6.3 and 6.4 Flashcards by Lily-Rose Williamson

Describe the structure of a neuromuscular junction:

Very similar to a synapse except:
Receptors are on muscle fibre sarcolemma instead of postsynaptic membrane and there are more
Muscle fibre forms clefts to store enzyme (acetylcholinesterase) to break down neurotransmitter)

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Compare transmission across cholinergic synapses and neuromuscular junctions:

Both unidirectional

Cholinergic:
Neurone to neurone
Neurotransmitters can be excitatory or inhibitory
Action potential may be initiated in postsynaptic neurone

Neuromuscular junction:
Motor neurone to muscle
Always excitatory
Action potential propogates along sarcolemma down T tubules

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How do muscles work?

Antagonistic pairs so pull in opposite directions:
- one contracts (agonist) pulling on bone
- other relaxes (antagonist)

Skeleton is incompressible so muscle can transmit force to bone

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Describe the gross and microscopic structure of skeletal muscle:

Made of many bundles of muscle fibres packaged together
Attached to bones by tendons
Muscle fibres contain:
- sarcolemma which folds inwards to form transverse T tubules
- sarcoplasm
- multiple nuclei
- many myofibrils
- sarcoplasmic reticulum
- many mitochondria

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Describe the ultrastructure of a myofibril:

Made of two types of long protein filaments, arranged in parallel:
- myosin (thick)
- actin (thin)

Arranged in functional units called sarcomeres
- ends= z lines
- middle= m line
- H zone= only myosin
- A band= all of myosin
- I band= just actin

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Explain the banding pattern seen in myofibrils:

I-bands- light bands containing only actin
A-bands- dark bands containing myosin and some actin
H zone contains only myosin
Darkest regions contain overlapping myosin and actin

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Give an overview of muscle contraction:

Myosin heads slide actin along myosin causing the sarcomere to contract
Simultaneous contraction of many sarcomeres causes myofibrils and muscle fibres to contract
WHen sarcomeres contract:
- H zones get shorter
- I band gets shorter
- A band stays the same
- Z lines get closer

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Describe the roles of actin, myosin, Ca2+, tropomyosin and ATP in myofibril contraction:

Depolarisation spreads down sarcolemma via T tubules causing Ca2+ release from sarcoplasmic reticulum which diffuses to myofibrils
Ca2+ bind to tropomyosin causing it to move- exposing binding sites on actin
Allowing myosin head, with ADP attached, to bind to binding sites on actin- forming actinomyosin cross bridge
Myosin heads change angle, pulling actin along myosin, using energy from ATP hydrolysis
New ATP binds to myosin head causing it to detach from binding site
Hydrolysis of ATP by ATPase releases energy for myosin heads to return to original position
Myosin reattaches to a different binding site further along actin, and process is repeated as long as Ca2+ conc. is high

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What happens during muscle contraction?

Ca2+ actively transported back into the endoplasmic reticulum using energy from ATP
Tropomyosin moves back to block myosin binding site on actin again so no actinomyosin crossbridges can form

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Describe the role of phosphocreatine in muscle contraction:

A source of Pi rapidly phosphorylates ADP to regenerate ATP
- ADP + phosphocreatine –> ATP + creatine
Runs out after a few seconds- used in short bursts of vigorous exercise
Anaerobic and alactic

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Describe the general properties, structure and location of slow twitch muscle fibres:

Properties:
Specialised for slow, sustained contractions
Produce more ATP slowly from aerobic respiration
Fatigues slowly

Location
High proportion in muscles used for posture
Legs of long distance runners

Structure:
High conc. of myoglobin- stores oxygen for aerobic respiration
many mitochondria- high rate of aerobic respiration
Many capillaries- supply high conc of oxygen/glucose for aerobic respiration and to prevent build up of lactic acid causing muscle fatigue

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Describe the general properties, location and structure of fast twitch muscle fibres:

General properties:
Specialised for brief, intensive contractions
Produces less ATP rapidly from anaerobic respiration
Fatigues quickly due to high lactate conc.

Location:
High proportion found in muscles used for fast movement e.g biceps, eyelids
Legs of sprinters

Structure:
Low levels of myoglobin
Lots of glycogen- hydrolysed to provide glucose for glycolysis (anaerobic) which is inefficient so large quantities needed
High conc of enzymes involved in anaerobic respiration
Store phosphocreatine

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Describe homeostasis:

Maintenance of a stable internal environment within restricted limits
By physiological control systems

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Explain the importance of maintaining stable core temp:

If too high
- H bonds in tertiary structure of enzymes break
- enzymes denature; active site changes shape and substrates can’t bind
- so fewer E-S complexes formed

If too low:
- not enough kinetic energy so fewer E-S complexes

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Explain the importance of maintaining stable blood pH:

Above or below optimal pH, ionic/H bonds in tertiary structure break
Enzymes denature; active sites change shape and substrate can’t bind
So fewer E-S complexes

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Explain the importance of maintaining stable blood glucose conc.

Hypoglycaemia (too low):
Not enough glucose for respiration
So less ATP produced
Active transport can’t happen- cell death

Hyperglycaemia (too high):
Water potential of blood decreases
Water lost from tissue to blood via osmosis
Kidneys can’t absorb all glucose- more water lost in urine causing dehydration

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Describe the role of negative feedback in homeostasis:

Receptors detect change from optimum
Effectors respond to counteract change
Returning levels to normal/optimum

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Explain the importance of conditions being controlled by separate mechanisms involving negative feedback:

Departure in different directions from the original state can all be controlled/reversed
Giving a greater degree of control

Describe positive feedback:

Receptors detect change from normal
Effectors respond to amplify change
Producing a greater deviation from normal

Describe the factors that influence blood glucose conc.

Consumption of carbs
Rate of respiration of glucose

Describe the role of the liver in glycogenesis, glycogenolysis
and gluconeogenesis:

Glycogenesis: Converts glucose to glycogen
Glycogenolysis: converts glyocgen to glucose
Gluconeogenesis: Converts amino acids and/or glycerol to glucose

Explain the action of insulin in decreasing blood glucose concentration:

Beta cells in islets of langerhans in pancreas detect blood glucose conc. is too high and secrete insulin
Attaches to specific receptors on cell surface membranes of target cells e.g liver/muscles

This causes more glucose channel proteins to join cell surface membrane
- increasing permeability to glucose
- so more glucose can enter cell by facilitated diffusion

This also activates enzymes involved in conversion of glucose to glycogen (glycogenesis)
- Lowering glucose conc. in cells creating a conc. gradient
- so glucose enters cell by facilitated diffusion

Explain the action of glucagon in increasing blood glucose conc.

Alpha cells in islets of langerhans in pancreas detect blood glucose conc is too low and secrete glucagon
Attaches to specific receptors on cell surface membranes of target cells (e.g liver)

Activates enzymes involved in hydrolysis of glycogen to glucose (glycogenolysis)
Activates enzymes involved in conversion of glycerol/ amino acids to glucose (gluconeogenesis)
- This establishes a conc gradient and glucose enters blood by facilitated diffusion

Explain the role of adrenaline in increasing blood glucose conc.

Fear/stree/exercise - adrenal glands secrete adrenaline

Attaches to specific receptors on cell surface membranes of target cells (e.g liver)
Activates enzymes involved in hydrolysis of glycogen to glucose
Establishes a conc gradient so glucose enters blood by facilitated diffusion

Describe the second messenger model of adrenaline and glucagon action:

Adrenaline/glucagon attach to specific receptors on cell membrane which: Activates enzyme adenylate cyclase WHich converts many ATP to cyclic AMP (cAMP) cAMP acts as the second messenger- activates protein kinase enzymes Protein kinase activates enzymes to break down glycogen to glucose

Suggest an advantage of the second messenger model:

A,plifies signal from hormone As each hormone can stimulate production of many molecules of second messenger (cAMP) Which can in turn activate many enzymes for rapid increase in glucose

Compare the causes of type I and type II diabetes:

Type I: Beta cells in islets of Langerhans produce insufficient insulin Normally develops in childhood due to an autoimmune response destroying B cells Type II: Receptor loses responsiveness/sensitivity to insulin So fewer glucose transport proteins, less uptake of glucose, less conversion of glucose to glycogen Risk factor=obesity

How can type I diabetes be controlled?

Injections of insulin Blood glucose conc monitored with biosensors so dose of insulin matched to glucose intake Eat regularly and control carb intake

Why can't insulin be taken as a tablet by mouth?

Insulin is a protein Would be hydrolysed by endopeptidases/exopeptidases

Describe how type II diabetes can be controlled:

NOT insulin injections but may use drugs which target insulin receptors to increase their sensitivity Reduce sugar intake Reduce fat intake More regular exercise Lose weight to increase sensitivity of receptors to insulin

Summarise the role of different parts of the nephron:

Bowman's capsule: formation of glomerular filtrate (ultrafiltration) Proximal convoluted tubule: Reabsorption of water and glucose (selective reabsorption) Loop of Henle: Maintenance of a gradient of sodium ions in the medulla Distal convoluted tubule and Collecting duct: reabsorption of water

Describe the formation of glomerular filtrate:

High hydrostatic pressure in glomerulus - as diameter of afferent ateriole is wider than efferent arteriole Small substances (water/glucose/ions/urea) forced into glomerular filtrate, filtered by: - Pores between capillary endothelial cells - Capillary basement membrane - Podocytes Large proteins/blood cells remain in blood

Describe the reabsorption of glucose by proximal convoluted tubule:

Na+ actively transported out of epithelial cells to capillary Na+ moves by facilitated diffusion into epithelial cells down a conc. gradient bringing glucose against its conc. gradient Glucose moves into capillary by facilitated diffusion down its conc. gradient

Describe the reabsorption of water by the proximal convoluted tubule:

Glucose in capillaries lowers water potential so water moves by osmosis down a water potential gradient

Describe and explain how features of the PCT allow the rapid reabsorption of glucose into the blood:

Microvilli provides a large SA Many channel/carrier proteins for facilitated diffusion/co transport Many carrier proteins for active transport Many mitochondria to produce ATP for active transport Many ribosomes to produce carrier and channel proteins

Suggest why glucose is found in urine of an untreated diabetic person:

Blood glucose conc. is too high so not all glucose reabsorbed at PCT As glucose carrier/cotransporter proteins are saturated/working at max rate

Explain the importance of maintaining a gradient of sodium ions in the medulla:

So water potential decreases down the medulla So a water potential gradient is maintained between the collecting duct and the medulla To maximise reabsorption of water by osmosis from filtrate

Describe the role of the loop of Henle in maintaining a gradient of Na+ in the medulla:

In the ascending limb: Na+ actively transported out Water remains as ascending limb in impermeable to water This increases conc of Na+ in the medulla, lowering water potential Descending limb: - Water moves out by osmosis then reabsorbed by capillaries - Na+ recycled (diffuses back in) Loop of henle acts as a countercurrent multiplier

Why do animals needing to conserve water have long loops of Henle?

More Na+ moved out so gradient is maintained for longer in medulla/higher Na+ conc So water potential gradient is maintained longer So more water can be reabsorbed from collecting duct by osmosis

Describe the reabsorption of water by the DCT and collecting ducts:

Water moves out of DCT and collecting duct by osmosis down a water potential Controlled by ADH which increases their permeability

What is osmoregulation?

Control of water potential of blood

Describe the role of the hypothalamus in osmoregulation:

Contains osmoreceptors which detect increase or decrease in blood water potential Produces more ADH when water potential is low or less ADH when water potential is high

Describe the role of the posterior pituitary gland in osmoregulation:

Secretes more/less ADH into blood due to signals from the hypothalamus

Describe the role of antidiuretic hormone in osmoregulation:

Attaches to receptors on collecting duct (and DCT) Simulating addition of channel proteins (aquaporins) into cell surface membranes So increases permeability of cells of collecting duct and DCT to water So increases water reabsorption from collecting duct/DCT by osmosis SO decreases volume and increases concentration of urine produced