Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

PHYSL 210B > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

What are the 3 classification of hormones?

A
  1. Proteins (small peptides, polypeptides, glycopeptides)
  2. Lipids (steroids, eicosanoids)
  3. Monoamines (catecholamines, thyroid)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What is the process of steroid hormone synthesis?

A

Cholesterol > Pregnenolone > Progesterone
Pregnenolone/Progesterone > Testosterone > Estrogen
Progesterone > Aldosterone/Cortisol

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the 4 ways that hormones reach their target?

A
  1. Endocrine (via blood)
  2. Neuroendocrine (via nerves and into the blood)
  3. Paracrine (sharing with nearby neighbouring cells)
  4. Autocrine (leave but act for itself)
  5. Intra (does not leave cell and act for itself)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

How do hormones interact with their targets?

A

Binds to a receptor, which then interacts with other molecules leading to a response

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 2 sites for receptors?

A
  1. Cell surface receptors
    Protein which bind to protein hormone and to catecholamines
  2. Intracellular receptors
    Proteins which bind to steroid hormones and to thyroid hormones
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are some examples of cell surface receptors?

A
  1. G-Protein Linked Receptors
    Regulates intracellular second messengers (eg cAMP, DAG, Ca2+) (eg receptors for adrenaline, glucagon, FSH, LH, TSH, PTH)
  2. Catalytic Receptors
    Either have enzyme activity themselves, or are closely associated with an enzyme after binding to a ligand
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

(Example) What happens when adrenaline is secreted?

A

Conformation of a receptor (adrenergic receptor) > G Protein > Enzyme (adenylate cyclase) > second messenger (cAMP) > Protein kinase (PKA) > Phosphorylation of proteins > Response of target cell

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the 3 sites of the intracellular receptor?

A
  1. Cytoplasm (steroid hormones)
  2. Nucleus ( sex steroids)
  3. Bound to DNA (thyroid hormone)

going to end up in the nucleus anyway

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What is the difference between the negative feedback and positive feedback?

A

Negative feedback decreases variation from “ideal” or “usual” value whereas positive feedback increases variation from “usual” value

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What are the 6 factors affecting hormone activity?

A
  • Synthesis
  • Secretion
  • Binding to plasma protein
  • Metabolism
  • Number of receptors
  • Response to hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What are the 7 difference between protein and steroid?

A
  • Protein is water soluble
  • Protein is synthesized from amino acids while steroid is synthesized from cholesterol
  • Protein is stored in granules and excreted by exocytosis ; steroids are not stored and excreted by diffusion
  • Protein do no need solubilization in blood ; steroid are mainly bound to plasma proteins
  • Hormone receptors for protein are on target cell surface membrane; steroid is mainly intracellular
  • Protein changes in intracellular signalling pathways whereas steroid regulate gene expression in target cell nucleus
  • Proteins are relatively faster
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What is the arrangement of the hypothalamus-pituitary unit?

A

Anterior pituitary, posterior pituitary, pituitary stalk, medium eminence, hypothalamus

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Where is the secondary plexus located (hypothalamus)?

A

Anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What are the 2 nucleus that acts on the posterior pituitary?

A

Supraoptic nucleus (SON), Paraventricular nucleus (PVN)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is the difference between the hormone transmission of anterior and posterior pituitary?

A

In the anterior pituitary, the neurotransmitter travel as far as the median eminence. Then transfer the hormone into the portal blood vessels. They are then carried down the pituitary stalk and then act on the receptors of the target cells in the anterior pituitary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What are the hormones and 5 target organ in the anterior pituitary?

A
  1. Ovaries & Testes
    • Follicle-stimulating hormone (FSH)
    • Luteinizing hormone (LH)
  2. Adrenal Cortex
    • Adrenocorticotropic hormone (ACTH)
  3. Thyroid Gland
    • Thyroid-Stimulating hormone (TSH)
  4. Mammary Gland
    • Prolactin (PRL)
  5. Tissues
    • Growth hormone (GH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What are the hypothalamic hormones and its effects?

A
  1. Increases secretion of FSH and LH
    • Gonadotropin releasing hormone (GnRH)
  2. Increases ACTH
    • Corticotropin releasing hormone (CRH)
  3. Increases TSH
    • Thyrotropin releasing hormone (TRH)
  4. Decreases PRL
    • Prolactin inhibiting hormone (PIH)
  5. Increases GH
    • Growth hormone releasing hormone (GHRH)
  6. Decreases GH
    • Somatosatin (SS) or Growth hormone inhibiting hormone (GHIH)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Which is the most abundant anterior pituitary hormone?

A

Growth hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What type of hormone is the growth hormone?

A
  • Protein hormone
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Why does growth hormone does not work on other animals?

A

Shows specificity

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

How is growth hormone secreted?

A

Pulsatile secretion; circadian rhythm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Where does growth hormone act on (receptor)?

A

Cell-surface receptors ( which are associated with protein kinase activity)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

What are the effects of growth hormone?

A

Increases growth, affects metabolism

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

What are the 3 sections of a bone?

A
  1. Diaphysis (shaft; middle part)
  2. Epiphyseal plate (cartilage)
  3. Epiphysis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

How do bones grow longer?

A

The progenitor cells (fibroblasts) in the cartilage differentiates into cartilage cells (chondrocytes). They then multiply. Salts deposit on the cartilage cells which triggers ossification, hence, forming bones.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Why does growth hormone act in vivo (human) but not in vitro?

A

Because the human body produces insulin growth hormone which aids in growth; but it is not always consistent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

What are the effects of GH on fats?

A

Increase lipolysis (breaking down fats) > increases fatty acids for energy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

What are the effects of GH on proteins?

A

Increase amino acid uptake into cells > increase protein synthesis > increase cell size (hypertrophy)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

What are the effects of GH of carbohydrates?

A

Decrease glucose uptake into cells which causes hyperglycaemia (diabetogenic)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

What hormone increases GH secretion?

A

Ghrelin, growth hormone releasing hormone

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What hormone decreases the release of GH?

A

Somatostatin, GH, IGF

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

How does carbohydrates and protein increase GH secretion?

A

Hypoglycaemia; increase in amino acids (arginine)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

How does carbohydrates and fats decreased GH secretion?

A

Hyperglycaemia; Increase in fatty acids

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

What physiological actions increase GH secretion?

A

Deep sleep; stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

What physiological actions decrease GH secretion?

A

Ageing

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

What if someone has too much GH?

A
  1. Gigantism (increase in linear growth in children)

2. Acromegaly (thickening of bones, large hands and feet; adults)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What if someone has too little GH?

A
  1. Dwarfism (stunted growth in children)

2. Metabolic effects

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

What are the two main hormones in the posterior pituitary and where are their target organs?

A
  1. Antidiuretic hormone (kidney, blood vessels)

2. Oxytocin (uterus, mammary glands)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Where does ADH bind to?

A

Cell surface receptor

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

What happens when ADH binds to the cell surface receptor (G-protein linked)?

A

Increase in cAMP which causes insertion of water (via channels) into the apical membrane.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

What receptors affects the release of ADH from the hypothalamus?

A

Osmoreceptors (e.g dehydration) and baroreceptors (e.g hemorrhage)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

What happens when you have too much ADH?

A

Syndrome of inappropriate antidiuretic hormone secretion (SIADH) which causes increased H20 retention and blood volume

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

What are the 2 syndromes associated to too little ADH?

A
  1. Central or neurogenic diabetes insipidus
    Lack of ADH; large volumes of dilute urine
  2. Nephrogenic diabetes insipidus
    Abnormal ADH receptors in kidney; large volumes of dilute urine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Where are the adrenal gland located?

A

One above each kidney

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

What are the sections in the cortex of the adrenal gland?

A

Zona glomerulosa, zona fasciculata, and zona reticularis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

What is located in the medulla of the adrenal gland?

A

Chromaffin cells

47
Q

What hormone family is located in the glomerulosa, faciculata, and reticularis? What are their functions?

A
  1. Minerals-corticoids (control salt levels)
  2. Glucose-corticoids (control sugar levels)
  3. Androgens (control sex hormones)
48
Q

What are the 4 major actions of aldosterone?

A
  1. Increase Na+ reabsorption by kidney
  2. Increase H2O reabsorption by kidney
  3. Increase K+ secretion by kidney
  4. Increase H+ secretion by kidney
49
Q

What happens when there is a decrease in ECF/BP/Na?

A

There is an increase in sympathetic activities > release of renin > angiotensinogen converts to angiotensin I > converted to angiotensin II (through ACE) > increase in BP, act on adrenal cortex> release of aldosterone

50
Q

How does cortisol affect the metabolism?

A

Increases:
- protein breakdown (increase in amino acids)
- fat breakdown (increase in glycerol and FFA)
- glucose formation in liver
- glycogen formation in liver
- blood glucose
- glucose available for CNS
Decreases:
- glucose utilization by peripheral tissue

51
Q

How does cortisol affect the immune system?

A 
Decreases:
- lymph node size
- lymphocyte number
- humoral /cellular immunity
- production of inflammatory substances (anti-inflammatory, anti-rejection)
Increases:
- infections
52
Q

How is the cortisol secretion controlled?

A

The hypothalamus acts on the anterior pituitary by the corticotrophin-releasing hormone (CRH) which releases the adrenin cortico trophin hormone (ACTH). ACTH binds to receptors in adrenal cortex and increase the output of cortisol. Negative feedback then occurs on the hypothalamus and anterior pituitary.

53
Q

What happens when you have too much aldosterone?

A

Cohn’s Syndrome (increase of ECF, BP, hypokalemia, metabolic alkalosis)

54
Q

What happens when you have too little aldosterone?

A

Addison’s disease (hypotension, metabolic acidosis), hyperkalemia

55
Q

What happens when you have too much cortisol?

A

Cushing’s disease (increase blood glucose, muscle wasting, “moon face”, “buffalo hump”, decrease resistance to infection)

56
Q

What happens when you have too little cortisol?

A

Addison’s disease (decrease blood glucose, increase skin pigmentation)

57
Q

What happens when you have too much adrenal androgens?

A

Virilization in men

58
Q

What happens when you have too little adrenal androgens?

A

Less sexual hair growth, and low libido in women

59
Q

How is catecholamine synthesized?

A

Tyrosine > dihydroxyphenylalanine (DOPA) > dopamine > noradrenaline (norepinephrine) > Adrenalin (epinephrine)

60
Q

What are the major actions of catecholamines (adrenaline and noradrenaline) on cardiovascular system?

A

Increase HR, force of contraction, cardiac output, blood pressure.
There is a redistribution of blood flow (from skin, gut to heart, brain and skeletal muscle)

61
Q

What are the major effects of cathecholamines (adrenaline and noradrenaline) in smooth muscle?

A

Dilation of pupils, bronchodilation, and decrease GI motility

62
Q

What are the major actions of catecholamines (adrenaline and noradrenaline) on metabolism?

A

Increase glycogenolysis (skeletal muscle and liver), lipolysis and gluconeogenesis

63
Q

How is the control of catecholamine secretion happen?

A

The splanchnic nerve (sympathetic preganglionic) innervates the chromaffin cells in the adrenal medulla. Ach acts on chromaffin cells to stimulate the release of adrenaline and noradrenaline.

64
Q

What are the two main structure of the thyroid gland?

A

Active follicle and resting follicle

65
Q

What’s the difference between the active follicle and resting follicle?

A

The active follicle has larger parafollicular cells (c-cells, secrete calcitonin) but less storage

66
Q

How is the thyroid hormone synthesized?

A

From tyrosine and iodine (iodination)

67
Q

What are the intermediates and active hormones when synthesizing the thyroid hormone?

A 
Intermediate:
1. Monoiodotyrosine
2. Di-iodotyrosine
Active hormone:
1. Tri-iodothyronine
2. Tetra-iodothyronine or thyroxine
68
Q

What is the life history of the thyroid hormone?

A
  1. Uptake of iodide form blood
  2. Synthesis of thyroglobulin
  3. Iodination of TYR
  4. Coupling of iodotyrosines
  5. Storage of colloid
  6. Endocytosis of colloid, breakdown by lysosomal enzymes
  7. Secretion of hormones into blood
  8. Transport in blood, mainly in bound form
  9. T4 as prohormone
  10. Thyroid hormone receptors
  11. Half life
69
Q

How is iodide taken into the cell?

A

Na+/I- pump

70
Q

What does thyroid globulin contain (residue)?

A

Tyrosine residue

71
Q

What binds to the nucleus more strongly T3 or T4?

A

T3

72
Q

What is the half life of T3 and T4?

A

T3: 1 day
T4: 7 day

73
Q

What are the physiological actions of thyroid hormones?

A
  1. Act on most tissues > change in transcription and translation
  2. Increase metabolism
  3. Necessary for growth and development
74
Q

How does thyroid hormone affect metabolism (catabolism and anabolism)?

A 
Increases:
- BMR, associated with increase O2 consumption and heat production in many tissues
- CHO absorption and utilization
- Protein breakdown (muscle)
- Fat breakdown
- Cholesterol metabolism (including excretion in bile)
Decreases:
Blood cholesterol level
75
Q

How does thyroid hormone affect growth and development?

A
  • act as tissue growth factors
  • small amounts increase protein synthesis
  • increase GH/IGF production
  • essential for CNS maturation in fetus/newborn
76
Q

What are the 4 other effects of the thyroid hormone?

A
  • increase HR/force (cardiovascular system)
  • increase adrenergic receptors (potentiation of sympathetic nervous system)
  • necessary for normal function and fertility (reproductive system)
  • increase turnover of bones
77
Q

How is the thyroid hormone secretion controlled?

A

The hypothalamus releases thyrotropin-releasing hormone (TRH) which signals the anterior pituitary to secrete thyroid stimulating hormone (TSH) which stimulates the thyroid gland. The thyroid gland then releases T3 and T4 resulting a negative feedback on the hypothalamus and anterior pituitary.

78
Q

What happens if you have an overproduction of thyroid gland?

A

Graves’ disease (autoimmune disorder), associated with increase BMR, exophthalmos, goitre

79
Q

What happens when there is an under activity of thyroid gland?

A
  • Hashimoto’s thyroiditis (autoimmune disorder which destroys thyroid gland or blocks hormone synthesis) hypothyroidism associated with myxedema, goitre, cretinism in children
  • Iodine deficiency
80
Q

What is the importance of calcium?

A
  • structural role
  • blood coagulation (absence = no clotting)
  • intracellular messenger
  • regulation of excitability
81
Q

What is the importance of phosphate?

A
  • structural role
  • metabolism
  • buffer
82
Q

What are the 3 major hormones and what are their targets?

A
  1. Parathyroid hormone (PTH)
  2. Active vitamin D
  3. Calcitonin
    Targets: Bone, GI Tract, Kidneys
83
Q

What is the bone made up of?

A

Calcified matrix:

  • protein framework (osteoid); mainly collagen
  • calcium and phosphate salts (mainly hydroxyapatite)
84
Q

What cell does the parathyroid gland contain?

A

Chief cells (parathyroid hormone, PTH)

85
Q

What does PTH do?

A

Increase [Ca] decrease phosphate levels

86
Q

What is the osteocytes osteolysis?

A

Ca moves from the osteocyte (embedded in ECF) to the osteoblasts through Ca channels and out to the blood through Ca Pump.

87
Q

How does osteoclastic resorption occur?

A
  • The osteoclast contain a ruffled border that is attached to the bone
  • It releases enzymes to the ruffled border and decreases the pH (eats away the bone and collagen)
  • osteoclast move away and osteoblasts moves in
  • osteoblasts secretes osteoid
  • the osteoblasts that is submerged in osteoid transitions to osteocytes
88
Q

Why does PTH increases [Ca] but decreases [P]?

A

This is because PTH acts differently in the kidney as P is taken away by the kidney but Ca is reabsorbed back to the blood plasma

89
Q

How does the chief cell of parathyroid gland controls Ca secretion?

A

There are Ca sensors in chief cells

90
Q

What are the two sources of vitamin D3?

A
  1. 7-dehydrocholesterol (in skin)

2. Diet (fish, eggs)

91
Q

What is the synthesis of active vitamin D3?

A

7-dehydrocholesterol/diet > cholecalciferol (vitamin D3) > (in liver) 25-hydroxycholecalciferol > (kidneys, in presence of 1-alpha-hydroxydase) active vit D

92
Q

How does the absorption of calcium occur?

A
  • Ca moves from the lumen of the gut into the duodenal cell (enterocyte) via Ca channels.
  • Joins with the calbindin complex to form Ca and calbindin
  • Ca moves out to the blood through Ca ATPase
93
Q

What are the 3 major actions of PTH?

A
  1. Increase resorption from bone
  2. Increase resorption of Ca and decrease reabsorption of P in kidney
  3. Increase reabsorption of Ca and P in GIT
94
Q

What are the 3 major actions of Vit D3?

A
  1. Bone (works together with PTH)
  2. Increase reabsorption of Ca and P in kidneys
  3. Increase reabsorption of Ca and P in GIT
95
Q

What is the major actions of calcitonin?

A
  1. Decrease resorption in bones
96
Q

What’s the difference between rickets and osteomalaids?

A

Rickets is a bone deformity whereas osteomalaids in adults are considered adults having weak bones

97
Q

What are the types of cells in the exocrine and endocrine pancreas?

A

Exocrine: Duct cells, acinar cells
Endocrine: Alpha cell, beta cell

98
Q

What are the major pancreatic hormone and which islet cell type does it come from?

A 
Glucagon- alpha
Insulin; amylin- beta
Somatostatin: Delta
Pancreatic polypeptide: F or PP
Vasoactive intestinal polypeptide (VIP): D1
99
Q

What is the overall action of insulin?

A

Convert nutrients into the storage form and inhibits the breakdown of the storage form

100
Q

What is the function of glucagon?

A

Breakdown the storage form of nutrients

101
Q

What is the function of insulin in muscle?

A

Converts glucose to glycogen; amino acids to protein

102
Q

What is the function of insulin in adipose tissue?

A

Converts FA to Triglyceride; glucose to FA

103
Q

What is the function of insulin in the liver?

A

Converts glucose to glycogen and energy and FA; converts amino acids to protein

104
Q

How is the action of insulin activated?

A

Insulin binds to the alpha subunit which binds to the beta subunit (insulin receptor) on the ECF which activates the tyrosine kinase in the ICF. Tyrosine kinase changes the insulin receptor substrates (IRS). Hence affecting the transport systems, enzyme activity and gene expression.

105
Q

How is glucose transported?

A
  1. Secondary active transport (Uphill, Na dependent)
    SGLT 1, 2
  2. Facilitated transport (Downhill, Na dependent)
    GLUT 1,2
    (GLUT 4 is insulin sensitive)
106
Q

Where does glucose come from (short, long-term)?

A

Short-term: glucose is readily available in blood soon after a meal is eaten
Long-term: Liver glycogen stores are broken down; New glucose made from non-carbohydrate sources, especially from amino acids

107
Q

How is glucose sensed?

A
  • Glucose enter the beta-cell via GLUT2 channel
  • Glucose is metabolize and increases ATP
  • Increase ATP cause a closure of K channels which causes depolarization
  • Depolarization causes Ca channels to open = inflow of Ca
  • Increase of insulin secretion
108
Q

Why is glucagon secretion increased by amino acid?

A

In a protein rich meal, there would be a rise in amino acid in blood. Because there is no sufficient carbohydrates, there is a increase in glucagon to increase the blood glucose.

109
Q

What are the causes for too much insulin?

A

Insulin-secreting tumour, insulin overdose

110
Q

What are the consequences of having too much insulin?

A
  • Lowering of blood glucose level (hypoglycaemia)
  • Brain requires glucose, lack of glucose leads to autonomic and hormonal responses
    e. g. increased sympathetic activity (sweating)
    e. g. increased production of counter-regulatory hormones (glucagon, adrenalin)
  • Hunger, confusion and drowsiness (convulsions and coma for severe situation)
111
Q

What is type 1 diabetes?

A
  • autoimmune disease
  • beta cells destroyed
  • absolute insulin deficiency
112
Q

What is type 2 diabetes?

A
  • increased resistance to insulin
  • initial increase in insulin secretion
  • relative insulin deficiency
  • strong associated with obesity
113
Q

What are some of the problems associated with diabetes?

A
  • abnormalities in carbohydrates, fats, and proteins
  • increased blood glucose level (hyperglycemia)
  • decrease uptake of glucose into insulin-dependent tissues
  • increase uptake of glucose into insulin-independent tissues
  • chronic problems
114
Q

What are the potential treatments for type 1 and 2 diabetes?

A 
Type 1:
- administration of insulin
- pancreatic transplant
- islet cell transplant
- gene therapy
- increase growth of new islet cells
Type 2:
- dietary control with exercise
- drugs which increase insulin secretion and/or response to insulin
- insulin

PHYSL 210B (5 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions