Artery

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35
Q

What is the primary blood supply source of the posterior pituitary?

A

Middle & Inferior Hypophyseal Arteries

(P.I.M.)
P - Posterior
I - Inferior Hypophyseal artery
M - middle hypophyseal artery

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36
Q

Where is the blood supply the pituitary received from? Where does it drain into?

A

Pituitary blood supply is received from the interal carotid arteries, which branches into the superior, middle, and inferior hypophyseal arteries.

The blood drains from the pituitary into the cavernous sinus.

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37
Q

What sinus does the instrument pass through during transsphendoidal surgery?

A

The sphenoid sinus

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38
Q

What condition is transsphenoidal surgery performed to treat?

A

Transsphendoidal surgery is the removal of pituitary tissue to treat hyperpituitarism.

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39
Q

What factors stimulate ADH secretion?

A
  • increased serum osmolality (solute concentration)
  • large decrease in blood pressure/extracellular fluid (ECF) volume
  • angiotensin 2 synthesis
  • pain/nausea
  • HYPOglycemia (low blood sugar)
  • nicotine, opiates
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40
Q

What are the inhibitory factors of ADH?

A
  • decreased serum osmolality (solute concentration)
  • increased blood pressure/ECF volume
  • Atrial natriuretic peptide (ANP)
  • Alcohol
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41
Q

What is the target tissue(s) of ADH/Vasopressin?

A

Vasopressin receptors of the Kidneys, sweat glands, & circulatory system

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42
Q

What are the symptoms of low serum ADH/vasopressin?

A
  • excretion of large volumes of dilute urine
  • decreased water reabsorption
  • vasodilation
  • low blood pressure
  • increased osmolarity of the blood
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43
Q

What are the symptoms of high serum ADH/vasopressin?

A
  • small volumes of concentrated urine being excreted
  • increased water reabsorption
  • vasocontriction
  • increased blood pressure
  • decreased osmolarity of the blood ( solute concentration)
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44
Q

What is the Renin Angiotensin System?

A

A system that is stimulated to restore blood pressure when there it gets low.

  1. The liver produces the enzyme angiotensinogen, which is responsible for producing Angiotensin 1.
  2. Low blood pressure triggers juxtaglomerular cells of the kidney to produce an enzyme Renin.
  3. These two enzymes work together to produce Angiotensin 1
  4. An enzyme produced in the lungs, known as ACE, will then convert Angiotensin 1 to Angiotensin 2.
  5. Angiotensin 2 will then effect multiple target organs to raise the blood pressure
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45
Q

What is Diabetes insipidus?

A

“Water diabetes”

  • Water imbalance due to ADH DEFICIENCY
  • Symptoms:
  • excretion of large amounts of dilute urine (polyuria, (glucose free, unlike DM)
  • excessive thirst (polydispia)
  • nocturia
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46
Q

What condition is causes ADH hypersecretion?

A

Syndrome of Inappropriate ADH secetion (SIADH)

  • water imbalance due toADH hypersecretion
  • typically caused by paraneoplastic syndrome
    -Symptoms
  • severe water retention causing water intoxication
  • brain swelling causing neurological problems
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47
Q

What inibits oxytocin secretion?

A
  • anxiety
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48
Q

What are the 3 parts of the anterior pituitary (adenohypophysis)?

A
  1. Pars distalis (90% the lobe)
  2. Pars intermedia (regresses; not found in adults)
  3. Pars tuburalis (wraps around the pituitary stalk/infundibulum)
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49
Q

What are the 5 endocrine cell types in the pars distalis?

A

Basophils:
- Corticotropes
- Thyrotropes
- Gonadotropes

Acidophils:
- Somatotropes
- Lactotropes

50
Q

Trace the hormone secretion along the endocrine axis from all the major hormones secreted from the hypothalamus to target tissues.

A
51
Q

What hormones stimulate & inhibits prolactin? What hormones can prolactin inhibit or stimulate?

A

Stimulated by:
- TRH
- Oxytocin
- VIP
-Neurotensin
- Pregnancy (low estrogen levels due to prolactin inhibitionofGnRH)

Inhibited by:
- Dopamine

Prolactin Stimulates:
-Dopamine secretion (negative feedback loop)

Prolactin Inhibits:
- Gonadotrophin Releasing Hormone (GnRH), which also indirectly inhibits FSH & LH

52
Q

What hormones stimulate & inhibit TSH secretion? What hormones can TSH stimulate or inhibit?

A

Stimulated by:
-TRH

Inhibited by:
- T3 & T4 (negative feedback)
- somatostatin

53
Q

What hormones stimulate & inhibit ACTH secretion? What hormones can ACTH stimulate or inhibit?

A

Stimulated by:
- Stress, which induces CRH secretion from hypothalamus
- hypoglycemia

Inhibited by:
- steroid hormones
- metabolic effects of steroid hormones released as a product of stress response pathway

*ACTH released throughout the day but peaks in the morning

54
Q

What hormones stimulate & inhibit GH secretion? What hormones can GH stimulate or inhibit?

A

Stimulated by:
- GHRH
- stress
-trauma
-hypoglycemia
-exercise
-sleep

Inhibited by:
- somatostatin
- GHRH inhibition directly by GH (negative feedback loop)
- GHRH inhibition via IGF secretion from the liver (negative feedback loop)

*Peaks at night

Hypersecretion:
- giantism in children
- acromegaly in adults

Hyposecretion:
- dwarfism in children

55
Q

What are the stimulatory & inhibitory factors of FSH & LH?

A
56
Q

Where is melanocyte stimulating hormone (MSH) produced?

A

In the pars intermedia of the anterior lobe ( regresses as we age).

MSH stimulates melanin production in melanocytes of the skin after UV exposure & in certain areas of the body in women during pregnancy

57
Q

What are the 3 ways in which the anterior pituitary can be disregulated?

A
58
Q

What are the target organs and the effects of each of the anterior pituitary hormones?

A
59
Q

What intermediate in the renin-angiotensin pathway is responsible for thirst sensation and sympathetic nervous system activation?

A

Angiotensin 2

60
Q

Aldosterone increases water reabsorption & raises the blood pressure by:

A) Stimulating the Na-H exchanges within the nephron
B) Increase sodium reabsorption in the nephron, colon, sweat, and salivary glands
C) Increasing potassium secretion in the kidney & colon
D) All of the above

A

D) All of the above

61
Q

True or false:

Cortisol binds to intracellular receptors at target tissues to induce or repress gene transcription

A

True

62
Q

What are the 3 main effects of cortisol secretion on target tissues?

A
  1. Increase blood glucose levels
  2. Vasocontriction (thus increase blood pressure)
  3. Anti-inflammatory effects
63
Q

When does cortisol hormone usually peak in the day?

A

In the morning

64
Q

What are the 3 anti-inflammatory actions of cortisol?

A
  1. Induces the synthesis of lipocortin, an inhibitor of the enzyme phospholipase A 2 .
    - this inhibits the synthesis of the precursor to prostaglandins and leukotrienes.
  2. Inhibits the production of interleukin-2 (IL-2) and the proliferation of T lymphocytes.
  3. Inhibits the release of histamine and serotonin from mast cells and platelets.
65
Q

What are the two main sex hormones & their androgen precursors?

A

Androgens/sex hormones: testosterone & estradiol/estrogen

Androgen precursors: DHEA & androstenedione
- produced by the adrenal cortex in the zona reticularis
- converted to sex hormones in the testis & ovaries

66
Q

What are the 3 categories of adrenalcortical steroids? What do each of them do?

A
67
Q

True or False:

The adrenal medulla is an extensionof thesympathetic nervous system?

A

True

68
Q

True or False:

Production of Catecholamines & dopamine in the adrenal medulla are stimulated by ACTH.

A

True

69
Q

What is PNMT and what it is regulated by?

A

PNMT = enzyme that converts norepinephrine to epinephrine.

PNMT is upregulated (increased activity/activated) by cortisol secretion (stress response/ sympathoadrenal response)

70
Q

What is the Sympathoadrenal response?

A
  • Autonomic (Sympathetic) Nervous System action in response to adrenal hormone release:

•Increased heart rate, high blood pressure
•Conversion of glycogen to glucose (liver)
•Decreased activity of GI tract
•Dilation of bronchioles

71
Q

What is Addison’s Disease?

A

•Have low cortisone and aldosterone
•Autoimmune destruction of adrenal gland
•Symptoms
•Skin hyperpigmentation
•Low blood pressure
•Weight loss
•Weakness
•Nausea, vomiting, diarrhea
•Treatment
•Glucocorticoids and mineralocorticoids

72
Q

What is Cushing’s Disease?

A

•Excess cortisol
•Pituitary secretes excess ACTH
•Symptoms
•Fragile skin
•Obesity (“moon” face)
•Elevated BP
•Hyperglycemia
•Depression
•Excessive body hair
•Treatment
•Surgical removal of tumor (radiation)
•Medication

73
Q

True or false:

Somatostatin inhibits insulin & glucagon secretion.

A

True

74
Q

True or False:

Somatostatin inhibits the Adenylyl cylase/cAMP pathway.

A

True

75
Q

What is secreted by pancreatic delta cells?

A

Somatostatin

76
Q

What is secreted by pancreatic epsilon cells?

A

Ghrelin

77
Q

What is secreted by pancreatic gamma cells?

A

Pancreatic polypeptide (regulates pancreatic secretions)

78
Q

What arethe endocrine cells of the pancreas called? What are the exocrine cells of the pancreas called?

A

Endocrine cells = islets of Langerhans

Exocrine cells = Acinar cells

79
Q

Whereis preproinsulin cleaved?

A

In the rough ER

80
Q

Where is proinsulin cleaved?

A

In the golgi apparatus.

81
Q

True or false:

Insulin is packaged into secretory vesicles along with a C peptide (a connecting peptide) or a zinc complex

A

True

82
Q

Explain how insulin is secreted in response to glucose

A
  1. Glucose is taken up by transporters (Glut-2)
  2. Glucose is metabolized to generate ATP
  3. High ATP closes K+/ATP channels
  4. Closure of K+/ATP channels causes depolarization
  5. Depolarization opens VDCC (voltage-dependent Calcium channels)
  6. Rise in intracellular Ca2+ = insulin secretion
83
Q

Explain how insulin is secreted in response to glucose

A
  1. Glucose is taken up by transporters (Glut-2)
  2. Glucose is metabolized to generate ATP
  3. High ATP closes K+/ATP channels
  4. Closure of K+/ATP channels causes depolarization
  5. Depolarization opens VDCC (voltage-dependent Calcium channels)
  6. Rise in intracellular Ca2+ = insulin secretion
84
Q

What are incretins?

A

Gastrointestinal hormones that potentiate insulin secretion.

•stimulated by fat and protein ingestion
•Include Glucose-dependent insulinotropic peptide (GIP) and glucagon-like peptide 1 (GLP-1)
•“Incretin effect”: the reason you will see a greater response to oral glucose than to intravenous glucose
•Incretins stimulate the release of insulin and inhibit the release of glucagon

85
Q

True or false:

Intravenous fusion of glucose will cause a larger increase in insulin secretion than oral glucose

A

False.

Oral glucose causes a larger increase in insulin secretion than intravenous infusion due to incretin effect

86
Q

How does Ach stimulate insulin secretion?

A

By enhancing calcium release from intracellular depots.

Remember insulin is secreted in response to increase inintracellular calcium concentrations.

87
Q

Activation of what two sympathetic pathway receptors inhibits insulin secretion?

A

Activation of alpha2 & beta2 adrenergic receptors

88
Q

What second messenger signaling pathway does glucagon activate?

A

Glucagon activates the Adenylyl cyclase/PKA pathway which causes inhibition of glycolysis and promotion of gluconeogenesis & glyconeogenesis

89
Q

What second messenger pathway does somatostatin inhibit?

A

Somatostatin inhibits the Adenyl cyclase cAMP Pathway, decreasing intracellular cAMP and calcium levels thus inhibiting both insulin and glucagon.

90
Q

What is the principle role of somatostatin?

A

The principle role of somatostatin is to extend the period over which the food nutrients are assimilated into the blood (prevent the nutrients from being absorbed too quickly)

91
Q

What is asthenia?

A

Lack of energy; a symptom associated with Type 1 Diabetes

92
Q

What is polyphagia?

A

Eating large amounts of food; a symptom of Type-1 Diabetics where despite the increased food intake, they experience rapid weight loss and asthenia (lack of energy)

93
Q

What are the various forms of treatment for Type-2 Diabetes & how do they work?

A
  • Metformin = suppresses glucose production in the liver
  • TZDs = increase insulin sensitivity
  • Sulfonylureas = cause additional release of insulin by the pancreas
  • Ozempic/Mounjaro (synthetic GLP-1& GIP/agonists) = drugs that mimic the incretin actions of GLP-1
  • inhibition of DPP-4 enzyme, which will inactivate incretin hormones GLP-1 & GIP
94
Q

Describe the structure & location of the thyroid gland

A

•Structure
•Right & left lobes
•Isthmus
•Pyramidal lobe – 50% of population
•On superior surface of isthmus
•Embryological remnant
•Location
•Posterior to sternothyroid & sternohyoid mm.
•Anterior to Larynx & trachea
•Level of C5-T1

95
Q

Which thyroid hormones are secreted by follicular cells?

A

T3 & T4

96
Q

Which thyroid cells are secreted by parafollicular (C) cells?

A

Calcitonin

97
Q

What are the functons of the 3 thyroid hormones?

A
98
Q

True or false:

T3 is much more potent than T4.

A

True

99
Q

True or false:

T4 comprises most of the circulating thyroid hormones (thyroxines) and is mostly converted to T3 within peripheral tissues

A

True

100
Q

How is the production of the thyroid hormones regulated?

A
  • Low metabolism is sensed by hypothalamus and TRH is secreted
101
Q

How is the production of the thyroid hormones regulated?

A
  • Low metabolism is sensed by hypothalamus and TRH is secreted
102
Q

What are colloids?

A

Thyroid hormones attached to thyroglobulin

103
Q

Where does synthesis of thyroid hormones occur and where are they stored?

A

Synthesis occurs part intracellularly & part extracellularly.

They are then stored in the follicular lumen

104
Q

What are the steps of thyroid hormone synthesis?

A
105
Q

True or false:

Thyroid hormones require binding proteins to circulate inthe blood stream?

A

True;

Although it istechnically an amino acid hormone, derived from tyrosine, the thyroid hormones ten to behave like steroid hormones.

106
Q

What are the 4 ‘s of thyroid hormones and what do they represent?

A

The 4 B’s represent the 4 man functions of T3 (active) thyroid hormone:
- Brain maturation
- Bone growth
- Beta-adrenergic effects
- Basal metabolic rate (BMR)

107
Q

What is Hashimoto’s Disease?

A

Hypothyroidism

108
Q

What is the major blood supply to the parathyroid gland?

A

Inferior thyroid atery

109
Q

What is the minor blood supply to the parathyroid glands?

A

Superior thyroid artery

110
Q

What is the primary function of the Chief cells of the parathyroid?

A

Synthesis & secretion of the parathyroid hormone (PTH)

111
Q

True or false:

PTH is degraded by the liver

A

True

112
Q

Which cell membrane receptors are present on chief cells of the parathyroid gland and what effects do these receptors have on synthesis and release of parathyroid hormone?

A

Chief cells of the parathyroid gland contain Gq protein coupled protein receptors coupled w/ PLC (phospholipase C). These receptors have a signaling pathway that will increase calcium and protein kinase C levels which will subsequently inhibity PTH synthesis & release.

Thus these receptors act as a regulatory mechanism on Chief cells for PTH synthesis& secretion

113
Q

Which of these are effects of PTH secretion?

A) Increase in plasma calcium & osteoclast activity
B) Increased expression of calcium binding protein in small intestine & increased absorption of Ca2+ by intestinal mucosal
C)Activation of Vitamin D & calcium reabsorption in kidney (activates 1α-hydroxylase)
D)Increases renal Phosphate excretion
E) All of the above

A

E) All of the above

114
Q

How is PTH secretion regulated?

A
115
Q

What are the signs in symptoms of hyper and hypocalcemia?

A
116
Q

True or false:

Vit D2 is obtained from plants & Vit D3 canbe synthesized in humans.

A

True

117
Q

What are the two commonVit D deficiency conditions

A

Children - rickets

Adults - osteomalacia (if deficiency is prolonged)

118
Q

How is Vitamin D synthesized?

A
119
Q

What dysfuntonal hormone secretions causes “bones, stones, groans (contripation), and psychiatric overtones” symptoms?

A

Hyperparathyroidism - high serum calcium levels; typically caused by a Benign parathyroid adenoma ~80% of cases, or parathyroid gland hyperplasia ~20%; causes bone wasting, constipation, and psychiatric symptoms; treatmentis to surgically remove the tumor or the entire parathyroid gland.

120
Q

What hormone secretion dysfunction causes tetany (sustained muscle contractions) & respiratory paralysis (diaphragm dysfunction)

A

Hypoparathyroidism – blood calcium levels that are too low; impairs muscle relaxation

121
Q

What’s pregnenolone?

A

Steroid hormone precursor that is converted to steroid hormones in the adrenal gland

BHS 550 Endocrinology (2 decks)

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