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Biochemistry 2nd Year > Chp 19; Hormones > Flashcards

Chp 19; Hormones Flashcards

1
Q
  1. Classify hormones based on chemical nature?

2.classify hormones based on mechanism of action?
Give examples of both?

A
  1. Protein/peptides (e.g insulin, Glucagon
    ADH, Oxytocin)
    Steroid hormones
    (Glucocoticoids, mineralocorticoids, sex hormones)
    Amino acid derivatives
    (Epinephrine, norepinephrine
    Thyroxine (T4), triiodothyronine (T3))
  2. Categories;
    Group 1 (lipophilic)—- bind to intracellular receptors
    E.g cholesterol derivatives (except T3 & T4);
    Androgens
    Estrogen
    Glucocorticoids
    Calcitriol

Group 2 (hydrophilic) — bind to cell surface receptors—- release second messenger
E.g when 2nd messenger is;
cAMP
(Glucagon
Calcitonin
ACTH
PTH
FSH
LH)

Phosphotidylinositol/calcium
(TRH
GnRH
Gastrin
CCK)

Unknown
(Growth hormone
Insulin
Prolactin
Oxytocin)

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2
Q
  1. Group 1 hormone bind to what on DNA?
  2. Formula and structure of cyclic AMP?
  3. How cyclic AMP is formed? By which enzyme?
  4. How cAMP is degraded?
  5. Synthesis of cAMP is mediated by which proteins?
A
  1. They first bind to intracellular hormone receptors —— hormone-receptor complex—–
    Binds to Hormone Responsibe Element (HRE) on DNA—- protein synthesis
  2. 3’, 5’ - monophosphate
    Contains;
    Adenine
    Ribose
    Phosphate
  3. Membrane bound adenylate cyclase converts ATP to cyclic AMP
  4. Hydrolysis by
    Phoshphodiesterase
    To 5’ AMP
  5. G proteins (that bind to guanine nucleotide)
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3
Q
  1. Structure of protein kinase A ? Second messenger for it?
  2. Second messenger for protein kinase C?
  3. Effect of Caffeine and thyophilline (methylxantine derivatives) on cAMP?
  4. Give selected examples of group 1 and group 2 hormones?
A
    • A heterotetramer containing
      2 —– Regulatory subunits (R)
      2 —– Catalytic subunits (C)
  • second messenger cAMP
    Dissociates heterotetramer and activates it—- phosphrylation of proteins
  1. Diacylglycerol
  2. Inhibit —– phosphodiesterase
    Increase —- intracellular level of cAMP
  3. Group 1
    Steroids
    T3 & T4
    Calcitriol

Group 2
Proteins
Polypeptides
Catecholamines

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4
Q
  1. Name the hypothalamic hormones??
  2. How many amino acids does these hormone contains?
    CRH
    GRH
    GRIH
  3. Which of these hormones is a decapeptide?
    Tripeptide
A
  1. 6 hormones or factors;
    Thyrotrophin-releasing hormone (TRH)
    Corticotrophin releasing hormone (CRH)
    Gonadotrophin releasing hormone (GnRH)
    Growth hormone releasing hormone (GRH) (somatotropin)
    Growth hormone release inhibiting hormone (GRIH)
    (Somatostatin)
    Prolactin release-inhibiting hormone (PRIH)
  2. CRH —- 41 amino acids
    GRH (somatotropin) —- 44 amino acids
    GRIH (somatostatin) —- 14 amino acids
  3. Decapeptide—Gonadotropin releasing hormone
    Tripeptide—- thyrotropin releasing hormone
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5
Q
  1. Master endocrine gland?
  2. Classify its hormones?
  3. What is chorionic somatomammotropin?
A
  1. Adenohypophysis (anterior pituitary)
  2. 3 categories;
    Growth hormone - prolactin group
    Glycoprotein hormones
    Pro-opiomelanocortin peptide family
  3. Chorionic somatomammotrophin (CS), also known as human placental lactogen (hPL), is a hormone produced by the placenta during pregnancy. It plays a key role in fetal development and maternal metabolism. The hormone is structurally similar to growth hormone and prolactin, and its main functions include:
  4. Regulating maternal metabolism: hPL alters the mother’s metabolism to ensure that the fetus gets enough nutrients. It increases insulin resistance in the mother, which raises maternal blood glucose levels, allowing more glucose to be available for the developing fetus.
  5. Stimulating milk production: hPL also prepares the breasts for lactation by promoting the development of mammary glands, although actual milk production doesn’t occur until after birth.
  6. Fetal growth: It supports fetal growth by increasing the availability of nutrients to the fetus and stimulating the production of certain hormones.

The levels of hPL rise throughout pregnancy, reaching their peak towards the end of gestation. It is often measured as part of prenatal tests to assess placental function.

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6
Q
  1. Largest increase in growth hormone occurs?
  2. The growth effects of GH are mediated by?
  3. Effect of GH on protein metabolism?
  4. Effect of GH on carbohydrate metabolism? Antagonistic to?
  5. Effect of GH on lipid metabolism?
A
  1. After the onset of sleep
  2. Somatomedin C produced in liver (insulin like growth factor ((IGF-I)))
  3. Anabolic effect
    -protein synthesis
    - positive nitrogen balance
    - increase in body weight
  4. Antagonisitic to insulin
    -hyperglycemia
  5. Promotes lipolysis
    -free fatty acids oxidation
    - ketogenesis in diabetes
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7
Q
  1. Overproduction of GH leads to?
  2. Underpoduction leads to?
  3. Other names for prolactin?
  4. Main functions of prolactin?
  5. Name the structural similar glycoproteinic hormones?
    Which of these are gonadotrophs?
    HcG is release by?
A
  1. Gigantism
    - in children
    - before epiphyseal plate close

Acromegaly
- in adults
- after epiphyseal closure

  1. Dwarfism
  2. Lactogenic hormone
    Luteotrophic hormone
    Mammotropin or luteotropin
  3. Lactation in mammals
    - growth of corpus luteum
    - stimulates progesterone
    - lipid biosynthesis (opposite to GH)
  4. TSH
    FSH
    LH
    human chorionic gonadotrophin (HCG)

-gonadotrophs
S
FSH
LH
hCG

  • placenta (not pituitary)
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8
Q
  1. From where these hormones are released;
    Thyrotropin releasing hormone (TRH)
    Thyroid stimulating hormone (TSH)
  2. How TSH works?
  3. What is organification?
  4. Functions of FSH in
    Females
    Males
  5. Functions of LH (luteinzing hormone) in
    Females
    Males
A
  1. TRH —- hypothalamus
    TSH —- anterior pituitary
  2. Thru cAMP
    - promotes uptake of iodide by thyroid gland
    - conversion of iodide ( I-) to active iodide (I+) (Organification)
    - proteolysis of thyroglobin to release T3 & T4
  3. conversion of iodide ( I-) to active iodide (I+)
  4. Females
    - follicular growth
    - increase weight of ovaries
    - enhance estrogen production

Males
- testosterone production
- spermatogenesis
- growth of semineferous tubules

  1. Female
    - progesterone release from corpus luteum

Males
- testesterone production from interstitial cells of leydig
- LH + FSH collectively ——- developemnt of secondary sex characters in males

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9
Q
  1. hCG is produced by??
    - resembles?
  2. Levels increase when?
  3. Significance?
  4. Name hormones of the pro-opiomelanocortin peptide family (POMC)
  5. All members of POMC are produced from??
  6. How many amino acid of POMC?
    - why is ot called pro-opiomelano-cortin?
A
  1. Syncitiotrophoblast cells of placenta
    - resembles LH structurally
  2. In plasma & urine
    Immediately after implantation of fertilized ovum
  3. hCG in urine — early detection (within a week after missing menstrual cycle)
    Of pregnancy
  4. ACTH
    lipotropin hormone (LPH)
    Melanocyte Stimulating Hormone (MSH)
    Neuromodulators (endorphins & enkephalins)
  5. A single gene of
    Anterior & intermediate pituitary
  6. 285
    - bcz;
    Prohormone to opioids melanocyte-stimulating hormone and corticotropin
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10
Q
  1. What hormones give rise to MSH;
    a-MSH
    B-MSH
    y-MSH
  2. Corticotropin like intermediate lobe peptide (CLIP) is formed by?
  3. How many amino acids does ACTH has?
    3 functions?
  4. Overproduction of ACTH leads to?
  5. How many amino acids in B-lipotropin?
    - found only in?
    - most important role?
  6. Name two pentapeptide derivatives of B-endorphins?
A
  1. a-MSH —- ACTH
    B-MSH —- B-Lipoptropin
    y-MSH —- N-terminal peptide
  2. ACTH
  3. 39
    - converts cholesterol —- pregnenolone
    - RNA & protein synthesis
    - lipolysis by activating lipase
  4. Cushing’s syndrome (due to tumor)
    - impaired glucose tolerance
    - negative nitrogen balance ( protein breakdown)
    - hypertension
    - muscle atrophy
    - edema
  5. 93 carboxyterminal aminoacids
    - pituitary
    - precursor for B-endorphin & enkephalin
  6. Methionine enkephalins
    Leucine enkephalins
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11
Q
  1. What type of neurotransmitters are endorphins and enkephalins? And what is their effect like?
    Also called?
    Control?

2.they bind to the same receptors as?

  1. Which type of MSH is important in human?
    - its activity is controlled in?
  2. Name the nonapeptide hormones? (9 amino acids)?
  3. Give 3 functions of oxytocin?
A
  1. Peptide neurotransmitters
    - opiate- like effects
    - opioid peptides
    - endogenous pain perception
  2. Morphine opiates
  3. y-MSH
  4. y-LPH or its precursor B-LPH
  5. Oxytocin
    ADH

5.
• Induces labor (uterus contraction)
• milk ejection ( contraction of myoepithelial cells of breast)
• inhibits steroids synthesis in ovary

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12
Q
  1. Release of ADH is controlled by which receptors?
  2. ADH acts on?
  3. Urine output
    With ADH
    Absence of ADH
  4. ADH action is mediated thru?
  5. Diabetes insipidus is characterized by?
A
  1. Osmoreceptors —- hypothalamus
    Baroreceptors —- heart
  2. Distal convulated tubule
  3. With ADH —- 0.5 -1.5 l/day
    Absence of ADH —- 20 l/day
  4. cAMP
  5. Excretion of large volumes of dilute urine (polyuria)
    - due to insufficient ADH
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13
Q
  1. Hormones secreted by thyroid gland?

2 . Precursor for synthesis of T3 & T4?

  1. Tyrosine of thyroglobin is iodinated at?
  2. How T3 & T4 are formed from MIT & DIT?
  3. Which mineral is essential for synthesis fir thyroid hormones?
  4. Uptake of iodide is
    Promoted by
    Inhibited by
  5. Iodide is converted to active iodine I+ by?
    Rxn requires
    Catalysed by?
    This oxidation is promoted by?
  6. Name the drugs that inhibits oxidation of iodide to active iodine?
A
  1. Thyroxine (T4)
    Triiodothyronine (T3)
    Calcitonin
  2. A glycoprotein thyroglobin
  3. Position 3 —– monoiodotyrosine (MIT)
    Position 5 —– Diiodotyrosine (DIT)
  4. 2 molecules of DIT couple to form —– T4
    1 molecule of MIT couples with 1 molecule of DIT to form —- T3
  5. Iodine

Promoted by —- TSH
Inhibited by —- Thyocyanate
Perchlorate

  1. -Requires H202
    - thyroperoxidase
    - TSH
  2. Antithyroid drugs;
    Thiourea
    Thiouracil
    Methimazole
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14
Q
  1. Which one is more active, T3 Or T4?
  2. Thyroid hormones increase O2 consumption in most tissues except;?
  3. Diminished Na+—K+ Atpase activity leads to?
  4. Effect of thyroid hormone in protein metabolism?
    1. Effect of thyroid hormone in carbs metabolism?
  6. Hypothyrodism effects lipids?
A
  1. T3 is 4 times more active than T4
  2. Brain
    Lungs
    Testes
    Retina
  3. Obesity
  4. Positive nitrogen effect
    Protein synthesis
  5. Cause glycogenolysis
    Gluconeogenesis
    Hyperglycemia
  6. Elevated plasm cholesterol
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15
Q
  1. Why thyroid gland becomes enlarged in goitre?
    Caused by?
  2. Name some goitrogenic substances?
  3. Simple endemic goitre is caused due to?
    - patient is given?
  4. Hyperthyroidism.is caused due to?
    Symptoms?
  5. Graves disease is due to?
  6. Treatement of hyperthyroidism?
A
  1. To compensate for decreased synthesis of thyroid hormones
    - associated with elevated TSH
    - deficiency of iodine ( needed for synthesis of thyroid hormones)
  2. That interfere with thyroid hormone production;
    Thiocyanates
    Nitrates
    Perchlorates
    And some drugs;
    Thiourea
    Thiouracil
    Thiocarbamide
  3. Deficiency of iodine in diet
    - iodized salt
  4. Graves disease
    - exopthalmos (protuding eyeballs)
    -higher BMR
  5. elevated thyroid stimulating igG also called (LATS)
    Long Acting Thyroid Stimulator
    — activated TSH
  6. Antithyroid drugs;
    Methimazole
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16
Q
  1. Hypothyroidism is assoviated with?
  2. Which disorder is associated woth?
    Graves disease
    Cretinism
    Myxoedema
  3. Natural painkillers in brain??
A
  1. Cretinism — in children
    Physical and mental retardation
    Myxoedma —- in adults
    Swelling around eyes (baggy eyes)
    Edema
    Weight gain

2.
Graves disease —- hyperthyroidism
Cretinism — hypothyroidism
Myxoedema —- hypothyroidism

  1. Endorphins
    Enkephalins
17
Q
  1. What is pheocytochroma?
    Diagnosis?
  2. Normal level of VMA in urine?
  3. Name the metabolic products of catecholamine excreted in urine?
  4. Name the enzymes acting on catecholamines?
  5. Both epinephrine & Norepinephrine are amine derivatives of?
  6. How epinephrine is formed from Norepinephrine?
A
  1. A tumor of adrenal medulla
    - excessive production of epinephrine & Norepinephrine (catecholamines)
    - urinary VMA (vanillyl mandelic Acid) (metabolite of catecholamine breakdown)
  2. < 8mg/day
  3. Metanephrine
    Vanillyl mandelic acid (VMA)
  4. Catechol-O-methyl transferase (COMT)
    Monoamine oxidase (MAO)
  5. Catechol nucleus (dihydroxylated phenyl ring)
  6. methyl derivative
18
Q
  1. Precursor for synthesis of catecholamine?
  2. Effect of catecholamine on:
    Carbohydrate
    Lipids
  3. How catecholamine affects smooth muscles of blood vessels in
    Skeletal muscle, bronchi, GIT
    Skin & kidney
  4. How it affects platelets?
    Oxygen consumption?
    Blood pressure
    Heart rate
A
  1. The amino acid - - - - Tyrosine
  2. Carbohydrate - - - - increase glucose level
    Lipids—- lipolysis
  3. Skeletal muscle, bronchi, GIT- - - - relax
    Skin & kidney—– contract
  4. Inhibits platelet aggregation
    O2- increases
    BP- increases
    HR- increases

Biochemistry 2nd Year (9 decks)

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