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PHYSL 210B > Endocrinology > Flashcards

Endocrinology Flashcards

1
Q

Hormones classified based on structure or

A

solubility in plasma ; structure dictates site of receptor and mechanism of action

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2
Q

Water soluble hormones

A

protein hormones and catecholamines

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3
Q

Lipid soluble hormones

A

steroids, thyroid hormones, eicosanoids

don’t like aqueous environments

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4
Q

Protein vs Steroid hormones

A 
proteins = stored after synthesis
steroids = not stored, made on demand
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5
Q

Two types of receptors

A
  1. cell surface receptors (proteins and catecholamines; carried by blood to target cell - receptors need to be at surface)
  2. intracellular receptors that bind to steroid and thyroid hormones
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6
Q

An increase in the number of receptors for a hormone

A

up-regulation
- decrease is down-regulation (bringing down number of receptors on surface of cells for water hormones for ex and usually happens during abundance/too much of hormones around target cell and constantly available for binding to hormones)

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7
Q

A hormone that controls the secretion of another hormone

A

tropic (trophic) hormone

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8
Q

Hypo-responsiveness

A

reduced responsiveness of target cells; abnormal receptors (LAron Dwarfism), defective cell signalling, defective enzyme function in target cells

** normal amounts of hormones but target cells may have problems so don’t respond properly; usually have to do with target cells **

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9
Q

Hyper-responsiveness

A

increased responsiveness of target cells

** normal amounts of hormones but target cells may have problems so don’t respond properly; usually have to do with target cells **

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10
Q

Hypo- vs. Hypersecretion

A
  • hypo = secretion of too little hormone

- hyper = secretion of too much hormone

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11
Q

Posterior vs. Anterior Pituitary

A

Post = lots of similarities w neural structures; downward development of neural tissues in brain area

Ant pit = developed during embryological development; as an outward growth from the part that developed ultimately into mouth, pharynx, etc.

** Ant is quite different from post even though they are laid juxtapositionally from each other **

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12
Q

What connects the hypothalamus to the anterior pituitary gland?

A

hypothalamic-hypophyseal portal system

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13
Q

The hormones of the anterior pituitary gland

A
  • FSH (ovaries & testes)
  • LH (ovaries & testes)
  • ACTH (causes release of another hormone at adrenal cortex)
  • TSH (thyroid gland)
  • PRL (does not act on a target organ to secrete another hormone but actually works on development of target gland = mammary gland or breast tissue)
  • GH (most tissues like bone)

** all are protein hormones and come from different cell types except FSH and LH which are secreted from the same cell type

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14
Q

Hormones of the hypothalamus and their effects on anterior pituitary hormones

A
  • GnRH = increases LH & FSH secretion
  • CRH = increases ACTH secretion
  • TRH = increases TSH secretion
  • GHRH = increases GH secretion
  • GHIH or SS = decreases GH secretion
  • PIH (dopamine/DA) = decreases PRL

** all are peptides except PIH

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15
Q

Posterior pituitary hormones

A
  • oxytocin and ADH
  • produced in the cell bodies of the hypothalamus
  • carried by the axons to the posterior pituitary
  • released fron the nerve endings in the posterior pituitary
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16
Q

Growth Hormone

A
  • most abundant anterior pituitary hormones
  • a protein hormone
  • acts on cell surface receptors and is associated with protein kinase activity
  • secreted throughout life
  • promotes growth mainly after birth (not in fetal stage)
  • pulsatile secretion
  • follows circadian rhythm
  • increases growth of most issues
  • affects metabolism
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17
Q

T or F. Growth hormone is necessary for fetal growth

A

F! after birth

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18
Q

Bone growth by GH

A
  • prior to puberty, usually growth of bone = shaft area
  • as shaft grows, the person grows in linear length
  • end of puberty = epiphyseal area (cartilage type) = seals up; closure of epiphyseal growth plate => no more increase in linear growth (height)
  • onset of puberty = sharp rise of total body height then linear growth stops = plateaus
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19
Q

Why does GH cause linear growth in vivo but not in vitro?

A

in human body, specifically in stage when growth can happen, GH is produced in the body or if u added GH to body => GH can work to produce another hormone in the liver and other cells = insulin-like growth factors ==> overall action of insulin-like growth factor = acts on target cells and helps overall growth (can’t happen in vitro!)

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20
Q

Effects of GH on metabolism

A
  • increases protein synthesis and increases growth of most tissues
  • FATS: GH increases lipolysis and increases FFAs for energy
  • CARBS: GH decreases glucose uptake into muscles (anti-insulin like effects); hyperglycemia, “diabetogenic”; increases gluconeogenesis by liver
  • PROTEINS: increses AA uptake into cells;increases protein synthesis; increases cell size (hypertrophy); increases # of cells in connective tissues (hyperplasia)
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21
Q

Actions of GH are actually mediated by IGF-1…

A

sometimes GH does not have to induce growth by acting directly on target cells to cause growth - indirect manner = GH working on liver to induce IGF-1

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22
Q

Too much GH

A
  • symptoms depend on time of onset
  • Gigantism = seen in children, increased linear growth
  • Acromegaly = seen in adults, thickening of bone, large hands, feet, jaw, accompanied with coarse features
  • associated with metabolic effects (eb. hyperglycemia)
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23
Q

Too little GH

A
  • Dwarfism (proportion looks normal) = in children, stunted growth due to decreased GHRH release, decreased GH synthesis and secretion
  • Laron dwarfism = mutation of GH receptor
  • metabolic effects
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24
Q

Mechanism of ADH action

A

ADH carried by blood to kidney and works on receptors on basolateral side of collecting ducts –> AC - cAMP - PKA - phosphorylation of substrate proteins - translocation of channels (aquaporin 2 ) - surface of luminal membrane

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25
Q

Too much ADH

A

increased water retention, increased blood volume (syndrome of inappropriate antidiuretic hormone secretion, SIADH)

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26
Q

Too little ADH

A
  • central or neurogenic diabetes insipidus (lack of ADH, large volume of dilute urine
  • nephrogenic diabetes insipidus (Abnormal ADH receptors in collecting duct cells, do not respond to circulating levels of ADH, large volumes of dilute urine)
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27
Q

Factors affecting oxytocin secretion

A
  • parturition, lactation
  • cervical stretch = uterine contraction —> hypothal to trigger cells that release oxytocin – through bloodstream – uterine muscles for further contractions = positive feedback; increases as more bind to receptors
  • pregnancy develops breast tissue for synthesis of milk but suckling from baby = positive stimulation of oxytocin release –> milk released ; milk ejection reflex induced by suckling of newborn that causes oxytocin production and regulates whole reflex production
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28
Q

Major actions of aldosterone

A
  • increased Na+ reabsorption by the kidney (i.e. increased Na+ retention by the body)
  • increased water reabsorption by the kidneys (this happens secondary to Na+ reabsorption)
  • increased K+ secretion by the kidneys (i.e. increased loss of K+ in urine)
  • increased H+ secretion by the kidney (i.e. increased loss of H+ in urine)
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29
Q

T or F. Aldosterone secretion is not primarily under the control of anterior pituitary tropic hormone

A

T! ACTH could probably maintain healthy status of cells but no regulatory control on aldosterone secretion

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30
Q

General functions of cortisol

A

affects metabolism of glucose and hence the name glucocorticoids

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31
Q

Cortisol “non-stress” responses

A

has permissive action on epinephrine and norepinephrine that exert control on vascular tone; this way cortisol helps in maintaining blood pressure around a normal level
- help to maintain vascular tone of blood vessels even in small amounts of cortisol

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32
Q

Metabolic effects of cortisol

A
  • increase in blood glucose (hyperglycemia)
  • increase in glucose availability for CNS
  • decrease in glucose utilization by peripheral tissues of the body
  • increase in glucose formation in the liver (gluconeogenesis)
  • increase in glycogen synthesis in the liver
  • increase in protein breakdown
  • increase in fat breakdown
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33
Q

Cortisol increases glucose availability for CNS

A

we need to keep blood glucose levels elevated to make glucose available to CNS = immediately after meal, blood glucose is high but starts dropping after two hours , when blood glucose starts to go down, how does blood supply glucose to brain tissue?? SO CORTISOL provides glucose to CNS when the levels of sugar has started to drop after meal
- after blood glucose drops this is when cortisol kicks in !!

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34
Q

______ glucose production in between meals

A

hepatic

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35
Q

Major actions of cortisol on immune system

A
  • decrease in lymphocyte number
  • decrease in lymph node size
  • reduced humoral and cellular immunity
  • decreased production of inflammatory substances, such as leukotrienes and prostaglandins
  • decreased capillary permeability and prevention of neutrophil diapedesis to the site of infection and edema
  • reduction in proteolytic content release from lysosomes
  • increased susceptibility to infection

** actually cortisol puts a break from your immune system to become hyperactive such that ur body does not become too active and respond to any antigen it sees and in this manner prevents the development of an autoimmune disease

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36
Q

Pharmacological use of cortisol

A

suppress organ rejection after transplantation

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37
Q

Other effects of cortisol

A
  • effects during fetal and neonatal life
    > required for development of CNS (brain)
    > GIT, adrenal gland
    > lungs (surfactant synthesis)

** GH is needed for growth of tissues following birth but this is an example where u can see that even if GH is not involved for fetal growth - cortisol is there which is essential for fetal development and neonatal life as well **

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38
Q

Diurnal rhythm

A
  • cortisol produced in our body also follows a diurnal rhythm associated with sleep-wake cycle
  • released and high during early hours of morning just before waking up = cortisol
    & low during night hours

^ pattern reversed in indivs that work night shift jobs, etc. (sleep in day and work in night)

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39
Q

Conn’s syndrome

A
  • too much aldosterone
  • hypernatremia
  • increase in volume of ECF
  • increase in BP (hypertension)
  • hypokalemia
  • metabolic alkalosis
40
Q

Cushing’s disease

A
  • too much cortisol
  • increase in blood glucose
  • muscle wasting
  • moon face, buffalo hump
  • decreased resistance to infection
41
Q

Too much adrenal androgens

A

virilization (masculinization) in females

42
Q

Addison’s disease

A
  • too little aldosterone
  • hypotension
  • metabolic acidosis
  • hyperkalemia
43
Q

Too little cortisol

A

also Addison’s disease

  • decrease in blood glucose, increased skin pigmentation
  • ACTH (causes release of cortisol) is produced along with another hormone in the anterior pituitary cells = melanocyte-stimulating hormone .. when feedback of cortisol is low, removes neg feedback on ant pituitary and as a result, high production of ACTH but also same cells produce MSH - once released = works on skin pigment cells = darkening of skin colour
44
Q

Too little adrenal androgens

A
  • reduced hair growth

- decreased sexual response in females (?)

45
Q

Regulation of catecholamine secretion

A

Splanchnic nerve innervates chromaffin cells within the adrenal medulla => release Ach on chromaffin cells => start to produce adrenaline and noradrenaline

Stimulus for synthesis and release = Ach from splanchnic nerve

46
Q

Major actions of catecholamines on CV system

A

increased:

heart rate, force of contraction, cardiac output, blood pressure

47
Q

Major actions of catecholamines on smooth muscle

A

dilation of pupils, bronchodilation, decreased GIT motility

48
Q

Major actions of catecholamines on metabolism

A

increased glycogenolysis (skeletal muscle & liver), increased lipolysis and gluconeogenesis (liver also helped by catecholamines to help body make more glucose; sources = non-carb source)

49
Q

What secretes calcitonin?

A

Parafollicular cells (thyroid hormone)

50
Q

T or F. T4 is found in a much larger proportion compared to T3 although T3 is the biologically active hormone produced by thyroid gland

A

T!

51
Q

Where is T4 converted to T3?

A

in peripheral cells and liver; T3 binds to nuclear receptors

52
Q

The thyroid produces:

A

90% T4

and 10% T3

53
Q

Physiological actions of thyroid hormones

A
  • acts on most tissues: change in transcription and translation process
  • increase metabolism
  • required for growth and development
54
Q

Growth and development actions of thyroid hormones

A
  • act as ‘tissue growth factors’
  • small amounts stimulate protein synthesis
  • increase GH/IGF-1- production
  • essential for CNS maturation during fetal stage
  • maternal hypothyroidism results in poor fetal CNS development and mental development disability
55
Q

Metabolic actions of thyroid hormones

A
  • catabolism and anabolism both increased
  • increased BMR, associated with increased O2 consumption and increased heat production
  • increased carb absorption and utilization
  • increased protein breakdown
  • increased cholesterol metabolism
  • decreased serum cholesterol (LDL)
56
Q

Other permissive effects of TH

A
  • CV system (beta adrenergic receptors): increased HR and contractility, increased BP
  • potentiation of sympathetic nervous system (beta-2 adrenergic receptors)
  • reproductive system: necessary for normal function and fertility
57
Q

T or F. T3 and T4 are transported in blood mainly in bound form TBP

A

T, T3 freer than T4

58
Q

T or F. Men are more likely than women to develop a thyroid condition

A

F! Women more likely

59
Q

Graves’ Disease

A
  • overactivity of thyroid gland
  • autoimmune disorder
  • Ab to the TSH receptor stimulates thyroid hormone production
  • associated with increased BMR (degeneration of muscle tissue, very thin, etc.)
  • exophthalmos, goitre, puffiness around eyes too
  • increased growth of thyroid follicles by Abs mimicking effects of TSH
60
Q

Hashimoto’s thyroiditis

A
  • underactivity of gland
  • most common autoimmune cause of hypothyroidism
  • autoimmune disorder where thyroid peroxidase (TPO) antibodies destroy thyroid gland to block hormone synthesis
  • hypothyroidism associated with myxedema (adult onset; associated to some of mental effects that these patients display when experiencing hypothyroidism = not present in all patients, sometimes there ), goitre, cretinism (in children only; not optimal growth or mental development due to hyposecretion )
61
Q

Symptoms of hypothyroidism

A 
lethargy
weight gain
cold intolerance
constipation
nausea/low appetite
Menorrhagia (heavy periods)
edema
shortness of breath
"myxedema madness"
dry skin
brittle hair and nails
62
Q

T or F. Goitres can happen for both hypo- and hypoerthyroidism

A

T!

63
Q

Most common cause of hypothyroidism, goitre, developmental/intellectual disability and preventable brain damage

A

Iron deficiency in diet

64
Q

Goitre formation in both cases

A

Hyper = increase T3 and T4 = strong negative feedback at ant pit and hypothalamus level; decreased in thyrotropin releasing hormone… etc. => low TSH; decreased in TSH hormone = goitre

Hypo = iodine deficiency in diet; less T3 and T4 => in the long run, taking away the effects of neg feedback, low amounts indirectly encourages hypothal to start releasing more TRH (works on ant pit) which increases TSH secretion
due to def in iodine, T3 and T4 will remain low but due to excessive TSH around in blood = do other anabolic, growth or tropic effects so thyroid gland will enlarge; colloid will have same or higher thyroglob made under effects of TSH

65
Q

Single best screening test for thyroid function

A

TSH measurement

  • changes in TSH occur often before measurable changes in T4 or T3 are present
  • TSH reflects the true state of free T4, free T3
66
Q

T or F. Concentration of free ionized calcium is greater in the ECF than the ICF

A

T! PTH increases Ca and decreases phosphate in the plasma (part of ECF)

67
Q

Dynamic calcium balance

A
  • bone formation - lots of ionized ca is taken up by bone; Ca moves from plasma to bone during bone formation (mineralization - depositing Ca salts)
  • adding Ca back to plasma = resorption by bone breakdown or demineralization
  • Ca can be secreted from blood and taken up in to small intestine
    Ca can be absorbed from dietary source from small int to take back into blood plasma
  • in kidneys, Ca can be filtered in Bowman’s Capsule and filtrate enters and Ca can be reabsorbed in body depending on the balance it needs to attain or if needed, it can be secreted out from kidney and finally it ends up being excreted from body through urine and some through fecal waste as well
68
Q

Osteoblasts vs. Osteocytes vs. Osteoclasts

A

Osteoblasts = involved in the development of new cells, new bones, etc. (addition of Ca 2+ tobone)

Osteocytes = bone cells provide lots of interconnected messages b/w cells while bone is developing

Osteoclasts = involved in BREAKDOWN of both tissue during remodelling of bone (release of Ca 2+ to bone)

69
Q

T or F. During resorption, osteoclasts generate H+ ion

A

T! does it by letting CO2 combine w H2O in presence of carbonic anhydrase = bicarbonate and H+ ion

  • H+ creates an acidic environment where lots of enzymes are activated and can help in osteoclastic resorption or breakdown of bone
    • bone has to broken down first then things can heal **
70
Q

T or F. Another hormone is regulating PTH

A

F! Levels of free ionized Ca is

71
Q

Active vit D

A

1,25-(OH)2D

72
Q

Vitamin D3 structure

A

structure that almost like steroid hormone; can permeate through plasma membrane of cells and has intracell receptors that can bind to D3 and bring about changes in certain proteins within target cell and all this happens by enhancing gene transcription, protein translation, etc.

73
Q

Absorption of Calcium

A
  • in presence of vit D, Ca channels are opened up in luminal side of duodenal cells which allows ionized Ca to enter and then binds to protein known as calbindin to form a complex => allows for transport of Ca in a complex form on the basolateral side where there is an active transporter of Ca ATPase which allows Ca to move out and get absorbed in the blood
  • vit D is a hormone, target is duodenal cell; makes proteins = allows for Ca absorption

** once Ca enters, calbindin helps in translocation process and once transported to basolateral side, Ca comes off complex and calbindin is re-circulated in cell as a free protein **

74
Q

Osteomalacia

A

softening of bones in adults; rickets in children

75
Q

Rickets in children

A

deficiency in mineralization of bone matrix, bones remain soft

  • not reversible
  • vit D supplements at early age = no rickets
76
Q

Low plasma calcium increases nerve and muscle excitability vi opening of Na+ channels

A

Hypocalcemic Tetany

  • hyposecretion of PTH
  • spasms; abduction of thumb over palm = typical contracture
77
Q

Central duct system of pancreas

A

acinar cells which pushes out to duct cells

  • pancreatic juices to small intestine
  • exocrine
78
Q

Islet of Langerhans

A
  • prancreatic hormones to blood; endocrine
  • beta cells (predominant = insulin and amylin (100:1)
  • alpha cells = glucagon
  • delta = somatostatin
79
Q

Insulin

A
  • hormone of feasting
  • increases uptake and storage of fuels
  • is an anabolic hormone (helps to retain nutrients to grow your body)
80
Q

Glucagon

A
  • hormone of fasting
  • increases mobilization of fuels when needed
  • is a catabolic hormone (helps in mobilizing stored nutrients when body needs fuel for its functions)
81
Q

Predominant anabolic hormone in our body

A

Insulin; all others have a role to play in breakdown (glucagon, epinephrine, cortisol, GH)

82
Q

Targets for insulin actions (3)

A
  • skeletal/cardiac muscle
  • adipocytes
  • hepatocytes
83
Q

When a person exercises or insulin is present, what happens to muscle/adipose tissues?

A

IRS activation causes translocation of transporters onto membrane surface = glucose uptake by facilitated diffusion

84
Q

Where does glucose come from?

A

short term
- glucose is readily available in blood immediately after a meal

long term
- glycogen stores from liver is broken down by glycogenolysis (12-24 hrs)

even longer
- “new glucose” is made from non=-carbohydrate sources such as AAs and fatty acids by the process of gluconeogenesis

85
Q

Primary role of glucagon

A

defend against hypoglycemia (low blood glucose)

86
Q

Primary target of glucagon

A

liver

  • promotes breakdown of hepatic glycogen
  • provision of substrates for increased glucose production by increased lipolysis
87
Q

Dominant hormone during fasting

A

glucagon

  • main effect = breaking down fat
  • get glucose into blood (net effect)
88
Q

Hypersecretion of insulin

A
  • causes: insulin secreting tumor, overdose
  • reduction of blood glucose level (hypoglycemia)
  • brain requires glucose: lack of glucose leads to autonomic and hormonal response changes
    > increased symp activity (such as palpitations or sweating)
    > increased production of counter regulatory hormones (such as glucagon, adrenaline
    > person feels tired, becomes confused and drowsy
    > severe cases = person can have convulsions and go into coma
89
Q

Hyposecretion of insulin

A
  • hyperglycemia (increased blood glucose)
  • diabetes mellitus
  • ketoacidosis
90
Q

Type 1 Diabetes Mellitus

A
  • autoimmune disorder
  • often seen in young people
  • b cells destroyed
  • absolute insulin deficiency
  • 5-10% of cases in NA
91
Q

Type 2 Diabetes Mellitus

A
  • increased resistance to insulin
  • strongly associated with obesity
  • traditionally more common in adults, observed lately in obese young children
  • relative insulin deficiency
  • 90-95% of all cases in NA
92
Q

this leads to a catabolic state characterized by hyperglycemia, generalized wasting, acidosis and ketogenesis = diabetic ketoacidosis

A

Insulin deficiency

93
Q

Diabetic ketoacidosis

A
  • a short term complication of DM
  • decreased insulin
  • increased counter-regulatory hormones (glucagon, epi/norepi, cortisol, GH)
  • leads to severe metabolic decompensation
  • characterized by: hyperglycemia, high ketone bodies, acidosis, hyperosmolarity, dehydration, death
  • acetone breath
  • thirst = polydipsia
  • polyphagia
  • glucosuria = increase urine vol
94
Q

Cardinal symptoms of DM

A
  • polyuria = increase urine vol, increase frequency in urination
  • glucosuria = glucose in urine
  • polyphagia = increased hunger
  • polydipsia = increased thirst
95
Q

Long term high levels of glucose leads to…

A

blindness, renal failure, atherosclerosis, changes in sensation, poor wound healing

96
Q

Treatment of Type 1 DM

A
  • administration of insulin by injection, programmable pump, inhalation, along with amylin analogs
  • islet cell transplant
  • gene therapy
97
Q

Treatment of Type 2 DM

A
  • dietary control and exercise
  • drugs which increase insulin secretion and/or response to insulin
  • insulin administration

PHYSL 210B (4 decks)

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