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Cell Biology > Tim Cheek > Flashcards

Tim Cheek Flashcards

1
Q

Which is the only body fluid compartment that wont contain protein?(1)

A

The interstitial fluid.

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2
Q

What % of water is in which body fluid compartments?(1)

A

67 in intracellular

33 in ecf (mainly in interstitial fluid,25%)

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3
Q

How does [Na+] compare in bfcs?Cl-?K+?Ca2+?(4)

A

High outside and relatively the same in interstitial and plasma
high outside and equal in ecf, low in icf
Low outside, same in both roughly, high in icf
Lower in ICF in membranous organelle, higher outside but equal.

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4
Q

Osmolarity of human fluids?(1)

A

300mOsm.

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5
Q

What is a uniporter?give an example.(1)

A

A protein channel that transports 1 molecule, GLUT transporters e.g. GLUT2 in a liver cell.

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6
Q

Na+/K+ atpase.(5)

A
  • Pump hydrolyses ATP to ADP to simultaneously transport 3 Na+ out of cell and 2 K+ into the cell per pump cycle
  • Accounts for >30% of total ATP consumption
  • Maintains gradient for Na+ (out>in) and K+ (in>out)
  • Many secondary active transport processes are coupled to the inward Na+ gradient
  • 1 cycle is approx 10ms
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7
Q

Difference between an antiporter and symporter?(1)

A

antiporter=oppoite molecule transfer e.g. sodium and calcium ion exchange.
symporter=same.

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8
Q

What is an action potential(1)

A

An action potential is a rapid change in membrane potential.

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9
Q

What is resting potential membrane (RMP) maintained by?(2)

A

-high permeability to K+ (K+ leak channel)
-active transport of Na+ out of membrane (Na+/K+ atpase=making it electrogenic)
leads to slightly more negative charge inside the membrane.

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10
Q

What is the equilibrium potential of K+?Na+?Cl-?RMP-why?(5)

A
  • -86mV
    -+60mV
  • -70mV
  • -70mV, closer to ion that is more permeable therefore closer to potassium than Na+ as permeability goes:
    k+>na+>cl->protein.
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11
Q

What is AP voltage?(1)

A

+30mV, become closer to Ena as Na permeability increase.

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12
Q

Describe what occurs during an action potential on a graph.(5)

A
  • Slow rising phase, SOME Na+ VGC open and Na+ influx occurs
  • reaches -55mV threshold voltage, Rapid rising phase, SOME K+ VGC open and K+ moves out of cell leading to further depolarisation, ALL Na+ VGC open!
  • Early repolarisation, ALL K+ VGC open, SOME Na+ VGC become inactivated
  • Hyperpolarisation, ALL Na+ VGC become inactivated, SOME K+ VGC close but some still open so overshoot
  • Resting state, both Na+ and K+ VGC close.
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13
Q

K+ VGC.(3)

A
  • opens when the membrane is depolarised, but more slowly than the Na+ channel
  • closes slowly in response to membrane repolarisation thus hyperpolarisation
  • only open or closed (no inactivation stage like Na+).
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14
Q

What is the trigger for Na+ VGC inactivation gates?(1)

A

Time dependant and is a different part of the protein!

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15
Q

What is the difference between the absolute and relative refractory periods?(2)

A

Absolute, inactivation gates closed NO AP generation
Refractory, SOME Na+ channels recovered so BIG stimuli can generate another AP, some K+ still open-reason why you need a bigger stimuli is further from threshold whilst in hyperpolarisation!.
these prevent backward movement of APs!

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16
Q

Where do APs occur?

A

Axon Hillock as high conc of Na+ VGC, AP travels via current loops nd induced depolarisation on nearby axon.

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17
Q

How big is the synpatic cleft?(1)

A

50nm.

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18
Q

When Ach binds to postsynaptic neuron what happens?(1)

A

Na+ ligand gated channels open, causing influx of Na+, also note that K+ ALSO can move through this and moves out of postsynaptic neurone.

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19
Q

What is an EPP what is its voltage?(2)

A

Ena+ Ek/2=-15mV, happens in junctional folds(JFs) and it results in aps in postsynaptic neurone nearby where Na+ VGC do occur (arent present in JFs)

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20
Q

What is the size of a mEPP?(3)

A

0.5mV-random vesicle secretion, vesicles release all or none of their contents and mEPP is 1/100th amplitude of EPP therefore 100 required for full EPP
200-300 secreted in usual timulation at NMJ though as safety margin.

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21
Q

How is Ach removed, why?(2)

A

Acetylcholinesterase breaks it down, acetate and choline then reuptaken and combined with acetyl coA to form Ach
If not broken down then Na+ ligand gated channels would be open constantly and so therefore the AP would not be transient.

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22
Q

Curare.(3)

A

South American arrow poison
blocks Ach receptor, causes paralysis
used as muscle relaxant by anaesthetists.

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23
Q

Botulism (Botulinum toxin).(4)

A

produced by bacteria in badly tinned foods (Clostridium botulinum)
inhibits exocytosis so Ach release stopped. Muscles therefore relax
in severe case paralysis can be fatal
active ingredient in BOTOX, more youthful appearance

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24
Q

Myasthenia Gravis.(3)

A

-autoimmune disorder, in which antibodies destroy Ach receptors
-because of safety factor, transmission at NMJ does not fail until many antibodies have accumulated
-EPPs not large enough to stimulate a.p. in muscle; death results from paralysis of respiratory muscles
treatment:
give inhibitors of Ach-ase (e.g. neostigmine)

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25
Q

1 muscle fibre=

A

1 muscle cell=many myofibrils.

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26
Q

Bands in myofibrils.(4)

A

A=overlap of thick and thin
I=thin filaments only, g-actin molecules make f-actin strands (2 wind together in a double helix) and tropomyosin winds around this helix, each g-actin has one myosin binding site, troponin binds to actin and tropomyosin wiht its T and I units.
H=thick filaments only, m line holds the filaments (several hundred myosin molecules) together
Z=length of sacromere.

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27
Q

What is a triad?(1)

A

T tubule with terminal cisternae on either side.

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28
Q

Describe how musuclar contraction occurs.(4)

A
  • Ca2+ influx from sarcolemma binds to tropinin-C revealing the myosin binding site and resulting in cross-bridge formation
  • Having hydrolysed ATP to ADP and Pi myosin is in a high energy state
  • myosin changes direction known a the powerstroke and pulls actin closer to M line, ATP binds breaking cross link
  • ATP is hydrolysed again and the process repeats provided Ca2+ is present (removed during relaxtion by Ca2+-ATPase pump) and ATP is present-why rigour mortis occurs after death as no ATP bind so continual semi contraction.
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29
Q

What is the speed of a muscular contraction?(1)

A

A typical muscle fibre has 500 myosin heads, each going through 5 cycles/sec during rapid contraction

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30
Q

Where do GPs occur?(1)

A

Occur in dendrites, cell bodies or axon terminals; not in axons

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31
Q

How do IPSPs work?(1)

A

Cl- enter or K+ leave-resulting in hyperpolarisation.

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32
Q

Why are frequency signals better?(3)

A
  • are digital and therefore less prone to ‘noise’ either on or off
  • have greater fidelity (signal to noise ratio high)
  • Other biological signals are also frequency encoded
    e. g. hormone-induced intracellular Ca2+ signals
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33
Q

What special characteristics do neurones have?(3)

A

Do not divide – foetal neurones lose their ability to undergo mitosis
Longevity – can live and function for a lifetime
High metabolic rate – require abundant oxygen and glucose

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34
Q

Special about intermediate CNS neurones?(1)

A

Dense dentritic tree.

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35
Q

What are bipolar neurones responsible?(1)

A

2 processes eminating from cell body and resposible for smell and vision, differ from pseudo-unipolar one process that leaves cell body but then immediately splits into 2, which are myelinated and for somatic purposes.

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36
Q

What are multipolar neurones?(1)

A

efferent (motor) and CNS neurones-many dendrites eminate from cell bodies.

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37
Q

What is postsynaptic inhibition?(1)

A

spatial summation involving presence of an IPSP, just presence of one will result in this.

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38
Q

What are the 2 types of receptors for neurotrnasmitters?(2)

A
  • Ligand-gated ion channels-inotropic receptors (fast synaptic potential)
  • G-protein coupled receptors that activate second messenger models-metabotropic receptors (short synaptic potential i.e. long term effects).
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39
Q

Examples of neurotransmitters that have inotropic receptors.(3)

A
  • Ach, Na+, K+
  • Glutamate, Na+, K+, Ca2+
  • GABA and Glycine, Cl-
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40
Q

Examples of neurotransmitters that have metabotropic receptors.(5)

A 
adrenaline
histamine
cholocytokinin
ATP
Ach.
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41
Q

What is Long-term potentiation (LTP)?(1)

A

LTP is the process by which repetitive stimulation at a synapse increases the efficacy of transmission at that synapse.

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42
Q

How does LTP occur?(3)

A
  • Glutamate released and binds to 2 inotropic receptors AMPA and NMDA (cant bind as Mg2+ blocks it)
  • wiht reptitive stimulation Mg2+ is ejected from NMDA recptor so Ca2+ can flow through and activate 2nd messenger system as well as the Na+ inlux occuring at the AMPA receptor resulting in an EPSP
  • This results in bith further glutamate release as well as greater sensitivity to glutamate and thus the synaptic connection becomes stronger.
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43
Q

How are proteins modified?(2)

A
  • confirmational change

- covalent modification i.e. phosphorylation.

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44
Q

5 steps in signalling pathway.(5)

A 
Signal
Reception-receptor
Transduction-transducer proteins
Amplification-secondary/signalling messenger cascades
Response.
45
Q

Different types of cell signalling and their increasing signal.(4)

A
  • Gap junctions occur in metabolites and NOT macromolecules
  • Contact dependant, important in immunity and development
  • autocrine signalling (self signalling or same cells)and paracrine-proximal cells, important during development
  • endocrine and synaptic
46
Q

Examples of intracellular receptors.(2)

A

Small hydrophobic molecules e.g. steroid hormones ad NO gas can diffuse across PLB and bind to intracellular receptors
Nuclear hormone receptors, confirmatonal change in response to ligand binding, recptor-ligand complex controls gene transcripton

47
Q

What is androgen sensitivity hormone?(1)

A

Males produce enough testosterone but no/little androgen receptors therefore phenotypically a woman.

48
Q

Role of NO receptors in muscle relaxation.(2)

A

Ligand binds causing confirmational change and thus NO synthase
this binds to guanylyl cyclase resulting in cGMP from GTP which us a second messenger which results in muscle relaxation.

49
Q

What are the 3 types of extracellular receptors?(3)

A

By hydrophillic or large molecules.

  • ion couple
  • g protein coupled (GPCRs)
  • enzyme coupled.
50
Q

What are the 2 types of G proteins?(2)

A

G proteins act as transducers
trimeric-with Gprotein coupled receptors
monomeric-with enzyme receptors

51
Q

What do G proteins do?(3)

A

Bind guanosine di/triphosphate (GDP/GTP), bind to target proteins on plasma membrane
they inactivate themselves through GTP hydrolyis ad both alpha and beta-gamma subunits rejoin to form an inactive g protein.

52
Q

How do GPCRs work?(3)

A

Activation of GCPR causing a confimational change and release of g protein

  • in resting state alpha sub unit of gp binds GDP as it is a GTPase
  • once stimulated a confirmation change occurs releasing GDP and binding GTP, the beta-gamma subunits and alpha sub units both dissociate.
53
Q

How does cAMP result in information being passed down the pathway?(3)

A

cAMP binds to the 2 regulatory subunits of cAMP dependant protein kinase (PKA)
this results in confirmational change
causes the 2 catalytic subunits of PKA to be released and activated thus able to transmit information.

54
Q

3 roles of GTP and ATP in cells.(3)

A
  • Nucleic acid synthesis (RNA)
  • Signal transduction
    • cGMP and G-protein activation (GTP)
    • cAMP and phosphorylation (ATP)
  • Carrying energy
55
Q

What controls the fight or flight mechanism?(1)

A

GPCRs via epinephrine, results in secondary messenger and phosphorylation casacade.

adenylyl cyclase–>cAMP—>PKA activation—>active enzyme—>product.

56
Q

What does phospholipase C do?(1)

A

Cleaves phosoinositol 4,5 biphosphate (PIP2) resulting in IP3 (causes Ca2+ release from ER) and DAG which with Ca2+ works to active protein kinase C (PKC)

57
Q

Ca2+.(2)

A

=Small changes in Ca2+ are easily detected, because cytosolic Ca2+ levels are maintained at a low level (~10-7M), compared to extracellular Ca2+ (~10-3M)
=Ca2+ can bind tightly to proteins inducing conformational change

58
Q

Calmodulin.(2)

A
  • Each calmodulin molecule binds 4 Ca2+ ions

- The resulting conformational change allows the calmodulin/Ca2+ complex to wrap around and activate target proteins.

59
Q

Enzyme linked receptors.(2)

A
  • Single-span transmembrane proteins

- Cytosolic domain has intrinsic enzymatic activity or is associated with an enzyme

60
Q

What are receptor tyrosine kinases (RTKs)?(

A

most common type of enzyme linked receptor, examples include growth related and insulin recptors

61
Q

How RTKs work.(3)

A
  • Binding of the ligand to growth factor receptors leads to cross-linking of two receptor chains
  • Oligomerisation of the receptor chains allows cross-phosphorylation (autophosphorylation)
  • these phosphorylated TK residues act as docking sites for other signalling proteins
  • Insulin receptors are tetramers; ligand binding causes realignment of the polypeptide chains activating cross-phosphorylation
62
Q

What is Ras and what is it responsible for?(1)

A

-small monomeric G protein main transducer responsible for cell growth factors eg fibroblast and epidermal growth factors (FGF and EGF).

63
Q

How does a monomeric protein such as Ras result in GTP hydrolysis?(3)

A
  • Not directly linked to receptor
  • GDP release activated by GEF (guanine nucleotide exchange factor)
  • Weak intrinsic GTPase activity – needs GAP (GTPase activating protein) to drive GTP hydrolysis.
64
Q

What mediates between RTK and Ras-GEF in Ras-MAPK pathway?(1)

A

Adaptor protein Grb-2.

65
Q

Steps of Ras-MAPK pathway.(4)

A

-Phosphorylation occurs starting with activation of Ras which through protein interaction results in
MAP kinase kinase kinase (Raf)
-(phosphorylated to) MAP kinase kinase (Mek)
-(phosphorylated to) MAP kinase (Erk)
-this then alter proteins and gene expression through phosphorylation

66
Q

How is RAS signalling linked to cancer?(5)

A
  • RAS is a proto-oncogene
  • RAS mutations are found in 20% of human cancers
  • Most common RAS mutations reduce GTP hydrolysis activity
  • GTP stays bound longer and the signalling pathway is continuously switched on
  • Leads to cell proliferation, even in the absence of growth factors such as EGF
67
Q

3 different types of signalling complex:

A
  • Stable: components of the signalling pathway are linked by a scaffold protein
  • Transient: the signalling complex assembles after the receptor is activated
  • Transient: modification of plasma phospholipid molecules.
68
Q

How G protein hydrolysis (or lack of it) plays a role in cholera.(5)

A
  • ADP-ribosylation of Gα prevents hydrolysis of GTP
  • Locks G-protein in an active state
  • Adenylyl cyclase remains activated
  • Increase in cAMP leads to loss of Cl- and water into intestinal lumen
  • Severe watery diarrhoea > dehydration > death
69
Q

Where are all the cytoskeleton components found within a cell?(3)

A

Actin-movement on c=surafce and cell shape, concentrated under plasma membrane
Microtubules-mitosis, transport e.g. vesicles, driv cilia and flagella
Intermediate filaments-mechanical strength, found in nucleus and cytoplasm

70
Q

Intermediate filaments.(6)

A
  • Found in both cytoplasm AND nucleus (known as lamins then and provide support as well as attachment of chromosomes, breakdown and are phosphorylated during mitosis)
  • connect cells via desmosomes
  • Diameter – 10 nm
  • Polymers of 8 tetramers of alpha helix that has 2 heads at boht N and C terminus
  • Flexible but most stable
  • Primary function is to prevent excessive stretching.
71
Q

Microtubules.(6)

A

-Diameter = 25nm, Tube polymer with globular monomers; tubulins, dimers of alpha and beta tubulin combine and then a tube is made of 13 protofilaments composed of these dimers, they are polar
-Use GTP to build up
-Cytoplasm,Grow out from centrosome
-Rigid and unstable
-Dynamic
-Function: Segregation of chromosomes during mitosis
Organelle and vesicle shuttling
Facilitate movement –sensory structures

72
Q

Microtubule motor proteins.(9)

A
  • Kinesins and dyneins (unrelated)
  • These proteins have ‘head’ and ‘tail’ regions
  • Globular heads bind ATP
  • Heads bind to microtubule
  • Hydrolysis of ATP drives movement
  • Kinesins towards plus end
  • Dyneins towards minus end
  • Tails bind “cargo”
  • Includes e.g. ER, golgi apparatus..
73
Q

Microtubule arrangement in cilia.(1)

A

9+2 arrangement driven by dyenins.

74
Q

Actin.(7)

A

-Diameter 6-8nm
-Polymers of Actin monomers
-Use ATP to build not GTP like microtubules
Regulated by binding proteins
-Cytoplasm: Cortex (gel-like networks), Bundles, 2D networks, 3D gels
Flexible
-Polar filaments + grows quicker
-Dynamic polymerisation and depolymerisation
-Function: Cell motility and contraction, Adhesion and mechanosensing

75
Q

Myosin I.(3)

A
  • All cells
  • One head/tail
  • Moves cargo along the actin filament.
76
Q

Myosin II.(4)

A
  • Muscle (& others)
  • Dimer
  • Forms filaments
  • Contractile structures.
77
Q

Spectrin.(4)

A

-Inner plasma membrane (pentagonal, hexagonal)
-Mechanical strength, stability , shape (plasma membrane integrity)
-Link membranes to the motors proteins and all major filament systems (scaffold)
-First isolated as a major component of human red blood cells membrane
Red blood cell “ghost” (spectre).

78
Q

Steroid hormones.(5)

A

•Small hydrophobic (lipophilic) molecules synthesised primarily from cholesterol.
•Released immediately following synthesis.
•Circulate in bound form (bound to plasma proteins@0
•Act on intracellular receptors which
then bid to DNA (hormone response
elements) and regulate gene
transcription.
•Have slow long lasting effects.

79
Q

Peptide hormones.(3)

A

•Peptide hormones are between 3 and 332 amino acids in length
•Synthesised as preprohormones (inactive hormones) and stored prior to release
•Act on cell surface receptors then via 2nd messenger systems
to cause effect in target cells

80
Q

Amino acid hormones.(4)

A 
•Amino acid hormones include
thyroid hormone and epinephrine
•Most synthesised from tyrosine
•Stored for instant release
•Different modes of action (TH
has intracellular receptor, others
act at surface)
81
Q

Describe action of hormone on body.(1)

A

Hormones are secreted by specialised cells into the blood and act on specific receptors in target tissues.

82
Q

Name some non-classical hormone producers in the human body.(6)

A
  • Kidney
  • Heart muscle
  • Endothelium
  • Platelets
  • Adipocytes
  • White blood cells.
83
Q

Features of some hormones.(5)

A
  • High affinity: Hormones are effective at low concentrations
  • Synergistic: The effect of two hormones is greater than one alone e.g. thyroid hormone and norepinephrine on heart rate
  • Permissive: The presence of one hormone is necessary for another to have an effect e.g. thyroid hormone and aldosterone on Na/K pumps in kidney
  • Antagonistic: Two hormones oppose each other’s effects e.g. insulin vs glucagon
  • Competitive: Two hormones, similar in structure, compete for the same receptor e.g. epinephrine and norepinephrine
84
Q

Provide a statement which best describes steroid hormone storage and synthesis.(1)

A

Synthesised from cholesterol on demand and are not stored inside the cell.

85
Q

Why do steroid hormones generally have slow long lasting effects?(1)

A

Protein expression depends on rate of production and half-life of the protein which limits the speed and longevity of the effect.
Remember steroid hormones act on intracellular receptors.

86
Q

Describe how steroid hormones act on their receptors.(3)

A

Receptor is composed of DNA binding region, hormone binding site (connected to DNA binding site by hinge region) and trancription activating domain
In the inactive for Hsp90 protein is bound to the receptor, blocking the DNA binding site thus preventing transcription
The steroid hormone binds to the hormone binding site (acting like an allosteric inhibitor) nd this causes ejection of the Hsp90 exposing the DNA binding site, hinge region opens the receptor thus allowing for binding to DNA and transcription can occur.

87
Q

What types of hormone release are there?(4)

A
  • Continuous: e.g. Thyroid hormone under control of TSH.
  • Pulsatile: e.g.GHRH—>different release at different time of day, peaks
  • Circadian: e.g. Melatonin—>act on day and night cycle and sensing blue light.
  • Exocytosis on stimulus: e.g. insulin.
88
Q

Epinephrine & Norepinephrine can cause vasoconstriction or vasodilation depending on the receptor type in the tissue. Which of the following is correct?

1) Alpha-1 and beta-2 receptors both act through activation of phospholipase C but they cause opposite effects on Ca2+ release
2) Alpha-1 and beta-2 receptors both act through activation of adenylate cyclase but they cause opposite effects on Ca2+ release
3) Alpha-1 receptors mediate smooth muscle relaxation through the cAMP pathway
4) Beta-2 receptors mediate smooth muscle relaxation through the cAMP pathway

A

4.
alpha 1 causes vasoconstriction through IP3 pathway (why 3 is wrong)
beta 2 cAMP pathways inhibits contractile proteins through phosphorylation thus causes relaxation

89
Q

How do we control the effects of hormones?(4)

A
  • Modification: Increases/decreases hormone activity e.g. Vitamin D
  • Degradation: Hormone broken down or excreted e.g.oestrogen
  • Receptor down-regulation: e.g. adrenergic receptors (become desensitised)
    Termination of intracellular effects: e.g. phosphatases
  • Negative feedback:
    By the regulated metabolite (e.g. glucose/insulin)
    By the hormone itself (e.g. cortisol)
    By the trophic hormone released by the pituitary
90
Q

What is the hypothalamic-pituitary axis?(3)

A

Aka the hypothalamohypophyseal system.
Major site of interaction between the nervous and endocrine systems.
Exerts control over several endocrine glands and a number of physiological activities.

91
Q

The structure of the pituitary gland.(3)

A
  • Aka the hypophysis, consists of two lobes:
  • Posterior pituitary: The posterior lobe is of neural origin and is know as the neurohypophysis. Consists of axons and nerve endings of neurones whose cell bodies reside in the hypothalamus (considered extension of hypothalmus)
  • Anterior pituitary: Anterior lobe originates from Rathke’s pouch and is known as the adenohypophysis. Consists of endocrine tissue
92
Q

What hormones are secreted in the posterior pituitary gland?Where abouts and where are they store?What are their role?(3)

A

Produced in magnocellular neurones and stored in posterior prior to release
Oxytocin-uterine contraction and breast myoepitleial contraction
ADH-water retention by kidney.

93
Q

What hormones are secreted in the anterior pituitary gland?Where abouts and where are they store?What are their role?(3)

A

refer to phone.

94
Q

Anterior pituitary hormone site of production and storage.(1)

A

Release hormones into the systemic circulation. Release is controlled by hypothalamic hypophysiotropic hormones in the portal hypophyseal vessels.

95
Q

What is the difference between pituitary gigantism and acromegaly?(1)

A

PG occurs early in life resulting in extremely tall person (giant)
A results in growth of extremeties with soft tissue such as jaw, hands and feet but not giant as after development cartiliage and bone no longer can divide and grow in excess in presence of GH.

96
Q

What is hypo-pituitary dwarfism?How can this be rectified?(2)

A

Lack of pituitary GH in childhood leading to dwarfism.
rhGH (replacement GH) can be provided if detected early enough and shouldl give normal height prediction of the individual.

97
Q

Growth hormone.(5)

A
  • Aka somatotropin, a 191 amino acid peptide hormone synthesised by somatotrophs in the anterior pituitary
  • Released in response to growth hormone-releasing hormone (GHRH) from the hypothalamus
  • Release inhibited by growth hormone-inhibiting hormone (somatostatin) from the hypothalamus
  • Stimulates growth, cell reproduction and regeneration
  • Functions of growth hormone can be direct or indirect via insulin-like growth factor 1 (IGF-1)
98
Q

What are the acute (direct) actions of GH.(4)

A
  • Release fatty acids from adipose tissue and enhances their conversion to acetly-CoA
  • Reduced glucose metabolism and uptake in to cells, especially the liver. Diabetogenic, i.e. anti-insulin
  • Increased gluconeogenesis in the liver
  • Increased production of insulin-like growth factor (IGF-1) - hepatic
99
Q

What are the long term effects of GH via IGF-1?(3)

A
  • Growth promoting action on bone, epiphyseal cartilage, soft tissue, gonads, viscera
  • Promotes amino acid uptake and protein synthesis
  • Insulin-like endocrine effects on tissues
100
Q

Function of thyroid.(4)

A

-Cardiovascular
Increases cardiac output and systolic pressure (heart rate & stroke volume)
-Metabolic
Increased basal metabolic rate (glycolysis, oxygen consumption and thermogenesis)
-Neurological
Essential for maintaining emotional tone
Improves alertness, memory, reflexes and wakefulness
-Growth and Development
Essential for foetal neural development, and bone growth after birth.

101
Q

What does the thyroid produce?(3)

A

Major product of the thyroid is Tetraiodothyronine, aka thyroxine or T4
Most active thyroid hormone physiologically is Triiodothyronine, aka T3
The thyroid also produces calcitonin which is involved in calcium homeostasis

102
Q

Structure of thryoid.(8)

A

-About 25g in adults
-Two lobes with connecting isthmus
-Rich blood supply
-2-4 pairs of parathyroids imbedded in posterior of thyroid
-Functional unit of thyroid are follices
-Single layer of cells surrounding a pool of colloid
-Production and storage of thyroid hormones in colloid
Amount of colloid varies:
More when is thyroid inactive
Little when iodine deficient
-C cells secrete calcitonin
involved in calcium homeostasis

103
Q

How are thyroid hormones synthesises?(3)

A

Thyroid hormones are produced by iodination and coupling of tyrosine
Thyroglobulin:
Glycoprotein synthesised by follicular cells and released into the follicular lumen (colloid) by exocytosis
At the apical follicular membrane-colloid boarder, tyrosine residues within thyroglobulin are iodinated in the presence of the enzyme thyroperoxidase
Thyroid hormones:
Precursors are monoidotyrosine (T1) and diidotyrosine (T2) which are coupled under the control of thyroperoxidase to form active hormones:
Thyroxine (T4)
Triiodothyronine (T3)

104
Q

Secretion amounts of thyroid hormone.(3)

A

Daily secretion: 100nmoles of T4 and about 5nmoles of T3
T3 is 3 -8 times more active than T4
Only 0.4% of T3 and 0.04% of T4 are “free” in blood

105
Q

What are the three main thyroid hormone transport proteins?(3)

A

Thyroxine-binding globulin (~ 70% of T3 & T4 bound with high affinity)
Thyroxine-binding prealbumin (~ 10% of T4, tenfold greater affinity for T4 than T3)
Albumin (~ 15% circulating T3 & T4, rapid dissociation makes it major source of free hormone to tissues)

106
Q

What are the affects of TSH on the thyroid?(6)

A

Increase iodine uptake
Increase thyroglobulin synthesis
Increase iodination of thyroglobulin
Increase pinocytosis of colloid (fluid into cell)
Increase lysosomal activity
Increase in size of thyroid cells (cuboidal to columnar)

107
Q

How are T3&4 interconverted?(4)

A
  • Most plasma T3 is derived from peripheral metabolism of T4 produced by the thyroid. This can be a “step up” or “step down” process:
  • 1 5’-deiodinase: most abundant, provides T3 to plasma, “step up”
  • 2 5’-deiodinase: brain and pituitary, provides T3 in CNS, “step up”
  • 3 5’-deiodinase: inactivates T4 by converting it to rT3, “step down”
108
Q

Impact of hypothyroidism on children and infants.(2)

A

New-born/infants:
Decreased metal capacity
Short stature

In children:
Decreased metal capacity and growth

109
Q

Impact of hypothyroidism on adults.(8)

A 
General tiredness and lethargy
Bradycardia
Mental slowness
Cold intolerance
Weight gain
Depression (in about 50% of cases)
Dry skin
Puffy hands and face.

Cell Biology (1 decks)

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