Hormonal communication Flashcards
1
Q
endocrine glands
A
secrete hormones directly into blood
2
Q
exocrine glands
A
- don’t secrete hormones
- have small duct that secrete chemicals to where they’re needed eg. salivary glands
3
Q
how does a hormone cause a response on a target cell?
A
- cells receiving hormonal signal (target cells) must have complementary receptor on plasma membrane which hormone binds to
- each hormone is different and has different receptor
4
Q
protein and peptide (non-steroid) hormones
A
- hydrophillic so cannot pass through plasma membrane
- attach to receptor on plasma membrane which triggers secondary messenger
- eg. adrenaline, insulin, glucagon
5
Q
steroid hormones
A
- derived from cholesterol
- lipid soluble so can pass through plasma membrane and attach to receptors in cytoplasm or nucleus
- they are transcription factors - act to facilitate or inhibit transcription of specific gene
- eg. testosterone, oestrogen
6
Q
differences between endocrine system and nervous system
A
- endocrine - communication by hormones, nervous - communication by nerve impulses
- transmission in blood vs by neurones
- slow vs rapid
- widespread vs localised
- long-lasting vs short-lived
- effect can be permanent vs temporary
7
Q
adrenal glands structure and location
A
- each gland divided into cortex on outside and medulla on inside
- located on top of each kidney
8
Q
adrenal glands and adrenaline function
A
- release adrenaline in response to stress eg. pain or shock
- outer layer - capsule, next layer in - cortex, inner section - medulla
- effect prepares body for action
- increased heart rate, increased stroke volume, vasocontriction (raises blood pressure), relax smooth muscle in bronchioles, dilate pupils, increase mental awareness, inhibit gut action, hairs erect, converts glycogen to glucose
9
Q
adrenal cortex function
A
- uses cholesterol to produce steroid hormones
- mineralcorticoids eg. aldosterone - controls salts (potassium and sodium) and water balance in blood - impact on blood pressure
- glucocorticoids eg. cortisol - main stress hormone - helps regulate metabolism by controlling how body converts fats, proteins, carbs to energy
- androgens - sex hormones eg. testosterone after puberty
10
Q
adrenal medulla function
A
- releases hormones when sympathetic NS activated
- adrenaline - increases heart rate to send blood to muscles and brain, increases blood glucose levels by converting glycogen to glucose
- noradrenaline - increases heart rate, widens pupils, widens air passages in lungs, narrows blood vessels in non-essential organs - high BP
11
Q
fight or flight responses overall
A
- an instinct possessed by all animals
- threat is perceived by autonomic NS, hypothalamus communicates with sympathetic NS and adrenal cortical system
- effects result in ‘fight or flight’
Responses: - increased HR - pump more oxygenated blood around body
- pupils dilated - more light taken in for better vision
- blood glucose levels increase - more respiration
- smooth muscle of airways relax - more oxygen in lungs
- digestion stops - focus more resources on emergency functions
12
Q
fight or flight in adrenal cortical system
A
- hypothalamus stimulates pituitary gland to secrete ACTH
- ACTH arrives at adrenal cortex and releases about 30 cortisol hormones to bloodstream
- fight or flight
13
Q
fight or flight in sympathetic NS
A
- hypothalamus activates sympathetic NS
- this activates glands and smooth muscle
- also activates adrenal medulla which releases noradrenaline and adrenaline to bloodstream
- fight or flight
14
Q
adrenaline effect on liver cells
A
- process has a cascade effect
- adrenaline (first messenger) binds to specific receptor on liver cell plasma membrane
- this activates the enzyme adenylyl cyclase to turn ATP into cAMP
- cAMP- secondary messenger, binds and activates a protein kinase enzyme which activates other enzymes
- the final enzyme triggers conversion of glycogen into glucose
15
Q
ways of increasing blood glucose concentrations
A
glycogenolysis - glycogen in liver and muscle cells is broken down into glucose - released into bloodstream, increasing blood glucose conc
gluconeogenesis - production of glucose from non-carbohydrate sources eg. liver makes it from glycerol and amino acids, it’s then released into the bloodstream to increase blood glucose conc
16
Q
ways of decreasing blood glucose concentration
A
Respiration - glucose in blood used by cells to release energy
Glycogenesis - production of glycogen from excess glucose is stored in liver
17
Q
pancreas exocrine function
A
- secretes alkaline pancreatic juices which pass into duodenum via pancreatic duct
- alkaline because of sodium carbonate - helps neutralise contents which have left acidic stomach
- pancreatic juice contains enzymes such as:
lipase - hydrolysis of lipids to fatty acids and glycerol
amylase - hydrolysis of starch to maltose
trypsin - hydrolysis of proteins to amino acids
18
Q
acinar cells
A
- groups of them surround tiny tubules that produce digestive juices
- make up most of the pancreas
19
Q
pancreas endocrine function
A
- islets of Langerhans - endocrine cells - made up of beta or alpha cells
- they secrete peptide hormones which control glucose levels
- endocrine cells are close to lots of capillaries which they can secrete hormones into
20
Q
alpha cells in pancreas - how do they increase blood glucose conc?
A
- alpha cells detect glucose level falling and secrete glucagon into bloodstream
- glucagon binds to receptors in liver cell plamsa membrane activating enzyme which breaks down glycogen into glucose - glycogenolysis, this glucose is transported out liver cells by facilitated diffusion
- glycogen also reduces amount of glucose absorbed by liver cells
- increases gluconeogenesis - new glucose made from amino acids and glycerol
- when alpha cells detect blood glucose cons above a certain level, secretion stops (negative feedback
21
Q
beta cells in pancreas - how they decrease blood glucose conc
A
- manufacture and secrete insulin
1. usually K+ channels are open so K+ diffuses outside the membrane, maintaining -70mV on inside of cell
2. when glucose moves inside the cell by a transporter, it’s metabolised in mitochondria into ATP
3. ATP sensitive K+ channels close when ATP binds to them, reducing electrochemical grad to -30mV inside the cell - depolarisation
4. this causes voltage gated Ca2+ channles open and Ca2+ floods into the cell - depolarisation
5. Ca2+ help form and move the vesicles containing insulin so insulin can be released by exocytosis
22
Q
normal blood glucose level
A
3.5-7 mmol/dm3
23
Q
hyperglycaemic blood glucose level, why it’s a problem and symptoms
A
- 15 mmol/dm3
- cells have higher water potential than the blood and lose water to the blood
- symptoms - extreme thirst, blurred vision, ketoacidosis
- ketoacidosis - ketone bodies are formed by fatty acids in the liver causing an acidosis that can be fatal
24
Q
hypoglycaemic blood glucose level and why it’s a problem
A
- below 3mmol/dm3
- can lead to inadequete glucose for respiration in cells
- symptoms: dizziness, feeling weak, nausea
25
Q
glycogen
A
- store of glucose in liver and muscle cells
- large insoluble polysaccharide linked by alpha 1-4 glycosidic bonds and alpha 1-6 side branches
26
Q
insulin effect on muscle cell
A
- insulin binds to receptor on plasma membrane
- receptor signals to cell to make vesicles with transporter protein (GLUT4) merge with the plasma membrane
- allows glucose to enter the cell and reduce the blood glucose level
- the cell can then utilise the glucose for respiration
27
Q
how does insuin cause glycogenesis?
A
- driven by raised insulin level
- insulin binds to receptors on plasma membrane of liver cells, activating enzyme called glucokinase
- glucokinase phosphorylates glucose, trapping it inside the cell as it can’t pass through the membrane tranporters
- phosphofructokinase and glycogen synthase catalyse formation of glycosidic bonds between glucose to make glycogen
- as glucose levels drop, beta cells reduce amount of insulin reduced
28
Q
type 1 diabetes
A
- usually occurs in childhood
- destruction of beta cells, usually as an autoimmune response - immune system attacks beta cells
- insulin not produced at all
29
Q
type 2 diabetes
A
- onset later in life
- insulin resistance - it’s released but receptor on cell doesn’t work correctly - cells don’t take up enough glucose
- beta cells don’t release enough insulin
- link to high BMI and high visceral fat
30
Q
symptoms of diabetes
A
- urine with glucose level over 9 mmol/dm3
- tired (cells can’t respire as glucose can’t get in), thirsty (low water pot. compared to glucose level in blood), urinary frequency (drinking more water bc low water pot.)
31
Q
how do you monitor diabetes?
A
- clinistix or diastix - urine dip sticks
- blood testing - spot test with biosensor
32
Q
treatment of type 1 diabetes
A
- blood glucose level is tested by pricking finger and a machine analysing it
- amount of insulin injected is dependent on blood glucose level
- insulin will reduce blood glucose levels
33
Q
treatment of type 2 diabetes
A
- diet control
- exercise
- insulin injections
- drugs that affect glucose absorption - reduce glycogenesis and enhance insulin production eg. metformin prevents glucose being absorbed
34
Q
where can insulin injections come from?
A
- pancreas of pigs or cows
- genetically modified bacteria - pure form (less allergic reaction), higher quantities, cheaper, more ethical
35
Q
stem cells in diabetes treatment and advantages
A
- totipotent - can grow into any type of cell
- usually come from embryo - ‘spare’ from infertility treatments/terminated pregnancies
- advantages: doesn’t require a donor, reduced likelihood of rejection, doesn’t require insulin injection
36
Q
how does the body know there needs to be a heart rate change?
A
- baroreceptors in the aorta, vena cava or carotid arteries detect a blood pressure change
- chemoreceptors in carotid artery, aorta and medulla detect a chemical change eg. pH of blood rising as CO2 levels rise
- baroreceptors send nerve impulse along sensory neurones to medulla oblongata which
37
Q
what happens when high bp is detected?
A
- cardioinhibitory centre sends nerve impulse along parasympathetic neurones to the SAN
- acetylcholine is secreted at the parasympathetic neurone and binds to receptors in the SAN
- this reduces the rate of impulses sent from the SAN to heart muscle to reduce heart rate
38
Q
what happens when low bp is detected?
A
- cardioacceleratory centre in medulla oblongata sends nerve impulse along sympathetic neurones to SAN
- noradrenaline is secreted by sympathetic neurone and binds to receptors on SAN
- this increases the rate of impulses sent from the SAN to the heart muscle so heart rate increases
