hormonal communication Flashcards

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1
Q

what is an endocrine gland

A
  • group of cells
  • specialised to secrete chemical (hormones)
  • directly into the blood stream
  • pancreas + adrenal glands
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2
Q

pituitary gland

A
  • growth hormone
  • controls bones and muscles growth
  • ADH
  • increases water reabsorption in kidneys
  • gonadotrophins
  • control development of ovaries and testes
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3
Q

thyroid

A
  • thyroxine
  • controls metabolism rate
  • rate at which glucose is used up in respiration
  • promotes growth
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4
Q

adrenal gland (role)

A
  • adrenaline
  • increase heart/breathing rate
  • raise blood sugar levels.
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5
Q

testis

A
  • testosterone
  • control sperm production
  • secondary sexual characteristics
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6
Q

pineal gland

A
  • melatonin

- affects reproductive development and daily cycles.

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7
Q

thymus

A
  • thymosin

- promotes production and maturation of WBC

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8
Q

pancreas

A
  • insulin
  • glucose to glycogen
  • glucagon
  • glycogen into glucose
  • in the liver
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9
Q

ovary

A
  • oestrogen
  • controls ovulation
  • secondary sexual characteristics
  • progesterone
  • prepares uterus lining for receiving an embryo
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10
Q

what is an exocrine gland

A
  • secrete hormones
  • through ducts
  • into organs
  • or to the surface of the body
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11
Q

steroid hormones

A
  • lipid-soluble
  • pass through lipid component of CM
  • bind to steroid hormone receptors on CM
  • hormone/receptor complex is formed
  • complex can inhibit or facilitate the transcription of a gene
  • E.g. oestrogen
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12
Q

non-steroid hormones

A
  • hydrophilic
  • can’t pass directly through the cell membrane
  • bind to specific receptor on surface of target cells membrane
  • causes a cascade reaction mediated by secondary messengers
  • E.g adrenaline
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13
Q

compare the hormonal and nervous systems

A
  • H: communication is by hormones
  • N: communication by nervous impulses
  • H: transmission by blood
  • N: transmission by neurones
  • H: slow transmission
  • N: very rapid transmission
  • H: widespread response
  • N: localised response
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14
Q

why is hormonal communication slow

A
  • not released directly onto their target cells

- they aren’t broken down as quickly as NT so have a longer-lasting more widespread effect.

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15
Q

where are the adrenal glands

A
  • on top of each kidney
  • cortex : outer region + produces hormones vital to life (cortisol and aldosterone)
  • medulla : inner regions + produces non-vital hormones (adrenaline)
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16
Q

Glucocorticoids

A
  • adrenal cortex
  • regulates metabolism
  • control how fats, proteins and carbs are converted into energy
  • regulates blood pressure
  • cardiovascular responses to stress
  • another gluc hormone = corticosterone
  • works with cortisol
  • both regulate immune responses
  • suppress inflammatory reactions
  • release of hormones controlled by hypothalamus.
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17
Q

mineralocorticoids

A
  • adrenal cortex
  • aldosterone
  • control blood pressure
  • maintain balance of water and salt in blood and body fluids
  • release is controlled by signals trigger by kidneys.
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18
Q

androgens

A
  • adrenal cortex
  • small amounts of male/female sex hormones
  • by ovaries/testis
  • important for women after menopause.
19
Q

when are adrenal medulla hormones released

A
  • when sympathetic NS stimulated

- body is stressed

20
Q

adrenaline

A
  • adrenal medulla
  • increases heart/breathing rate
  • blood flows to brain and muscles
  • rapidly increases BGC
  • glycogen converted to glucose in the liver = glycogenolysis
21
Q

nor-adrenaline

A
  • adrenal medulla
  • works with adrenaline
  • increases heart rate
  • dilates pupils
  • widens air passages in lungs
  • narrows blood vessel near non-essential organs (inc blood pressure)
22
Q

function of the pancreas

A

Exocrine gland : producing and releasing enzymes into the duodenum via a duct
Endocrine glands : produce and releasing hormones into the blood.

23
Q

role of pancreas as an exocrine gland

A
  • made up of exocrine glandular tissue
  • produces digestive enzymes
  • alkaline fluid : pancreatic juice
  • enzymes + juice released into pancreatic duct and then to the duodenum (top of small I(
  • amylase : starch into simple sugars
  • protease : protein into amino acids
  • lipase : lipids into FA and glycerol
24
Q

role of pancreas as an endocrine gland

A
  • controls BGC
  • small regions of endocrine tissue
  • these are Islets Of Langerhans
  • produce insulin and glucagon
  • secrete them directly into the bloodstream.
25
Q

endocrine tissue under microscope

A
  • Islets of Langerhans
  • lightly stained
  • large, spherical clusters
26
Q

exocrine tissue under microscope

A
  • acini
  • darker stained
  • small clusters
27
Q

Alpha IOL

A
  • produce and secrete glucagon

- larger and more than beta in IOL

28
Q

Beta IOL

A
  • produce and secrete insulin
29
Q

reasons as to why BGC can increase

A
  • Diet : when you eat carb-rich foods, the carb is broken down into glucose by DS. Glucose is absorbed by bloodstream and BGC rises
  • Glycogenolysis : glycogen stored in liver and muscle cells is broken down into glucose which is absorbed into blood stream - inc BGC
  • Gluconeogenesis - glucose is formed from non-carb sources : glycerol (from lipids) and amino acids in the liver form glucose. Released into blood stream and inc BGC.
30
Q

how can BGC be decreased

A
  • respiration : glucose used by cells to release energy for muscle cells to contract. The more intense physical activity, the more BGC decreases.
  • Glycogenesis : Excess glucose converted to glycogen and stored in the liver.
31
Q

role of insulin

A
  • high BGC
  • detected by beta cells
  • secrete insulin directly into blood stream
  • insulin binds to glycoprotein receptor
  • tertiary structure of glucose transport protein channels change
  • channels open
  • glucose enters cell
  • insulin activates enzymes to convert glucose to glycogen and fat
  • increased cellular resp
  • glycogenesis.
  • insulin broken down by enzymes by cells in liver
  • BGC returns to normal
  • detected by beta cells
  • when it falls below a set level, beta cells reduce insulin secretion
  • negative feedback.
32
Q

how does insulin lower BGC

A
  • increases rate of glucose to fat conversion
  • increases rate of glycogenesis
  • increases respiratory rate of cells (need for glucose)
  • increases rate of glucose absorption by cells (skeletal muscle cells)
  • inhibits glucagon from alpha IOL
33
Q

role of glucagon

A
  • BGC is too low
  • detected by alpha IOL
  • glycogen secreted directly into bloodstream
  • only liver and fat cells have glucagon receptors
  • BGC increases by :
  • glycogenolysis
  • reducing absorption of glucose by liver cells
  • gluconeogenesis
  • BGC returns to normal
  • detected by alpha cells
  • when rises above a set level
  • alpha cells reduce glycogen secretion
  • negative feedback
34
Q

control of insulin secretion

A
  • at normal BGC, K+ channels in plasma membrane of beta cells are open
  • K+ diffuses out of cells
  • inside of cell = -70mV
  • BGC rises
  • glucose enters cell via glucose transporter
  • glucose metabolised inside mitochondria
  • ATP produced
  • ATP binds to K+ channels
  • K+ close
  • channels are ‘ATP sensitive’
  • K+ no longer diffuse out
  • CM depolarizes to -30mV
  • depolarization causes VG Ca2+ to open
  • Ca2+ diffuse in
  • secretory vesicles release insulin by exocytosis.
35
Q

Type 1 diabetes

A
  • beta cells don’t produce insulin
  • no known cause, prevention or treatment
  • Suggest that condition caused by autoimmune response where own immune system attacks the beta cells
  • begins in childhood.
36
Q

type 2 diabetes

A
  • beta cells don’t produce enough insulin or persons body cells don’t respond properly to insulin
  • due to glycoprotein insulin receptor on CM not working properly
  • cells lose responsiveness to insulin
  • don’t take up enough glucose leaving it in the bloodstream
  • risk increases with age
  • result of excess body weight, physical inactivity.
37
Q

symptons of diabetes

A
  • high BGC
  • glucose in urine
  • excessive thirst + need to urinate
  • weight loss
  • blurred vision
  • tiredness
38
Q

Treatement for type 1

A
  • regular insulin injection
  • regularly test BGC (prick)
  • analysed using machine, tells person BGC, person can work out does of insulin needed
  • if injected with too much insulin - hypoglycaemia
39
Q

treatment for type 2

A
  • regulate carb intake through diet
  • matching to exercise levels
  • lose weight if overweight
  • drugs can be used that stimulate insulin production / slow down the rate at which body absorbs glucose from intestine
  • insulin injections.
40
Q

adv of genetically modified insulin by bacteria

A
  • pure form (less likely to cause allergic reactions)
  • insulin produced in higher quantities
  • cheaper
  • overcomes religious/ethical reasons of using animal products.
41
Q

use of stem cells in treating diabetes

A
  • stem cells could be grown in beta cells
  • beta cells implanted into the pancreas (with type 1)
  • person could make insulin as normal
  • if effective can cure type 1
  • this means donor availability wouldn’t be an issue (unlimited source of beta cells)
  • reduce rejection likelihood because embryonic stem cells are unlikely to be rejected
  • no longer have to inject with insulin
  • limited knowledge : we don’t know if the transplantation might induce tumours due to unlimited cell growth.
42
Q

describe flight or fight response

A
  • autonomic NS detects danger
  • hypothalamus triggers sympathetic NS
  • nervous impulse triggers release of hormones from adrenal medulla
  • noradrenaline increases heart rate
  • adrenaline causes glycogenolysis in liver cells
  • BGC increases
  • used for respiration
  • provides ATP for muscle contraction
  • pituitary gland stimulates the adrenal-cortical system by secreting ACTH
  • hormones released from adrenal cortex that prepare body to deal with threat.
43
Q

action of adrenaline

A
  • non-steroid hormone
  • binds to specific receptors on liver CM
  • activates adenylyl cyclase
  • activated enzyme coverts ATP to cAMP (S-messenger)
  • increase in cAMP activates protein kinases
  • these phosphorylate and activate other enzymes
  • trigger conversion of glycogen into glucose